Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 50-year-old woman was transported to a hospital complaining of marked general malaise and epigastralgia with diarrhea and vomiting. Her electrocardiogram showed sinus arrest with a duration of nearly 8 sec. Atrial pacing with an external pacemaker improved her symptoms promptly. Following transfer to our hospital 3 days later, bradyarrhythmia was not detected despite the removal of the external pacemaker. Transient atrial fibrillation was found in our hospital, and she was diagnosed as hyperthyroidism based on findings of finger tremor, exophthalmos, diffuse goiter and an abnormally high level of thyroid hormone. On cardiac catheterization, left ventriculography showed anterior wall hypokinesis and mild mitral regurgitation. Coronary arteriography showed the absence of organic stenosis. Right ventricular endomyocardial biopsy showed myocardial hypertrophy and partial disarray, but no findings of myocarditis. Electrophysiological study showed the normal upper range of AH-time (120 msec) and HV-time (50 msec), and prolongation of corrected sinus recovery time (CSRT, 955 msec). After a euthyroid state was successively induced for about 10 days by methylmercaptoimidazole therapy, AH-time, HV-time and CSRT were shortened to 85, 35 and 290 msec respectively. Her complaints and sick sinus syndrome disappeared after the treatment of hyperthyroidism without a pacemaker.
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PMID:Hyperthyroidism complicated with sick sinus syndrome. 878 74

We report a 85-year-old woman who had an onset of gait disturbance at 80 years of the age. She had a dizzy spell when she was 80-year-old. She was evaluated at another hospital where paroxysmal tachycardia and sinus arrest lasting as long as 5.8 seconds were found. She was diagnosed as having sick sinus syndrome and a pace maker was inserted. She had a gradual onset of disturbance of gait shortly after the above dizzy spell. She became unable to walk fast and her steps became small. Neurologic examination at age 83 revealed small step gait with freezing episodes. Retropulsion was present. No motor weakness or origidity was noted. She had no tremor. Mentally she was alert and sound. Cranial nerves were essentially normal. Cranial CT scan revealed slight diffuse low density change in the bilateral cerebral white matter. She was treated with amantadine HCI and levodopa with carbidopa. Her gait and balance showed some improvement. She developed pneumonia and worsening of her gait when she was 85 years of the age, and she was admitted again to our hospital. She was mentally alert and sound but she showed marked freezing of gait with loss of postural reflex; she would have fallen down unless supported upon standing. Cranial nerves were again essentially normal. Her hospital course was complicated by pneumonia, DIC, and renal failure. She expired suddenly on the 10th day of her last admission. She was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had vascular parkinsonism due to lacunar state. However, paucity of vascular changes in her CT scan remained as a question. Other participants thought that she had nigral cell loss secondary to her aging and circulatory disturbance which would have been caused by her sick sinus syndrome. Post-mortem examination revealed marked loss of nigral pigmented cells; the cell loss was diffusely seen in the substantia nigra. Neurofibrillary tangles were seen in the remaining neurons. In addition, gliosis was noted in the globus pallidus and the subthalamic nucleus, however, neuronal loss was very mild in those nuclei. In the superior colliculus, neuronal loss was mild, however, gliosis was seen. No clear neuronal loss was observed in the locus coeruleus, however, Lewy bodies were seen in the remaining neurons. Furthermore, Lewy bodies were also found in the substantia sigra. It was thought that she had progressive supranuclear play (PSP). Question was whether or not she was complicated by Parkinson's disease. Clinically, she had no rigidity or tremor. Pathologically, locus coeruleus did not show neuronal loss. Therefore, incidental Lewy body disease was raised as a possibility. Finally, it should be pointed out that she had no oculomotor disturbance or dementia, yet she had PSP. Her clinical features were those of pure akinesia. Pathologic changes were also relatively mild except for those in the substantia nigra. Possibility of post-encephalitic parkinsonism without encephalitis was also discussed, however, over all distribution of her pathologic changes was more consistent with PSP.
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PMID:[A 85-year-old woman with the onset of progressive gait disturbance at 80 years of the age]. 912 48