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)

We describe a patient with a clinical picture characterized by subacute onset of confusion, myoclonus, tremor and generalized convulsive seizures with a relapsing course, which was attributed to Hashimoto's encephalopathy. EEG and MRI were diffusely abnormal. High titers of antithyroid antibodies were detected in her serum. She responded well to corticosteroids and her condition remained good during a one-year follow-up.
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PMID:Hashimoto's encephalopathy: clinical and laboratory findings. 911 67

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

We report a case of Parkinsonism due to interferon alpha (IFN alpha) therapy for chronic hepatitis C. A 51-year-old female received IFN alpha (Sumipheron@6 x 10(6) IU), three times a week by intramuscular injection. Six months after the initiation of IFN alpha therapy, she noticed tremor of bilateral fingers, and was admitted to our hospital. Neurological examination revealed muscle rigidity, bilateral finger tremor, mild bradykinesia. Tremor was more extreme at posture rather than at rest. She was diagnosed as Parkinsonism, and carbidopa-levodopa therapy was effective. Attention must be paid to Parkinsonism, when IFN alpha is administered.
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PMID:[Parkinsonism in a patient receiving interferon alpha therapy for chronic hepatitis C]. 914 76

A 20-year-old asthmatic woman who ingested 300 mg of salbutamol (Albuterol) and 30 g of paracetamol is presented. She had sinus tachycardia up to 160/min, hypotension (80/50 mmHg), tremor, hypokalemia (2.1 mEq/l) and hyperglycemia (12.1 mEq/l). Treatment was by gastric lavage, fluids, potassium and N-acetylcysteine. Symptoms resolved in 24 hours.
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PMID:[Salbutamol intoxication]. 915 36

A common observation in neurological practice is parkinsonism with concomitant cognitive decline, an association that usually arises from various underlying degenerative or vascular conditions, most of which are untreatable. An elderly woman with no history of psychiatric disease presented complaining of memory and cognitive impairment serious enough to interfere with daily life activities over the preceding year. She soon developed a predominantly left-sided tremor, rigidity and bradykinesia. She had had only 2 years of formal education. Neuropsychological assessment showed poor performance on Wechsler memory scale sub-items, as well as constructional apraxia, dyscalculia, reasoning difficulties and gross information deficits. A 3-month trial course of levodopa was followed by dramatic improvement in both parkinsonian symptoms and cognitive performance, including a 7-point gain in the Mini-Mental Status Examination score. At the same time, the Beck Depression Inventory score fell from 27 (baseline) to 18. Over the 10-year follow-up period the patient developed late levodopa syndrome and a persistent but mild dysthymic disorder, but never manifested dementia as defined by DSM-III-R criteria. This patient's case illustrates three important principles. First, although parkinsonism is known to be preceded by depressive episodes, particularly in a subgroup of younger patients, the symptoms of the elderly patient whose Parkinson's disease is foreshadowed by depression can mimic depressive pseudodementia, potentially leading to diagnostic confusion. Second, impaired motivation and disturbances in cognitive function are different from mood disorders, as the former involve the mesolimbic/mesocortical dopamine system, explaining the beneficial effect of levodopa on motivation and cognition in this patient even as mood was unaffected. Finally, depressive pseudodementia in Parkinson's disease does not necessarily herald the development of organic dementia in the long term.
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PMID:[Depressive pseudodementia in early Parkinson's disease: lessons from a case with long-term follow-up]. 919 54

Various neurodegenerative diseases have been reported to be associated with rapid eye movement (REM) sleep behavior disorder (RBD). This is the first report of a patient with corticobasal degeneration (CBD) associated with subclinical RBD. A 72-year-old woman was admitted complaining of fine tremor of the right hand and weakness of the right lower extremity. She was diagnosed as having CBD on the basis of clinical features and neuroimaging studies. Her family noticed snoring and increase in sleep talk, but they did not regard them as pathological. All-night polysomnography (PSG) revealed REM sleep without atonia (RWA) during which 14 episodes of talking and singing were observed. They ranged from the utterance of one word to that of comprehensible words of a song for about 3 minutes accompanied by various nonpurposeful movements of the mouth, hands, and limbs. These episodes were not associated with any sleep-disturbed breathing. Future PSG studies on CBD patients together with postmortem analysis of brain stem structures that are crucial for generating REM sleep-related atonia are warranted for further understanding of the pathophysiological mechanism of RBD.
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PMID:Subclinical REM sleep behavior disorder in a patient with corticobasal degeneration. 941 50

We report a 37-year-old Japanese woman with hereditary progressive dystonia with marked diurnal fluctuation and dopa-responsive dystonia. She developed dystonia in the lower limbs at the age of 11 years, followed by spasmodic torticollis and resting tremor of the feet, which responded remarkably to low doses of levodopa (100 mg/day). Concentrations of biopterin and neopterin in CSF were decreased. Polymerase chain reaction analysis of the guanosine 5'-triphosphate cyclohydrolase I gene revealed a novel mutation (Thr186-->Lys).
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PMID:A novel mutation of the GTP-cyclohydrolase I gene in a patient with hereditary progressive dystonia/dopa-responsive dystonia. 948 87

A 58-year-old woman developed slowly progressive tremulous myoclonus provoked mainly by action and posture. She had neither seizure nor dementia. No one in her family had similar symptoms. The presence of giant somatosensory evoked potentials (SEP) with enhanced long loop reflex and premovement cortical spikes demonstrated by the jerk-locked averaging method suggest that the involuntary movement is cortical reflex myoclonus. Magnetoencephalogram revealed that the generator sources of giant SEPs were the post-central somatosensory cortex and probably also the pre-central motor cortex. Symptoms improved after treatment with zonisamide, clonazepam and valpolate. This kind of involuntary movement might be called cortical myoclonic tremor.
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PMID:[A case of cortical reflex myoclonus manifesting tremor]. 950 72

A 39-year-old female suffered from diffuse goiter, palpitation, finger tremor and body weight loss for about one year. Then she developed acute onset of myalgia and swelling of calves, and muscle weakness of proximal limbs. She could not walk because of myalgia and muscle weakness, and was admitted to our hospital 4 days after the onset of muscle symptoms. On admission, her pulse was 110 per minute and she had finger tremor of 11-12 Hz. The thyroid gland was markedly and diffusely enlarged with an elastic soft surface. She presented muscle weakness of proximal limbs and neck, and had intermittent swelling and myalgia on calves. Deep tendon reflexes were increased in all extremities. The erythrocyte sedimentation rate was 22 mm per hour. Eosinophilia was not recognized. Serum CK level was elevated to 671 IU/l. Serum free T3 was higher than 21.7 pg/ml and free T4 was also elevated to 10.19 ng /dl. Serum TSH was lower than 0.05 microU/ml and thyroid stimulating antibody was 1,302.0%. Muscle biopsy of her left gastrocnemius muscle revealed markedly hypertrophic fascia with inflammatory cellular infiltration on HE staining. Inflammatory change was also recognized in muscle tissue and in perivascular region of perimysium. Variation of fiber size, necrotic fibers, and central nuclei were also seen. From these clinical and laboratory findings she was diagnosed as having Basedow's disease associated with fasciitis and polymyositis. Her thyroid function was improved by anti-thyroid drug, and swelling and myalgia of sural regions and weakness of proximal limbs were also improved by steroid therapy. Only one case of Basedow's disease associated with fasciitis and seven cases of that associated polymyositis have so far been reported. This is the first case report of fasciitis associated with Basedow's disease and polymyositis.
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PMID:[A case of fasciitis associated with Basedow's disease and polymyositis]. 959 6

We report a 74-year-old woman with parkinsonism and dementia, who died 4 years after the onset of the disease. She was well until 70 years of the age (1993) when she noted slowness in the movement in her left hand. She also developed gait disturbance and the similar symptoms spread to the right upper and lower extremities. Two years after the onset, she had difficulty in walk, and was admitted to our hospital on March 9, 1995. Her daughter had the onset of hand tremor at 50 years of the age and gait disturbance at 52. Her gait improved after levodopa treatment, but her MRI revealed a liner T2-high signal lesion along the outer surface of each putamen. On admission, the patient was alert but slighted demented. Higher cerebral functions were normal. She had a masked face and small voice. Her gait was of small step without arm swing. Retropulsion was present. Rigidity was noted in the neck but not in the limbs. She was bradykinetic but tremor was absent. She was treated with levodopa/carbidopa, dops, and bromocriptine with considerable improvement and was discharged on March 30, 1995. On January 19, 1996, she developed fever and hallucination; she became more akinetic and admitted again. She showed marked dementia and stage IV parkinsonism. She was treated by supportive measures with improvement in the general condition, but she was found to have a gastric cancer for which a subtotal gastrectomy was performed on March 11, 1996. Post-operative course was uneventful, but her parkinsonism progressed to stage V. She was transferred to another hospital on May 13, 1996. In July 21, 1996, she developed dyspnea and fever and was admitted to our hospital again. She was somnolent. Rigidity was moderate to marked and she was unable to stand or walk. By supportive cares, her general condition improved and was discharged to home on November 4, 1996. She developed fever on June 13, 1997 and admitted to our service again. Her BP was 150/90 mmHg. She was alert but markedly demented. Laboratory examination revealed increases in liver enzymes (GOT 75 IU/l, GPT 101 IU/l) and renal dysfunction (BUN 68 mg/dl, creatinine 3.27 mg/dl). Subsequent hospital course was complicated by renal failure and thrombocytopenia (33,000/ml). She expired on July 1, 1997. The patient was discussed in a neurologic CPC, and a chief discussant arrived at the conclusion that the patient had diffuse Lewy body disease and her daughter striatonigral degeneration. Some participants thought both the patient and her daughter had diffuse Lewy body disease. Post-mortem examination revealed marked degeneration of the substania nigra and the locus coeruleus. The medial part of the nigra also showed marked cell loss. Lewy bodies were found in the remaining nigral and coeruleus neurons. Cortical Lewy bodies were very few and the striatum was intact. Pathologic diagnosis was Parkinson's disease. Dementia was in part attributed to the marked degeneration of the medial part of the substantia nigra.
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PMID:[A 74-year-old woman with parkinsonism and dementia who died four years after the onset]. 973 28


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