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)

A 74-year-old man developed progressive deafness and unsteady gait two years after gastrectomy for a gastric cancer. Neurological examination revealed an alert and intelligent Japanese male in no acute distress. The optic fundi were normal. The pupils and the extraocular muscles were normal, however, horizontal nystagmus was noted in right and left gaze. He showed marked bilateral deafness, and loss of caloric response bilaterally. No muscle atrophy nor weakness was noted. His gait was wide-based and ataxic. Tandem gait was impossible. Romberg sign was present. No cerebellar ataxia was noted in the finger-to-nose or the heel-to-knee test. No adiadochokinesis was noted. Hyperextensibility was noted in the lower extremities. Deep reflexes were normal in the upper limbs, and diminished in the lower extremities. Sensation was intact. He showed the jumbling phenomenon, and the disturbance of the righting reflex in the tilt-table examination. Neuroradiological as well as laboratory studies were unremarkable except for the high titer of CEA in the CSF. Four months after his admission, malignant tumor cells were found in the CSF. It seemed likely that he had completely lost bilateral vestibular and auditory functions caused by meningeal carcinomatosis. His disturbance of gait and station was apparently similar to cerebellar ataxic gait, however, he did not have limb ataxia. The cranial CT scans failed to show cerebellar atrophy. It was our impression that his motor disturbance was in all likelihood caused by the bilateral loss of vestibular functions, i.e., vestibular ataxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Vestibular ataxia caused by meningeal carcinomatosis]. 236 34

A 65-year-old woman was operated for gastric adenocarcinoma in 1989. Six years later, peritonitis carcinomatosa, swelling of periaortic lymphnodes and high serum CA-125 were discovered. She received chemotherapy with 5-FU and cisplatin resulting in reduction of ascites. In September, 1998, the swelling of left supraclavicular lymphnodes and the elevation of serum CA-125 reappeared. Pathological diagnosis of supraclavicular lymphnodes was adenocarcinoma. Serum CA-125 was normalized by chemotherapy using cisplatin, farumorubicin and endoxan. However, unsteadiness appeared since December 10, 1998 followed by dysarthria and involuntary movement of neck and upper limbs. These symptoms progressed subacutely. The physical examination on admission revealed swelling of left suraclavicular lymphnodes, nystagmus on lateral gaze, saccadic eye movement on smooth pursuit and severe cerebellar ataxia. In addition, resting tremor of 3-4 Hz was observed at right hand, left wrist and neck which tended to increase amplitude by calculation. Similar movements were seen in the left first toe, though the frequency was lower. Brain MRI revealed mild cerebellar atrophy. She was diagnosed as paraneoplastic cerebellar degeneration (PCD) by serum anti Yo antibody and clinical course. The study of HLA showed positive link to A4 without A24. The primary focus of adenocarcinoma in cervical lymphnodes was suggested to be ovary rather than stomach due to the pattern of immunostaining for cytokeratin, CEA and CA125, although no carcinoma was found in ovarium clinically. The feature of this case is a PCD with resting tremor of frequency of 3-4 Hz and negative link to HLA-A24 in Japanese.
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PMID:[A case of paraneoplastic cerebellar degeneration with resting tremor]. 1143 63