Thalamic infarcts

Bogousslavsky, Julien; Régli, F; Uské, A

doi:10.1212/wnl.38.6.837

Cited by 622 publications

(370 citation statements)

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“…In our case, decreased consciousness was the result of infarctions in both paramedian thalami and the left rostral midbrain, which then made us suspect an occlusion of the AOP, since vertebrobasilar and posterior circulations were unaffected. Like previous studies [3,4,[6][7][8][9][10][11][12][13], our case showed severe cognitive dysfunctions, especially in attention and verbal long-term memory. Symptoms rapidly improved during early rehabilitation periods.…”

Section: Discussionsupporting

confidence: 87%

Clinical Features of an Artery of Percheron Infarction: a Case Report

et al. 2017

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Highlights• Altered mentality, memory impairment, and gaze palsy are the typical symptom triad.• Rehabilitative goals were set to improve the patient's alertness, cognitive functions, and gait.• Alertness and cognitive functions were improved during early rehabilitation period. ABSTRACTThe artery of Percheron (AOP) is an uncommon variant of the paramedian artery, a solitary trunk branching off from the posterior cerebral arteries, supplying both paramedian thalami, and also often the rostral midbrain and the anterior thalamus. The typical clinical manifestations of the AOP infarction include altered mental status, cognitive impairment, and oculomotor dysfunction. We report a rare case with AOP infarction, and the clinical characteristics and rehabilitation courses for alertness disorder, cognitive dysfunction, and other accompanied symptoms.

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Section: Discussionsupporting

confidence: 87%

Clinical Features of an Artery of Percheron Infarction: a Case Report

et al. 2017

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“…We speculate that this may have been caused by a transient dysfunction of the bilateral thalami, given the striking signal alteration in this region on MRI. Dysfunction of the right thalamus can cause visuospatial hemineglect on the left side (Bogousslavsky, Regli, & Uske, 1988;De Witte et al, 2011;Watson & Heilman, 1979), and dysfunction of the left thalamus can cause aphasia (Bogousslavsky et al, 1988;De Witte et al, 2011;Kumar, Masih, & Pardo, 1996). For example, in the literature a case has been described where a patient with deep cerebral venous thrombosis with bithalamic infarction presented with a transient left-side visuospatial neglect, aphasia and amnesia (Benabdeljlil et al, 2001), which resembles our case.…”

Section: Discussionsupporting

confidence: 66%

Bithalamic Dysfunction in Wernicke’s Encephalopathy

Nariai

Mittelmann

Farmakidis

et al. 2017

EJBM

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We describe a 65-year-old, nonalcoholic, right-handed female with multiple vascular risk factors who developed transient visuospatial hemineglect and global aphasia after presenting with the classic triad of Wernicke’s encephalopathy (mental status changes, nystagmus/ophthalmoplegia, and ataxia). A brain MRI showed no evidence of acute infarction, but demonstrated signal change in the medial thalami and mammillary bodies. Intravenous thiamine therapy was given, and visuospatial hemineglect and ophthalmoplegia disappeared while the aphasia improved. The occurrence of these acute transient clinical features has not been previously reported in Wernicke’s encephalopathy.

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“…CPSP occurs most often after strokes that involve the thalamus [4][5][6][7][8][9]. The quality of life of patients with CPSP is very poor due to daily paroxysms of persistent spontaneous pain and hypersensitivity to noxious (hyperalgesia and allodynia) and non-noxious stimuli (paresthesia and dysesthesia) [10][11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Gabapentinoid Insensitivity after Repeated Administration is Associated with Down-Regulation of the α2δ-1 Subunit in Rats with Central Post-Stroke Pain Hypersensitivity

Yang

et al. 2016

Neurosci. Bull.

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The a 2 d-1 subunit of the voltage-gated Ca 2? channel (VGCC) is a molecular target of gabapentin (GBP), which has been used as a first-line drug for the relief of neuropathic pain. GBP exerts its anti-nociceptive effects by disrupting trafficking of the a 2 d-1 subunit to the presynaptic membrane, resulting in decreased neurotransmitter release. We previously showed that GBP has an antiallodynic effect in the first two weeks; but this is followed by insensitivity in the later stage after repeated administration in a rat model of central post-stroke pain (CPSP) hypersensitivity induced by intra-thalamic hemorrhage. To explore the mechanisms underlying GBP insensitivity, the cellular localization and time-course of expression of the a 2 d-1 subunit in both the thalamus and spinal dorsal horn were studied in the same model. We found that the a 2 d-1 subunit was mostly localized in neurons, but not astrocytes and microglia. The level of a 2 d-1 protein increased in the first two weeks after injury but then decreased in the third week, when GBP insensitivity occurred. Furthermore, the a 2 d-1 down-regulation was likely caused by later neuronal loss in the injured thalamus through a mechanism other than apoptosis. In summary, the present results suggest that the GBP receptor a 2 d-1 is mainly expressed in thalamic neurons in which it is up-regulated in the early stage of CPSP but this is followed by dramatic down-regulation, which is likely associated with GBP insensitivity after long-term use.Keywords Central post-stroke pain Á Calcium channel a 2 d subunit Á Gabapentinoid Á Thalamic hemorrhagic stroke Á Thalamus Á Spinal dorsal horn

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Thalamic infarcts

Cited by 622 publications

References 0 publications

Clinical Features of an Artery of Percheron Infarction: a Case Report

Clinical Features of an Artery of Percheron Infarction: a Case Report

Bithalamic Dysfunction in Wernicke’s Encephalopathy

Gabapentinoid Insensitivity after Repeated Administration is Associated with Down-Regulation of the α2δ-1 Subunit in Rats with Central Post-Stroke Pain Hypersensitivity

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