Sensorimotor stroke due to thalamocapsular ischemia.
A 61-year-old hypertensive diabetic man awoke with a numb, heavy right arm and leg; symptoms progressed within 30 hours to a dense right hemisensory syndrome involving head, face, trunk, arm, and leg, accompanied by a right hemiparesis, involving tongue, face, arm, and leg with extensor plantar response, leaving him barely able to move the arm and leg against gravity. No impairment in alertness, memory, language, praxic, or visual functions was evident at any time. Improvement in motor function began in 24 hours and progressed to walking status by discharge on day 23. Eight days passed before the sensory deficit showed improvement, and it was still prominent at discharge. Autopsy three months later showed a 4 X 2 X 4-mm lacune in the ventral posterior nucleus of the left thalamus, with a zone of pallor on stained microscopic sections extending into the immediately adjacent posterior limb of the internal capsule. This case appears to be unique in that a sensorimotor stroke has been produced by a confirmed thalamocapsular infarct.
D002561:Cerebrovascular Disorders / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D003342:Corpus Striatum / Q000098:blood supply* / Q000473:pathology; D048909:Diabetes Complications; D006801:Humans; D002542:Intracranial Embolism and Thrombosis / Q000150:complications*; D008297:Male; D008875:Middle Aged; D013577:Syndrome; D013787:Thalamic Nuclei / Q000098:blood supply* / Q000473:pathology