The DOI matches its Crossref record; 25 of the 25 references it cites were found in a registry or an index; 16 of the 32 sources its claims cite were checked for support.
Loss of hypocretin (orexin) neurons with traumatic brain injury
Open accessAbstract
Chronic, daytime sleepiness is a major, disabling symptom for many patients with traumatic brain injury (TBI), but thus far, its etiology is not well understood. Extensive loss of the hypothalamic neurons that produce the wake‐promoting neuropeptide hypocretin (orexin) causes the severe sleepiness of narcolepsy, and partial loss of these cells may contribute to the sleepiness of Parkinson disease and other disorders. We have found that the number of hypocretin neurons is significantly reduced in patients with severe TBI. This observation highlights the often overlooked hypothalamic injury in TBI and provides new insights into the causes of chronic sleepiness in patients with TBI. Ann Neurol 2009;66:555–559
Overview
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Written from the paper’s full text.
TL;DR
In postmortem hypothalami from 4 patients with severe TBI versus 4 controls, hypocretin neuron number was significantly reduced by 27%. This suggests that hypothalamic hypocretin neuron loss may contribute to chronic sleepiness after TBI.
Key findings
- TBI subjects had 27% fewer hypocretin neurons than controls (23,655 ± 5,035 vs. 32,318 ± 3,060 neurons, p = 0.001).
- MCH neurons were 31% fewer in TBI subjects (39,540 ± 10,900 vs. 57,176 ± 24,016), but this was not quite statistically significant (p = 0.06); excluding one female control with low MCH neuron numbers, TBI subjects had 29% fewer hypocretin neurons (p = 0.002) and 40% fewer MCH neurons (p = 0.003).
- GFAP-labeled astrocyte density was higher in TBI patients than controls (21 ± 12 vs. 7 ± 2 per mm², p < 0.001), and patients with more severe hypocretin neuron loss had more GFAP-labeled astrocytes (r = −0.46, p = 0.01).
- TBI hypothalami also showed intense perivascular hypocretin immunoreactivity, and many hypocretin neurons were small and pyknotic with reduced hypocretin fiber density.
Methods
- Autopsy brains from 4 patients who died 7 to 42 days (mean 19) after severe TBI and 4 control subjects with no clinical evidence of TBI or other neurological disorders; TBI patients were younger (51 ± 19 years) than controls (69 ± 18 years), and all subjects were male except one woman in the control group.
- Immunohistochemistry for hypocretin-1, MCH, and GFAP; hypocretin and MCH neurons were counted across a 1:24 series of the entire hypothalamus with Abercrombie correction, and GFAP-immunolabeled astrocytes were counted in 30 randomly selected 400 by 400 µm sites within the lateral and posterior hypothalamus.
- Cell counts were compared between groups using Student’s t-tests.
Limitations
- Stated by the paper: the study examined a small number of brains, control subjects were not fully matched, other wake-promoting systems were not examined, and the patients had fatal TBI, probably introducing selection bias; non-fatal TBI may be associated with less severe hypocretin neuron loss.
- Evident from the text: this is described as a pilot study with severe/fatal TBI cases, so findings may not generalize to milder or non-fatal TBI, and the autopsy design cannot directly establish that hypocretin loss causes chronic sleepiness.
Model-written summary. Check it against the paper before relying on it.
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Claims the paper makes
16 of 32 cited sources checked · 3 supported · 0 flagged · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Injury to ascending arousal pathways from the brainstem may contribute, but recent findings suggest a key role for the neuropeptides hypocretin-1 and -2 (also known as orexin-A and -B).2,4,5”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Introduction
What the sources say
- Partly supportedcites [2] Baumann CR Werth E Stocker R Sleep-wake disturbances 6 months after traumatic brain injury: a prospective study Brain 2007 130 1873 1883 17584779 sourceExperimental — accuracy not yet measured
The section on clinical characteristics and potential causes proposes that TBI may damage hypocretin neurons or their axons, contributing to post-traumatic sleepiness. It does not identify injury to ascending arousal pathways from the brainstem as that mechanism. The risk-factors section reports no association between lesion location and sleep-wake disturbances; outcomes in patients with visible brainstem or hypothalamic lesions did not differ from those of other patients. Page numbers were not available in our copy. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [4] Baumann CR Stocker R Imhof HG Hypocretin-1 (orexin A) deficiency in acute traumatic brain injury Neurology 2005 65 147 149 16009905 source
- Partly supportedcites [5] España RA Scammell TE Sleep neurobiology for the clinician Sleep 2004 27 811 820 15283019 sourceExperimental — accuracy not yet measured
The review’s Arousal Network section says lesions of the rostral reticular formation can disrupt wakefulness because they also damage arousal fibers. Its introductory discussion reports excessive sleepiness after injury to wake-promoting regions, but it does not establish that brainstem pathway injury contributes to chronic sleepiness specifically after head trauma. Page numbers are unavailable in our copy. (LLM, conf=0.84)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Even after 6 months recovery, many TBI patients with EDS have persistently low hypocretin-1 levels.2”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Introduction
What the sources say
- Partly supportedcites [2] Baumann CR Werth E Stocker R Sleep-wake disturbances 6 months after traumatic brain injury: a prospective study Brain 2007 130 1873 1883 17584779 sourceExperimental — accuracy not yet measured
The Laboratory studies section reports that hypocretin-1 remained low in 4 of 21 patients at six months, while it was normal in 17. The Clinical characteristics section says levels were lower in patients with EDS, but does not establish that many patients with EDS had persistently low levels. The claim overstates the prevalence of persistent deficiency. (LLM, conf=0.88)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Selective loss of the hypocretin-producing neurons causes sleepiness and cataplexy in over 90% of patients with narcolepsy,5–9”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Introduction
What the sources say
- Partly supportedcites [5] España RA Scammell TE Sleep neurobiology for the clinician Sleep 2004 27 811 820 15283019 sourceExperimental — accuracy not yet measured
The Orexin/Hypocretin section (page unavailable) links loss of orexin neurons to difficulty maintaining wakefulness and describes cataplexy with deficient orexin signaling. But its figure is about 90% of patients with narcolepsy *and cataplexy* having undetectable cerebrospinal-fluid orexin—not over 90% of all patients with narcolepsy having selective neuronal loss that causes both symptoms. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [6] Adamantidis AR Zhang F Aravanis AM Neural substrates of awakening probed with optogenetic control of hypocretin neurons Nature 2007 450 420 424 17943086 PMC6744371 source
- Not checked — no full text of the sourcecites [7] Peyron C Faraco J Rogers W A mutation in a case of early onset narcolepsy and a generalized absence of hypocretin peptides in human narcoleptic brains Nat Med 2000 6 991 997 10973318 source
- Not checked — no full text of the sourcecites [8] Thannickal TC Moore RY Nienhuis R Reduced number of hypocretin neurons in human narcolepsy Neuron 2000 27 469 474 11055430 PMC8760623 source
- Partly supportedcites [9] Crocker A España RA Papadopoulou M Concomitant loss of dynorphin, NARP, and orexin in narcolepsy Neurology 2005 65 1184 1188 16247044 PMC2254145 sourceExperimental — accuracy not yet measured
The Conclusions (page unavailable) say that narcolepsy with cataplexy is likely caused by loss of orexin-producing neurons, and the Discussion links disrupted orexin signaling to sleepiness and cataplexy. The paper does not establish that this occurs in over 90% of patients: its Results report roughly 90% or greater neuron loss in two people with narcolepsy and cataplexy, not a percentage of patients. (LLM, conf=0.87)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Coma and obtundation are common during the acute period, but even after 6 months recovery, 43% of patients have symptoms of sleep disorders.2,3”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Introduction
What the sources say
- Partly supportedcites [2] Baumann CR Werth E Stocker R Sleep-wake disturbances 6 months after traumatic brain injury: a prospective study Brain 2007 130 1873 1883 17584779 sourceExperimental — accuracy not yet measured
The Fig. 3 caption (Single patient reports; page unavailable) reports that 28 of 65 patients (43%) had sleep–wake disturbances for which no cause other than traumatic brain injury was identified. But it reports sleep–wake disturbances in 47 of 65 patients overall, so 43% is the rate for a narrower group, not the overall rate implied by the claim. (LLM, conf=0.88)
- Partly supportedcites [3] Castriotta RJ Wilde MC Lai JM Prevalence and consequences of sleep disorders in traumatic brain injury J Clin Sleep Med 2007 3 349 356 17694722 PMC1978308 sourceExperimental — accuracy not yet measured
The Discussion reports that 47% of the TBI sample had a diagnosed sleep disorder, and Table 4 includes patients studied more than six months after injury. It does not report that 43% had symptoms after six months of recovery; the stated percentage, measure, and time-specific estimate are unsupported. (LLM, conf=0.84)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Partly supported
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
“Double immunofluorescence staining showed that patients with more severe loss of hypocretin neurons had more GFAP-labeled astrocytes (r=−0.46, p=0.01).”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Results
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA 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
“Though TBI brains contained fewer hypocretin neurons, the neurons were distributed in a normal pattern, thus demonstrating the reliability and completeness of the cell counts (Figure 2).”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Results
Strength:boosted· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA 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
“The number of hypocretin neurons in TBI subjects was 27% less than in controls (23,655±5,035 vs. 32,318±3,060 neurons, p = 0.001) (Figure 1).”
- Also stated in: § Abstract · plain
“We have found that the number of hypocretin neurons is significantly reduced in patients with severe TBI.”
- Also stated in: § Discussion · plain
“In this pilot study, we found that patients with severe TBI have a significant loss of hypocretin-producing neurons.”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Abstract · plain
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
“The density of astrocytes as assessed by GFAP staining was significantly higher (21±12 vs. 7±2 per mm2, p<0.001) in TBI patients than in controls (Supplemental Figure B).”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Results
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA 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
“This amorphous staining was present around small vessels in the posterior and lateral hypothalamus but not elsewhere.”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Results
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA 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
“Hypothalami from TBI patients also contained intense perivascular hypocretin immunoreactivity (Figure 3).”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Results
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes
- Probably not a substantial claim. 17
- It may state two separate claims as one. 14
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“and identical symptoms occur in mice genetically lacking hypocretins.10”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Introduction
What the sources say
- Partly supportedcites [10] Chemelli RM Willie JT Sinton CM Narcolepsy in orexin knockout mice: molecular genetics of sleep regulation Cell 1999 98 437 451 10481909 sourceExperimental — accuracy not yet measured
The Discussion reports that mice lacking orexin (hypocretin) have narcoleptic attacks and sleep dysregulation remarkably similar to human narcolepsy. It does not establish that the symptoms are identical: the authors say they cannot clearly distinguish the mice’s narcoleptic from cataplectic episodes and note an EEG feature not reported in humans or dogs. (LLM, conf=0.82)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Chronic, daytime sleepiness is a major, disabling symptom for many patients with traumatic brain injury (TBI), but thus far, its etiology is not well understood.”
- Also stated in: § Introduction · plain
“Though chronic sleepiness is common after head trauma, the cause remains unclear.”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Abstract
What the sources say
- Supportedcites [2] Baumann CR Werth E Stocker R Sleep-wake disturbances 6 months after traumatic brain injury: a prospective study Brain 2007 130 1873 1883 17584779 source
The Clinical characteristics and potential causes section reports excessive daytime sleepiness in 38% of patients six months after TBI. The quality-of-life section says that sleep–wake complaints, particularly daytime sleepiness, significantly affect quality of life and social functioning; the Circadian sleep–wake disorders section says their neurobiological bases are unknown. Page numbers are unavailable in our copy. (LLM, conf=0.91)
- Partly supportedcites [3] Castriotta RJ Wilde MC Lai JM Prevalence and consequences of sleep disorders in traumatic brain injury J Clin Sleep Med 2007 3 349 356 17694722 PMC1978308 sourceExperimental — accuracy not yet measured
The Discussion reports a high prevalence of excessive daytime sleepiness after TBI and poorer cognitive and vigilance performance in sleepy subjects. It says functional disability is possible but that the impact on day-to-day functioning has not been established; it also cannot determine whether some sleep disorders preceded the injury. The paper therefore supports the prevalence and uncertainty about cause, but not the stronger claim that chronic sleepiness is an established major disabling symptom. (LLM, conf=0.85)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Introduction · plain
Every source the paper cites for this claim was checked and supports it.
In the paper
“In a prospective study of 65 TBI patients, 1 in 4 patients reported excessive daytime sleepiness (EDS) irrespective of the location or severity of the head trauma.2”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Introduction
What the sources say
- Supportedcites [2] Baumann CR Werth E Stocker R Sleep-wake disturbances 6 months after traumatic brain injury: a prospective study Brain 2007 130 1873 1883 17584779 source
The Abstract (page unavailable) reports 65 patients and subjective excessive daytime sleepiness in 18 (28%), consistent with roughly one in four patients reporting EDS. The Identification of risk factors section (page unavailable) reports no association between injury localization and post-traumatic sleep–wake disturbances, and says severe TBI was not associated with disturbances other than hypersomnia. (LLM, conf=0.90)
Strength:plain· not yet calibratedn = 65Tests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Another study of 87 patients revealed similar results, with sleepiness in 25% after TBI.3”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Introduction
What the sources say
- Supportedcites [3] Castriotta RJ Wilde MC Lai JM Prevalence and consequences of sleep disorders in traumatic brain injury J Clin Sleep Med 2007 3 349 356 17694722 PMC1978308 source
The Results report 87 TBI subjects, and Table 1 lists 22 (25%) in the sleepy group, defined by an MSLT score below 10. The Discussion likewise reports excessive daytime sleepiness in approximately 26% of the sample. (LLM, conf=0.94)
Strength:plain· not yet calibratedn = 87Tests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Hypocretins are made by a small cluster of neurons in the lateral hypothalamus that play an essential role in promoting wakefulness.”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Introduction
What the sources say
- Partly supportedcites [5] España RA Scammell TE Sleep neurobiology for the clinician Sleep 2004 27 811 820 15283019 sourceExperimental — accuracy not yet measured
The Orexin/Hypocretin section says hypocretins are produced by neurons in the lateral and posterior hypothalamus and that these neurons play an essential role in stabilizing wakefulness. It does not establish that they form a small cluster, and it names the posterior hypothalamus as well as the lateral hypothalamus. (LLM, conf=0.79)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In controls, the total number of hypocretin neurons and their distribution across the lateral and posterior hypothalamus were similar to prior reports.7,8,14,15”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Results
What the sources say
- Not checked — no full text of the sourcecites [7] Peyron C Faraco J Rogers W A mutation in a case of early onset narcolepsy and a generalized absence of hypocretin peptides in human narcoleptic brains Nat Med 2000 6 991 997 10973318 source
- Not checked — no full text of the sourcecites [8] Thannickal TC Moore RY Nienhuis R Reduced number of hypocretin neurons in human narcolepsy Neuron 2000 27 469 474 11055430 PMC8760623 source
- Partly supportedcites [14] Fronczek R Overeem S Lee SY Hypocretin (orexin) loss in Parkinson's disease Brain 2007 130 1577 1585 17470494 sourceExperimental — accuracy not yet measured
The Hypocretin-1 cell number section reports a control median of 36,842 neurons, and the Hypocretin-1 histochemistry section says their distribution matched an earlier description in the perifornical lateral hypothalamus. Our copy does not compare the control total with prior reports or explicitly describe a distribution across both the lateral and posterior hypothalamus. Page numbers were not available in the indexed passages. (LLM, conf=0.83)
- Partly supportedcites [15] Thannickal TC Lai YY Siegel JM Hypocretin (orexin) cell loss in Parkinson's disease Brain 2007 130 1586 1595 17491094 PMC8762453 sourceExperimental — accuracy not yet measured
The Materials and methods and Quantitative analysis sections say the authors examined five normal brains and determined hypocretin-cell number and distribution. The passages available from our copy do not give a total control-neuron count or say that the count and lateral/posterior hypothalamic distribution were similar to prior reports (pages not provided). (LLM, conf=0.70)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Other reports describe pituitary and hypothalamic dysfunction,17,18”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Discussion
What the sources say
- Partly supportedcites [17] Karavitaki N Wass J Henderson Slater JD Wade D A case of post-traumatic isolated ACTH deficiency with spontaneous recovery 9 months after the event J Neurol Neurosurg Psychiatry 2006 77 276 277 16421141 PMC2077606 sourceExperimental — accuracy not yet measured
The case report describes isolated ACTH deficiency after traumatic brain injury, supporting pituitary dysfunction. The Discussion mentions the hypothalamus as a possible site of injury but does not report hypothalamic dysfunction; page numbers are unavailable in our copy. (LLM, conf=0.83)
- Not checked — no full text of the sourcecites [18] Schneider HJ Aimaretti G Kreitschmann-Andermahr I Hypopituitarism Lancet 2007 369 1461 1470 17467517 source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
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 pattern of gliosis differed across the TBI patients.”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Results
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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
“Many hypocretin neurons in TBI patients were small and pyknotic, and the density of hypocretin fibers appeared reduced.”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Results
Load-bearingStrength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“Among the TBI patients, the number of hypocretin neurons differed moderately between the left and right sides of the hypothalamus and between individuals, reflecting the asymmetry and heterogeneity of TBI.”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Results
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt 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
“However, our TBI patients had significantly fewer hypocretin neurons even though they were younger than the controls.”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“TBI patients also had 31% fewer MCH neurons than controls (39,540±10,900 vs. 57,176±24,016), but this reduction was not quite statistically significant (p = 0.06), probably because of variable numbers of MCH neurons.”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Results
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt 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
“If one excludes the female control subject with surprisingly low numbers of MCH neurons (control subject 2), then the TBI subjects had 29% fewer hypocretin neurons than controls (33,342±2,785; p=0.002) and 40% fewer MCH neurons (66,434±18,730; p=0.003).”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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 perivascular staining may represent phagocytized hypocretin peptide following damage to the hypocretin neurons.”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Results
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“In addition, we did not examine other wake-promoting systems, and the extent of injury to other arousal pathways should be further investigated in larger human and animal studies.”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Discussion
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“We examined a small number of brains, and the control subjects were not fully matched.”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Discussion
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“One early study showed damage to the hypothalamus in 42% of deceased TBI patients.11”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Discussion
What the sources say
- Not checked — no full text of the sourcecites [11] Crompton MR Hypothalamic lesions following closed head injury Brain 1971 94 165 172 5552160 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“In this pilot study, the TBI patients were younger (51 ± 19 years) than the controls (69 ± 18 years), and all subjects were male except for one woman in the control group.”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Results
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“To estimate accurately the numbers of hypocretin and MCH neurons in each section, we performed Abercrombie corrections based on the size of the cell nuclei in each subject.13”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Methods > Cell counts
What the sources say
- Not checked — no full text of the sourcecites [13] Guillery RW On counting and counting errors J Comp Neurol 2002 447 1 7 11967890 source
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Postmortem delays were similar in both groups (TBI: 12±3 hours, controls: 13±3 hours) (Supplemental Table).”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Results
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Only clearly-immunolabeled neurons with neuronal morphology, outgoing axons and dendrites, and a nuclear void were counted.”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Methods > Cell counts
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
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
“This injury was not limited to the hypocretin neurons as there was a partial loss of neurons producing MCH and patchy gliosis throughout the hypothalamus.”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“It is possible that non-fatal TBI is associated with a less severe loss of hypocretin neurons.”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Discussion
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
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In the paper
“To prevent miscounting, we used a fine-scale counting grid that encompassed no more than 10 neurons per grid sector.”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Methods > Cell counts
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Hypersomnolence is common with hypothalamic and rostral brainstem injuries, but is uncommon with selective loss of the hypocretin neurons.21”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Discussion
What the sources say
- Not matchedcites [21] Scammell TE Culebras A Secondary Narcolepsy Sleep Disorders and Neurologic Diseases 2007 2nd edition New York Informa Healthcare 117 134
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Not matched
In the paper
“About one-third of TBI patients have brainstem injuries, often near the midbrain tegmentum, that may disrupt ascending monoaminergic or cholinergic wake-promoting pathways.20”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Discussion
What the sources say
- Not checked — no full text of the sourcecites [20] Crompton MR Brainstem lesions due to closed head injury Lancet 1971 1 669 673 4101614 source
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Though TBI brains contained fewer hypocretin neurons, the neurons were distributed in a normal pattern, thus demonstrating the reliability and completeness of the cell counts (Figure 2).”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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In the paper
“In all subjects, the complete hypocretin neuron field was examined (Supplemental Figure A).”
§ Loss of hypocretin (orexin) neurons with traumatic brain injury > Results
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
The authors state this as an assumption.
Partial loss of hypocretin neurons causes the generally milder sleepiness of narcolepsy without cataplexy and Parkinson's disease.
“some hypothesize that a partial loss of these cells causes the generally milder sleepiness of narcolepsy without cataplexy and Parkinson’s disease.14,15,19”
“This assumption is supported by our recent finding of reduced CSF hypocretin-1 levels in sleepy TBI patients who survived their injury.2”
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?
The cited source says what the claim attributes to it.
In the citing paper
“Baumann et al. 2009 found that in 4 TBI patients, the number of hypocretin neurons was decreased by 27% compared to controls.47”
From Effects of Traumatic Brain Injury on the Orexin/Hypocretin System (2025) · cites this paper as [47]
The cited source says what the claim attributes to it.
In the citing paper
“some studies have evidence of reduced numbers of MCH neurons after injury. However, this outcome was observed after severe TBI,46,47”
From Effects of Traumatic Brain Injury on the Orexin/Hypocretin System (2025) · cites this paper as [47]
Citations
Cites
Narcolepsy in orexin Knockout Mice
Chemelli, R. M., Willie, J. T., Sinton, C. M., Elmquist, J. K., Scammell, T., Lee, C., Richardson, J. A., Williams, S. C., Xiong, Y., Kisanuki, Y., et al. (1999) · Cell · doi:10.1016/s0092-8674(00)81973-x · Cited by 3,095 · cited 1×
“Selective loss of the hypocretin-producing neurons causes sleepiness and cataplexy in 90% of patients with narcolepsy, and identical symptoms occur in mice genetically lacking hypocretins.(10) Injury to the hypothalamus is common in patients with TBI,(11) but its clinical impact remains unclear.”
BackgroundSelf-citationPeyron, C., Faraco, J., Rogers, W., Ripley, B., Overeem, S., Charnay, Y., Nevsimalova, S., Aldrich, M., Reynolds, D., Albin, R., et al. (2000) · Nature Medicine · doi:10.1038/79690 · Cited by 2,118 · cited 1×
“In controls, the total number of hypocretin neurons and their distribution across the lateral and posterior hypothalamus were similar to prior reports.(7,8,14,15) Hypothalami from TBI patients also contained intense perivascular hypocretin immunoreactivity (Fig 3).”
ResultReduced Number of Hypocretin Neurons in Human Narcolepsy
Thannickal, T. C., Moore, R. Y., Nienhuis, R., Ramanathan, L., Gulyani, S., Aldrich, M., Cornford, M., & Siegel, J. M. (2000) · Neuron · doi:10.1016/s0896-6273(00)00058-1 · Cited by 2,089
Neural substrates of awakening probed with optogenetic control of hypocretin neurons
Adamantidis, A. R., Zhang, F., Aravanis, A. M., Deisseroth, K., & de Lecea, L. (2007) · Nature · doi:10.1038/nature06310 · Cited by 1,341
Incidence of Traumatic Brain Injury in the United States, 2003
Rutland-Brown, W., Langlois, J. A., Thomas, K. E., & Xi, Y. L. (2006) · Journal of Head Trauma Rehabilitation · doi:10.1097/00001199-200611000-00009 · Cited by 836
Hypocretin (orexin) cell loss in Parkinson's disease
Thannickal, T. C., Lai, Y.-Y., & Siegel, J. M. (2007) · Brain · doi:10.1093/brain/awm097 · Cited by 566 · cited 2×
“Clearly, extensive loss of hypocretin neurons is sufficient to cause the sleepiness of narcolepsy with cataplexy, and some hypothesize that a partial loss of these cells causes the generally milder sleepiness of narcolepsy without cataplexy and Parkinson disease.(14,15,19) This assumption is supported by our recent fi…”
ResultHypocretin (orexin) loss in Parkinson's disease
Fronczek, R., Overeem, S., Lee, S. Y. Y., Hegeman, I. M., van Pelt, J., van Duinen, S. G., Lammers, G. J., & Swaab, D. F. (2007) · Brain · doi:10.1093/brain/awm090 · Cited by 463 · cited 2×
“Clearly, extensive loss of hypocretin neurons is sufficient to cause the sleepiness of narcolepsy with cataplexy, and some hypothesize that a partial loss of these cells causes the generally milder sleepiness of narcolepsy without cataplexy and Parkinson disease.(14,15,19) This assumption is supported by our recent fi…”
ResultHassani, O. K., Lee, M. G., & Jones, B. E. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0811400106 · Cited by 451 · cited 1×
“Loss of the MCH neurons may also contribute to the pathophysiology of post-traumatic sleep-wake disturbances, as these cells are hypothesized to regulate rapid eye movement sleep.(22,23) Overall, it seems likely that the persistent sleepiness in some TBI patients is due to a combination of reduced hypocretin signaling…”
BackgroundSleep-wake disturbances 6 months after traumatic brain injury: a prospective study
Baumann, C. R., Werth, E., Stocker, R., Ludwig, S., & Bassetti, C. L. (2007) · Brain · doi:10.1093/brain/awm109 · Cited by 380 · cited 7×
“Injury to ascending arousal pathways from the brainstem may contribute, but recent findings suggest a key role for the neuropeptides hypocretin-1 and -2 (also known as orexin-A and -B).(2,4,5) Hypocretins are made by a small cluster of neurons in the lateral hypothalamus that play an essential role in promoting wakefu…”
BackgroundMethodResultInfluentialSelf-citationOn counting and counting errors
Guillery, R. W. (2002) · Journal of Comparative Neurology · doi:10.1002/cne.10221 · Cited by 343 · cited 1×
“To estimate accurately the numbers of hypocretin and MCH neurons in each section, we performed Abercrombie corrections based on the size of the cell nuclei in each subject.(13) We then calculated the total numbers of hypocretin and MCH neurons by multiplying the cell counts per section by the section sampling frequenc…”
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Items 101–185 of 185
Effects of intrathecal baclofen therapy in subjects with disorders of consciousness: a reappraisal
Nardone, R., Sebastianelli, L., Brigo, F., Golaszewski, S., Trinka, E., Pucks-Faes, E., Saltuari, L., & Versace, V. (2020) · Journal of neural transmission · doi:10.1007/s00702-020-02233-8 · Cited by 9
Sleep disorders in traumatic brain injury
Paredes, I., Navarro-Main, B., & Lagares, A. (2020) · Neurocirugía (English Edition) · doi:10.1016/j.neucie.2020.12.001 · Cited by 15
Treating sleep disorders following traumatic brain injury in adults: Time for renewed effort?
Stewart, K., Shakarishvili, N., Michalak, A., Maschauer, E. L., Jenkins, N. D., & Riha, R. L. (2022) · Sleep Medicine Reviews · doi:10.1016/j.smrv.2022.101631 · Cited by 12
Kousi, C., Lampri, E., Voulgaris, S., Vougiouklakis, T., Galani, V., & Mitselou, A. (2021) · Forensic Science International · doi:10.1016/j.forsciint.2021.110961 · Cited by 10
Christensen, J., MacPherson, N., Li, C. N., Yamakawa, G. R., & Mychasiuk, R. (2023) · The Journal of Headache and Pain · doi:10.1186/s10194-023-01608-y · Cited by 10
“The pathological reduction in hypothalamic volume following a severe TBI [65], and the 27% loss of orexinergic neurons post fatal TBIs comparatively [66], indicates the vulnerability of the orexinergic neurons to shearing forces [65].”
BackgroundSleep in traumatic brain injury
Mazwi, N., Fusco, H. N., & ZAFONTE, R. D. (2015) · Handbook of clinical neurology · doi:10.1016/b978-0-444-63521-1.00035-2 · Cited by 11
[Brazilian guidelines for the diagnosis of narcolepsy].
Aloe, F., Alves, R., Araújo, J., Azevedo, A., Bacelar, A., Bezerra, M., Bittencourt, L., Bustamante, G., Cardoso, T. A. M. D. O., Éckeli, Á., et al. (2010) · Revista Brasileira de Psiquiatria · doi:10.1590/s1516-44462010005000014 · Cited by 12
“narcoleptic patients to acquire access to stimulant medication or some other form of compensation.(52)”
BackgroundAnatomy and Physiology of Normal Sleep
Schneider, L. D. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-804074-4.00001-7 · Cited by 17
Sugeno, N., Kawaguchi, N., Hasegawa, T., et al. (2012) · Neurological Sciences · doi:10.1007/s10072-012-1009-x · Cited by 9
Chiu, H.-Y., Li, W., Lin, J.-H., Su, Y.-K., Lin, E.-Y., & Tsai, P.-S. (2018) · Brain Injury · doi:10.1080/02699052.2018.1432893 · Cited by 9
“Deficiency in CSF hypocretin has been found to be associated with increased sleep following acute TBI (41,42).”
BackgroundTan, L. P., Wang, N., Gu, Z., Zhu, J., Liu, C., & Xu, Z. (2021) · Evidence-based Complementary and Alternative Medicine · doi:10.1155/2021/6611461 · Cited by 10
“[53] found that the number of orexin neurons in the hypothalamus after TBI was 29% lower than that in a normal group, assessed through pathological examination of four patients who died because of TBI.”
BackgroundSleep Disorders in Traumatic Brain Injury
Kaleyias, J., & Kothare, S. V. (2022) · Journal of Clinical Neurophysiology · doi:10.1097/wnp.0000000000000661 · Cited by 10
Characteristics and Neural Mechanisms of Sleep–Wake Disturbances After Traumatic Brain Injury
Yan, G., Wei, Y., Wang, D., Wang, D., Ren, H., & Hou, B. (2024) · Journal of Neurotrauma · doi:10.1089/neu.2023.0647 · Cited by 7
“56,57 This is also reflected in the clinical features, which show that most patients with so-called post-TBI narcolepsy do not have typical cataplexy, but often have hypersomnia (as opposed to the normal amount of sleep per 24 h in narcolepsy patients).”
Jang, S. H., Kim, S., & Kwon, Y. H. (2018) · Frontiers in Neuroscience · doi:10.3389/fnins.2018.00348 · Cited by 9
Trastornos del sueño en el traumatismo craneoencefálico
Paredes, I., Navarro-Main, B., & Lagares, A. (2020) · Neurocirugía · doi:10.1016/j.neucir.2020.09.001 · Cited by 7
Neuropathology of Sudden Infant Death Syndrome: Hypothalamus
Waters, K. A., Hunt, N. J., & Machaalani, R. (2018) · University of Adelaide Press eBooks · doi:10.20851/sids-28 · Cited by 5
Ye, M., Solarana, K., Rafi, H., Patel, S., Nabili, M., Liu, Y., Huang, S., Fisher, J. A. N., Krauthamer, V., Myers, M. R., et al. (2019) · Scientific Reports · doi:10.1038/s41598-019-51876-5 · Cited by 6
Mannino, G. S., Green, T. R. F., Murphy, S. M., Sierks, M. R., Opp, M. R., & Rowe, R. K. (2025) · Neurobiology of Sleep and Circadian Rhythms · doi:10.1016/j.nbscr.2025.100127 · Cited by 6
Hoyer, D., & Jacobson, L. H. (2024) · Medicine in Drug Discovery · doi:10.1016/j.medidd.2024.100190 · Cited by 6
Sleep Disorders after Traumatic Brain Injury: Milestones in Perspective
Castriotta, R. J., & Wilde, M. C. (2015) · Springer eBooks · doi:10.1007/978-1-4939-2089-1_36 · Cited by 5
Christensen, J., Vlassopoulos, E., Barlow, C. K., Schittenhelm, R. B., Li, C. N., Sgro, M., Warren, S., Semple, B. D., Yamakawa, G. R., Shultz, S. R., et al. (2024) · Experimental Neurology · doi:10.1016/j.expneurol.2024.114969 · Cited by 4
“Moreover, given that both severe and mild TBI have been associated with a loss of orexin neurons (also known as hypocretin) (Baumann et al., 2009; Christensen et al., 2023a), this could explain modafinil ’ s ability to ameliorate excessive daytime sleepiness following TBI.”
BackgroundAnwer, M., Bolkvadze, T., Puhakka, N., Ndode‐Ekane, X. E., & Pitkänen, A. (2019) · Neuroscience · doi:10.1016/j.neuroscience.2019.07.040 · Cited by 4
Sleep disturbance in specific neurodevelopmental disorders
Stores, G. (2014) · Cambridge University Press eBooks · doi:10.1017/cbo9780511972935.005 · Cited by 4
Narcolepsy and Idiopathic Hypersomnia
Ahmed, I., & Thorpy, M. J. (2011) · Humana Press eBooks · doi:10.1007/978-1-60761-735-8_16 · Cited by 4
“A 2007 study found that the CSF hypocretin-1 levels were decreased in these TBI patients, and a follow-up study in 2009 demonstrated the number of hypocretin neurons in the hypothalamus was signifi cantly reduced [ 53, 54 ] .”
BackgroundSherman, D. L., Williams, A., Sahithi, G. D., et al. (2021) · Critical Care Explorations · doi:10.1097/cce.0000000000000349 · Cited by 3
“Our studies on asphyxial cardiac arrest (24, 25) and cardiopulmonary resuscitation (CPR) (15, 16) were approved by the Animal Care and Use Committee of the Johns Hopkins Medical Institutions (protocol number RA19M498).”
MethodGerald, B., Ortiz, J. B., Green, T. R. F., Brown, S. D., Adelson, P. D., Murphy, S. M., & Rowe, R. K. (2022) · Biology · doi:10.3390/biology11040600 · Cited by 3
“Using a mouse model, we previously demonstrated that altered sleep after a diffuse TBI was temporally associated with inflammation and elevated cytokines [62,70,71].”
BackgroundSleep Disturbances Following Traumatic Brain Injury
Mathews, A. A., Halsey, S. L., & Bell, K. R. (2022) · Current Physical Medicine and Rehabilitation Reports · doi:10.1007/s40141-022-00351-w · Cited by 3
Dickerman, R. D., Williamson, J., & Mathew, E. (2020) · Neurosurgery · doi:10.1093/neuros/nyaa518 · Cited by 3
Primary and Secondary Neurogenic Hypersomnias
Bassetti, C. L. (2012) · Sleep Medicine Clinics · doi:10.1016/j.jsmc.2012.03.016 · Cited by 3
Self-citationOuellet, M., Beaulieu‐Bonneau, S., & Morin, C. M. (2019) · Elsevier eBooks · doi:10.1016/b978-0-12-813014-8.00010-x · Cited by 3
Effects of Traumatic Brain Injury on the Orexin/Hypocretin System
Somach, R. T., Lim, M. M., & Cohen, A. S. (2025) · Neurotrauma Reports · doi:10.1089/neur.2024.0111 · Cited by 2
“Baumann et al. 2009 found that in 4 TBI patients, the number of hypocretin neurons was decreased by 27% compared to controls.”
InfluentialJoão, R. B., Pacheco-Barrios, N. V., Leite, M. G. H. S. J., Soares, Y. R. R. G., Bakir, Z. E., Veiga, M. E., & Dantas, J. M. (2025) · Brain Injury · doi:10.1080/02699052.2025.2502424 · Cited by 3
Awakening Recovery: Enhancing Orexinergic Tone After Acute CNS Damage
Otero-López, P., Madrid-González, X., Fernández‐Dueñas, V., & Flores, Á. (2025) · Pharmaceuticals · doi:10.3390/ph18121879 · Cited by 2
“Post-mortem analysis shows reduced orexin immunoreactivity, consistent with functional suppression or structural loss of lateral-hypothalamic neurons [93].”
The interplay between neuroendocrine and sleep alterations following traumatic brain injury
Howell, S., & Griesbach, G. S. (2018) · Neurorehabilitation · doi:10.3233/nre-182483 · Cited by 2
More than a bump to the head: An overview of the long-term effects of concussion
Coffman, C. A., Covassin, T., & Pontifex, M. B. (2024) · The Psychology of learning and motivation/The psychology of learning and motivation · doi:10.1016/bs.plm.2024.06.003 · Cited by 2
Singh, K., & Kothare, S. V. (2016) · Springer eBooks · doi:10.1007/978-3-319-41742-4_12 · Cited by 2
Bassetti, C. L. (2011) · Springer eBooks · doi:10.1007/978-1-4419-8390-9_29 · Cited by 4
“Traumatic brain injury (acute phase) [39, 75–77]”
Self-citationTraumatic Brain Injury and Sleep-Wake Disorders
Baumann, C. R. (2012) · Sleep Medicine Clinics · doi:10.1016/j.jsmc.2012.08.002 · Cited by 2
Self-citationPost-Traumatic Narcolepsy Associated with Thalamic/Hypothalamic Injury
Yi, K., Chung, S., Park, B., & Kim, J. S. (2015) · Sleep Medicine Research · doi:10.17241/smr.2015.6.2.81 · Cited by 2
Pathophysiology of Sleep-Wake Disturbances After Traumatic Brain Injury
Gosselin, N., & Baumann, C. R. (2016) · Elsevier eBooks · doi:10.1016/b978-0-323-24288-2.00025-8 · Cited by 4
Self-citationAnwer, M., Lara-Valderrábano, L., Karttunen, J., Ndode‐Ekane, X. E., Puhakka, N., & Pitkänen, A. (2019) · Journal of Neurotrauma · doi:10.1089/neu.2019.6739 · Cited by 2
“29,30 11 The lack of hypothalamic injury-specific biomarkers, however, limits the detection of TBI-induced endocrinopathy.”
Elliott, J. E., Brewer, J. S., Keil, A. T., Ligman, B. R., Bryant‐Ekstrand, M., McBride, A. A., Powers, K., Sicard, S. J., Twamley, E. W., O'Neil, M. E., et al. (2025) · PLoS ONE · doi:10.1371/journal.pone.0305305 · Cited by 2
Left Temporopolar Impairment in a Case of Posttraumatic Hypersomnia
Farisse, J., Guedj, É., Richieri, R. M., Cock, V. C. D., Lançon, C., & Boyer, L. (2013) · Journal of Head Trauma Rehabilitation · doi:10.1097/htr.0b013e3182803eda · Cited by 1
Alóe, F., Alves, R. C., Araújo, J. F., de Azevedo, A. P., Bacelar, A., Bezerra, M. L. D. S., Rita, L., Bittencourt, A. C. R., Bustamante, G., Éckeli, Á. L., et al. (2010) · Cited by 1
The Influence of Neuroendocrine and Sleep Disturbances on Recovery from Traumatic Brain Injury
Kreber, L. A. (2017) · Physical Medicine and Rehabilitation - International · doi:10.26420/physmedrehabilint.2017.1122
“A number of studies have identified hypothalamic abnormalities in patients with brain injury, more specifically, to the wake promoting hypocretin/orexin neurons concentrated within the hypothalamus [96,101,102].”
BackgroundSleep Disorders After Traumatic Brain Injury
Valko, P. O., & Baumann, C. R. (2016) · Elsevier eBooks · doi:10.1016/b978-0-323-24288-2.00099-4 · Cited by 1
Self-citationThe link between sleep and quality of life in childhood traumatic brain injury
Botchway-Commey, E. N., Godfrey, C., Ryan, N. P., Sood, N. T., Yumul, J. N., Anderson, V. A., & Catroppa, C. (2022) · Elsevier eBooks · doi:10.1016/b978-0-12-823036-7.00025-6 · Cited by 1
Sleep Issues and Mild Traumatic Brain Injury
Goldrich, D. Y., Woodson, B. T., Hundal, J. S., & Wackym, P. A. (2019) · Elsevier eBooks · doi:10.1016/b978-0-12-812344-7.00014-5 · Cited by 1
Ouellet, M., Beaulieu‐Bonneau, S., Savard, J., & Morin, C. M. (2019) · Elsevier eBooks · doi:10.1016/b978-0-12-811316-5.00001-x · Cited by 1
Wenn Belastungen zum Dauerzustand werden: Erschöpfung
Klösch, G., Hauschild, P., & Zeitlhofer, J. (2020) · Springer eBooks · doi:10.1007/978-3-662-59139-0_6 · Cited by 1
Esterov, D., & Schultz, B. A. (2020) · Elsevier eBooks · doi:10.1016/b978-0-323-65385-5.00046-9 · Cited by 1
SOMNOLENCE, FATIGUE ET FONCTIONNEMENT ATTENTIONNEL SUITE À UN TRAUMATISME CRANIOCÉRÉBRAL
Beaulieu‐Bonneau, S. (2012) · Corpus Université Laval (Université Laval) · Cited by 1
Sleep–Wake Disorders Following Traumatic Brain Injury
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Self-citationNarkolepsja - czy poznaliśmy wszystkie tajemnice choroby?
Wierzbicka, A., Wichniak, A., & Jernajczyk, W. (2014)
Future Directions in Hypersomnias: Diagnosis and Treatment
Culebras, A. (2013) · Elsevier eBooks · doi:10.1016/b978-0-12-378610-4.00256-4
Sleep‐Wake Disorders following Traumatic Brain Injury
Baumann, C. R. (2010) · doi:10.1002/9781444315158.ch17
Self-citationBaumann, C. R. (2011) · Cambridge University Press eBooks · doi:10.1017/cbo9780511762697.031
Self-citationEPILEPSY, SLEEP DISTURBANCES, AND PSYCHIATRIC CONSEQUENCES
Parko, K., Abrams, G., Campbell, J. S., & Glass, G. A. (2010) · CONTINUUM Lifelong Learning in Neurology · doi:10.1212/01.con.0000391455.22676.09
The Roles of Hypocretin/Orexin in Narcolepsy, Parkinson’s Disease, and Normal Behavior
Siegel, J. M. (2011) · Springer eBooks · doi:10.1007/978-1-4419-8390-9_4
Farah, F. H. (2017) · Journal of Analytical & Pharmaceutical Research · doi:10.15406/japlr.2017.04.00096
Response to the letter from Professor Helena Hachul and colleagues
Suzuki, Y., Arbour, C., Khoury, S., & Lavigne, G. J. (2017) · Sleep Medicine · doi:10.1016/j.sleep.2017.07.004
Sleep Disorders after Typical Concussive Brain Injury: Classification, Diagnosis, and Management
McKnight, C. A., & Victoroff, J. (2019) · Cambridge University Press eBooks · doi:10.1017/9781139696432.027
Lateral Hypothalamic Control of Sleep in the Context of Cancer
Borniger, J. C., & Nevárez, N. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-816658-1.00012-0
Post-Traumatic and Post-Neurosurgical Hypersomnia
Pelayo, R. (2014) · Elsevier eBooks · doi:10.1016/b978-1-4557-0318-0.00021-8 · Cited by 1
“Sleep disturbances emerged as significant predictors of poorer functional outcomes in children with moderate or severe TBI.”
BackgroundInfluentialSleep After Traumatic Brain Injury
Mollayeva, T. (2022) · Springer eBooks · doi:10.1007/978-981-16-0123-1_32
Kryger, M. H., Rosenberg, R. P., Pegram, G. V., et al. (2011) · Elsevier eBooks · doi:10.1016/b978-1-4377-2651-0.00007-8
Šonka, K., & Šusta, M. (2014) · Springer eBooks · doi:10.1007/978-88-470-5388-5_23
Baumann, C. R., & Poryazova, R. (2011) · Springer eBooks · doi:10.1007/978-1-4419-8390-9_31
Self-citationLam, J. C., & Reesman, J. L. (2018) · Springer eBooks · doi:10.1007/978-3-319-98414-8_26
Future directions in hypersomnias: diagnosis and treatment
Culebras, A. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-822963-7.00056-6
Traumatismes crâniens et sommeil : une revue narrative
Hartley, S., Baillieul, S., Azouvi, P., & Léotard, A. (2022) · Médecine du Sommeil · doi:10.1016/j.msom.2022.06.002
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Traumatic brain injury: Inter-relationship with sleep
Green, T. R. F., Ortiz, J. B., & Rowe, R. K. (2022) · Elsevier eBooks · doi:10.1016/b978-0-12-823036-7.00037-2
Narcolepsy and Idiopathic Hypersomnia
Ahmed, I., & Thorpy, M. J. (2022) · Respiratory medicine · doi:10.1007/978-3-030-93739-3_15
Neuroanatomical and Etiological Approaches to Secondary Narcolepsy
Şenel, G., & Karadeniz, D. (2022) · Neurological Sciences and Neurophysiology · doi:10.4103/nsn.nsn_5_22
Sommeil, fatigue, troubles du sommeil et troubles cognitifs
Ponsford, J. L., Connolly, L. J., Grima, N., & Ymer, L. (2021) · De Boeck Supérieur eBooks · doi:10.3917/dbu.azouv.2021.01.0137
Sathiamoses, L. O., Reshmi, R., & Prasanth, S. R. (2023) · International Journal of Science and Research (IJSR) · doi:10.21275/sr231106085038
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Metadata
- Authors
- Baumann, C. R., Bassetti, C. L., Valko, P. O., Haybaeck, J., Keller, M., Clark, E., Stocker, R., Tolnay, M., & Scammell, T. E.
- Affiliations
- Beth Israel Deaconess Medical Center (US)
- University Hospital Zurich (CH)
- Corresponding author
- Baumann, Christian R.
- ORCID
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2009-10
- Volume
- 66
- Issue
- 4
- Pages
- 555-559
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- PMC
- PMC2770195
- OpenAlex
- W2025705478
- Semantic Scholar
- 1dbac4f5e899ccafddf7329f779db1028a085914
- Cited by
- 185
- References
- 25
- Citations by year
- 2026: 2 · 2025: 8 · 2024: 6 · 2023: 4 · 2022: 13 · 2021: 10 · 2020: 13 · 2019: 11 · 2018: 22 · 2017: 10 · 2016: 10 · 2015: 19 · 2014: 12 · 2013: 10 · 2012: 12
- FWCI
- 5.33
- Type
- journal article
- Language
- en
- Open access
- green
- www.zora.uzh.ch
- Licence
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, other-oa)
- PubMed Central (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich)
- Funders
- National Institute of Mental Health (R01 MH062589, MH062589)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
- Keywords
- orexin, traumatic brain injury, hypothalamic neurons, narcolepsy, Parkinson's disease, wakefulness
- MeSH terms
- Orexins, Adult, Aged, Aged, 80 and over, Brain Injuries, Cell Count, Female, Humans, Hypothalamus, Male, Middle Aged, Neurons, Neuropeptides, Pilot Projects, Wakefulness, Intracellular Signaling Peptides and Proteins
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