The DOI matches its Crossref record; 186 of the 187 references it cites were found in a registry or an index; none of the 273 sources its claims cite is checked for support yet.
Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside
Open accessAbstract
SummaryNeuropathic pain is a debilitating form of chronic pain resulting from nerve injury, disease states, or toxic insults. Neuropathic pain is often refractory to conventional pharmacotherapies, necessitating validation of novel analgesics. Cannabinoids, drugs that share the same target as Δ9-tetrahydrocannabinol (Δ9-THC), the psychoactive ingredient in cannabis, have the potential to address this unmet need. Here, we review studies evaluating cannabinoids for neuropathic pain management in the clinical and preclinical literature. Neuropathic pain associated with nerve injury, diabetes, chemotherapeutic treatment, human immunodeficiency virus, multiple sclerosis, and herpes zoster infection is considered. In animals, cannabinoids attenuate neuropathic nociception produced by traumatic nerve injury, disease, and toxic insults. Effects of mixed cannabinoid CB1/CB2 agonists, CB2 selective agonists, and modulators of the endocannabinoid system (i.e., inhibitors of transport or degradation) are compared. Effects of genetic disruption of cannabinoid receptors or enzymes controlling endocannabinoid degradation on neuropathic nociception are described. Specific forms of allodynia and hyperalgesia modulated by cannabinoids are also considered. In humans, effects of smoked marijuana, synthetic Δ9-THC analogs (e.g., Marinol, Cesamet) and medicinal cannabis preparations containing both Δ9-THC and cannabidiol (e.g., Sativex, Cannador) in neuropathic pain states are reviewed. Clinical studies largely affirm that neuropathic pain patients derive benefits from cannabinoid treatment. Subjective (i.e., rating scales) and objective (i.e., stimulus-evoked) measures of pain and quality of life are considered. Finally, limitations of cannabinoid pharmacotherapies are discussed together with directions for future research.
Overview
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Written from the paper’s full text.
TL;DR
This review synthesizes preclinical and clinical evidence that cannabinoids and endocannabinoid modulators suppress neuropathic pain via CB1 and CB2 mechanisms. Clinical studies largely support efficacy in neuropathic pain, but side effects, small trials, and long-term safety questions remain.
Key findings
- In animals, cannabinoids attenuate neuropathic nociception in at least nine surgically induced traumatic nerve/nervous system injury models and in disease/toxic models (diabetes, chemotherapy, HIV, demyelination, post-herpetic neuralgia); mixed CB1/CB2 agonists, CB2-selective agonists, and FAAH/MGL/transport inhibitors are effective, often via CB1 and/or CB2, with nonneuronal microglial CB2 mechanisms implicated.
- Clinical studies largely affirm benefit: in HIV-associated sensory neuropathy, 52% (13/25) receiving cannabis cigarettes had >30% pain reduction; smoked cannabis was superior to placebo on DDS/VAS without negative impact on CD4/CD8/T-cell counts or viral load.
- In MS-related neuropathic pain, dronabinol, Cannador, and Sativex improved pain/spasticity/sleep; one 1-year follow-up reported 74% of placebo vs 45% cannabinoid patients discontinued for lack of benefit; Sativex open-label: 95% entered, 54% completed 1 year, 44% completed 2 years, 25% withdrew due adverse events, 95% had ≥1 adverse event.
- Adverse-event review: 96.6% of medical cannabinoid adverse events were not serious and no serious adverse events were exclusively cannabinoid-related; 99% of serious adverse events from randomized trials came from only two trials. Negative clinical studies were small (≤8 subjects) and used oral dronabinol.
Methods
- Narrative review of preclinical and clinical literature on cannabinoids for neuropathic pain, covering nerve injury, diabetes, chemotherapy, HIV, MS, and herpes zoster.
- Compares mixed CB1/CB2 agonists, CB2-selective agonists, endocannabinoid transport/degradation inhibitors, and genetic knockout models; clinical review includes smoked marijuana, synthetic Δ9-THC analogs (Marinol, Cesamet), and cannabis preparations with Δ9-THC and cannabidiol (Sativex, Cannador).
- No systematic search strategy, meta-analysis, or formal risk-of-bias assessment is described.
Limitations
- Stated: psychoactive effects of centrally acting CB1 agonists and side effects (dizziness, balance impairment, intoxication, dry mouth, dysgeusia, sedation, hunger) challenge therapy; high-quality long-term safety trials are needed.
- Stated: two negative clinical studies were small (≤8 subjects), used oral dronabinol titrated to 25 mg/day (mean 16.6 ± 6.5 mg and 15 ± 6 mg), and had prominent side effects/high dropout; patients had mixed refractory neuropathic pain.
- Evident from text: as a narrative review, it does not systematically quantify evidence; preclinical pharmacological specificity was not consistently assessed, and many clinical studies were small, mixed-population, or open-label extensions.
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253 Not checked yet · 30 Own interpretation · 23 No basis given · 4 Own result
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In the paper
“None of the studies we reviewed evaluated the presence of cold allodynia.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“WIN55,212-2 is the only compound that has been evaluated in the SCI model.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“However, mediation by cannabinoid receptors has not been assessed for agonists tested in this model.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Met-F-AEA, a CB1-specific agonist based upon the structure of anandamide, the mixed cannabinoid agonist WIN55,212-2 and the CB2-specific agonist AM1241, administered chronically, suppressed mechanical hyperalgesia associated with STZ-induced diabetic neuropathy.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Side-effects were reported in all studies in a proportion of patients receiving cannabinoid-based medications.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Cannabinoid-based medications have more frequently been evaluated for efficacy in suppressing MS-related spasticity.142”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
What the sources say
- Not checked yetcites [142] Malfitano, 2008, Cannabinoids in the management of spasticity associated with multiple sclerosis, Neuropsychiatr Dis Treat
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Two studies have examined effects of smoked cannabis for the treatment of HIV-associated sensory neuropathy (resulting from HIV infection, dideoxynucleoside antiretroviral therapy, or both) and have reported positive results (Table 7).”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > HIV-associated neuropathy
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The most frequently reported side-effects were dizziness, impairment of balance, feelings of intoxication, dry mouth and dysgeusia (most commonly observed with oral-mucosal sprays), sedation, and hunger.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“However, pharmacological specificity has not been consistently assessed in this model.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Post Herpetic Neuralgia
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“A single study has examined patients with neuropathic pain resulting exclusively from a brachial plexus avulsion (Table 8).”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Brachial Plexus Avulsion-induced Neuropathy
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Two studies have examined the effects of cannabinoid-based medications in patients suffering from spinal cord injuries.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Mixed Neuropathic Pain
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Changes in experimental design after initiation of the study complicate interpretation of these latter findings.163”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Mixed Neuropathic Pain
What the sources say
- Not checked yetcites [163] Hagenbach, 2007, The treatment of spasticity with Delta9-tetrahydrocannabinol in persons with spinal cord injury, Spinal Cord source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“We are aware of only two clinical studies that have failed to report efficacy of cannabinoids, relative to placebo, for treatment of mixed neuropathic pain.164, 165”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Caveats
What the sources say
- Not checked yetcites [164] Attal, 2004, Are oral cannabinoids safe and effective in refractory neuropathic pain?, Eur J Pain source
- Not checked yetcites [165] Clermont-Gnamien, 2002, The therapeutic use of D9-tetrahydrocannabinol (dronabinol) in refractory neuropathic pain, Presse Med
hedged- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Densities of CB1 receptors are low in brainstem sites critical for controlling heart rate and respiration. This distribution explains the low toxicity and absence of lethality following marijuana intoxication.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Receptor Pharmacology
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Cannabinoids, drugs that share the same target as Δ9-tetrahydrocannabinol (Δ9-THC), the psychoactive ingredient in cannabis, have the potential to address this unmet need.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Abstract
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Rests on an assumption: Neuropathic pain is a debilitating form of chronic pain caused by damage to the nervous system, resulting from peripheral nerve injury, toxic insults, or disease states.
- Rests on an assumption: Neuropathic pain is often refractory to conventional pharmacotherapies, necessitating validation of novel analgesics.
In the paper
“Fatty-acid amide hydrolase (FAAH) is the principle catabolic enzyme for fatty-acid amides including AEA and N-palmitoylethanolamine (PEA).25”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Endocannabinoids
What the sources say
- Not checked yetcites [25] Fezza, 2008, Fatty acid amide hydrolase: a gate-keeper of the endocannabinoid system, Subcell Biochem source
plaindirect- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Clinical studies largely affirm that neuropathic pain patients derive benefits from cannabinoid treatment.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“CB2 receptor protein has been reported in the DRG,13 brainstem,14 thalamus,15 PAG,15 and cerebellum15, 16 of naive rats.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Receptor Pharmacology
What the sources say
- Not checked yetcites [13] Ross, 2001, Actions of cannabinoid receptor ligands on rat cultured sensory neurones: implications for antinociception, Neuropharmacology source
- Not checked yetcites [14] Van Sickle, 2005, Identification and functional characterization of brainstem cannabinoid CB2 receptors, Science source
- Not checked yetcites [15] Gong, 2006, Cannabinoid CB2 receptors: immunohistochemical localization in rat brain, Brain Res source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“In animals, cannabinoids attenuate neuropathic nociception produced by traumatic nerve injury, disease, and toxic insults.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“CB1 and CB2 receptors exhibit disparate anatomical distributions.3”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Receptor Pharmacology
What the sources say
- Not checked yetcites [3] Munro, 1993, Molecular characterization of a peripheral receptor for cannabinoids, Nature source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“However, an upregulation of CB2 receptor immunoreactivity or mRNA is observed in sites implicated in nociceptive processing under conditions of induced neuropathy.17, 18”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Receptor Pharmacology
What the sources say
- Not checked yetcites [17] Beltramo, 2006, CB2 receptor-mediated antihyperalgesia: possible direct involvement of neural mechanisms, Eur J Neurosci source
- Not checked yetcites [18] Wotherspoon, 2005, Peripheral nerve injury induces cannabinoid receptor 2 protein expression in rat sensory neurons, Neuroscience source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In CCI rats, chronic administration of either AM404 or URB597 suppresses plasma extravasation, a condition associated with neuropeptide release at peripheral levels.54, 55”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [54] La Rana, 2008, AM404, an anandamide transport inhibitor, reduces plasma extravasation in a model of neuropathic pain in rat: role for cannabinoid receptors, Neuropharmacology source
- Not checked yetcites [55] Russo, 2007, The fatty acid amide hydrolase inhibitor URB597 (cyclohexylcarbamic acid 3′-carbamoylbiphenyl-3-yl ester) reduces neuropathic pain after oral administration in mice, J Pharmacol Exp Ther source
plaindirect- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Cannabinoids suppress neuropathic nociception in at least nine different animal models of surgically-induced traumatic nerve or nervous system injury.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Models of Surgically-induced Traumatic Nerve Injury
plaindirectn = 9- Asserted: passes — The authors put it forward as true.
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In the paper
“Chronic administration of synthetic analogues of natural cannabinoid ligands containing cannabidiol attenuate or reverse established thermal and mechanical hyperalgesia in the CCI model.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Tolerance, a feature which may contribute to loss of analgesic efficacy of currently available analgesics, failed to develop following repeated administration the CB2-specific agonist of A-836339.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [51] Yao, 2009, J Pharmacol Exp Ther source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Not surprisingly, several classes of cannabinoids have been shown to suppress CCI-induced neuropathic nociception in rodents and include mixed cannabinoid agonists which target both CB1 and CB2 receptors, CB2-selective agonists and modulators of the endocannabinoid system that inhibit FAAH or MGL (Tables 2 and 3).”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
boosteddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“AM404, administered chronically or acutely, does not affect locomotor behavior, indicating a low propensity of this agent to produce unwanted motor side-effects associated with direct activation of CB1 receptors.52, 53”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [52] Costa, 2006, AM404, an inhibitor of anandamide uptake, prevents pain behaviour and modulates cytokine and apoptotic pathways in a rat model of neuropathic pain, Br J Pharmacol source
- Not checked yetcites [53] La Rana, 2006, Modulation of neuropathic and inflammatory pain by the endocannabinoid transport inhibitor AM404 [N-(4-hydroxyphenyl)-eicosa-5,8,11,14-tetraenamide], J Pharmacol Exp Ther source
plain- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, not all effects of AEA are mediated by cannabinoid receptors.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Endocannabinoids
plain- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Endocannabinoid modulators suppress neuropathic pain symptoms associated with CCI (Tables 2 and 3).”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Interestingly, GW405833, a CB2-specific agonist, also reduces depression-like behavior associated with this mononeuropathy in the forced swim test.50”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [50] Hu, 2009, Depression-like behaviour in rats with mononeuropathy is reduced by the CB2-selective agonist GW405833, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“Anandamide and PEA exerts effects, at least in part, through a peripheral mechanism; both fatty-acid amides suppressed release of calcitonin gene-related peptide and somatostatin evoked by the irritant resiniferotoxin without altering peptide release under basal conditions.65”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [65] Helyes, 2003, Inhibitory effect of anandamide on resiniferatoxin-induced sensory neuropeptide release in vivo and neuropathic hyperalgesia in the rat, Life Sci source
hedgeddirect- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“All classes of cannabinoids evaluated produced anti-allodynic and anti-hyperalgesic effects in the Seltzer model (Table 4).”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The fatty acid PEA, administered chronically, attenuated the development of thermal hyperalgesia and mechanical allodynia in the CCI model through CB1, PPARγ and TRPV1-mediated mechanisms.60”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [60] Costa, 2008, The endogenous fatty acid amide, palmitoylethanolamide, has anti-allodynic and anti-hyperalgesic effects in a murine model of neuropathic pain: involvement of CB(1), TRPV1 and PPARgamma receptors and neurotrophic factors, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“whereas 2-AG produced anti-hyperalgesic and anti-allodynic effects through activation of both peripheral CB1 and CB2 receptors.67”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [67] Desroches, 2008, Modulation of the anti-nociceptive effects of 2-arachidonoyl glycerol by peripherally administered FAAH and MGL inhibitors in a neuropathic pain model, Br J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“CCI increases AEA and 2-AG levels in the PAG and RVM, sites implicated in the descending modulation of pain.56”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [56] Petrosino, 2007, Changes in spinal and supraspinal endocannabinoid levels in neuropathic rats, Neuropharmacology source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“OL135 and URB597 attenuate cold and mechanical allodynia in a manner that is dependent upon activation of both CB1 and CB2 receptors.59”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [59] Kinsey, 2009, Blockade of endocannabinoid-degrading enzymes attenuates neuropathic pain, J Pharmacol Exp Ther source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“Chronic administration of PEA also normalized levels of three neutrophic factors (NGF, GDNF, and NT-3) that were increased by CCI.60”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [60] Costa, 2008, The endogenous fatty acid amide, palmitoylethanolamide, has anti-allodynic and anti-hyperalgesic effects in a murine model of neuropathic pain: involvement of CB(1), TRPV1 and PPARgamma receptors and neurotrophic factors, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Exogenously applied endocannabinoids, AEA and 2-AG, suppress changes in neuropathic nociception induced by partial sciatic nerve ligation.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Thermal hyperalgesia was present in all studies reviewed here that evaluated this measure with one exception.62”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [62] Jayamanne, 2006, Actions of the FAAH inhibitor URB597 in neuropathic and inflammatory chronic pain models, Br J Pharmacol source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Further support for this hypothesis is derived from the observation that overexpression of the CB2 receptor attenuated enhanced expression of microglia.63”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [63] Racz, 2008, Crucial role of CB(2) cannabinoid receptor in the regulation of central immune responses during neuropathic pain, J Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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None of the sources cited for this claim have been checked yet.
In the paper
“Interestingly, anandamide produced anti-hyperalgesic and anti-allodynic effects through a CB1 mechanism,65, 66”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [65] Helyes, 2003, Inhibitory effect of anandamide on resiniferatoxin-induced sensory neuropeptide release in vivo and neuropathic hyperalgesia in the rat, Life Sci source
- Not checked yetcites [66] Guindon, 2006, Antihyperalgesic effects of local injections of anandamide, ibuprofen, rofecoxib and their combinations in a model of neuropathic pain, Neuropharmacology source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“Chronic administration of AM404 significantly decreased CCI-induced Fos expression in the lumbar spinal cord through CB1/CB2 and TRPV1-mediated mechanisms.58”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [58] Rodella, 2005, AM404, an inhibitor of anandamide reuptake decreases Fos-immunoreactivity in the spinal cord of neuropathic rats after non-noxious stimulation, Eur J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Moreover, CB2 receptors in the spinal cord contribute to CB2-mediated suppression of mechanical allodynia.70”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [70] Yamamoto, 2008, Involvement of central cannabinoid CB2 receptor in reducing mechanical allodynia in a mouse model of neuropathic pain, Eur J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These results suggest that genetic disruption of the CB2 receptor has a disinhibitory effect on the responses of glial cells following partial sciatic nerve ligation.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“However, CB2-/- mice notably exhibit increased microglial and astrocyte expression in the contralateral spinal dorsal horn – a mechanism which may help to explain differences in neuropathic nociception between wild-types and knockouts.63”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [63] Racz, 2008, Crucial role of CB(2) cannabinoid receptor in the regulation of central immune responses during neuropathic pain, J Neurosci source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Compounds targeting three distinct mechanisms for modulating endocannabinoid levels also suppress neuropathic nociception following partial sciatic nerve ligation.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Structurally distinct CB2-specific agonists are efficacious in suppressing neuropathic nociception in this model.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Deletion of a putative novel cannabinoid receptor, GPR55, is also associated with the failure to develop mechanical hyperalgesia following partial sciatic nerve ligation.72”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [72] Staton, 2008, The putative cannabinoid receptor GPR55 plays a role in mechanical hyperalgesia associated with inflammatory and neuropathic pain, Pain source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Mechanical hyperalgesia and allodynia are observed following partial ligation of the sciatic nerve.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [61] Seltzer, 1990, A novel behavioral model of neuropathic pain disorders produced in rats by partial sciatic nerve injury, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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In the paper
“Chronic administration of WIN55,212-2 produced anti-allodynic effects up to six days following the final injection.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [81] Leichsenring, 2009, Analgesic and antiinflammatory effects of cannabinoid receptor agonists in a rat model of neuropathic pain, Naunyn Schmiedebergs Arch Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“CP55,940 produces antinociception in CB1+/+, CB2+/+, CB2-/-, but not CB1-/- mice subjected to SNL, suggesting that activity at CB1 dominates the antinocieptive profile of mixed CB1/CB2 agonists following systemic administration.45”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [45] Sain, 2009, Antinociceptive effects of the non-selective cannabinoid receptor agonist CP 55,940 are absent in CB1(−/−) and not CB2(−/−) mice in models of acute and persistent pain, Neuropharmacology source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Upregulation of CB2 receptor immunoreactivity on sensory afferent terminals in the spinal cord has also been reported following SNL.18”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [18] Wotherspoon, 2005, Peripheral nerve injury induces cannabinoid receptor 2 protein expression in rat sensory neurons, Neuroscience source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Multiple CB2-specific agonists suppress neuropathic nociception induced by SNL.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“The CB2 agonist AM1241 suppresses both thermal hyperalgesia and mechanical allodynia following SNL in both rats17, 44, 85 and mice44.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [17] Beltramo, 2006, CB2 receptor-mediated antihyperalgesia: possible direct involvement of neural mechanisms, Eur J Neurosci source
- Not checked yetcites [44] Ibrahim, 2003, Activation of CB2 cannabinoid receptors by AM1241 inhibits experimental neuropathic pain: pain inhibition by receptors not present in the CNS, Proc Natl Acad Sci U S A source
- Not checked yetcites [85] Naguib, 2008, MDA7: a novel selective agonist for CB2 receptors that prevents allodynia in rat neuropathic pain models, Br J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These findings collectively document the presence of regulatory changes in endocannabinoid levels associated with SNL, a finding which may contribute to the efficacy of peripherally administered cannabinoid agonists that activate CB1 receptors in this model.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“All studies reviewed here documented the presence of mechanical allodynia following SNL.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“An emerging body of literature now suggests that antinociceptive effects of CB2 agonists may be mediated by suppression of microglial activation.4”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [4] Guindon, 2008, Cannabinoid CB2 receptors: a therapeutic target for the treatment of inflammatory and neuropathic pain, Br J Pharmacol source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Increases in CB1 mRNA are observed in the uninjured (but abnormal) L4 DRG ipsilateral to injury.83”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [83] Mitrirattanakul, 2006, Site-specific increases in peripheral cannabinoid receptors and their endogenous ligands in a model of neuropathic pain, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Acute WIN55,212-2 suppresses all forms of neuropathic nociception tested in this model.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“CB1-/- mice receiving AM1241 showed enhanced antihyperalgesia.44”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [44] Ibrahim, 2003, Activation of CB2 cannabinoid receptors by AM1241 inhibits experimental neuropathic pain: pain inhibition by receptors not present in the CNS, Proc Natl Acad Sci U S A source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“All studies with the exception of one78 indicated the presence of thermal hyperalgesia when animals were tested.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [78] De Vry, 2004, 3-[2-cyano-3-(trifluoromethyl)phenoxy]phenyl-4,4,4-trifluoro-1-butanesulfo nate (BAY 59-3074): a novel cannabinoid Cb1/Cb2 receptor partial agonist with antihyperalgesic and antiallodynic effects, J Pharmacol Exp Ther source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The CB1-specific agonist ACEA inhibits pERK expression induced by in vitro application of capsaicin to the spinal cords of SNL rats.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [84] Kawasaki, 2006, Different effects of opioid and cannabinoid receptor agonists on C-fiber-induced extracellular signal-regulated kinase activation in dorsal horn neurons in normal and spinal nerve-ligated rats, J Pharmacol Exp Ther source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“SNL produces regulatory changes in CB1 mRNA and endocannabinoid levels.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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In the paper
“This observation contrasts with effects of opioids (i.e. morphine and DAMGO) which lose the ability to inhibit C-fiber induced ERK activation in the L5 spinal cord following SNL.84”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [84] Kawasaki, 2006, Different effects of opioid and cannabinoid receptor agonists on C-fiber-induced extracellular signal-regulated kinase activation in dorsal horn neurons in normal and spinal nerve-ligated rats, J Pharmacol Exp Ther source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“PEA abolished mechanical hyperalgesia following partial sciatic nerve ligation through a mechanism that was blocked by a CB2 antagonist.65”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [65] Helyes, 2003, Inhibitory effect of anandamide on resiniferatoxin-induced sensory neuropeptide release in vivo and neuropathic hyperalgesia in the rat, Life Sci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Paracetomol may undergo local metabolic transformation into AM404, resulting in increased levels of endocannabiniods.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The structurally distinct CB2-specific agonist, JWH133, also attenuates mechanically-evoked responses of WDR neurons in both naive and spinal nerve ligated rats.86”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [86] Elmes, 2004, Cannabinoid CB2 receptor activation inhibits mechanically evoked responses of wide dynamic range dorsal horn neurons in naive rats and in rat models of inflammatory and neuropathic pain, Eur J Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“WIN55,212-2 was more efficacious in suppressing mechanical allodynia vs. thermal hyperalgesia in the CCI-ION model.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [94] Liang, 2007, The synthetic cannabinoids attenuate allodynia and hyperalgesia in a rat model of trigeminal neuropathic pain, Neuropharmacology source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Compound 17, a novel FAAH inhibitor, reversed mechanical allodynia in SNL rats with the same potency as a 5-fold higher dose of gabapentin.90”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [90] Sit, 2007, Novel inhibitors of fatty acid amide hydrolase, Bioorg Med Chem Lett source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Local injection of JWH133 into the ventroposterolateral nucleus of the thalamus attenuated spontaneous and mechanically-evoked neuronal activity in SNL, but not sham rats, in a CB2-dependent manner.87”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [87] Jhaveri, 2008, Evidence for a novel functional role of cannabinoid CB(2) receptors in the thalamus of neuropathic rats, Eur J Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Cannabinoids alleviate neuropathic nociception in several other injury models.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“These and earlier findings from the same group95 indicate that cannabinoids are negative modulators of nociceptive transmission at the superficial layer of the trigeminal caudal subnucleus.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [95] Liang, 2004, Cannabinoid-induced presynaptic inhibition at the primary afferent trigeminal synapse of juvenile rat brainstem slices, J Physiol source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, CB2 receptor activation may exert little functional control under nonpathological conditions.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Importantly, co-localization of CB2 immunoreactivity with markers of microglia and perivascular cells was observed on day 4 post-surgery.96”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [96] Romero-Sandoval, 2008, Spinal microglial and perivascular cell cannabinoid receptor type 2 activation reduces behavioral hypersensitivity without tolerance after peripheral nerve injury, Anesthesiology source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Additionally, OL135, a compound that accesses the CNS and inhibits FAAH, suppressed mechanical allodynia in a CB2-dependent manner.91”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [91] Chang, 2006, Inhibition of fatty acid amide hydrolase produces analgesia by multiple mechanisms, Br J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“A four-fold higher dose was required for reduction of mechanically-evoked WDR neuronal responses in SNL rats; these rats showed no corresponding increase in endocannabinoid levels, suggesting that contributions of FAAH to endocannabinoid metabolism may be modified under conditions of neuropathic nociception.92”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [92] Jhaveri, 2006, Analgesic effects of fatty acid amide hydrolase inhibition in a rat model of neuropathic pain, J Neurosci source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Systemic and spinal administration of the novel CB2 agonist, A-836339, also attenuates spontaneous and mechanically-evoked neuronal firing of spinal WDR neurons in a CB2-dependent manner in SNL but not sham rats.88”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [88] McGaraughty, 2009, A CB(2) receptor agonist, A-836339, modulates wide dynamic range neuronal activity in neuropathic rats: contributions of spinal and peripheral CB(2) receptors, Neuroscience source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“CB2 receptor immunoreactivity96 is increased in the ipsilateral dorsal horn following L5 spinal nerve transection (L5-SNT).97”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [96] Romero-Sandoval, 2008, Spinal microglial and perivascular cell cannabinoid receptor type 2 activation reduces behavioral hypersensitivity without tolerance after peripheral nerve injury, Anesthesiology source
- Not checked yetcites [97] Tanga, 2005, The CNS role of Toll-like receptor 4 in innate neuroimmunity and painful neuropathy, Proc Natl Acad Sci U S A source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The antinociceptive effects of URB597 were blocked by a CB1-specific antagonist in both sham and SNL rats.92”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [92] Jhaveri, 2006, Analgesic effects of fatty acid amide hydrolase inhibition in a rat model of neuropathic pain, J Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“and this effect is likely to result from downregulation of FAAH gene expression, an effect which has also been observed in adipocytes sampled from obese women.110”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
What the sources say
- Not checked yetcites [110] Engeli, 2005, Activation of the peripheral endocannabinoid system in human obesity, Diabetes source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“WIN55,212-2, administered systemically, suppressed all forms of hyperalgesia and allodynia present.98”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [98] Walczak, 2005, Behavioral, pharmacological and molecular characterization of the saphenous nerve partial ligation: a new model of neuropathic pain, Neuroscience source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The neurobiological rearrangement of cannabinoid and mu-opioid receptors may contribute to the antinociceptive efficacy of WIN55,212-2 and morphine in this model.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Diabetic rats exhibit a decrease in the density of CB1 receptor protein in DRG.108”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
What the sources say
- Not checked yetcites [108] Zhang, 2007, Expression of cannabinoid CB1 receptors in models of diabetic neuropathy, J Pharmacol Exp Ther source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Daily pre-treatment with indomethacin (COX-1 inhibitor) or L-NOArg (non-selective NOS inhibitor) increased the anti-hyperalgesic actions of low doses of WIN55,212-2, AM1241 and MET-F-AEA in STZ rats to a greater extent than the cannabinoid administered alone, suggesting the presence of antinociceptive synergism between cannabinoid and COX pathways.107”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
What the sources say
- Not checked yetcites [107] Bujalska, 2008, Effect of cannabinoid receptor agonists on streptozotocin-induced hyperalgesia in diabetic neuropathy, Pharmacology source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“An increase in the number of apoptotic cells and impaired neurite growth was observed in PC12 cells cultured under hyperglycemic conditions and these effects were effectively treated by HU-210.114”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
What the sources say
- Not checked yetcites [114] Dagon, 2007, The synthetic cannabinoid HU-210 attenuates neural damage in diabetic mice and hyperglycemic pheochromocytoma PC12 cells, Neurobiol Dis source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“suggesting the presence of antinociceptive synergism between cannabinoid and COX pathways.107”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
What the sources say
- Not checked yetcites [107] Bujalska, 2008, Effect of cannabinoid receptor agonists on streptozotocin-induced hyperalgesia in diabetic neuropathy, Pharmacology source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Comparable responses to WIN55,212-2 were only observed at doses high enough to induce sedation and rigidity in all mice.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [7] Agarwal, 2007, Cannabinoids mediate analgesia largely via peripheral type 1 cannabinoid receptors in nociceptors, Nat Neurosci source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“TNI injury resulted in an upregulation of CB1 receptor mRNA in the contralateral thalamus on day 1 post-surgery,106 indicating cannabinoid receptor regulation within an important relay nucleus in the ascending pain pathway.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [106] Siegling, 2001, Cannabinoid CB(1) receptor upregulation in a rat model of chronic neuropathic pain, Eur J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Moreover, a non-nociceptive dose of Δ9-THC, administered in conjunction with morphine, enhanced the antinociceptive properties of morphine in both diabetic and naive mice.115”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
What the sources say
- Not checked yetcites [115] Williams, 2008, Decreased basal endogenous opioid levels in diabetic rodents: effects on morphine and delta-9-tetrahydrocannabinoid-induced antinociception, Eur J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Cannabinoids may show greater therapeutic potential for treating painful diabetic neuropathy compared to opioids.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“COX inhibitors may block oxidative metabolism of endocannabinoids, thereby increasing endocannabinoids available to interact with cannabinoid receptors.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
In the paper
“Mu-opioid, CB1 and CB2 receptor protein was increased in the ipsilateral spinal cord and hindpaw skin at 7 days post-surgery.99”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [99] Walczak, 2006, Characterization of chronic constriction of the saphenous nerve, a model of neuropathic pain in mice showing rapid molecular and electrophysiological changes, J Neurosci Res source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Systemic WIN55,212-2 suppressed all forms of neuropathic nociception present in this model, including thermal hyperagesia, cold allodynia, mechanical hyperalgesia and mechanical allodynia.99”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [99] Walczak, 2006, Characterization of chronic constriction of the saphenous nerve, a model of neuropathic pain in mice showing rapid molecular and electrophysiological changes, J Neurosci Res source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In rats, SPL increased μ-opioid, CB1, and CB2 receptor protein in ipsilateral hindpaw skin, DRG and lumbar spinal cord.98”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [98] Walczak, 2005, Behavioral, pharmacological and molecular characterization of the saphenous nerve partial ligation: a new model of neuropathic pain, Neuroscience source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These findings are suggestive of a negative feedback mechanism that could result in downregulation of the endocannabinoid signaling system.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Thus, CB1 receptors on nociceptors in the periphery account for much of the antinociceptive effects of cannabinoids.7”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [7] Agarwal, 2007, Cannabinoids mediate analgesia largely via peripheral type 1 cannabinoid receptors in nociceptors, Nat Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“However, these effects were not blocked by a CB1-specific agonist.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
What the sources say
- Not checked yetcites [114] Dagon, 2007, The synthetic cannabinoid HU-210 attenuates neural damage in diabetic mice and hyperglycemic pheochromocytoma PC12 cells, Neurobiol Dis source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Systemic and intrathecal, but not intraplantar, WIN55,212-2 suppressed vincristine-induced mechanical allodynia through activation of CB1 and CB2 receptors.122”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chemotherapy-induced Neuropathy
What the sources say
- Not checked yetcites [122] Rahn, 2007, Activation of cannabinoid CB1 and CB2 receptors suppresses neuropathic nociception evoked by the chemotherapeutic agent vincristine in rats, Br J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“By contrast, DAMGO failed to produce an effect.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Demyelination-induced Neuropathy
What the sources say
- Not checked yetcites [125] Wallace, 2003, Focal lysolecithin-induced demyelination of peripheral afferents results in neuropathic pain behavior that is attenuated by cannabinoids, J Neurosci source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, activated microglia may be a common target underlying cannabinoid-mediated suppressions of neuropathic nociception.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > HIV-associated Sensory Neuropathy
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Systemic administration of either the CB2 agonist (R,S)-AM1241 or its receptor-active enantiomer (R)-AM1241 produced CB2-mediated suppressions of paclitaxel-induced mechanical allodynia.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chemotherapy-induced Neuropathy
What the sources say
- Not checked yetcites [89] Rahn, 2008, Selective activation of cannabinoid CB2 receptors suppresses neuropathic nociception induced by treatment with the chemotherapeutic agent paclitaxel in rats, J Pharmacol Exp Ther source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“A more recent study using the same paclitaxel dosing paradigm118 reported the presence of mechanical allodynia and the absence of thermal hyperalgesia.85”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chemotherapy-induced Neuropathy
What the sources say
- Not checked yetcites [118] Polomano, 2001, A painful peripheral neuropathy in the rat produced by the chemotherapeutic drug, paclitaxel, Pain source
- Not checked yetcites [85] Naguib, 2008, MDA7: a novel selective agonist for CB2 receptors that prevents allodynia in rat neuropathic pain models, Br J Pharmacol source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Administration of Δ9-THC to diabetic rats restored CSF levels of endogenous dynorphin and leu-enkephalin to levels observed following morphine administration to non-diabetic rats.115”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
What the sources say
- Not checked yetcites [115] Williams, 2008, Decreased basal endogenous opioid levels in diabetic rodents: effects on morphine and delta-9-tetrahydrocannabinoid-induced antinociception, Eur J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Systemic (R,S)-AM1241 also partially reversed vincristine-induced mechanical allodynia in a CB2-dependent manner.122”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chemotherapy-induced Neuropathy
What the sources say
- Not checked yetcites [122] Rahn, 2007, Activation of cannabinoid CB1 and CB2 receptors suppresses neuropathic nociception evoked by the chemotherapeutic agent vincristine in rats, Br J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Thigmotaxis was present in animals receiving ddc, either alone or in conjunction with HIV-gp120, indicating the presence of anxiety-like behavior in these rats.123”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > HIV-associated Sensory Neuropathy
What the sources say
- Not checked yetcites [123] Wallace, 2007, Characterization of rodent models of HIV-gp120 and anti-retroviral-associated neuropathic pain, Brain source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Cannabinoids have been shown to suppress cisplatin-induced emesis in the least shrew.117”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chemotherapy-induced Neuropathy
What the sources say
- Not checked yetcites [117] Ray, 2009, Delta 9-tetrahydrocannabinol suppresses vomiting behavior and Fos expression in both acute and delayed phases of cisplatin-induced emesis in the least shrew, Behav Brain Res source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“WIN55,212-2-induced decreases in spontaneous motor activity were nonetheless observed.119”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chemotherapy-induced Neuropathy
What the sources say
- Not checked yetcites [119] Pascual, 2005, A cannabinoid agonist, WIN 55,212-2, reduces neuropathic nociception induced by paclitaxel in rats, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Notably, the anti-hyperalgesic and anti-allodynic effects of WIN55,212-2 were reversed by a CB1-specific antagonist in both tests.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Demyelination-induced Neuropathy
What the sources say
- Not checked yetcites [125] Wallace, 2003, Focal lysolecithin-induced demyelination of peripheral afferents results in neuropathic pain behavior that is attenuated by cannabinoids, J Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Increases in the density of microglia and astrocytes were observed in the ipsilateral dorsal horn following HIV-gp120 treatment.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > HIV-associated Sensory Neuropathy
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Diabetic rats exhibit lower levels of dynorphin and β-endorphins in cerebrospinal fluid (CSF) relative to non-diabetic rats treated under the same conditions.115”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
What the sources say
- Not checked yetcites [115] Williams, 2008, Decreased basal endogenous opioid levels in diabetic rodents: effects on morphine and delta-9-tetrahydrocannabinoid-induced antinociception, Eur J Pharmacol source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“(S)-AM1241, the enantiomer exhibiting lower affinity for the CB2 receptor, failed to produce an anti-allodynic effect.89”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chemotherapy-induced Neuropathy
What the sources say
- Not checked yetcites [89] Rahn, 2008, Selective activation of cannabinoid CB2 receptors suppresses neuropathic nociception induced by treatment with the chemotherapeutic agent paclitaxel in rats, J Pharmacol Exp Ther source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The novel cannabilactone, AM1714, also reversed mechanical allodynia associated with paclitaxel treatment in a CB2-dependent manner.89”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chemotherapy-induced Neuropathy
What the sources say
- Not checked yetcites [89] Rahn, 2008, Selective activation of cannabinoid CB2 receptors suppresses neuropathic nociception induced by treatment with the chemotherapeutic agent paclitaxel in rats, J Pharmacol Exp Ther source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Lynch and colleagues126 reported the presence of thermal hyperalgesia (tail immersion) and mechanical allodynia in mice that were infected with Theiler's murine encephalomyelitis virus (TMEV).”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Multiple Sclerosis-associated Neuropathy
What the sources say
- Not checked yetcites [126] Lynch, 2008, Analysis of nociception, sex and peripheral nerve innervation in the TMEV animal model of multiple sclerosis, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In this model, rats showed signs of mechanical allodynia up to 72 days post-paclitaxel.89”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chemotherapy-induced Neuropathy
What the sources say
- Not checked yetcites [89] Rahn, 2008, Selective activation of cannabinoid CB2 receptors suppresses neuropathic nociception induced by treatment with the chemotherapeutic agent paclitaxel in rats, J Pharmacol Exp Ther source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These findings implicate the spinal cord as an important site of action mediating anti-allodynic effects of cannabinoids.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chemotherapy-induced Neuropathy
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The anti-allodynic effects of WIN55,212-2 and (R,S)-AM1241 were observed at doses that did not produce intrinsic effects on motor behavior in the bar test.122”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chemotherapy-induced Neuropathy
What the sources say
- Not checked yetcites [122] Rahn, 2007, Activation of cannabinoid CB1 and CB2 receptors suppresses neuropathic nociception evoked by the chemotherapeutic agent vincristine in rats, Br J Pharmacol source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The mixed cannabinoid agonist WIN55,212-2 is an effective anti-hyperalgesic agent in three distinct animal models of HIV-associated sensory neuropathy (Table 6).”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > HIV-associated Sensory Neuropathy
plaindirectn = 3- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, combinations of opioids and cannabinoids may show promise as adjunctive analgesics in humans.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“CBD may compete with cannabinoid agonists for cannabinoid receptor binding sites, thereby minimizing psychoactivity of drugs that employ a combination of Δ9-THC and CBD.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
What the sources say
- Not checked yetcites [144] Mechoulam, 2007, Cannabidiol—recent advances, Chem Biodivers source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“One study reported severe gastrointestinal effects for 10% of patients taking Sativex® versus 0% reporting similar problems in the placebo group.133”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies
What the sources say
- Not checked yetcites [133] Nurmikko, 2007, Sativex successfully treats neuropathic pain characterised by allodynia: a randomised, double-blind, placebo-controlled clinical trial, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Evidence to date from clinical studies suggests that these compounds show therapeutic efficacy in suppressing neuropathic pain (Table 7 and 8).”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Abrams and colleagues135 reported that 52% of patients (i.e. 13 out of 25 receiving cannabis cigarettes) experienced a greater than 30% reduction in pain (visual analogue scale daily ratings; VAS).”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > HIV-associated neuropathy
What the sources say
- Not checked yetcites [135] Abrams, 2007, Cannabis in painful HIV-associated sensory neuropathy: a randomized placebo-controlled trial, Neurology source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Based upon our reviews of the literature, cannabinoids exhibit their greatest efficacy when employed for the management of neuropathic pain (Tables 7 and 8).132”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies
What the sources say
- Not checked yetcites [132] Beaulieu, 2007, Reassessment of the role of cannabinoids in the management of pain, Curr Opin Anaesthesiol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Cannabinoids and fatty-acid amides suppress neuropathic nociception in an animal model of post herpetic neuralgia (Table 6).”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Post Herpetic Neuralgia
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“However, L-29 nonetheless suppressed neuropathic nociception in the Seltzer model via activation of CB1 and CB2 receptors (see Table 4).”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Post Herpetic Neuralgia
What the sources say
- Not checked yetcites Table 4
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“However, unwanted side-effects, in contrast to analgesic effects, may undergo tolerance.134”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies
What the sources say
- Not checked yetcites [134] Svendsen, 2004, Does the cannabinoid dronabinol reduce central pain in multiple sclerosis?, BMJ source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, several features of cannabinoid pharmacology are particularly desirable for an analgesic intervention aimed at managing neuropathic pain in AIDS and cancer patients.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > HIV-associated neuropathy
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Cannabidiol is a natural constituent in cannabis, which has very low affinity for cannabinoid CB1 and CB2 receptors.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
What the sources say
- Not checked yetcites [144] Mechoulam, 2007, Cannabidiol—recent advances, Chem Biodivers source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Moreover, CD4+, CD8+, and T-cell counts were not negatively impacted by cannabinoid treatment in HIV patients.136”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > HIV-associated neuropathy
What the sources say
- Not checked yetcites [136] Abrams, 2003, Short-term effects of cannabinoids in patients with HIV-1 infection: a randomized, placebo-controlled clinical trial, Ann Intern Med source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Cold and mechanical allodynia, but not thermal hyperalgesia, have been reported in a model of autoimmune encephalomyelitis in which mice were immunized with myelin oligodendrocyte glycoprotein (MOG(35-55))128”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Multiple Sclerosis-associated Neuropathy
What the sources say
- Not checked yetcites [128] Olechowski, 2009, Neuropathic pain behaviours in a chronic-relapsing model of experimental autoimmune encephalomyelitis (EAE), Pain source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“However, neither a CB1- nor CB2-specific antagonist suppressed L-29 mediated suppression of VZV-induced mechanical allodynia.64”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Post Herpetic Neuralgia
What the sources say
- Not checked yetcites [64] Wallace, 2007, The effect of the palmitoylethanolamide analogue, palmitoylallylamide (L-29) on pain behaviour in rodent models of neuropathy, Br J Pharmacol source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Stimulus-evoked pain testing revealed that the group receiving cannabis experienced a reduction in the area sensitive to mechanical allodynia (with a foam brush or 26g von Frey hair) in the heat and capsaicin sensitization model.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > HIV-associated neuropathy
What the sources say
- Not checked yetcites [135] Abrams, 2007, Cannabis in painful HIV-associated sensory neuropathy: a randomized placebo-controlled trial, Neurology source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Animals treated subchronically with PEA showed improvements in tests of motor performance, measures that were impaired following TMEV infection.129”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Multiple Sclerosis-associated Neuropathy
What the sources say
- Not checked yetcites [129] Loria, 2008, Study of the regulation of the endocannabinoid system in a virus model of multiple sclerosis reveals a therapeutic effect of palmitoylethanolamide, Eur J Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“This finding is perhaps unsurprising given that PPAR-α mediates effects of PEA in suppressing neuronal sensitization.130”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Post Herpetic Neuralgia
What the sources say
- Not checked yetcites [130] LoVerme, 2006, Rapid broad-spectrum analgesia through activation of peroxisome proliferator-activated receptor-alpha, J Pharmacol Exp Ther source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“By contrast, opioid analgesics produce deleterious effects on sleep architecture, including reductions in slow wave sleep and promotion of sleep apnea.157, 158”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Mixed Neuropathic Pain
What the sources say
- Not checked yetcites [157] Walker, 2007, Chronic opioid use is a risk factor for the development of central sleep apnea and ataxic breathing, J Clin Sleep Med source
- Not checked yetcites [158] Dimsdale, 2007, The effect of opioids on sleep architecture, J Clin Sleep Med
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“A similarly structured study reported improved pain ratings (VAS) and spasticity severity following CBD and Δ9-THC in patients with mixed neuropathic pain.159”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Mixed Neuropathic Pain
What the sources say
- Not checked yetcites [159] Wade, 2003, A preliminary controlled study to determine whether whole-plant cannabis extracts can improve intractable neurogenic symptoms, Clin Rehabil source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“A recent meta-analysis examining six studies of cannabinoid-based medications used for the treatment of MS-related neuropathic pain revealed that cannabis preparations were superior to placebo.148”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
What the sources say
- Not checked yetcites [148] Iskedjian, 2007, Meta-analysis of cannabis based treatments for neuropathic and multiple sclerosis-related pain, Curr Med Res Opin source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In a retrospective review of patient charts at the Pain Center of the McGill University Health Center from 1999-2003,161 75% of patients received some benefit from taking nabilone (whether that came in the form of pain relief, improved sleep, decreased nausea or increased appetite).”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Mixed Neuropathic Pain
What the sources say
- Not checked yetcites [161] Berlach, 2006, Experience with the synthetic cannabinoid nabilone in chronic noncancer pain, Pain Med source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“These observations correspond to preclinical observations of cannabinoid receptor upregulation following nerve injury.18”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Brachial Plexus Avulsion-induced Neuropathy
What the sources say
- Not checked yetcites [18] Wotherspoon, 2005, Peripheral nerve injury induces cannabinoid receptor 2 protein expression in rat sensory neurons, Neuroscience source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“MS patients receiving Sativex® (a medicinal cannabis extract containing approximately a 1:1 ratio of CBD:Δ9-THC, administered as an oral-mucosal spray) reported significant reductions in pain symptoms as measured with the NRS-11 and neuropathic pain scale (NPS) in a 4-week treatment period double-blind, placebo-controlled study.146”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
What the sources say
- Not checked yetcites [146] Rog, 2005, Randomized, controlled trial of cannabis-based medicine in central pain in multiple sclerosis, Neurology source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“This study reported that 74% of the patients in the placebo group, versus 45% of the patients receiving cannabinoid-based medications, cited a lack of benefit derived from experimental medication as the reason for discontinuation of the trial.145”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
What the sources say
- Not checked yetcites [145] Zajicek, 2005, Cannabinoids in multiple sclerosis (CAMS) study: safety and efficacy data for 12 months follow up, J Neurol Neurosurg Psychiatry source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Sleep quality disturbance scores were improved in patients receiving either active drug versus placebo.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Brachial Plexus Avulsion-induced Neuropathy
What the sources say
- Not checked yetcites [150] Berman, 2004, Efficacy of two cannabis based medicinal extracts for relief of central neuropathic pain from brachial plexus avulsion: results of a randomised controlled trial, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“This study reported that cannabinoids compounded the decreased neurocognitive performance of patients that was present at baseline.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Mixed Neuropathic Pain
What the sources say
- Not checked yetcites [155] Wilsey, 2008, A randomized, placebo-controlled, crossover trial of cannabis cigarettes in neuropathic pain, J Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Sativex® improved pain ratings as measured with the NRS in a five-week double-blind, placebo-controlled study performed in patients experiencing unilateral neuropathic pain.133”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Mixed Neuropathic Pain
What the sources say
- Not checked yetcites [133] Nurmikko, 2007, Sativex successfully treats neuropathic pain characterised by allodynia: a randomised, double-blind, placebo-controlled clinical trial, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Eighteen of those same patients participated in stimulus-evoked pain testing during the study and patients showed a trend towards decreased mechanical allodynia following CT-3 administration.153”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Mixed Neuropathic Pain
What the sources say
- Not checked yetcites [153] Salim, 2005, Pain measurements and side effect profile of the novel cannabinoid ajulemic acid, Neuropharmacology source
hedgedconditionaln = 18- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Nabilone (Cesamet®) decreased measures of spasticity-related pain (11-Point Box Test) in patients experiencing chronic upper motor neuron syndrome (UMNS) associated with a number of pain syndromes.160”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Mixed Neuropathic Pain
What the sources say
- Not checked yetcites [160] Wissel, 2006, Low dose treatment with the synthetic cannabinoid Nabilone significantly reduces spasticity-related pain: a double-blind placebo-controlled cross-over trial, J Neurol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Ninety-five percent of the patients in the placebo-controlled study chose to enter a two year open-label study with Sativex®.147”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
What the sources say
- Not checked yetcites [147] Rog, 2007, Oromucosal delta9-tetrahydrocannabinol/cannabidiol for neuropathic pain associated with multiple sclerosis: an uncontrolled, open-label, 2-year extension trial, Clin Ther source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“CBD also acts as an agonist at serotonin 5-HT1a receptors.144”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
What the sources say
- Not checked yetcites [144] Mechoulam, 2007, Cannabidiol—recent advances, Chem Biodivers source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“A one year double-blind, placebo-controlled follow up study in MS patients demonstrated improved symptoms of pain, spasms, spasticity, sleep, shakiness, energy level, and tiredness following administration of either dronabinol or Cannador®.145”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
What the sources say
- Not checked yetcites [145] Zajicek, 2005, Cannabinoids in multiple sclerosis (CAMS) study: safety and efficacy data for 12 months follow up, J Neurol Neurosurg Psychiatry source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Quality of sleep was improved by all cannabinoid based medications156”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Mixed Neuropathic Pain
What the sources say
- Not checked yetcites [156] Notcutt, 2004, Initial experiences with medicinal extracts of cannabis for chronic pain: results from 34 ‘N of 1’ studies, Anaesthesia source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“CB2 receptor immunoreactivity has been reported in normal and injured human DRG neurons, brachial plexus nerves, and neuromas as well as peripheral nerve fibers.151”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Brachial Plexus Avulsion-induced Neuropathy
What the sources say
- Not checked yetcites [151] Anand, 2008, Cannabinoid receptor CB2 localisation and agonist-mediated inhibition of capsaicin responses in human sensory neurons, Pain source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“However, upregulation of CB2 receptor immunoreactivity was specifically observed in injured human nerve specimens and avulsed DRG obtained during surgery for brachial plexus repair.151”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Brachial Plexus Avulsion-induced Neuropathy
What the sources say
- Not checked yetcites [151] Anand, 2008, Cannabinoid receptor CB2 localisation and agonist-mediated inhibition of capsaicin responses in human sensory neurons, Pain source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Eighty percent of the patients chose to enter an open-label study with Sativex® following completion of this randomized study.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Brachial Plexus Avulsion-induced Neuropathy
What the sources say
- Not checked yetcites [150] Berman, 2004, Efficacy of two cannabis based medicinal extracts for relief of central neuropathic pain from brachial plexus avulsion: results of a randomised controlled trial, Pain source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Greater numbers of nonserious adverse events were observed following cannabinoid treatment, as expected.170”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Side-effects
What the sources say
- Not checked yetcites [170] Wang, 2008, Adverse effects of medical cannabinoids: a systematic review, CMAJ source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Moreover, 99% of serious adverse events from randomized clinical trials were reported in only two trials.170”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Side-effects
What the sources say
- Not checked yetcites [170] Wang, 2008, Adverse effects of medical cannabinoids: a systematic review, CMAJ source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Cannabinoids suppress hyperalgesia and allodynia (i.e. mechanical allodynia, mechanical hyperalgesia, thermal hyperalgesia and, where evaluated, cold allodynia), induced by diverse neuropathic pain states through CB1 and CB2-specific mechanisms.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Conclusions
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In this latter study,166 it was concluded that the weak opioid dihydrocodeine was a statistically better treatment for chronic neuropathic pain than nabilone.166”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Caveats
What the sources say
- Not checked yetcites [166] Frank, 2008, Comparison of analgesic effects and patient tolerability of nabilone and dihydrocodeine for chronic neuropathic pain: randomised, crossover, double blind study, Bmj source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The psychoactive effects of centrally-acting cannabinoid agonists, nonetheless, represent a challenge for pain pharmacotherapies that directly activate CB1 receptors in the brain.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Conclusions
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Benefits of an add-on treatment with nabilone have nonetheless been noted in patients with chronic therapy-resistant pain (observed in causal relationship with a pathological status of the skeletal and locomotor system).167”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Caveats
What the sources say
- Not checked yetcites [167] Pinsger, 2006, Benefits of an add-on treatment with the synthetic cannabinomimetic nabilone on patients with chronic pain—a randomized controlled trial, Wien Klin Wochenschr source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“An early case study reported pain relief and improvement in spasticity in a patient with a spinal cord injury following oral Δ9-THC.162”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Mixed Neuropathic Pain
What the sources say
- Not checked yetcites [162] Maurer, 1990, Delta-9-tetrahydrocannabinol shows antispastic and analgesic effects in a single case double-blind trial, Eur Arch Psychiatry Clin Neurosci source
plaindirectSingle case- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Intolerable side-effects were observed in all groups of patients receiving either gabapentainoids, tricyclic antidepressants, anticonvulsants, cannabinoids (nabilone or Sativex®) and topical agents).169”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Side-effects
What the sources say
- Not checked yetcites [169] Toth, 2008, A prospective identification of neuropathic pain in specific chronic polyneuropathy syndromes and response to pharmacological therapy, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Notably, the presence of intolerable side-effects was similar amongst the different classes of medications.169”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Side-effects
What the sources say
- Not checked yetcites [169] Toth, 2008, A prospective identification of neuropathic pain in specific chronic polyneuropathy syndromes and response to pharmacological therapy, Pain source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Oral dronanbinol produced significant pain relief versus placebo when combined with opioid therapy in both a double-blind, placebo-controlled crossover phase and a subsequent open-label extension.168”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Caveats
What the sources say
- Not checked yetcites [168] Narang, 2008, Efficacy of dronabinol as an adjuvant treatment for chronic pain patients on opioid therapy, J Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Clinical studies largely reaffirm that cannabinoids show efficacy in suppressing diverse neuropathic pain states in humans.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Conclusions
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
- Probably not a substantial claim. 23
- It may state two separate claims as one. 135
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Cannabinoid agonists have been evaluated in animal models of disease-related neuropathic pain, although pharmacological specificity has not been consistently assessed.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Disease-related Models of Neuropathic Pain
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Diabetic neuropathy induced by a single injection of streptozotocin (STZ) resulted in increased sensitivity to noxious and non-noxious levels of mechanical stimulation, and failed to induce thermal hyperalgesia in the studies reviewed here (Table 6).”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Animal models of multiple sclerosis (MS) have been described, although to our knowledge, no study to date has evaluated cannabinoid-mediated suppression of MS-induced neuropathic nociception.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Multiple Sclerosis-associated Neuropathy
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Three of the articles reviewed here used smoking as the route of administration, whereas the other thirteen employed oral preparations in the form of pills or oral-mucosal sprays.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“However, possible changes in CB1 receptor immunoreactivity, were not evaluated in the human tissue, and therefore cannot be excluded.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Brachial Plexus Avulsion-induced Neuropathy
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Both of these studies employed eight or fewer subjects and evaluated dronabinol titrated to a dose of 25 mg/day (where tolerated).”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Caveats
plainn = 8- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“PEA may indirectly alter levels of endocannabinoids by competing with anandamide and other fatty-acid amides for degradation by FAAH or by suppressing FAAH expression at the transcriptional level.27, 28”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Endocannabinoids
What the sources say
- Not checked yetcites [27] Re, 2007, Palmitoylethanolamide, endocannabinoids and related cannabimimetic compounds in protection against tissue inflammation and pain: potential use in companion animals, Vet J source
- Not checked yetcites [28] Bisogno, 2002, Fatty acid amide hydrolase, an enzyme with many bioactive substrates, Curr Pharm Des source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“CB1 receptors are localized to the central nervous system (CNS) and the periphery. CB1 receptors are found in sites associated with pain processing, including the periaqueductal gray (PAG),8 rostral ventromedial medulla (RVM),8 thalamus,9 dorsal root ganglia (DRG),10 amygdala,8 and cortex8.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Receptor Pharmacology
What the sources say
- Not checked yetcites [8] Herkenham, 1991, Characterization and localization of cannabinoid receptors in rat brain: a quantitative in vitro autoradiographic study, J Neurosci source
- Not checked yetcites [9] Matsuda, 1993, Localization of cannabinoid receptor mRNA in rat brain, J Comp Neurol source
- Not checked yetcites [10] Hohmann, 1999, Localization of central cannabinoid CB1 receptor messenger RNA in neuronal subpopulations of rat dorsal root ganglia: a double-label in situ hybridization study, Neuroscience source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“PEA does not bind cannabinoid receptors and has recently been described as an endogenous ligand for peroxisome proliferator receptor-α (PPAR-α).26”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Endocannabinoids
What the sources say
- Not checked yetcites [26] Lo Verme, 2005, The nuclear receptor peroxisome proliferator-activated receptor-alpha mediates the anti-inflammatory actions of palmitoylethanolamide, Mol Pharmacol source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Activation of the CB1 receptor also results in hypothermia, sedation, catalepsy, and altered mental status.11”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Receptor Pharmacology
What the sources say
- Not checked yetcites [11] Malan, 2001, CB2 cannabinoid receptor-mediated peripheral antinociception, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Both CB12 and CB23 receptors are G-coupled protein receptors that are negatively coupled to adenylate cyclase.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Receptor Pharmacology
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“The CB2 receptor was originally believed to be restricted to the periphery, primarily to immune cells (e.g. mast cells),12 although they may be present neuronally in some species.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Receptor Pharmacology
What the sources say
- Not checked yetcites [12] Facci, 1995, Mast cells express a peripheral cannabinoid receptor with differential sensitivity to anandamide and palmitoylethanolamide, Proc Natl Acad Sci U S A source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“CB2 receptor activation stimulates MAPK activity but does not modulate calcium or potassium conductances.4”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Receptor Pharmacology
What the sources say
- Not checked yetcites [4] Guindon, 2008, Cannabinoid CB2 receptors: a therapeutic target for the treatment of inflammatory and neuropathic pain, Br J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“FAAH-/- mice are hypoalgesic in models of acute and inflammatory pain; these effects are blocked by a CB1 antagonist.29, 30”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Endocannabinoids
What the sources say
- Not checked yetcites [29] Cravatt, 2001, Supersensitivity to anandamide and enhanced endogenous cannabinoid signaling in mice lacking fatty acid amide hydrolase, Proc Natl Acad Sci U S A source
- Not checked yetcites [30] Lichtman, 2004, Mice lacking fatty acid amide hydrolase exhibit a cannabinoid receptor-mediated phenotypic hypoalgesia, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“A neurophysiological basis for these findings is derived from the observation that WIN55,212-2 (i.v.) dose-dependently inhibits windup46 as well as CCI-induced increases in spontaneous firing47 of spinal wide dynamic range (WDR) neurons through a CB1-dependent mechanism.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [46] Strangman, 1999, Cannabinoid WIN 55,212-2 inhibits the activity-dependent facilitation of spinal nociceptive responses, J Neurophysiol source
- Not checked yetcites [47] Liu, 2006, Effects of a cannabinoid agonist on spinal nociceptive neurons in a rodent model of neuropathic pain, J Neurophysiol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Monoacylglycerol lipase (MGL) is a key enzyme implicated in the hydrolysis of 2-AG.33, 34”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Endocannabinoids
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“SR141716, administered acutely, is pro-hyperalgesic and pro-allodynic in this model. 42”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [42] Herzberg, 1997, The analgesic effects of R(+)-WIN 55,212-2 mesylate, a high affinity cannabinoid agonist, in a rat model of neuropathic pain, Neurosci Lett source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Several mixed cannabinoid CB1/CB2 agonists have been shown to suppress all forms of neuropathic nociception observed in the CCI model, primarily through CB1-mediated mechanisms.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“CB1 receptors are upregulated in the spinal cord following CCI; these effects are believed to be modulated by tyrosine kinase38 and glucocorticoid39 receptors.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [38] Lim, 2003, Upregulation of spinal cannabinoid-1-receptors following nerve injury enhances the effects of Win 55,212-2 on neuropathic pain behaviors in rats, Pain source
- Not checked yetcites [39] Wang, 2007, Central glucocorticoid receptors regulate the upregulation of spinal cannabinoid-1 receptors after peripheral nerve injury in rats, Pain source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, it is important to emphasize that the behavioral phenotype induced by antagonist treatment may depend upon level of endocannabinoid tone present in the system, the injection paradigm (chronic vs. acute), and presence of regulatory changes in cannabinoid receptors or endocannabinoids.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Both AEA and 2-AG can be metabolized by cyclooxygenase-2 (COX-2), a phenomenon that may contribute to the antinociceptive properties of non-steroidal anti-inflammatory drugs (NSAIDS) that act through inhibition of COX-2.4”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Endocannabinoids
What the sources say
- Not checked yetcites [4] Guindon, 2008, Cannabinoid CB2 receptors: a therapeutic target for the treatment of inflammatory and neuropathic pain, Br J Pharmacol source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“WIN55,212-2 also normalizes prostaglandin E2 (PGE2) levels and nitric oxide (NO) activity, two mediators of neuropathic pain that are increased following CCI.48”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [48] Costa, 2004, Repeated treatment with the synthetic cannabinoid WIN 55,212-2 reduces both hyperalgesia and production of pronociceptive mediators in a rat model of neuropathic pain, Br J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Thus, it is noteworthy that CB2 receptor mRNA is upregulated in the lumbar spinal cord following CCI. This upregulation is restricted to non-neuronal cells (e.g. glia).49”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [49] Zhang, 2003, Induction of CB2 receptor expression in the rat spinal cord of neuropathic but not inflammatory chronic pain models, Eur J Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“AEA can also activate the peroxisome proliferator receptor-γ (PPARγ) receptor.32”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Endocannabinoids
What the sources say
- Not checked yetcites [32] Bouaboula, 2005, Anandamide induced PPARgamma transcriptional activation and 3T3-L1 preadipocyte differentiation, Eur J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Anandamide also acts as an endovanalloid at the transient receptor potential cation channel (TRPV1) receptor.31 AEA shows affinity for TRPV1 that is 5-20 fold lower than its affinity for CB1.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Endocannabinoids
What the sources say
- Not checked yetcites [31] Ross, 2001, Structure-activity relationship for the endogenous cannabinoid, anandamide, and certain of its analogues at vanilloid receptors in transfected cells and vas deferens, Br J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“AM404 also normalizes CCI-induced changes in NO activity,52, 53 COX-253 activity, cytokine levels (e.g. TNF-α and IL10),52 and NF-κB52 levels.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [52] Costa, 2006, AM404, an inhibitor of anandamide uptake, prevents pain behaviour and modulates cytokine and apoptotic pathways in a rat model of neuropathic pain, Br J Pharmacol source
- Not checked yetcites [53] La Rana, 2006, Modulation of neuropathic and inflammatory pain by the endocannabinoid transport inhibitor AM404 [N-(4-hydroxyphenyl)-eicosa-5,8,11,14-tetraenamide], J Pharmacol Exp Ther source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“This basal hypoalgesia is absent in FAAH-/- mice subjected to nerve injury, where genotype differences in evoked neuropathic pain behaviors are not apparent.30”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Endocannabinoids
What the sources say
- Not checked yetcites [30] Lichtman, 2004, Mice lacking fatty acid amide hydrolase exhibit a cannabinoid receptor-mediated phenotypic hypoalgesia, Pain source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“However, anti-hyperalgesic effects observed with these compounds are likely to be independent of cannabinoid receptors, and may be mediated through TRPV1.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [40] Costa, 2007, The non-psychoactive cannabis constituent cannabidiol is an orally effective therapeutic agent in rat chronic inflammatory and neuropathic pain, Eur J Pharmacol source
- Not checked yetcites [41] Comelli, 2008, Antihyperalgesic effect of a Cannabis sativa extract in a rat model of neuropathic pain: mechanisms involved, Phytother Res source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“CCI produces mechanical allodynia as well as thermal allodynia and hyperalgesia in the ipsilateral paw as early as two days post-surgery.37”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [37] Bennett, 1988, A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“AM404, an endocannabinoid transport inhibitor, increases accumulation and, hence, bioavailability, of anandamide (and potentially other endocannabinoids) through a mechanism that remains incompletely understood.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Multiple CB2-selective agonists have been demonstrated to suppress CCI-induced mechanical allodynia, although pharmacological specificity has not been consistently assessed (Table 2).”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Mixed CB1/CB2 agonists, such as CP55,940 or WIN55,212-2, typically act as CB1-selective agonists following systemic administration,45 although CB2-mediated effects may be unmasked following administration of CB2-selective agents or following local administration of the same compounds.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [45] Sain, 2009, Antinociceptive effects of the non-selective cannabinoid receptor agonist CP 55,940 are absent in CB1(−/−) and not CB2(−/−) mice in models of acute and persistent pain, Neuropharmacology source
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“However, SR141716 (p.o.), administered chronically, suppresses thermal and mechanical hyperalgesia in both rats and CB1+/+ mice, while failing to produce an effect in CB1-/- mice. 43”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [43] Costa, 2005, Effect of the cannabinoid CB1 receptor antagonist, SR141716, on nociceptive response and nerve demyelination in rodents with chronic constriction injury of the sciatic nerve, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Thus, CB2 agonists may show therapeutic potential for suppressing neuropathic pain without producing tolerance when administered either alone or as adjuncts to exisiting treatments.51”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [51] Yao, 2009, J Pharmacol Exp Ther source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Pro-hyperalgesic effects of SR141716 and SR144528 have been reported in the Seltzer model,65 indicating a potential alteration in endocannabinoid tone following nerve injury.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [65] Helyes, 2003, Inhibitory effect of anandamide on resiniferatoxin-induced sensory neuropeptide release in vivo and neuropathic hyperalgesia in the rat, Life Sci source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The transport inhibitor AM404, administered systemically, suppressed mechanical allodynia in a CB1-dependent manner, without producing motor effects.73”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [73] Mitchell, 2007, Actions of the endocannabinoid transport inhibitor AM404 in neuropathic and inflammatory pain models, Clin Exp Pharmacol Physiol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Ajulemic acid (CT-3), which was developed as a peripherally restricted cannabinoid analogue, also produced activity in the tetrad but anti-hyperalgesic effects occurred at doses lower than those producing side-effects.69”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [69] Dyson, 2005, Antihyperalgesic properties of the cannabinoid CT-3 in chronic neuropathic and inflammatory pain states in the rat, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, activation of CB1 and CB2 receptors as well as pharmacological manipulation of endocannabinoid accumulation or breakdown suppresses neuropathic nociception in rodents.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Anti-hyperalgesic effects of AEA and PEA were blocked by a CB1 and CB2 antagonist, respectively.65”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [65] Helyes, 2003, Inhibitory effect of anandamide on resiniferatoxin-induced sensory neuropeptide release in vivo and neuropathic hyperalgesia in the rat, Life Sci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“CCI also increases levels of endogenous AEA, but not 2-AG, in the dorsal raphe – an observation which may help explain the anti-hyperalgesic efficacy of an anandamide transport inhibitor in this model.57”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [57] Palazzo, 2006, Neuropathic pain and the endocannabinoid system in the dorsal raphe: pharmacological treatment and interactions with the serotonergic system, Eur J Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Additionally both OL135 and URB597 are antinociceptive in FAAH+/+ mice, but fail to produce an effect in FAAH-/- mice.59”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [59] Kinsey, 2009, Blockade of endocannabinoid-degrading enzymes attenuates neuropathic pain, J Pharmacol Exp Ther source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The novel MGL inhibitor, JZL184, attenuates CCI-induced mechanical and cold allodynia through indirect activation of the CB1 receptor; JZL184 was efficacious in attenuating neuropathic nociception in both FAAH+/+ and FAAH-/- mice.59”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [59] Kinsey, 2009, Blockade of endocannabinoid-degrading enzymes attenuates neuropathic pain, J Pharmacol Exp Ther source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“CB2-/- mice reportedly develop thermal hyperalgesia and mechanical allodynia in the contralateral paw following surgery, whereas CB2+/+ do not.63”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [63] Racz, 2008, Crucial role of CB(2) cannabinoid receptor in the regulation of central immune responses during neuropathic pain, J Neurosci source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Several studies report efficacy of mixed cannabinoid CB1/CB2 agonists in this model, although CNS side-effects were nonetheless observed in the same dose range that resulted in full reversal of neuropathic nociception.68”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [68] Fox, 2001, The role of central and peripheral Cannabinoid1 receptors in the antihyperalgesic activity of cannabinoids in a model of neuropathic pain, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“CCI increases serotonin (5-HT) levels in the dorsal raphe and this effect was suppressed by both WIN55,212-2 and AM404 in a CB1-dependent manner.57”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chronic Constriction Injury (CCI)37
What the sources say
- Not checked yetcites [57] Palazzo, 2006, Neuropathic pain and the endocannabinoid system in the dorsal raphe: pharmacological treatment and interactions with the serotonergic system, Eur J Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“CB2 mRNA was also shown to be upregulated in the ipsilateral (versus the contralateral) spinal cord and DRG following SNL and the presence of CB2 mRNA was confirmed in spinal cord microglial cells in culture.17”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [17] Beltramo, 2006, CB2 receptor-mediated antihyperalgesia: possible direct involvement of neural mechanisms, Eur J Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The FAAH inhibitor URB597, administered locally in the paw,67 but not systemically62 suppressed both thermal hyperalgesia and mechanical allodynia through a CB1 mechanism.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [62] Jayamanne, 2006, Actions of the FAAH inhibitor URB597 in neuropathic and inflammatory chronic pain models, Br J Pharmacol source
- Not checked yetcites [67] Desroches, 2008, Modulation of the anti-nociceptive effects of 2-arachidonoyl glycerol by peripherally administered FAAH and MGL inhibitors in a neuropathic pain model, Br J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Gabapentin successfully attenuated mechanical allodynia in this model, however, several other commonly prescribed neuropathic pain medications including amitriptyline, fluoxetine and indomethacin failed to show similar effects.80”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [80] LaBuda, 2005, Pharmacological evaluation of the selective spinal nerve ligation model of neuropathic pain in the rat, J Neurosci Methods source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Increases in both AEA and 2-AG have also been reported in the ipsilateral injured L5, but not the uninjured L4 DRG.83”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [83] Mitrirattanakul, 2006, Site-specific increases in peripheral cannabinoid receptors and their endogenous ligands in a model of neuropathic pain, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The L29-induced suppression of thermal hyperalgesia was mediated by both the CB1 receptor and PPAR-α, whereas suppression of mechanical allodynia was mediated by CB1/CB2 and PPAR-α receptors.64”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [64] Wallace, 2007, The effect of the palmitoylethanolamide analogue, palmitoylallylamide (L-29) on pain behaviour in rodent models of neuropathy, Br J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Spinal, but not systemic, administration of HU-210 has been reported to reduce Aδ fiber-evoked responses on spinal WDR neurons in both shams and SNL rats, whereas HU-210 showed no effect on C-fiber responses of SNL rats.82”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [82] Chapman, 2001, Functional changes in the inhibitory effect of spinal cannabinoid (CB) receptor activation in nerve injured rats, Neuropharmacology source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The fatty-acid analogue of PEA, L-29, also suppressed thermal hyperalgesia and mechanical allodynia in the Seltzer model.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [64] Wallace, 2007, The effect of the palmitoylethanolamide analogue, palmitoylallylamide (L-29) on pain behaviour in rodent models of neuropathy, Br J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“CB2 mRNA was upregulated in the lumbar spinal cord following SNL,49 coincident with the expression of activated microglia.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [49] Zhang, 2003, Induction of CB2 receptor expression in the rat spinal cord of neuropathic but not inflammatory chronic pain models, Eur J Neurosci source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Chronic administration of WIN55,212-2 also attenuates the development of mechanical allodynia and suppresses glial activation in the spinal cord following SNL with no overt motor side-effects.81”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [81] Leichsenring, 2009, Analgesic and antiinflammatory effects of cannabinoid receptor agonists in a rat model of neuropathic pain, Naunyn Schmiedebergs Arch Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Intrathecal N-arachidonoyl glycine (NaGly), the arachodonic acid conjugate, also attenuated mechanical allodynia in this model, however, the anti-hyperalgesic actions of this compound are independent of spinal cannabinoid receptors.75”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [75] Vuong, 2008, Actions of N-arachidonyl-glycine in a rat neuropathic pain model, Neuropharmacology source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Thus, it is noteworthy that mixed cannabinoid agonists, cannabinoid CB2-selective agonists and FAAH inhibitors all attenuated neuropathic nociception induced by SNL (Table 5).”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The MGL inhibitor URB602 (which cannot be used systemically as a selective MGL inhibitor), administered locally in the paw, also suppressed neuropathic nociception in this model through activation of both CB1 and CB2 receptors.67”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [67] Desroches, 2008, Modulation of the anti-nociceptive effects of 2-arachidonoyl glycerol by peripherally administered FAAH and MGL inhibitors in a neuropathic pain model, Br J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Locally injected (i.paw) paracetamol suppressed mechanical allodynia and thermal hyperalgesia present following partial sciatic nerve ligation and these effects are blocked by local administration of either a CB1 or a CB2 antagonist.76”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Partial Sciatic Nerve Ligation (Seltzer Model)61
What the sources say
- Not checked yetcites [76] Dani, 2007, The local antinociceptive effects of paracetamol in neuropathic pain are mediated by cannabinoid receptors, Eur J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In the same study, spinal administration of URB597 was equally efficacious at attenuating mechanically-evoked responses and increasing levels of endogenous cannabinoids in SNL and sham rats and these effects were CB1-mediated.92”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [92] Jhaveri, 2006, Analgesic effects of fatty acid amide hydrolase inhibition in a rat model of neuropathic pain, J Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Chronic constriction injury of the infraorbital nerve (CCI-ION) results in thermal hyperalgesia and mechanical allodynia (as measured by head withdrawals) ipsilateral to the site of injury.93”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [93] Vos, 1991, Behavioral changes following ligation of the infraorbital nerve in rats: an animal model of trigeminal neuropathic pain
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Intrathecal JWH015 reduced SNT-induced increases in activated microglia in a CB2-dependent manner, further supporting a role for nonneuronal CB2 receptors in anti-hyperalesic effects of CB2 agonists. 96”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [96] Romero-Sandoval, 2008, Spinal microglial and perivascular cell cannabinoid receptor type 2 activation reduces behavioral hypersensitivity without tolerance after peripheral nerve injury, Anesthesiology source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“CP55,940 reversed mechanical allodynia in this model 1 h following a second intrathecal injection, although this dosing paradigm was also associated with motor effects.96”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [96] Romero-Sandoval, 2008, Spinal microglial and perivascular cell cannabinoid receptor type 2 activation reduces behavioral hypersensitivity without tolerance after peripheral nerve injury, Anesthesiology source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“WIN55,212-2 and HU-210 increased mechanical withdrawal responses and thermal withdrawal latencies on the ipsilateral side of the head in this model.94”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [94] Liang, 2007, The synthetic cannabinoids attenuate allodynia and hyperalgesia in a rat model of trigeminal neuropathic pain, Neuropharmacology source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“High antihyperalgesic doses of WIN55,212-2 decreased rotarod latencies and body temperature, whereas HU210, at the singular low dose used (10 μg/kg), had no effect on these dependent measures.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [94] Liang, 2007, The synthetic cannabinoids attenuate allodynia and hyperalgesia in a rat model of trigeminal neuropathic pain, Neuropharmacology source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The CB2-specific agonist GW405833, administered chronically, suppressed the development of mechanical allodynia concomitant with suppression of glial activation at the level of the spinal cord.81”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [81] Leichsenring, 2009, Analgesic and antiinflammatory effects of cannabinoid receptor agonists in a rat model of neuropathic pain, Naunyn Schmiedebergs Arch Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Interestingly, pre-treatment with the CB1 antagonist, SR141716, enhanced the effects of A-836339 when applied to the L5 DRG,88 indicating that blockade of CB1 receptors enhanced the antinociceptive effects of a CB2 agonist, as reported previously.89”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [88] McGaraughty, 2009, A CB(2) receptor agonist, A-836339, modulates wide dynamic range neuronal activity in neuropathic rats: contributions of spinal and peripheral CB(2) receptors, Neuroscience source
- Not checked yetcites [89] Rahn, 2008, Selective activation of cannabinoid CB2 receptors suppresses neuropathic nociception induced by treatment with the chemotherapeutic agent paclitaxel in rats, J Pharmacol Exp Ther source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Low doses of locally injected URB597 (i.pl.) reduced mechanically-evoked responses of WDR neurons and increased endocannabinoid levels in ipsilateral paw tissue of sham operated rats.92”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Spinal Nerve Ligation (SNL)77
What the sources say
- Not checked yetcites [92] Jhaveri, 2006, Analgesic effects of fatty acid amide hydrolase inhibition in a rat model of neuropathic pain, J Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Intrathecal JWH015 dose-dependently suppressed behavioral hypersensitivity following a second injection, indicating a cumulative anti-allodynic effect of this drug.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [96] Romero-Sandoval, 2008, Spinal microglial and perivascular cell cannabinoid receptor type 2 activation reduces behavioral hypersensitivity without tolerance after peripheral nerve injury, Anesthesiology source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“CB1 receptor upregulation was observed in both the ipsilateral and contralateral superficial layer of the trigeminal caudal nucleus, and this effect was greater on the ipsilateral side.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [94] Liang, 2007, The synthetic cannabinoids attenuate allodynia and hyperalgesia in a rat model of trigeminal neuropathic pain, Neuropharmacology source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Standard analgesics (e.g. morphine, gabapentin, amitryptiline) are efficacious in treating neuropathic nociception resulting from a crush injury of the sciatic nerve, but showed limited efficacy following SNI.101”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [101] Decosterd, 2004, Differential analgesic sensitivity of two distinct neuropathic pain models, Anesth Analg source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Lean males subjected to hyperinsulinemia show a 2-fold increase in FAAH mRNA expression whereas obese males subjected to the same conditions failed to show similar alterations in gene expression.111”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
What the sources say
- Not checked yetcites [111] Murdolo, 2007, Insulin differentially modulates the peripheral endocannabinoid system in human subcutaneous abdominal adipose tissue from lean and obese individuals, J Endocrinol Invest source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The spared nerve injury (SNI) model reliably produces thermal hyperalgesia and mechanical allodynia in studies that tested for both measures.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
In the paper
“Acute WIN55,212-2, administered systemically, suppressed SCI-induced mechanical allodynia in a CB1-dependent manner, although other parameters of neuropathic pain were not assessed.103”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [103] Hama, 2007, Antinociceptive effect of cannabinoid agonist WIN 55,212-2 in rats with a spinal cord injury, Exp Neurol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“A dose-escalation study with BAY 59-3074 in the SNI model indicated that tolerance rapidly develops to side-effects observed following chronic administration (e.g. hypothermia), whereas no loss in analgesic efficacy was observed.78”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [78] De Vry, 2004, 3-[2-cyano-3-(trifluoromethyl)phenoxy]phenyl-4,4,4-trifluoro-1-butanesulfo nate (BAY 59-3074): a novel cannabinoid Cb1/Cb2 receptor partial agonist with antihyperalgesic and antiallodynic effects, J Pharmacol Exp Ther source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Spinal cord injury (SCI)102 produces mechanical hyperalgesia and allodynia.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [102] Bruce, 2002, Chronic pain after clip-compression injury of the rat spinal cord, Exp Neurol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Interestingly, Δ9-THC exhibited enhanced antinociceptive efficacy in diabetic rats whereas morphine showed reduced antinociceptive efficacy.115”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
What the sources say
- Not checked yetcites [115] Williams, 2008, Decreased basal endogenous opioid levels in diabetic rodents: effects on morphine and delta-9-tetrahydrocannabinoid-induced antinociception, Eur J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“HU-210 did not alter the hyperglycemia index; however, it did normalize cerebral oxidative stress present in diabetic mice.114”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
What the sources say
- Not checked yetcites [114] Dagon, 2007, The synthetic cannabinoid HU-210 attenuates neural damage in diabetic mice and hyperglycemic pheochromocytoma PC12 cells, Neurobiol Dis source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Unlike morphine, chronic administration of WIN55,212-2 reduced mechanical allodynia in the SCI model with no decrease in effectiveness over time.104”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [104] Hama, 2009, Sustained antinociceptive effect of cannabinoid receptor agonist WIN 55,212-2 over time in rat model of neuropathic spinal cord injury pain, J Rehabil Res Dev source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Acute WIN55,212-2 suppressed thermal hyperalgesia and mechanical allodynia in both mice lacking CB1 receptors in primary nociceptors (SNS-CB1-) and their wild-type controls; however differences in the antinociceptive effects of WIN55,212-2 were observed between genotypes, and these effects were greater with mechanical than thermal sensitivity.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [7] Agarwal, 2007, Cannabinoids mediate analgesia largely via peripheral type 1 cannabinoid receptors in nociceptors, Nat Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Increased levels of endocannabinoids have been found in obese patients suffering from Type II diabetes109”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
What the sources say
- Not checked yetcites [109] Matias, 2006, Changes in endocannabinoid and palmitoylethanolamide levels in eye tissues of patients with diabetic retinopathy and age-related macular degeneration, Prostaglandins Leukot Essent Fatty Acids source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“STZ-diabetic mice showed a progressive decline in the radial arm maze and reduced neurological scores, both of which were recovered following treatment with HU-210.114”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
What the sources say
- Not checked yetcites [114] Dagon, 2007, The synthetic cannabinoid HU-210 attenuates neural damage in diabetic mice and hyperglycemic pheochromocytoma PC12 cells, Neurobiol Dis source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“SNS-CB1- mice showed exaggerated sensitivity to noxious levels of mechanical stimulation and a cold plate relative to their wild-type counterparts, whereas differential sensitivity was not observed between genotypes with non-noxious levels of mechanical stimulation and noxious levels of thermal stimulation.7”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [7] Agarwal, 2007, Cannabinoids mediate analgesia largely via peripheral type 1 cannabinoid receptors in nociceptors, Nat Neurosci source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Mechanical allodynia and thermal hyperalgesia were present in the initial study describing this technique105 as well as the study we reviewed.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [105] Hofmann, 2003, Pharmacological sensitivity and gene expression analysis of the tibial nerve injury model of neuropathic pain, Eur J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The CB1 antagonist rimonabant (Acomplia®) ameliorates insulin resistance and decreases weight gain in patients suffering from metabolic syndromes.112”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
What the sources say
- Not checked yetcites [112] Scheen, 2009, The endocannabinoid system: a promising target for the management of type 2 diabetes, Curr Protein Pept Sci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Systemic BAY 59-3074 was shown to attenuate both forms of neuropathic nociception, although pharmacological specificity was not assessed.78”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Other Nerve Injury Models
What the sources say
- Not checked yetcites [78] De Vry, 2004, 3-[2-cyano-3-(trifluoromethyl)phenoxy]phenyl-4,4,4-trifluoro-1-butanesulfo nate (BAY 59-3074): a novel cannabinoid Cb1/Cb2 receptor partial agonist with antihyperalgesic and antiallodynic effects, J Pharmacol Exp Ther source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In animal models, rimonabant improves resistance to insulin through pathways that are both dependent and independent of adiponectin, a hormone important for the regulation of glucose and catabolism of fatty acids.113”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > STZ-induced Diabetic Neuropathy
What the sources say
- Not checked yetcites [113] Watanabe, 2009, Rimonabant ameliorates insulin resistance via both adiponectin-dependent and adiponectin-independent pathways, J Biol Chem source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Rats receiving ddc displayed modest levels of gliosis whereas combined treatment with both HIV-gp120 and ddc increased levels of microglial activation.123”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > HIV-associated Sensory Neuropathy
What the sources say
- Not checked yetcites [123] Wallace, 2007, Characterization of rodent models of HIV-gp120 and anti-retroviral-associated neuropathic pain, Brain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“No hypersensitivity to thermal stimuli or motor deficits was observed following ddc treatment.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > HIV-associated Sensory Neuropathy
What the sources say
- Not checked yetcites [123] Wallace, 2007, Characterization of rodent models of HIV-gp120 and anti-retroviral-associated neuropathic pain, Brain source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Using the paclitaxel dosing paradigm described by Flatters and Bennett,120 mechanical allodynia, but not thermal hyperalgesia, was observed.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chemotherapy-induced Neuropathy
What the sources say
- Not checked yetcites [120] Flatters, 2004, Ethosuximide reverses paclitaxel- and vincristine-induced painful peripheral neuropathy, Pain source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“WIN55,212-2 prevented the development of mechanical allodynia induced by cisplatin, but failed to produce an anti-emetic benefit in this study.116”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chemotherapy-induced Neuropathy
What the sources say
- Not checked yetcites [116] Vera, 2007, WIN 55,212-2 prevents mechanical allodynia but not alterations in feeding behaviour induced by chronic cisplatin in the rat, Life Sci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Perineural HIV-gp120 together with ddc treatment resulted in mechanical allodynia that was greater than either treatment alone; no changes in paw withdrawal latencies to thermal stimuli or motor deficits reported.123”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > HIV-associated Sensory Neuropathy
What the sources say
- Not checked yetcites [123] Wallace, 2007, Characterization of rodent models of HIV-gp120 and anti-retroviral-associated neuropathic pain, Brain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, both mixed CB1/CB2 agonists and selective CB2 agonists suppress paclitaxel-evoked mechanical allodynia.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chemotherapy-induced Neuropathy
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Rats treated with the antiretroviral agent zalcitabine (ddc) developed mechanical allodynia that persisted up to 43 days post-injection and peaked between days 14 and 32.123”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > HIV-associated Sensory Neuropathy
What the sources say
- Not checked yetcites [123] Wallace, 2007, Characterization of rodent models of HIV-gp120 and anti-retroviral-associated neuropathic pain, Brain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“WIN55,212-2 attenuated mechanical allodynia and thermal hyperalgesia in this model and remained efficacious for up to one hour post injection.125”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Demyelination-induced Neuropathy
What the sources say
- Not checked yetcites [125] Wallace, 2003, Focal lysolecithin-induced demyelination of peripheral afferents results in neuropathic pain behavior that is attenuated by cannabinoids, J Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In one study, paclitaxel118 produced mechanical allodynia starting on day 5 that continued throughout the timecourse, although thermal hyperalgesia was only present from days 18-21.119”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chemotherapy-induced Neuropathy
What the sources say
- Not checked yetcites [118] Polomano, 2001, A painful peripheral neuropathy in the rat produced by the chemotherapeutic drug, paclitaxel, Pain source
- Not checked yetcites [119] Pascual, 2005, A cannabinoid agonist, WIN 55,212-2, reduces neuropathic nociception induced by paclitaxel in rats, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“WIN55,212-2 suppressed neuropathic nociception in this model but had no effect on body temperature or immobility.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chemotherapy-induced Neuropathy
What the sources say
- Not checked yetcites [119] Pascual, 2005, A cannabinoid agonist, WIN 55,212-2, reduces neuropathic nociception induced by paclitaxel in rats, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Interestingly, female mice showed an increased rate of development and greater allodynia than their male counterparts, a finding which mimics the greater prevalence of neuropathic pain symptoms reported by female MS patients.127”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Multiple Sclerosis-associated Neuropathy
What the sources say
- Not checked yetcites [126] Lynch, 2008, Analysis of nociception, sex and peripheral nerve innervation in the TMEV animal model of multiple sclerosis, Pain source
- Not checked yetcites [127] Buchanan, 2003, Gender analyses of nursing home residents with multiple sclerosis, J Gend Specif Med
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Vincristine produced mechanical allodynia, but not thermal hyperalgesia, in a 10 day injection paradigm121.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chemotherapy-induced Neuropathy
What the sources say
- Not checked yetcites [121] Weng, 2003, Changes in sensory processing in the spinal dorsal horn accompany vincristine-induced hyperalgesia and allodynia, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Heightened sensitivity to both non-noxious and noxious mechanical stimulation is observed in lysolecithin-treated rats; this hypersensitivity emerged 5 days post-exposure and peaked between 9-15 days post-exposure.125 Recovery to baseline levels was observed by day 23 post-lysolecithin.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Demyelination-induced Neuropathy
What the sources say
- Not checked yetcites [125] Wallace, 2003, Focal lysolecithin-induced demyelination of peripheral afferents results in neuropathic pain behavior that is attenuated by cannabinoids, J Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Naguib and colleagues85 demonstrated that a novel CB2-specific agonist, MDA7, suppressed paclitaxel-induced mechanical allodynia, although mediation by CB2 receptors was not assessed.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Chemotherapy-induced Neuropathy
What the sources say
- Not checked yetcites [85] Naguib, 2008, MDA7: a novel selective agonist for CB2 receptors that prevents allodynia in rat neuropathic pain models, Br J Pharmacol source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Dronabinol reduced spontaneous pain intensity as measured with a numerical rating scale (NRS) over a treatment period of 3 weeks134 and improved overall pain ratings on the category-rating scale over a treatment period of 15 weeks143.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
What the sources say
- Not checked yetcites [134] Svendsen, 2004, Does the cannabinoid dronabinol reduce central pain in multiple sclerosis?, BMJ source
- Not checked yetcites [143] Zajicek, 2003, Cannabinoids for treatment of spasticity and other symptoms related to multiple sclerosis (CAMS study): multicentre randomised placebo-controlled trial, Lancet source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“An anonymous cross-sectional questionnaire study revealed that as many as one-third of patients suffering from HIV have used cannabis to treat symptoms.138”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > HIV-associated neuropathy
What the sources say
- Not checked yetcites [138] Woolridge, 2005, Cannabis use in HIV for pain and other medical symptoms, J Pain Symptom Manage source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Additionally, this drug improved median radiating pain intensity and pressure threshold,134 sleep quality, spasms, and spasticity143 in MS patients.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
What the sources say
- Not checked yetcites [134] Svendsen, 2004, Does the cannabinoid dronabinol reduce central pain in multiple sclerosis?, BMJ source
- Not checked yetcites [143] Zajicek, 2003, Cannabinoids for treatment of spasticity and other symptoms related to multiple sclerosis (CAMS study): multicentre randomised placebo-controlled trial, Lancet source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“autoimmune encephalomyelitis has been postulated to underlie the development of neuropathic pain in MS.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Multiple Sclerosis-associated Neuropathy
What the sources say
- Not checked yetcites [128] Olechowski, 2009, Neuropathic pain behaviours in a chronic-relapsing model of experimental autoimmune encephalomyelitis (EAE), Pain source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Dronabinol (Marinol®) is used to counteract AIDS-related wasting and promote appetite in patients suffering from AIDS-related anorexia.139”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > HIV-associated neuropathy
What the sources say
- Not checked yetcites [139] Beal, 1995, Dronabinol as a treatment for anorexia associated with weight loss in patients with AIDS, J Pain Symptom Manage source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“CBD's antinociceptive effects have additionally been attributed to inhibition of anandamide degradation, the compound's antioxidant properties, or binding to an unknown cannabinoid receptor.144”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
What the sources say
- Not checked yetcites [144] Mechoulam, 2007, Cannabidiol—recent advances, Chem Biodivers source
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Interestingly, a mouse model of MS (TMEV infection) is also characterized by an upregulation of CB2 receptor mRNA and increases in levels of 2-AG and PEA.129”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Multiple Sclerosis-associated Neuropathy
What the sources say
- Not checked yetcites [129] Loria, 2008, Study of the regulation of the endocannabinoid system in a virus model of multiple sclerosis reveals a therapeutic effect of palmitoylethanolamide, Eur J Neurosci source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“This study found no changes in heart rate, blood pressure, plasma HIV RNA (viral load; VL), or blood CD4+ lymphocyte counts following cannabis treatment, suggesting that cannabis did not negatively impact the already compromised immune system in these patients.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > HIV-associated neuropathy
What the sources say
- Not checked yetcites [137] Ellis, 2009, Smoked medicinal cannabis for neuropathic pain in HIV: a randomized, crossover clinical trial, Neuropsychopharmacology source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Approximately 50% of rats exposed to the varicella-zoster virus (VZV) developed mechanical allodynia in the ipsilateral paw by 14 days post-infection; no thermal hyperalgesia or cold allodynia was observed.64”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Post Herpetic Neuralgia
What the sources say
- Not checked yetcites [64] Wallace, 2007, The effect of the palmitoylethanolamide analogue, palmitoylallylamide (L-29) on pain behaviour in rodent models of neuropathy, Br J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In 2009, Ellis and colleagues137 reported similar results in a crossover study employing multiple concentrations of Δ9-THC in cannabis cigarettes administered to patients. Cannabis was superior to placebo in either phase of the crossover as measured with the descriptor differential scale (DDS) or VAS.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > HIV-associated neuropathy
What the sources say
- Not checked yetcites [137] Ellis, 2009, Smoked medicinal cannabis for neuropathic pain in HIV: a randomized, crossover clinical trial, Neuropsychopharmacology source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Among the symptoms improved following cannabis were appetite (97% reported improvement), pain (improved in 94% of the patients with pain), nausea (93% reported improvement) and anxiety (93% reported improvement).138”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > HIV-associated neuropathy
What the sources say
- Not checked yetcites [138] Woolridge, 2005, Cannabis use in HIV for pain and other medical symptoms, J Pain Symptom Manage source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The benefits of Δ9-THC and nabilone for the treatment of chemotherapy-induced nausea and vomiting have also been validated.140, 141”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > HIV-associated neuropathy
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“It may act as a high potency antagonist of cannabinoid agonists and an inverse agonist at CB2 receptors.144”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
What the sources say
- Not checked yetcites [144] Mechoulam, 2007, Cannabidiol—recent advances, Chem Biodivers source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Systemic WIN55,212-2, administered from days 18-21 post infection, fully reversed mechanical allodynia to baseline levels in this model of post herpetic neuralgia, although pharmacological specificity was not assessed.131”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Post Herpetic Neuralgia
What the sources say
- Not checked yetcites [131] Hasnie, 2007, Further characterization of a rat model of varicella zoster virus-associated pain: Relationship between mechanical hypersensitivity and anxiety-related behavior, and the influence of analgesic drugs, Neuroscience source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The PEA analogue L-29 suppressed mechanical allodynia in this model with an earlier onset relative to gabapentin.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Nociception in Animal Models > Post Herpetic Neuralgia
What the sources say
- Not checked yetcites [64] Wallace, 2007, The effect of the palmitoylethanolamide analogue, palmitoylallylamide (L-29) on pain behaviour in rodent models of neuropathy, Br J Pharmacol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Additionally, patients did not increase the titration of their dose indicating that no tolerance developed to Sativex®.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
What the sources say
- Not checked yetcites [147] Rog, 2007, Oromucosal delta9-tetrahydrocannabinol/cannabidiol for neuropathic pain associated with multiple sclerosis: an uncontrolled, open-label, 2-year extension trial, Clin Ther source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Cannador®, administered over a treatment period of 15 weeks, improved overall pain ratings as well as sleep quality, spasms, and spasticity on category-rating scales in patients suffering from MS-related neuropathic pain.143”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
What the sources say
- Not checked yetcites [143] Zajicek, 2003, Cannabinoids for treatment of spasticity and other symptoms related to multiple sclerosis (CAMS study): multicentre randomised placebo-controlled trial, Lancet source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Δ9-THC and Sativex®, but not placebo or CBD, reduced the VAS rating of the two worst pain symptoms during the crossover phase.156”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Mixed Neuropathic Pain
What the sources say
- Not checked yetcites [156] Notcutt, 2004, Initial experiences with medicinal extracts of cannabis for chronic pain: results from 34 ‘N of 1’ studies, Anaesthesia source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Both Δ9-THC and Sativex® reduced the primary outcome measure (Box-Scale 11 ordinal rating scale) in patients suffering from brachial plexus avulsion, indicating a reduction in pain symptoms versus placebo.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Brachial Plexus Avulsion-induced Neuropathy
What the sources say
- Not checked yetcites [150] Berman, 2004, Efficacy of two cannabis based medicinal extracts for relief of central neuropathic pain from brachial plexus avulsion: results of a randomised controlled trial, Pain source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, cannabinoid-based pharmacotherapies consistently show efficacy for suppressing pain due to multiple sclerosis, a disease state associated with an upregulation of CB2 receptors in microglia.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“CT-3 has limited CNS availability,69 which translates into fewer CB1-mediated side-effects.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Mixed Neuropathic Pain
What the sources say
- Not checked yetcites [69] Dyson, 2005, Antihyperalgesic properties of the cannabinoid CT-3 in chronic neuropathic and inflammatory pain states in the rat, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Twenty-five percent withdrew due to adverse events and 95% experienced one or more adverse events during the course of treatment.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
What the sources say
- Not checked yetcites [147] Rog, 2007, Oromucosal delta9-tetrahydrocannabinol/cannabidiol for neuropathic pain associated with multiple sclerosis: an uncontrolled, open-label, 2-year extension trial, Clin Ther source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Increased CB2 immunoreactivity has been reported in spinal cords derived from multiple sclerosis patients.149 Here, greater numbers of microglia/macrophage cells expressing CB2 immunoreactivity were observed relative to controls.149”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
What the sources say
- Not checked yetcites [149] Yiangou, 2006, COX-2, CB2 and P2X7-immunoreactivities are increased in activated microglial cells/macrophages of multiple sclerosis and amyotrophic lateral sclerosis spinal cord, BMC Neurol source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In this study, Sativex® reduced mechanical dynamic and punctate allodynia, and improved sleep disturbances.133”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Mixed Neuropathic Pain
What the sources say
- Not checked yetcites [133] Nurmikko, 2007, Sativex successfully treats neuropathic pain characterised by allodynia: a randomised, double-blind, placebo-controlled clinical trial, Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Δ9-THC and Sativex® additionally improved muscle spasms and spasticity severity.159”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Mixed Neuropathic Pain
What the sources say
- Not checked yetcites [159] Wade, 2003, A preliminary controlled study to determine whether whole-plant cannabis extracts can improve intractable neurogenic symptoms, Clin Rehabil source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Most doses of Sativex® were administered between 6 PM and 12 AM demonstrating that pain symptoms may be at their worst during normal sleeping hours for MS patients.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
What the sources say
- Not checked yetcites [147] Rog, 2007, Oromucosal delta9-tetrahydrocannabinol/cannabidiol for neuropathic pain associated with multiple sclerosis: an uncontrolled, open-label, 2-year extension trial, Clin Ther source
boostedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The NRS-11, completed at the end of the trial or upon withdrawal, was not different from the earlier randomized study indicating that Sativex® was still suppressing pain.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
What the sources say
- Not checked yetcites [147] Rog, 2007, Oromucosal delta9-tetrahydrocannabinol/cannabidiol for neuropathic pain associated with multiple sclerosis: an uncontrolled, open-label, 2-year extension trial, Clin Ther source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“A 21 patient study reported that ajulemic acid (CT-3) suppressed mixed forms of neuropathic pain, as assessed with the VAS, in the morning (3 hours after drug administration), but not in the afternoon (8 hours following drug administration).152”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Mixed Neuropathic Pain
What the sources say
- Not checked yetcites [152] Karst, 2003, Analgesic effect of the synthetic cannabinoid CT-3 on chronic neuropathic pain: a randomized controlled trial, JAMA source
plaindirectn = 21- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“CT-3 binds with high affinity to both CB1 and CB2 receptors and also binds with low affinity to PPARγ receptors.154”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Mixed Neuropathic Pain
What the sources say
- Not checked yetcites [154] Liu, 2003, Activation and binding of peroxisome proliferator-activated receptor gamma by synthetic cannabinoid ajulemic acid, Mol Pharmacol source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Smoking cannabis cigarettes also improved spontaneous pain relief and pain unpleasantness VAS ratings in patients suffering from mixed forms of neuropathic pain, but failed to alter stimulus-evoked pain.155”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Mixed Neuropathic Pain
What the sources say
- Not checked yetcites [155] Wilsey, 2008, A randomized, placebo-controlled, crossover trial of cannabis cigarettes in neuropathic pain, J Pain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Fifty-four percent of the patients completed one year and 44% of patients completed two years of the study.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Multiple Sclerosis-induced Neuropathic Pain
What the sources say
- Not checked yetcites [147] Rog, 2007, Oromucosal delta9-tetrahydrocannabinol/cannabidiol for neuropathic pain associated with multiple sclerosis: an uncontrolled, open-label, 2-year extension trial, Clin Ther source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Seventy-one percent of the patients tested chose to continue to the open label study of Sativex® with 63% withdrawing by the end of the study for various reasons.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Mixed Neuropathic Pain
What the sources say
- Not checked yetcites [133] Nurmikko, 2007, Sativex successfully treats neuropathic pain characterised by allodynia: a randomised, double-blind, placebo-controlled clinical trial, Pain source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Patients additionally reported improvements in sleep problems and disturbances while experiencing an increase in sleep adequacy in the open-label phase of the study.168”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Caveats
What the sources say
- Not checked yetcites [168] Narang, 2008, Efficacy of dronabinol as an adjuvant treatment for chronic pain patients on opioid therapy, J Pain source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“One study reported side-effects that were more prominent in older patients and did not correlate with analgesia.164”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Caveats
What the sources say
- Not checked yetcites [164] Attal, 2004, Are oral cannabinoids safe and effective in refractory neuropathic pain?, Eur J Pain source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“A recent systematic review of adverse effects of medical cannabinoids concluded that most adverse events (96.6%) were not serious and no serious adverse events were related exclusively to cannabinoid administration.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Side-effects
What the sources say
- Not checked yetcites [170] Wang, 2008, Adverse effects of medical cannabinoids: a systematic review, CMAJ source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The present review suggests that cannabinoids show promise for treatment of neuropathic pain in humans either alone or as an add-on to other therapeutic agents.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Conclusions
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The mean dose was 16.6 ± 6.5 mg oral dronabinol in one study164 and 15 ± 6 mg in the other study.165”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Caveats
What the sources say
- Not checked yetcites [164] Attal, 2004, Are oral cannabinoids safe and effective in refractory neuropathic pain?, Eur J Pain source
- Not checked yetcites [165] Clermont-Gnamien, 2002, The therapeutic use of D9-tetrahydrocannabinol (dronabinol) in refractory neuropathic pain, Presse Med
plainn = 8- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“However, the authors noted that a small number of subjects responded well to nabilone and side-effects were generally mild and in the expected range.166”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Caveats
What the sources say
- Not checked yetcites [166] Frank, 2008, Comparison of analgesic effects and patient tolerability of nabilone and dihydrocodeine for chronic neuropathic pain: randomised, crossover, double blind study, Bmj source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Patients in this study exhibited a mean baseline VAS rating of 69.6 mm on a 0-100 mm VAS scale; mean VAS ratings were 59.93 ± 24.42 mm and 58.58 ± 24.08 mm for patients taking nabilone and dihydrocodeine, respectively.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Caveats
What the sources say
- Not checked yetcites [166] Frank, 2008, Comparison of analgesic effects and patient tolerability of nabilone and dihydrocodeine for chronic neuropathic pain: randomised, crossover, double blind study, Bmj source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“In this study, most forms of neuropathic pain had similar prevalence rates and responsiveness to the different pharmacotherapies evaluated.169”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Side-effects
What the sources say
- Not checked yetcites [169] Toth, 2008, A prospective identification of neuropathic pain in specific chronic polyneuropathy syndromes and response to pharmacological therapy, Pain source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These studies have elucidated neuronal as well as nonneuronal (i.e. activated microglia) sites of action for cannabinoids in suppressing pathological pain states and documented regulatory changes in cannabinoid receptors and endocannabinoid accumulation in response to peripheral or central nervous system injury.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Conclusions
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Side-effects were equally associated with the different cannabinoid pharmacotherapies; the average rate of nonserious adverse events was higher in patients receiving Sativex® or oral Δ9-THC than controls. 170”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Side-effects
What the sources say
- Not checked yetcites [170] Wang, 2008, Adverse effects of medical cannabinoids: a systematic review, CMAJ source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, nonserious adverse events (e.g. dizziness), which pose the major limitation to patient compliance with pharmacotherapy, are not unique to cannabinoids.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Conclusions
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Combination therapies including a cannabinoid show efficacy for treatment-resistant neuropathic pain and may be employed to limit doses of analgesics or adjuvants associated with adverse side-effects.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Caveats
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“During the last two decades, a large number of research papers have demonstrated the efficacy of cannabinoids and modulators of the endocannabinoid system in suppressing neuropathic pain in animal models.”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Conclusions
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
In the paper
“A later study reported that 18% of the patients with spinal cord injuries reported pain relief following treatment with oral dronabinol (mean 31 mg per day), whereas 23% experienced enhancement of pain, resulting in subsequent withdrawal by several patients.163”
§ Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside > Cannabinoid Modulation of Neuropathic Pain in Clinical Studies > Mixed Neuropathic Pain
What the sources say
- Not checked yetcites [163] Hagenbach, 2007, The treatment of spasticity with Delta9-tetrahydrocannabinol in persons with spinal cord injury, Spinal Cord source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
Neuropathic pain is a debilitating form of chronic pain caused by damage to the nervous system, resulting from peripheral nerve injury, toxic insults, or disease states.
“Neuropathic pain is a debilitating form of chronic pain resulting from nerve injury, disease states, or toxic insults.”
The paper relies on this without support.
Neuropathic pain is often refractory to conventional pharmacotherapies, necessitating validation of novel analgesics.
“Neuropathic pain is often refractory to conventional pharmacotherapies, necessitating validation of novel analgesics.”
The paper relies on this without support.
Neuropathic pain responds poorly to available therapies and remains a significant clinical problem.
“Neuropathic pain remains a significant clinical problem because it responds poorly to available therapies.”
The paper relies on this without support.
Adverse side-effect profiles may limit therapeutic dosing and contribute to inadequate pain relief.
“Moreover, adverse side-effect profiles may limit therapeutic dosing and contribute to inadequate pain relief.”
The paper relies on this without support.
Activation of CB1 receptors suppresses neuronal excitability and transmitter release by suppressing calcium conductance and inhibiting inward rectifying potassium conductance.
“Activation of CB1 receptors suppresses calcium conductance and inhibits inward rectifying potassium conductance, thereby suppressing neuronal excitability and transmitter release.”
The paper relies on this without support.
Microglia secrete pro-inflammatory factors and induce the release of mediators associated with synaptogenesis and plasticity, leading to changes in neuronal excitability.
“Microglia secrete pro-inflammatory factors and induce the release of several mediators (e.g. nitric oxide (NO), neurotrophins, free radicals) that are associated with synaptogenesis and plasticity, leading to changes in neuronal excitability.”
The paper relies on this without support.
Spontaneous firing of wide dynamic range neurons contributes to behavioral hypersensitivity and neuronal sensitization in neuropathic pain states.
“Spontaneous firing of WDR neurons is believed to contribute to behavioral hypersensitivity and neuronal sensitization in neuropathic pain states.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Using complementary genetic and pharmacological approaches, distinct components of the endocannabinoid system (ie, receptors and endocannabinoid-regulating enzymes) have emerged as promising targets to treat neuropathic pain (Table 5; for additional information, Guindon and Hohmann, 2009;Rahn and Hohmann, 2009).”
From The endogenous cannabinoid system: a budding source of targets for treating inflammatory and neuropathic pain (2018) · cites this paper as Rahn and Hohmann, 2009
In the citing paper
“The endocannabinoid system plays a key role in pain mechanisms [42], and, previously, cannabinoids were long used by women to alleviate dysmenorrhea [45].”
From Endocannabinoid involvement in endometriosis. (2010) · cites this paper as [42]
Citations
Cites
Isolation and Structure of a Brain Constituent That Binds to the Cannabinoid Receptor
Devane, W. A., Hanuš, L., Breuer, A., Pertwee, R. G., Stevenson, L. A., Griffin, G., Gibson, D., Mandelbaum, A., Etinger, A., & Mechoulam, R. (1992) · Science · doi:10.1126/science.1470919 · Cited by 5,633
A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man
Bennett, G. J., & Xie, Y.-K. (1988) · Pain · doi:10.1016/0304-3959(88)90209-6 · Cited by 5,376
Molecular characterization of a peripheral receptor for cannabinoids
Munro, S., Thomas, K. L., & Abu-Shaar, M. (1993) · Nature · doi:10.1038/365061a0 · Cited by 5,092
Structure of a cannabinoid receptor and functional expression of the cloned cDNA
Matsuda, L. A., Lolait, S. J., Brownstein, M. J., Young, A. C., & Bonner, T. I. (1990) · Nature · doi:10.1038/346561a0 · Cited by 5,011
Ledent, C. A., Valverde, O., Cossu, G., Petitet, F., Aubert, J.-F., Beslot, F., Böhme, G. A., Impérato, A., Pedrazzini, T., Roques, B. P., et al. (1999) · Science · doi:10.1126/science.283.5400.401 · Cited by 3,628
Ho Kim, S., & Mo Chung, J. (1992) · Pain · doi:10.1016/0304-3959(92)90041-9 · Cited by 3,069
Mechoulam, R., Ben-Shabat, S., Hanus, L., Ligumsky, M., Kaminski, N. E., Schatz, A. R., Gopher, A., Almog, S., Martin, B. R., Compton, D. R., et al. (1995) · Biochemical Pharmacology · doi:10.1016/0006-2952(95)00109-d · Cited by 2,913
Isolation, Structure, and Partial Synthesis of an Active Constituent of Hashish
Gaoni, Y., & Mechoulam, R. (1964) · Journal of the American Chemical Society · doi:10.1021/ja01062a046 · Cited by 2,389
Spared nerve injury: an animal model of persistent peripheral neuropathic pain
Décosterd, I., & Woolf, C. J. (2000) · Pain · doi:10.1016/s0304-3959(00)00276-1 · Cited by 2,317
2-Arachidonoylgylcerol: A Possible Endogenous Cannabinoid Receptor Ligand in Brain
Sugiura, T., Kondo, S., Sukagawa, A., Nakane, S., Shinoda, A., Itoh, K., Yamashita, A., & Waku, K. (1995) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1995.2437 · Cited by 2,196
Cited by
Sorted by citations
Taming THC: potential cannabis synergy and phytocannabinoid-terpenoid entourage effects.
Russo, E. B. (2011) · British Journal of Pharmacology · doi:10.1111/j.1476-5381.2011.01238.x · Cited by 1,535
Slominski, A. T., Zmijewski, M. A., Skobowiat, C., Zbytek, B., Slominski, R. M., & Steketee, J. D. (2012) · Advances in anatomy, embryology and cell biology · doi:10.1007/978-3-642-19683-6 · Cited by 505
Slominski (2012) · doi:10.1007/978-3-642-19683-6_1 · Cited by 461
Is lipid signaling through cannabinoid 2 receptors part of a protective system?
Pacher, P., & Mechoulam, R. (2011) · Progress in Lipid Research · doi:10.1016/j.plipres.2011.01.001 · Cited by 435
Modulating the endocannabinoid system in human health and disease – successes and failures
Pacher, P., & Kunos, G. (2013) · FEBS Journal · doi:10.1111/febs.12260 · Cited by 418
Metadata
- Authors
- Rahn, E. J., & Hohmann, A. G.
- Affiliations
- University of Georgia (US)
- Corresponding author
- Hohmann, Andrea G.
- ORCID
- Hohmann, Andrea G.
- Venue
- Neurotherapeutics
- Publisher
- Elsevier BV
- Published
- 2009-10
- Volume
- 6
- Issue
- 4
- Pages
- 713-737
- ISSN
- 1878-7479 (ISSN-L)
- PMC
- PMC2755639
- OpenAlex
- W2020010905
- Semantic Scholar
- 7daf2b1153c0a36249f6f7c9b8f70b259a9da126
- Cited by
- 305
- References
- 187
- Citations by year
- 2026: 9 · 2025: 7 · 2024: 14 · 2023: 17 · 2022: 18 · 2021: 25 · 2020: 22 · 2019: 17 · 2018: 19 · 2017: 22 · 2016: 26 · 2015: 20 · 2014: 24 · 2013: 15 · 2012: 20
- FWCI
- 1.71
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neurotherapeutics (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Psi Chi
- National Institute on Drug Abuse (DA022478, R21DA022478, R01DA021644, DA021644)
- Topics
- Health Sciences › Medicine › Pharmacology (medical) › Cannabis and Cannabinoid Research
- Health Sciences › Medicine › Physiology (medical) › Pain Mechanisms and Treatments
- Health Sciences › Medicine › Anesthesiology and Pain Medicine › Pain Management and Treatment
- Keywords
- cannabinoids, neuropathic pain, delta-9-tetrahydrocannabinol, endocannabinoid system, CB1 receptor, CB2 receptor, CB2 receptor agonist, endocannabinoid degradation, nerve injury, diabetic neuropathy, chemotherapy-induced peripheral neuropathy, HIV neuropathy, multiple sclerosis, herpes zoster, allodynia, hyperalgesia, cannabis smoking, Marinol, Sativex, analgesia
- MeSH terms
- Animals, Cannabinoids, Chronic Disease, Disease Models, Animal, Humans, Neuralgia, Peripheral Nervous System Diseases, Receptors, Cannabinoid, Cannabinoid Receptor Modulators
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-09, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-09 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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