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)

The clinical and pathological findings after a natural intra-uterine infection with BVD-virus in a Friesian dairy herd are described. The virological and serological aspects will be discussed in a separate paper (30). In a period of 4 years, 11 calves were born with the following nervous symptoms: more or less serious incoordination, tremor, oscillating nystagmus, and a negative blinking reflex. The pupillary and sucking reflexes were normal. No ocular defects, such as lenticular opacity or retinal atrophy were observed. The first calf was born in 1979. Within 6 months the symptoms disappeared. After a normal conception and pregnancy this animal gave birth to 2 clinically normal calves in 1981 and 1982. The second calf died at the age of 2 months, due to an ulcerating enteritis. In 1980, again 8 calves with the same nervous symptoms were born within a period of 3 months. Two calves died at the age of 3 days and 5 weeks respectively; 2 calves were sold when 10 days and 3 weeks old; one calf did not improve and was necropsied at the age of 17 days. The remaining 3 calves showed only a slight hypermetria when examined after 6 months. At that time nystagmus was only visible with ophthalmoscopy. Two calves were slaughtered when 10 months old. The last one, a bull, proved to be sterile and was necropsied at the age of 1 1/2 year. A calf, born in 1981, recovered within a week and was necropsied at the age of 15 days. The last calf, born in 1982, did not improve at all and was necropsied at the age of 14 days. During these 4 years none of the other animals in the herd showed any symptoms due to an acute or chronic BVD-virus infection. At post mortem examination of 6 animals no macroscopically visible malformations were found. Hypomyelination and abnormal glial cells were evident in 5 cases, especially in the two youngest calves which did not show any improvement. One of them had had an obvious thymic hypoplasia. The calf which recovered within a week showed only very slight changes. In one of the calves slaughtered at 10 months, inflammatory lesions were found in the brain. The diagnosis was confirmed by virological investigations. Clinically as well as pathologically there was a close resemblance to Border disease in lambs and congenital tremor in piglets after prenatal exposure to Hog cholera virus.
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PMID:Neurological disorders, virus persistence and hypomyelination in calves due to intra-uterine infections with bovine virus diarrhoea virus. I. Clinical symptoms and morphological lesions. 664 98

The prevalence of neurological abnormality was determined among Cree Indians of northern Quebec who were exposed to methylmercury through contamination of local fish. A medical team examined each subject, without knowledge of the subjects' methylmercury exposure, and assessed nystagmus, co-ordination and gait, tremor, movements and reflexes, sensation, stereognosis, 2 point discrimination, visual fields and hearing. Tremor, incoordination and abnormal reflexes were the most prevalent neurological abnormalities, but other major manifestations of methylmercury toxicity (impairment of peripheral sensation, astereognosis and concentric constriction of visual fields) were seen infrequently. Abnormalities in Quebec were much less severe than in previous reported outbreaks of methylmercury poisoning. Since no single clinical syndrome is pathognomonic of methylmercury poisoning, the presence of neurological abnormality does not establish that it is causally related to methylmercury exposure.
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PMID:Prevalence of neurological abnormality in Cree Indians exposed to methylmercury in northern Quebec. 665 82

Deltamethrin is a pyrethroid insecticide which produces reversible motor symptoms in mammals involving facial movements, progressive incoordination, and choreoathetosis. These symptoms were found to be preceded and accompanied by increases in blood flow in the caudate nucleus and cerebral cortex of conscious rats. Blood flow, measured by the hydrogen polarography method, showed a 2.8-3.8 fold increase in the caudate nucleus and a 1.9-2.6 increase in the cortex after intraperitoneal deltamethrin. The increase in caudate blood flow provided an early and sensitive indicator of the development of motor symptoms, and preceded development of EEG spike discharges. A different pattern of motor symptoms consisting largely of tremor with no choreoathetosis was produced for comparison using another pyrethroid, cismethrin. This, whilst producing a similar increase in cortical flow, did not produce the disproportionate increase in caudate flow characteristic of deltamethrin. Although the actions of deltamethrin were shown not to be restricted to the extrapyramidal system, the selectivity of the blood flow increases, and the nature of the symptoms produced show deltamethrin to be a useful tool for the production of experimental extrapyramidal motor hyperactivity.
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PMID:Changes in brain blood flow associated with deltamethrin-induced choreoathetosis in the rat. 679 14

Two patients are reported presenting with incoordination mimicking cerebellar disease in the upper and lower limbs, ataxia of gait, absent tendon reflexes and little or no clinically detectable wasting. Motor conduction velocity in the upper limbs was substantially reduced in one patient whereas it was normal and slightly reduced in the other. It is concluded that in Charcot-Marie Tooth disease incoordination may mimic cerebellar disease and when this is so it is due to the association of varying degrees of proprioceptive deafferentation and a dyskinesia similar to that produced by familial (essential) tremor.
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PMID:Unusual presentation of Charcot Marie-Tooth disease-incoordination with absent of minimal wasting-Report of 2 cases. 722 62

We generated mice, null mutant in the adhesion molecule on glia (AMOG), the beta 2 subunit of the murine Na,K-ATPase gene. These mice exhibit motor incoordination at 15 d of age, subsequently tremor and paralysis of extremities, and die at 17-18 d after birth. At these ages, the mutants have enlarged ventricles, degenerating photoreceptor cells, and swelling and degeneration of astrocytic endfeet, leading to vacuoles adjoining capillaries of brain stem, thalamus, striatum, and spinal cord. In tissue homogenates from entire brains of 16-17-d-old mutants, Na,K-ATPase activity and expression of the beta 1 subunit of the Na,K-ATPase and of the neural adhesion molecules L1, N-CAM, and MAG appear normal. We suggest that the mutant phenotype can be related primarily to reduced pump activity, with neural degeneration as a possible consequence of osmotic imbalance.
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PMID:Degeneration of neural cells in the central nervous system of mice deficient in the gene for the adhesion molecule on Glia, the beta 2 subunit of murine Na,K-ATPase. 752 97

The adhesion molecule on glia (AMOG) has been reported to function as cell adhesion molecule and also to constitute the beta 2-subunit of the murine Na,K-ATPase. In order to elucidate these functions in vivo, Magyar et al. have generated mice carrying a targeted deletion of the AMOG gene. These mice exhibit behaviourally normal development till postnatal day P16. At this time, they develop muscular weakness, incoordination, and tremor. Death invariably occurs 24-36 hours after onset of the symptoms. Histological and ultrastructural examination of brain sections show enlarged ventricles, brain edema, and swelling of astrocyte end feet. However, no disturbances of the architecture or cell migration in the brain can be detected. In order to identify long-term consequences of AMOG deficiency which might not yet be detectable at the time of death, we have established a CNS grafting model. The embryonal brain anlage (E10.5-E13.5) was grafted into the caudoputamen of wild type mice. The graft recipients are sacrificed up to 7 months after the procedure. Both wild type and AMOG deficient grafts develop and form solid neural tissue with neurons, myelinated axons, glial cells, and ventricular structures, as shown by histological and immunocytochemical analysis. However, no differences in grafts derived from wild type, heterozygous, and AMOG-deficient donors can be detected. Proliferation has been examined by BrdU immunocytochemistry. The blood-brain barrier as examined by repeated magnetic resonance imaging after injection of Gadolinium-DTPA has been shown to be largely reconstituted five weeks after grafting.
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PMID:[Morphology and development of neural transplants of AMOG-deficient mice]. 753 17

This is the first reported case of dystonia with a partial deletion of the long arm (q) of chromosome 18. Neurologic findings in the 18q- syndrome include mental retardation, seizures, nystagmus, incoordination, tremor, and chorea. A 36-year-old woman with an 18q terminal deletion [karyotype 46,XX,del(18)(q22.2)] had hypothyroidism, diabetes mellitus, borderline intelligence, short stature, short neck, sensorineural hearing loss, and sensorimotor axonal neuropathy. Parents' karyotypes were normal. She had had incoordination and writing difficulty since childhood. Posturing and tremor of the head began at age 16, followed by arm tremors. She had jaw deviation and tremor, neck tremor with retrocollis, involuntary pronation of the right arm, coarse postural and severe action tremor, and tight pen grip with dystonic wrist extension on writing. The 18q- syndrome should be added to the list of genetic causes of secondary dystonia. A karyotype analysis should be considered in secondary dystonias, particularly when there are associated features such as short stature and endocrinopathies.
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PMID:Dystonia in a patient with deletion of 18q. 756 32

A minority of patients treated with serotonergic agents develop a fulminant and potentially life-threatening illness characterized by changes in mental status, restlessness, myoclonus, hyperreflexia, tremor, shivering, incoordination, hyperthermia, diaphoresis and diarrhea. This condition of serotonergic hyperstimulation is called the "serotonin syndrome". The author describes an adverse response in a patient given fluoxetine and lithium. A 61-year-old woman presented to casualty exhibits nearly all of the diagnostic criteria proposed by Sternbach [17].
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PMID:[A case of serotonin syndrome]. 756 25

We report a case of juvenile Parkinson's disease which initially presented as bulbar incoordination at the age 12. The condition was characterized by dystonia of the upper extremities. The patient was a 14-year-old female. The patient's main symptoms were bulbar dysfunction. Resting and action tremor, akinesia, stooped posture, distortion of the trunk, dystonia of the upper extremities, oculogyric crisis, and impairment of the postural reflex were seen. The bulbar symptoms were considered to be attributable to circumoral uncoordination. Although L-dopa decarboxylase inhibitors were markedly effective in alleviating these symptoms, an adverse reaction due to the agent was observed as the form of oral dyskinesia. Since the changes in blood concentration of L-dopa after administration of the agent was clearly reflected in the surface electromyogram, we concluded that this diagnostic procedure is useful in evaluating the therapeutic efficacy of L-dopa.
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PMID:[Juvenile Parkinson's disease initially presenting as bulbar incoordination: a case report]. 818 82

The allocation of hypoglycaemic symptoms to autonomic or neuroglycopenic groups tends to occur on an a priori basis. In view of the practical need for clear symptom markers of hypoglycaemia more scientific approaches must be pursued. Substantial evidence is presented from two large scale studies we performed which support a three factor model of hypoglycaemic symptomatology, based on the statistical associations discovered among symptoms reported by diabetic patients. Study 1 involved 295 insulin-treated out-patients and found that 11 key hypoglycaemic symptoms segregated into three clear factors: autonomic (sweating, palpitation, shaking and hunger) neuroglycopenic (confusion, drowsiness, odd behaviour, speech difficulty and incoordination), and malaise (nausea and headache). The three factors were validated on a separate group of 303 insulin-treated diabetic out-patients. Confirmatory factor analyses showed that the three factor model was the optimal model for explaining symptom covariance in each group. A multi-sample confirmatory factor analysis tested the rigorous assumptions that the relative loadings of symptoms on factors across groups were equal, and that the residual variance for each symptom was identical across groups. These assumptions were successful, indicating that the three factor model was replicated in detail across these two large samples. It is suggested that the results indicate valid groupings of symptoms that may be used in future research and in clinical practice.
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PMID:Partitioning the symptoms of hypoglycaemia using multi-sample confirmatory factor analysis. 840 46


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