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)

An autopsy case of a 52-year-old man suffering from chronic manganese poisoning (CMP) is reported with determination of the manganese distribution in the brain. The patient had been working in a manganese ore crushing plant since 1965. In 1967 he began to complain of difficulties in walking and diminished libido. Later, he developed various neuropsychiatric symptoms including euphoria, emotional incontinence, masked face, monotonous speech, "cock-walk", increased muscle tone, weakness of upper and lower extremities, tremor of the eye lids, and exaggeration of knee jerks. The major neuropathological change was degeneration of the basal ganglia, in which the pallidum was severely affected. The pallidum disclosed a loss and degeneration of nerve cells, which was especially marked in the medial segment, a prominent decrease of myelinated fibers, and moderate astrocytic proliferation. The substantia nigra was intact. Distribution of manganese in the brain of the present case of CMP was determined using flameless atomic absorption spectrometry and compared with control cases and also a case of Parkinson's disease (PD). There was no significant difference between the control cases and the case of PD in average concentration of manganese and its distribution in the brain. The present case of CMP showed no elevation in average concentration of manganese in the brain. However, there were some changes in its distribution. Thus, the continuance of neurological disorders in CMP is not linked to an elevated manganese concentration itself in the brain. CMP appears to be different from PD in neuropathology and manganese behavior in brain.
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PMID:Chronic manganese poisoning: a neuropathological study with determination of manganese distribution in the brain. 376 27

We studied a 68-year-old man who died after 13 years of progressive dementia, rigidity, bradykinesia, mild tremor, stooped posture, slow and shuffling gait, dystonia, blepharospasm, apraxia of eyelid opening, anarthria, aphonia, and incontinence. At autopsy, he had generalized brain atrophy with large deposits of iron pigment in the globus pallidus, caudate, and substantia nigra. Axonal spheroids were found in the globus pallidus, substantia nigra, medulla, and spinal cord. The neurochemical analysis of the brain revealed marked loss of dopamine in the nigral-striatal areas, with relative preservation of dopamine in the limbic areas. This is the oldest case of familial Hallervorden-Spatz disease reported and the first with neurochemical analysis of the brain.
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PMID:Late-onset Hallervorden-Spatz disease presenting as familial parkinsonism. 396 11

One of the case of the angiographically disappeared giant aneurysm is reported, which was arising from the top of the basilar artery. A 52-year-old man was admitted in April, 1978. He had developed a recent memory disturbance, tremor in the both upper extremities, the rigidity of the four extremities, an ataxic gait and urinary incontinence. Enhanced CT scan on admission demonstrated a large oval mass in the suprasellar region indenting nearly total third ventricle. Bilateral lateral ventricles were significantly dilated. The initial vertebral angiogram shortly after the admission revealed an oval-shaped aneurysm, 27 mm in the longest diameter, arising from the top of the basilar artery. The aneurysm was considered to be inaccessible due to its anatomical location and size. A ventriculoperitoneal shunt was placed, which alleviated clinical symptoms and signs immediately. However, a vertebral angiogram 1 year following the initial angiogram showed significant enlargement of the aneurysm, in spite of hypotensive and coagulant drugs which had been administered, then the administration of hypotensive drugs was ceased. Ventriculo-peritoneal shunt was replaced by ventriculo-atrial shunt in Sep. 1980. Left vertebral angiogram in May, 1981, 3 years after the initial angiogram, demonstrated the aneurysm had completely disappeared. He has been followed-up by the repetitive angiography up to the present, which proved the aneurysm has not reappeared. The occurrence of a spontaneous angiographical disappearance of an intracranial aneurysm is relatively uncommon, especially of a giant aneurysm. A rare case of spontaneous angiographical disappearance of a giant aneurysm was presented in this report.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Spontaneous angiographical disappearance of an unruptured giant aneurysm of the basilar top demonstrated by a sequential series of angiograms. A case report]. 408 84

Comprehensive treatment, including pharmacotherapy, rehabilitation, psychotherapy and ultrasound stimulation of the lymphatic system by the method of Seltzer is given to multiple sclerosis patients at the hospital department for these patients. In the first year of treatment three courses of ultrasound sessions are given with 24 sessions in each course, in the second year two such courses are given, and in the following years one course is given yearly. The present material comprised 45 patients after 7 or 8 courses of treatment in the hospital. The neurological status of each patient was evaluated before the first course and after the last one using a score scale containing the most important clinical parameters. Is was found that these therapeutic methods had only a negligible effect on paresis of the extremities, but it seems that they influenced favourably eye signs, particularly nystagmus, and cerebellar tremor. The greatest improvement was obtained in sphincter disturbances, especially in pollakiuria and urinary incontinence. The effect of ultrasound alone on the obtained results could not have been assessed. Investigations would be necessary for this purpose which are not done in this hospital.
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PMID:[Complex treatment of patients with multiple sclerosis]. 664 25

A 68-year-old man who ingested an improperly prepared extract of pokeweed had sweating, confusion, tremor, weakness, incontinence, and syncope. Analysis of the symptoms from this and similar patients previously reported suggests that the pokeweed plant contains an agent that produces peripheral and central cholinergic stimulation.
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PMID:Pokeweed poisoning. 724 29

The clinical features and natural history of 100 patients diagnosed as probable multiple system atrophy (MSA) are described. In all 14 (of 41 deceased) cases who underwent post-mortem examination of the brain, the diagnosis was confirmed pathologically, providing some validation of the clinical diagnostic criteria used. There were 67 men and 33 women. Median age at onset (at time of first reported symptom) was 53 (range 33-76) years. Autonomic symptoms were the initial feature in 41% of the patients, but had subsequently developed in 97% at latest follow-up. The most frequent autonomic symptom in men was impotence, and in women was urinary incontinence. Symptomatic orthostatic hypotension, although present in 68%, was severe in only 15% of patients. Parkinsonism was the initial feature in 46%, but had subsequently developed in 91% of subjects at latest follow-up. It was the predominant motor disorder [striatonigral degeneration (SND) type] in 82% of the patients, and was usually asymmetric (74%). Although akinesia and rigidity predominated, tremor was present at rest in 29% of patients, but in only 9% had a classical pill-rolling parkinsonian rest tremor been recorded. Twenty-nine percent of MSA patients had a good or excellent levodopa response at some stage. However, only 13% maintained this response. Prominent orofacial dyskinesias and dystonias occurred in a quarter of treated patients with MSA. Early onset (before age 49 years) MSA patients tended to have a good levodopa response. Cerebellar symptoms or signs were the only initial feature in 5%. Although subsequently developing in a further 47% of cases, in only 18% was a cerebellar syndrome the only (9%) or predominant (9%) motor disorder [olivopontocerebellar (OPCA) type]. Pyramidal involvement at latest follow-up was noted in 61% of all cases. In a further seven patients the initial features involved more than one system, and one other had presented as a parasomnia. Multiple system atrophy of the OPCA type most commonly presented with gait ataxia. Tremor, pyramidal signs and myoclonus were less common than in MSA of the SND type. Cerebellar signs were present in 42% of patients with MSA of the SND type and parkinsonian signs in 50% of patients with MSA of the OPCA type. Disease progression was faster than in idiopathic Parkinson's disease, so that > 40% of patients were markedly disabled or wheelchair bound within 5 years of onset of motor disturbance. Median survival of the whole group as calculated by Kaplan-Meier analysis was 9.5 years.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical features and natural history of multiple system atrophy. An analysis of 100 cases. 792 69

A 24-year-old oil well tester was rendered semiconscious by hydrogen sulfide (H2S). He received oxygen and was hospitalized but released in 30 minutes. The next day, nausea, vomiting, diarrhea, and incontinence of urine and stool led to rehospitalization. These problems and leg shaking, dizziness, sweating, trouble sleeping, and nightmares prevented his return to work. A physical examination, chest x-ray, and pulmonary function tests were normal 39 months after the episode but vibration sense was diminished. Two choice visual reaction times were delayed. Balance was highly abnormal (5 to 6 cm/sec) with eyes closed. Blink reflex latency was slow (R-1 17.5 msec versus normal 14.3 msec). Numbers written on finger tips were not recognized. Verbal and visual recall were impaired but overlearned memory was intact. Cognitive functions measured by Culture Fair, block design, and digit symbol were impaired. Perceptual motor was slow. Scores for confusion, tension-anxiety, depression, and fatigue were elevated and vigor was reduced. Forty-nine months after exposure his reaction time, sway speed, and color vision had not improved. His recall and his cognitive, constructional, and psychomotor speeds had improved but remained abnormal. These deficits are most likely due to H2S. Similar testing of other survivors is recommended.
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PMID:Case report: profound neurobehavioral deficits in an oil field worker overcome by hydrogen sulfide. 823 84

We report a 20-year-old female with Hallervorden-Spatz syndrome (HSS). This patient is the product of consanguineous parents. She developed genu valgum, tendency to fall and mental deterioration at the age of 6, decrease of the number of spoken words at the age of 14, dysarthria, unsteady gait, postural tremor of the upper extremities, dystonic posture of hands and double incontinence at the age of 16. Her disease progressed slowly. Neurological examination on admission revealed severe mental retardation, optic atrophy, forced grasping, hyperactive tendon reflexes in the upper extremities and bilateral Babinski sign. An extensive laboratory investigation including the leukocyte lysosomal enzymes, serum amino acid analyses, copper studies and ceruloplasmin were almost within normal limits. MRI, T2 weighted images, showed markedly decreased signal intensity in the globus pallidus but substantia nigra and increased signal intensity in diffuse cerebral white matter. T1 weighted images showed marked atrophy of the brainstem and cerebellum. She met the diagnostic criteria for HSS by Swaiman; we diagnosed her as HSS group II. HSS is characterized by the presence of many spheroids in the central nervous system which is similar to neuroaxonal dystrophy (ND). However, clinical and pathological differences exist between HSS and ND, the precise classification of the two conditions has remained controversial. Although there are many reported cases in which both conditions overlap, this is the first reported case that simultaneously demonstrates increased iron deposition in the globus pallidus, marked atrophy of the brainstem and cerebellum and typical clinical course compatible with HSS.
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PMID:[A case of Hallervorden-Spatz syndrome with marked atrophy of the brainstem and cerebellum]. 836 59

An outbreak of hemorrhagic colitis associated with Escherichia coli O157:H7 occurred in a kindergarten in Saitama, Japan from September to November, 1990. Seven patients admitted to our hospital showed neurological manifestations: generalized seizures, impaired consciousness, urinary incontinence, gaze nystagmus, phrenic nerve palsy, action tremor and vertigo. Two patients died. On the basis of the clinical courses and laboratory findings of the seven patients and postmortem findings of one case, these neurological symptoms were suspected to be induced by the verotoxin elaborated by Escherichia coli O157:H7.
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PMID:Neurological manifestations of hemorrhagic colitis in the outbreak of Escherichia coli O157:H7 infection in Japan. 851 21

We report a 65-year-old man with parkinsonism, supranuclear gaze palsy, and dementia. The patient was well until 58 years of the age (1984) when he noted an onset of tremor in his right hand. He visited our neurology service two years after the onset; neurologic examination at that time revealed moderate restriction in down ward gaze, horizontal gaze nystagmus in left and right gaze, stooped posture with loss of arm swing when he walked, slight rigidity in the neck and the right upper and lower extremities, and resting tremor in his right hand and foot; mentation was intact. He was treated with 600 mg of levodopa with carbidopa; his tremor partially improved. He received left Vim thalamotomy on March 14 of 1987. His tremor disappeared after the thalamotomy. Post-operative course was complicated by transient clouding of consciousness due to subdural hematoma which developed after the surgery. Six months after the surgery, he noted increase in the unsteadiness of gait; he also experienced urinary incontinence once in a while, and he became mentally dull. In November of 1988, he had episodes of stiffening of his body. Although his spontaneous speech was very much reduced, he repeatedly hummed a same tune; no one could make him stop humming. In June of 1989, he was totally unable to move his eyes in the vertical direction. He was hospitalized to another hospital in May of 1990 where he died six month after admission because of pneumonia. The clinical course of this patient was characterized by the onset with parkinsonian resting tremor, and supranuclear gaze palsy and dementia in the later course. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had an overlap syndrome of progressive supranuclear palsy (PSP) and diffuse Lewy body disease. Majority of the participants thought that the patient had progressive supranuclear palsy, but many of them had an impression that parkinsonian tremor responding to levodopa as the initial symptom for PSP is rather unusual. Postmortem examination revealed severe loss of neurons in the substantia nigra, the globus pallidus, and the subthalamic nucleus with reactive gliosis; formy spheroids were seen in the substantia nigra, however, no Lewy bodies or neurofibrillary tangles were observed. Moderate neuronal loss was also seen in the dentate nucleus of the cerebellum. In addition, the precentral gyrus showed moderate neuronal loss, astrocytosis, and spongy change in the second layer; ballooned neurons were seen in the third and the fifth layers. Histologic characteristics were consistent with the pathologic diagnosis of corticobasal degeneration.
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PMID:[A 65-year-old man with Parkinsonism, gaze palsy, and dementia]. 867 36


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