Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two cases of phenytoin toxicity in patients with chronic liver disease who were taking 300 mg phenytoin daily are described. Each patient developed encephalopathy, characterized by confusion, disturbed conscious state, asterixis, and nystagmus, which was resistant to treatment with protein restriction, lactulose, and neomycin, but responsive to withdrawal of phenytoin. We suggest that the phenytoin did not precipitate hepatic encephalopathy, but caused an encephalopathy that mimicked it. We recommend that phenytoin be used cautiously in patients with liver disease, and that the drug's unbound serum level be measured if encephalopathy occurs.
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PMID:Phenytoin toxicity and hepatic encephalopathy: simulation or stimulation? 361 89

Five patients were examined suffering from bilateral paramedian thalamic infarction, caused by occlusion of the posterior paramedian thalamo-subthalamic arteries, when they begin from one single pedicle. All cases began with obnubilation or transitory coma, followed by hypersomnia. Four patients showed vertical gaze paralysis, and the fifth vertical nystagmus. In three cases, nuclear lesion of the III cranial nerve was observed along with alteration of the photomotor reflexes, and there was miosis in one case. All were suffering from weakness in one or another limb or facial paresis and generalised acute hypotonia: only one patient had hemihypostesia. All five had dysarthria, ataxy and dysmetria, one had asterixis and two spasmodic crying. Between 5 and 12 months later, one had akinetic mutism and vertical gaze paralysis as the most noteworthy signs. The neuroradiological images show a bilateral ischemic lesion in the paramedian thalamic region, which extends in some cases to the anterior nucleus and in one case to the pulvinars; the lesion continues through the subthalamic regions and the medial part of the mesencephalic tegmentum, with a clear extension to the medial region of the cerebral peduncles in three cases and to the tectum in one case.
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PMID:[Paramedian bithalamic infarct syndrome: report of five new cases]. 749 75

We prospectively studied motor symptoms in 32 patients with CT- or MRI-proven acute pure parietal stroke. A transient, mild, 'pseudoparesis' of the hand (90%), was noted, improved by visual attention and prompting, associated with non-awareness of muscle power (53%), transient soft pyramidal signs (50%), unilateral akinesia (100%) and motor hemineglect (37%) in non-dominant lesions. Lower motoneurone-type atrophy was not observed in this acute phase. We called 'poikilotonia' the striking unpredictable variations in muscle tone, ranging from extreme hypertonia to hypotonia, found in all patients. When maintaining postures, patients showed large oscillations (100%), laterodeviation or levitation of the arm (60%), especially in the case of large or posterior lesions, or, occasionally (3%), motor persistence or even hemicatalepsy (3%). Limb kinetic and manipulatory apraxia, with inadequate organization and anticipation of motor sequences and synergies, motor arrests, perplexity, unrecognizable gestures and loss of bimanual coordination, was a constant finding (100%). Other apraxias (62%) and difficulty in copying intransitive gestures of the hand (84%) were associated with posterior lesions involving the supramarginal gyrus. When reaching towards objects, all patients showed abnormal anticipatory hand shaping, but visuomotor ataxia (3%) was only seen with bilateral posterior stroke. Sensory (70%) or pseudocerebellar (4%) ataxia, was seen in both anterior and posterior lesions. Avoidance behaviors (34%) were not uncommon, but had no localizing value. Of the dyskinesias, hand dystonia (84%) was frequent, but athetosis (16%), asterixis (15%), postural tremor (15%), myoclonus (9%) and stereotypia (9%), were uncommon. The abnormal eye movements were unilateral hypo-akinesia of exploratory saccades (43%), abnormal ipsilateral pursuit and contralateral optokinetic nystagmus in the case of posterior lesions, and oculomotor apraxia with bilateral posterior lesions. In conclusion, parietal motor syndrome can be recognized during bedside examination, and probably reflects the loss of multiple sensory feedback to motor programs, especially those directed to the extrapersonal space.
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PMID:Parietal motor syndrome: a clinical description in 32 patients in the acute phase of pure parietal strokes studied prospectively. 987 53