Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a 62-year-old man with ballism confined to the right leg, so-called monoballism. He was admitted to our hospital complaining of gait disturbance due to violent involuntary movements in the right lower extremity which had developed seven days before. He had a ten-years' history of hypertension and at age 57 had been diagnosed as having asymptomatic multiple cerebral infarcts. Until admission, he was taking antiplatelet drugs for the purpose of preventing thrombotic stroke. On neurological examination, he showed mild impairment of higher brain function, Horner's sign in the left eye, and typical ballism in the right lower extremity. Involuntary movements were never observed in the face and the other extremities. Surface electromyography also showed reciprocal burst discharges at about 1 Hz related to the ballistic movements in the right lower extremity. CT scan revealed a high density lesion surrounded by a low density in the left subthalamic area. MRI examination demonstrated a dumbbell shaped hemorrhage extending from the left subthalamic nucleus to the dorsomedial nucleus of the ipsilateral thalamus. Adding to the hemorrhage, many ischemic lesions were observed in the bilateral basal ganglia and thalamus including the left pallidum. The causal end of the hemorrhage apparently located in the anterior dorsomedial portion of the subthalamic nucleus. There were few reports concerning monoballism, especially monoballism limited to the lower extremity. Recent researches indicate that a subthalamic lesion reduces the excitatory control from the subthalamus to the internal segment of the globus pallidus, which leads to a disinhibition of the thalamus and gives rise to ballism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of thalamo-subthalamic hemorrhage presenting monoballism in the contralateral lower extremity]. 130 Feb 59

We present two siblings with hereditary cortical cerebellar atrophy (CCA), who showed peculiar clinical features. Their unaffected parents are cousins. The mode of inheritance in this family was autosomal recessive. Both patients developed involuntary movement and ataxia during the fourth decade. The proband (patient 1) was the elder sister. She developed choreoathetoid involuntary movement and cerebellar ataxia at the age of 32. At the age of 39, she showed mental deterioration and marked gait disturbance due to severe ataxia and amyotrophy. At the age of 40, she took medication for hypertension. At the age of 42, she was bedridden and had generalized convulsions and dysautonomia. Involuntary movement continued until her death at age 44. She had amenorrhea since the age of 25 years. Neuropathological findings. The brain weighed 1,010 g. We found marked degeneration in the cerebellar cortex including the molecular, Purkinje cells, and granular cell layers, and in the inferior olivary nuclei. In the basal ganglia, the putamen and caudate nuclei were moderately affected, but the substantia nigra and globus pallidus were spared. The cerebral cortex was spared, but the cerebral white matter showed diffuse myelin pallor without fibrillary gliosis. In the pons, the volume of the tegmentum was moderately decreased, but the base was spared. The spinal cord was normal. The findings of the patient differed from those of the case originally reported by Gordon Holmes in 1907. Holmes autopsied a case showing severe degeneration in both the cerebellar cortex including all three layers and the inferior olivary nucleus as in our patient. However, the striatum of his case spared and the patient did not develop involuntary movement as did other patients. The patients presented here should be distinguished from Holmes' original case clinicopathologically.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Autosomal recessive hereditary cortical cerebellar atrophy with striatal degeneration--two siblings showing choreoathetoid movement, ataxia, dementia, and amenorrhea]. 806 39

A 79-year-old woman with hypertension was evaluated 3 hours and 20 minutes after the sudden onset of left-sided weakness which lasted about 15 minutes and was followed by involuntary, coarse, flinging movements of the left extremities (hemiballistic), occurring every few minutes, and facial asymmetry. Brain computed tomography revealed no abnormalities. The patient received intravenous thrombolysis with 0.9 mg/kg of alteplase 4 hours after the symptom onset. Involuntary movements and central facial nerve paresis subsided within 48 hours of the thrombolysis. Magnetic resonance imaging at day 5 revealed restricted diffusion within the right globus pallidus, which was a new ischemic lesion. Thrombolysis should be considered in hemiballism as a presenting symptom of acute stroke.
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PMID:Successful treatment with intravenous recombinant tissue plasminogen activator in an acute stroke patient presenting with hemiballism. 2621 30