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Thalamic strokes that severely impair arousal extend into the brainstem
Open accessAbstract
In this study, we evaluate the role of the thalamus in the neural circuitry of arousal. Level of consciousness within the first 12 hours of a thalamic stroke is assessed with lesion symptom mapping. Impaired arousal correlates with lesions in the paramedian posterior thalamus near the centromedian and parafascicular nuclei, posterior hypothalamus, and midbrain tegmentum. All patients with severely impaired arousal (coma, stupor) had lesion extension into the midbrain and/or pontine tegmentum, whereas purely thalamic lesions did not severely impair arousal. These results are consistent with growing evidence that pathways most critical for human arousal lie outside the thalamus. Ann Neurol 2018;84:926–930
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TL;DR
In 33 patients with ischemic thalamic lesions, severe arousal impairment (coma/stupor) occurred only when lesions extended into the brainstem, whereas purely thalamic lesions did not severely impair arousal. The findings challenge the view that the human thalamus is a critical relay for arousal.
Key findings
- Lesion-symptom mapping was significant (cross-validated correlation = 0.59; p < 0.001), with impaired arousal associated with bilateral ventromedial thalamus near the centromedian and parafascicular nuclei, posterior hypothalamus, and midbrain tegmentum; peak MNI coordinate: −3, −16, 3.
- All 4 patients with severe arousal impairment (2 coma, 2 stupor) had infarcts extensively involving the brainstem in addition to the thalamus.
- 12 patients with thalamic lesions with minimal to no brainstem extension were awake on presentation with no impairment of consciousness; 17 patients with intermediate midbrain extension had partial arousal impairments (obtunded, somnolent, or lethargic).
- The authors conclude that pathways most critical for human arousal likely lie outside the thalamus, and that historical thalamic involvement may reflect shared vascular supply with brainstem arousal structures.
Methods
- Retrospective study identifying patients from University of Iowa Hospitals and Clinics electronic medical records (2000–2017) with MR imaging showing abnormal diffusion signal in the thalamus; exclusions included sepsis, alcohol or drug overdose, seizure, or trauma.
- Sample: 23 Iowa patients (17 men, ages 63.30 ± 14.25) plus 10 patients from a previously published University of Utah artery of Percheron study (5 men, ages 50.30 ± 16.23), totaling 33 patients.
- Arousal during the first 12 hours after symptom onset was rated on a 6-point scale (coma, 1; stupor, 2; obtunded, 3; somnolent, 4; lethargic, 5; awake, 6) by 2 neurologists blinded to imaging; lesions were mapped onto the MNI152 template using FSL and analyzed with LESYMAP sparse canonical correlation lesion-symptom mapping, with 4-fold cross-validation and voxel coverage limited to areas with damage in ≥3 patients and ≥10% of the cohort.
Limitations
- Stated: the analysis is limited to 33 patients, and the authors cannot exclude the possibility that a purely thalamic lesion can severely impair consciousness, though they did not observe such a case.
- Stated: most literature cases of “thalamic coma” have radiographic evidence of extension into the hypothalamus and brainstem, exam findings not consistent with coma, or signs such as ophthalmoplegia indicating pontine or midbrain damage.
- Stated: the study focuses on arousal in the first 12 hours and does not evaluate hypersomnia or circadian rhythm disruptions reported with diencephalic lesions; future work with larger samples is needed. Evident from the text: the retrospective design and small sample limit generalizability and causal inference.
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Claims the paper makes
10 Not checked yet · 6 Own result · 5 Own method · 2 Check pending · 1 Partly supported · 1 Mixed support · 1 No full text of the sources · 1 No basis given · accuracy not yet measured
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 overall LSM is significant (cross-validated correlation = 0.59; p < 0.001).”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Results
plaincorrelational- Asserted: passes — The authors put it forward as true.
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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 remaining 17 patients with intermediate extension into the midbrain had partial impairments in level of arousal (obtunded, somnolent, or lethargic).”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Results
plaincorrelationaln = 17- Asserted: passes — The authors put it forward as true.
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In the paper
“All patients with severely impaired arousal (coma, stupor) had lesion extension into the midbrain and/or pontine tegmentum”
- Also stated in: § Results · plain
“The 4 patients with severe impairments in arousal (2 coma, 2 stupor) all had infarcts extensively involving the brainstem in addition to the thalamus (Fig 2).”
- Also stated in: § Conclusions · plain
“every patient with a thalamic lesion causing a severe impairment in arousal had extension into the brainstem”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Abstract
plaincorrelationaln = 4- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Results · 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
“Impaired arousal correlates with lesions in the paramedian posterior thalamus near the centromedian and parafascicular nuclei, posterior hypothalamus, and midbrain tegmentum.”
- Also stated in: § Results · plain
“Regions associated with impaired arousal extend from the bilateral ventromedial thalamus in the region of the centromedian and parafascicular nuclei (Fig 1B–E) with a peak at Montreal Neurological Institute (MNI) coordinate: −3, −16, 3.”
- Also stated in: § Conclusions · plain
“Our analysis identifies an association between impaired arousal and a bilateral region of the ventromedial thalamus near the centromedian and parafascicular nuclei, extending into posterior hypothalamus and midbrain.”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Abstract
plaincorrelationaln = 4- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Results · plain
None of the sources cited for this claim have been checked yet.
In the paper
“These findings are consistent with previous research highlighting the role of the brainstem and posterior hypothalamus as critical regions in the arousal pathway,1–4”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Conclusions
What the sources say
- Not checked yetcites [1] Fischer DB, Boes AD, Demertzi A, A human brain network derived from coma-causing brainstem lesions. Neurology 2016; 87: 2427– 2434. 27815400 PMC5177681 source
- Not checked yetcites [2] Eban-Rothschild A, Rothschild G, Giardino WJ, Jones JR, de Lecea L. VTA dopaminergic neurons regulate ethologically relevant sleep-wake behaviors. Nat Neurosci 2016; 19: 1356– 1366. 27595385 PMC5519826 source
- Not checked yetcites [3] Pedersen NP, Ferrari L, Venner A, Supramammillary glutamate neurons are a key node of the arousal system. Nat Commun 2017; 8: 1405. 29123082 PMC5680228 source
- Not checked yetcites [4] Parvizi J, Damasio AR. Neuroanatomical correlates of brainstem coma. Brain 2003; 126: 1524– 1536. 12805123 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Similarly, our findings are consistent with previous work linking dorsolateral pontine tegmentum lesions to coma in humans1,4 and coma-like outcomes in animals.9”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Conclusions
What the sources say
- Not checked yetcites [1] Fischer DB, Boes AD, Demertzi A, A human brain network derived from coma-causing brainstem lesions. Neurology 2016; 87: 2427– 2434. 27815400 PMC5177681 source
- Not checked yetcites [4] Parvizi J, Damasio AR. Neuroanatomical correlates of brainstem coma. Brain 2003; 126: 1524– 1536. 12805123 source
- Not checked yetcites [9] Fuller PM, Sherman D, Pedersen NP, Saper CB, Lu J. Reassessment of the structural basis of the ascending arousal system. J Comp Neurol 2011; 519: 933– 956. 21280045 PMC3119596 source
Checked before — its earlier verdict is held back until a new check runs.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“suggest that historically the thalamus was implicated because of its shared vascular supply with brainstem structures that are critical for arousal.19”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Conclusions
What the sources say
- Not checked yetcites [19] Schmahmann JD. Vascular syndromes of the thalamus. Stroke 2003; 34: 2264– 2278. 12933968
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Outside the thalamus, neurons in the posterior hypothalamus and basal forebrain appear more important than the thalamus for linking brainstem arousal- promoting projections to the cerebral cortex.”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Abstract
What the sources say
- Not checked yetcites [3] Pedersen NP, Ferrari L, Venner A, Supramammillary glutamate neurons are a key node of the arousal system. Nat Commun 2017; 8: 1405. 29123082 PMC5680228 source
A check is scheduled.
- Not checked yetcites [9] Fuller PM, Sherman D, Pedersen NP, Saper CB, Lu J. Reassessment of the structural basis of the ascending arousal system. J Comp Neurol 2011; 519: 933– 956. 21280045 PMC3119596 source
A check is scheduled.
- Not checked yetcites [11] Saper CB, Fuller PM. Wake-sleep circuitry: an overview. Curr Opin Neurobiol 2017; 44: 186– 192. 28577468 PMC5531075 source
A check is scheduled.
- Not checked yetcites [12] Xu M, Chung S, Zhang S, Basal forebrain circuit for sleep-wake control. Nat Neurosci 2015; 18: 1641– 1647. 26457552 PMC5776144 source
A check is scheduled.
- Not checked yetcites [13] Anaclet C, Pedersen NP, Ferrari LL, Basal forebrain control of wakefulness and cortical rhythms. Nat Commun 2015; 6: 8744. 26524973 PMC4659943 source
A check is scheduled.
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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A check of a cited source is scheduled, or we don’t hold its full text yet; the claim is checked once it runs.
In the paper
“Ablating the posterior hypothalamus or inhibiting corticopetal neurons in the basal forebrain nuclei produces coma, whereas exciting these regions is potently wake-promoting.3,9,11–13”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Abstract
What the sources say
- Not checked yetcites [3] Pedersen NP, Ferrari L, Venner A, Supramammillary glutamate neurons are a key node of the arousal system. Nat Commun 2017; 8: 1405. 29123082 PMC5680228 source
A check is scheduled.
- Not checked yetcites [9] Fuller PM, Sherman D, Pedersen NP, Saper CB, Lu J. Reassessment of the structural basis of the ascending arousal system. J Comp Neurol 2011; 519: 933– 956. 21280045 PMC3119596 source
A check is scheduled.
- Not checked yetcites [11] Saper CB, Fuller PM. Wake-sleep circuitry: an overview. Curr Opin Neurobiol 2017; 44: 186– 192. 28577468 PMC5531075 source
A check is scheduled.
- Not checked yetcites [12] Xu M, Chung S, Zhang S, Basal forebrain circuit for sleep-wake control. Nat Neurosci 2015; 18: 1641– 1647. 26457552 PMC5776144 source
- Not checked yetcites [13] Anaclet C, Pedersen NP, Ferrari LL, Basal forebrain control of wakefulness and cortical rhythms. Nat Commun 2015; 6: 8744. 26524973 PMC4659943 source
boosteddirect- Asserted: passes — The authors put it forward as true.
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- Not checked yet
- It may state two separate claims as one. 10
- Probably not a substantial claim. 12
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“Ablating the posterior hypothalamus or inhibiting corticopetal neurons in the basal forebrain nuclei produces coma, whereas exciting these regions is potently wake-promoting.3,9,11–13”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Abstract
What the sources say
- Partly supportedcites [3] Pedersen NP, Ferrari L, Venner A, Supramammillary glutamate neurons are a key node of the arousal system. Nat Commun 2017; 8: 1405. 29123082 PMC5680228 sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) reports that caudal hypothalamic lesions or inactivation caused marked, often prolonged somnolence, supporting a loss-of-arousal effect but not coma. The paper does not report that inhibiting corticopetal basal forebrain neurons produces coma. (LLM, conf=0.88)
- Not checked yetcites [9] Fuller PM, Sherman D, Pedersen NP, Saper CB, Lu J. Reassessment of the structural basis of the ascending arousal system. J Comp Neurol 2011; 519: 933– 956. 21280045 PMC3119596 source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked yetcites [11] Saper CB, Fuller PM. Wake-sleep circuitry: an overview. Curr Opin Neurobiol 2017; 44: 186– 192. 28577468 PMC5531075 source
Checked before — its earlier verdict is held back until a new check runs.
- Partly supportedcites [12] Xu M, Chung S, Zhang S, Basal forebrain circuit for sleep-wake control. Nat Neurosci 2015; 18: 1641– 1647. 26457552 PMC5776144 sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) reports that basal forebrain SOM+ neurons inhibit wake-promoting neurons and that activating SOM+ neurons increases NREM sleep. It does not report coma from posterior hypothalamus ablation or from inhibiting corticopetal basal forebrain neurons; those interventions and the claimed outcome are unsupported by this copy. (LLM, conf=0.78)
- Disputedcites [13] Anaclet C, Pedersen NP, Ferrari LL, Basal forebrain control of wakefulness and cortical rhythms. Nat Commun 2015; 6: 8744. 26524973 PMC4659943 sourceExperimental — accuracy not yet measured
The Results section on inhibition of basal forebrain GABAergic neurons reports a roughly 70% increase in slow-wave sleep over three hours in mice, not coma. The paper does not report posterior-hypothalamus ablation as an outcome of this study. (LLM, conf=0.86)
Checked by a reasoning model — may be wrong.
plaindirect- Asserted: passes — The authors put it forward as true.
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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
“For example, extensive ablation or inhibition of thalamic neurons fails to alter the normal pattern and amount of waking and sleeping behavior, and the only apparent electroencephalographic abnormality that results is a loss of spindle activity during sleep.8–10”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Abstract
What the sources say
- Not checked — no full text of the sourcecites [8] Villablanca J, Salinas-Zeballos ME. Sleep-wakefulness, EEG and behavioral studies of chronic cats without the thalamus: the “athalamic” cat. Arch Ital Biol 1972; 110: 383– 411. 4349191
- Partly supportedcites [9] Fuller PM, Sherman D, Pedersen NP, Saper CB, Lu J. Reassessment of the structural basis of the ascending arousal system. J Comp Neurol 2011; 519: 933– 956. 21280045 PMC3119596 sourceExperimental — accuracy not yet measured
The Results section reports that rats with extensive thalamic lesions had no significant changes in NREM or REM sleep amounts or circadian sleep pattern, and that sleep spindles disappeared. But it also reports decreased EEG theta power during the subjective night, so spindle loss was not the only apparent EEG abnormality. The cited experiment tested lesions; the paper’s Introduction also discusses earlier studies using thalamic inactivation. (LLM, conf=0.90)
- Partly supportedcites [10] Buzsaki G, Bickford RG, Ponomareff G, Nucleus basalis and thalamic control of neocortical activity in the freely moving rat. J Neurosci 1988; 8: 4007– 4026. 3183710 PMC6569493 sourceExperimental — accuracy not yet measured
The High-voltage spindles section (page unavailable) reports that thalamic lesions suppressed high-voltage spindles while EEG correlates of run–drink–immobility transitions remained essentially unchanged. It does not establish that the amount or pattern of waking and sleeping was unaffected; it describes the affected spindles as occurring during immobility with eyes open, not during sleep. (LLM, conf=0.88)
plain- 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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Probably not a substantial claim. 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
“whereas purely thalamic lesions did not severely impair arousal.”
- Also stated in: § Results · plain
“In contrast, 12 patients with thalamic lesions with minimal to no extension into the brainstem were awake on presentation with no impairment of consciousness.”
- Also stated in: § Conclusions · boosted
“no patients with lesions entirely limited to the thalamus demonstrated severe impairment in arousal.”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Abstract
boostedn = 12- 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.
- Also stated in: § Results · 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 lesion overlap (Fig 1A) demonstrates coverage of the thalamus and limited coverage of the brainstem and other structures supplied by the posterior circulation.”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Results
boosted- 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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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“this is not consistent with past evidence that ischemic strokes and other lesions limited to the brainstem cause coma.1,4”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Conclusions
What the sources say
- Not checked yetcites [1] Fischer DB, Boes AD, Demertzi A, A human brain network derived from coma-causing brainstem lesions. Neurology 2016; 87: 2427– 2434. 27815400 PMC5177681 source
- Not checked yetcites [4] Parvizi J, Damasio AR. Neuroanatomical correlates of brainstem coma. Brain 2003; 126: 1524– 1536. 12805123 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.
Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“These results are consistent with growing evidence that pathways most critical for human arousal lie outside the thalamus.”
- Also stated in: § Conclusions · plain
“These results are consistent with evidence from experimental animals that the thalamus is not critical for arousal,8–10”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Abstract
What the sources say
- Not checked — no full text of the sourcecites [8] Villablanca J, Salinas-Zeballos ME. Sleep-wakefulness, EEG and behavioral studies of chronic cats without the thalamus: the “athalamic” cat. Arch Ital Biol 1972; 110: 383– 411. 4349191
- Not checked yetcites [9] Fuller PM, Sherman D, Pedersen NP, Saper CB, Lu J. Reassessment of the structural basis of the ascending arousal system. J Comp Neurol 2011; 519: 933– 956. 21280045 PMC3119596 source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked yetcites [10] Buzsaki G, Bickford RG, Ponomareff G, Nucleus basalis and thalamic control of neocortical activity in the freely moving rat. J Neurosci 1988; 8: 4007– 4026. 3183710 PMC6569493 source
Checked before — its earlier verdict is held back until a new check runs.
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.
- Also stated in: § Conclusions · plain
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
“Level of arousal was rated on a 6-point scale (coma, 1; stupor, 2; obtunded, 3; somnolent, 4; lethargic, 5; awake, 6, terms defined previously17) by 2 neurologists blinded to patient imaging (J.C.G. and A.D.B.).”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Patients and Methods
plain- Asserted: passes — The authors put it forward as true.
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Probably 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
“Our findings are also limited in that we focus on level of arousal in the first 12 hours and do not evaluate hypersomnia or circadian rhythm disruptions that have been reported with diencephalic lesions.”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Conclusions
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.
None of the sources cited for this claim have been checked yet.
In the paper
“Early models of an ascending reticular activating system (ARAS) originating from diffuse neurons in the brainstem reticular formation have been revised to include discrete brainstem regions and individual nuclei that are preferentially involved in maintaining a state of wakefulness.1–5”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Abstract
What the sources say
- Not checked yetcites [1] Fischer DB, Boes AD, Demertzi A, A human brain network derived from coma-causing brainstem lesions. Neurology 2016; 87: 2427– 2434. 27815400 PMC5177681 source
- Not checked yetcites [2] Eban-Rothschild A, Rothschild G, Giardino WJ, Jones JR, de Lecea L. VTA dopaminergic neurons regulate ethologically relevant sleep-wake behaviors. Nat Neurosci 2016; 19: 1356– 1366. 27595385 PMC5519826 source
- Not checked yetcites [3] Pedersen NP, Ferrari L, Venner A, Supramammillary glutamate neurons are a key node of the arousal system. Nat Commun 2017; 8: 1405. 29123082 PMC5680228 source
- Not checked yetcites [4] Parvizi J, Damasio AR. Neuroanatomical correlates of brainstem coma. Brain 2003; 126: 1524– 1536. 12805123 source
- Not checked — no full text of the sourcecites [5] Moruzzi G, Magoun HW. Brainstem reticular formation and activation of the EEG. Electroencephalogr Clin Neurophysiol 1949; 1: 455– 473. 18421835 source
plain- Asserted: passes — The authors put it forward as true.
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Probably 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
“The previously published study did not perform lesion-symptom mapping, and their results do not overlap with the current analysis.”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Patients and Methods
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.
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
“This analysis is limited to 33 patients, and we cannot exclude the possibility that a purely thalamic lesion can severely impair consciousness, though we did not observe such a case.”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Conclusions
hedgedn = 33- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“dating back to Moruzzi and Magoun’s demonstration that the brainstem and caudal diencephalon show the lowest stimulation threshold for cortical arousal.5”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Conclusions
What the sources say
- Not checked — no full text of the sourcecites [5] Moruzzi G, Magoun HW. Brainstem reticular formation and activation of the EEG. Electroencephalogr Clin Neurophysiol 1949; 1: 455– 473. 18421835 source
boostedcorrelational- 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
“We also note that most, if not all, cases from the literature describing “thalamic coma” have radiographic evidence of lesions extending into the hypothalamus and brainstem, have exam findings not consistent with the diagnosis of coma, or have clinical signs like ophthalmoplegia that signify damage to the pons or midbrain.20–22”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Conclusions
What the sources say
- Not checked — no full text of the sourcecites [20] Bogousslavsky J, Regli F, Uske A. Thalamic infarcts: clinical syndromes, etiology, and prognosis. Neurology 1988; 38: 837– 848. 3368064 source
- Not checked — no full text of the sourcecites [21] Zappella N, Merceron S, Nifle C, Artery of Percheron infarction as an unusual cause of coma: three cases and literature review. Neurocrit Care 2014; 20: 494– 501. 24566980 source
- Not checked yetcites [22] Rivera-Lara L, Henninger N. Delayed sudden coma due to artery of percheron infarction. Arch Neurol 2011; 68: 386– 387. 21403026 source
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hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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It 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
“Lesion location was reproduced onto a 3D template brain (MNI152 atlas, 1 × 1 × 1 mm) using FSL (http://fsl.fmrib.ox.ac.uk/fsldownloads/), as performed previously,1 and accuracy of each lesion was reviewed independently by 2 neurologists blinded to clinical outcome (J.C.G. and A.D.B.).”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Patients and Methods
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.
Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“Yet the assumption that critical, arousal-promoting projections from the brainstem must synapse in the thalamus has been challenged by a growing body of research in experimental animals.”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Abstract
What the sources say
- Not checked — no full text of the sourcecites [8] Villablanca J, Salinas-Zeballos ME. Sleep-wakefulness, EEG and behavioral studies of chronic cats without the thalamus: the “athalamic” cat. Arch Ital Biol 1972; 110: 383– 411. 4349191
- Not checked yetcites [9] Fuller PM, Sherman D, Pedersen NP, Saper CB, Lu J. Reassessment of the structural basis of the ascending arousal system. J Comp Neurol 2011; 519: 933– 956. 21280045 PMC3119596 source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked yetcites [10] Buzsaki G, Bickford RG, Ponomareff G, Nucleus basalis and thalamic control of neocortical activity in the freely moving rat. J Neurosci 1988; 8: 4007– 4026. 3183710 PMC6569493 source
Checked before — its earlier verdict is held back until a new check runs.
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.
Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“Based on the idea that the ascending arousal system relays in the thalamus, patients with disorders of consciousness have had electrodes implanted into their thalami by several groups of investigators, with inconsistent results.15”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Abstract
What the sources say
- Not checked yetcites [15] Vanhoecke J, Hariz M. Deep brain stimulation for disorders of consciousness: systematic review of cases and ethics. Brain Stimul 2017; 10: 1013– 1023. 28966051 source
Checked before — its earlier verdict is held back until a new check runs.
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.
- Not checked yet
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
“As such, the question of whether the human thalamus is necessary for maintaining a basic level of arousal remains unanswered.”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Abstract
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.
Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“A study of atrophy patterns in a large cohort of patients with disorders of consciousness observed no association between thalamic atrophy and wakefulness, but this study could not determine whether the thalamus is necessary for maintaining a basic level of arousal.14”
§ Thalamic Strokes That Severely Impair Arousal Extend Into the Brainstem > Abstract
What the sources say
- Not checked yetcites [14] Lutkenhoff ES, Chiang J, Tshibanda L, Thalamic and extrathalamic mechanisms of consciousness after severe brain injury. Ann Neurol 2015; 78: 68– 76. 25893530 source
Checked before — its earlier verdict is held back until a new check runs.
hedged- 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.
Probably not a substantial claim. It may state two separate claims as one.
- Not checked yet
The paper relies on this without support.
Level of arousal during the first 12 hours can be reliably determined retrospectively from electronic medical records and neurological exam findings.
“The level of arousal displayed by each patient during the first 12 hours after the onset of symptoms was extrapolated from review of the electronic medical record based primarily on neurological exam findings.”
The paper relies on this without support.
The exclusion criteria of sepsis, alcohol or drug overdose, seizure, or trauma adequately exclude non-lesional causes of impaired arousal.
“Exclusion criteria included the presence of sepsis, alcohol or drug overdose, seizure, or trauma.”
The paper relies on this without support.
The 10 patients from the previously published Utah study can be combined with the Iowa patients because the cases were analyzed using the same protocols.
“Cases were analyzed using the same protocols as those from Iowa.”
Citations
Cites
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Supramammillary glutamate neurons are a key node of the arousal system
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Improved accuracy of lesion to symptom mapping with multivariate sparse canonical correlations
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Metadata
- Authors
- Hindman, J., Bowren, M. D., Bruss, J., Wright, B., Geerling, J. C., & Boes, A. D.
- Affiliations
- University of Iowa (US)
- University of Iowa Hospitals and Clinics (US)
- University of Utah (US)
- Corresponding author
- Geerling, Joel C.
- Boes, Aaron D.
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2018-12
- Volume
- 84
- Issue
- 6
- Pages
- 926-930
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- PMC
- PMC6344294
- OpenAlex
- W2900677790
- Semantic Scholar
- 4184d4c64c8b9221316dfc1d12e9db9ca0d787c1
- Cited by
- 53
- References
- 21
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 5 · 2023: 10 · 2022: 8 · 2021: 6 · 2020: 6 · 2019: 4 · 2018: 1
- FWCI
- 2.79
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (K08‐NS099425K12HD027748‐24K12NS098482‐01)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
- Health Sciences › Medicine › Clinical Neurology › Deep Brain Stimulation and Movement Disorders
- Health Sciences › Medicine › Clinical Neurology › Acute Ischemic Stroke Management
- Keywords
- thalamic infarction, arousal, coma, stupor, lesion-symptom mapping, posterior thalamus, centromedian nucleus, parafascicular nucleus, posterior hypothalamus, midbrain tegmentum, pontine tegmentum, brainstem, level of consciousness
- MeSH terms
- Arousal, Brain Mapping, Brain Stem, Coma, Female, Humans, Magnetic Resonance Imaging, Male, Retrospective Studies, Thalamus, Time Factors, Stroke, Imaging, Three-Dimensional, Stupor
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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.
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