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 previously unrecorded nervous disease in pigeons was investigated. The disease, characterized by paresis, paralysis of the extremities, head-shaking, and torticollis, is contagious and spreads slowly. The mortality rate of affected pigeons was very high. The disease appeared to spread among pigeon flocks in spring and summer. The predominant gross change in most cases examined was congestion of the visceral organs. Some cases had grayish spots on the pancreas and kidneys. The histologic changes are characterized by neuronal and myelin degeneration with mononuclear cell infiltration and perivascular cuffing. Degeneration of the parenchyma and marked congestion are prominent in the visceral organs. The causal agent, found to be a virus, produced pock lesions on chorioallantoic membranes of developing chick embryos and failed to aagglutinate chicken RBCs. Antisera against Newcastle disease virus and avian encephalomyelitis virus did not neutralize the isolated virus. The virus produced typical signs in experimentally inoculated pigeons.
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PMID:Viral encephalomyelitis of pigeons: pathology and virus isolation. 54 2

Estonian shale oil contains about 25--30% phenols, and their action determines the toxicity of shale oils. The clinical symptoms of intoxication are rather similar, regardless of route of administration. Due to neurotropic action, the coordination of movements is impaired, and clonic and tetanic convulsions, paresis and paralysis of extremities, and narcosis are observed. In subacute and chronic toxicity tests, dysfunction of the central nervous system was found. In long-term (4--6 month) experiments, changes in liver and kidney function were found. Shale oil has gonadotropic activity and causes changes in the sexual cycle as well as diminution of the number of primordial folicles in the ovaries or a decrease in the quantity of normal spermatogonia in testicular germinal epithelium. Shale oils produce local irritation of skin and mucous membranes. Shale oil can induce sensitization of the organism after repeated administration. The results of acute intoxication tests have proved that volatile and nonvolatile phenol fractions, isomeric dimethylphenols, and 5-methylresorcinol, must be characterized as moderately toxic substances; the LD50 ranges from 501 to 1500 mg/kg. The clinical symptoms of acute toxication are similar for all studied phenols (restlessness, unsteadiness, clonic tremor, paresis and paralysis of extremities, and death). In spite of the moderate toxicity of phenols in acute experiments, repeated administration of small doses can cause different changes in the nervous system and internal organs of experimental animals. For all the phenols studied, the maximum allowable concentration in water was limited by their effect on the organoleptic properties of water. The nonactive dose for warm-blooded animals is from 100 to 3000 times the threshold limit value of phenols on the basis of their organoleptic properties. The effect of commercial products of oil shale industry is generally determined by the toxicity of the main components: water-soluble oil shale phenols.
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PMID:Toxicological studies of shale oils, some of their components, and commercial products. 57 2

Tick-borne encephalitis is transmitted by the tick ixodes ricinus. After the second world war an increase in the number of cases of encephalitis was observed and the neurotropic virus was isolated for the first time in 1948. Reservoir animals are mouse-like wild animals and also agricultural domestic animals. The infection is transmitted to humans through tick bites. It becomes apparent subjectively in headaches, vomiting, tiredness, giddiness and insomnia, and objectively in meningeal symptoms, extrapyramidal tremor, cerebellar ataxia, vestibular nystagmus and paresis. The treatment consists of strict rest in bed for 10 days at least and symptomatic support of the general health. Good results are obtained with antiedematous therapy with hydrocortisone or pyritinol.
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PMID:[Clinical picture of Central European tick-borne encephalitis (author's transl)]. 82 10

A patent, who suffered from nonprogressive athetotic-myoclonic hyperkinesia of the left arm and spastic paresis of the underdeveloped left leg since early childhood, experienced a febrile episode at the age of 23, after which a weakness and ataxia of the right limbs with frequent falling persisted; at the age of 28, he developed a right-sided rigidity, tremor at rest and mask-like face as sequelae of encephalitis disseminata exacerbations. The violent intention myoclonus of the left side of the body could be abolished by stereotactic coagulation in the V.o.p and V.o.a and zona incerta until death 11 days later. The athetotic myoclonic hyperkinesia is the consequence of a left-sided severe status marmoratus of the right putamen with extensive loss of nerve cells and shrinkage. The additional nerve cell loss in the right substantia nigra due to demyelinating encephalitic foci did not produce Parkinson symptoms, because these require a normal striatum. This loss did, however, exaggerate the original hyperkinesia to a violent intention myoclonus, which was abolished by interruption of denatatothalamic afferents to the V.o.p nucleus and of pallidothalamic afferents to the V.o.a nucleus. The Parkinson syndrome of the right side is due to demyelinating foci of different ages. The Parkinson symptoms were manifest on the right side, because the left status marmoratus did not severely reduce the striatal nerve cells. In this case, there is no indication that the introduction of the stereotactic electrode has precipitated new demyelinating foci.
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PMID:Stereotactic treatment of action myoclonus in a case of combined status marmoratus and multiple sclerosis. A contribution to the pathophysiology of basal ganglia with multiple lesions in both the striatum and the substantia nigra. 109 75

Twenty-four 4-week-old poults, free from Mycoplasma meleagridis and M. gallisepticum, were inoculated with a velogenic viscerotropic strain of Newcastle disease virus. Clinical signs (gasping, coughing, and dyspnea) developed 4-5 days postinoculation, continued until nervous derangement appeared, and then (usually 3 days after initial clinical signs appeared) declined in severity. Prominent nervous signs were paresis and paralysis of the extremities, with pronounced head-shaking. The most constant gross lesions detected involved the airsacs. The abdominal sacs of a few poults contained a large accumulation of yellowish, cheesy exudate and there was cloudiness of the thoracic airsacs of all inoculated poults. A few turkeys had tracheitis with some catarrhal exudates and casts in the lower part of the tracheal lumen. Congestion of lepto-meningeal vessels usually correlated with the severity of the nervous signs. The histologic lesions were characterized by both degenerative and proliferative changes with predominantly mononuclear cell and heterophil infiltrations throughout the body. The obvious lesion seen in the recovery stage of the disease was proliferation of lymphofollicular nodules in the parenchymatous organs.
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PMID:Pathology of velogenic Newcastle Disease virus infection in turkeys. 116 10

We reported a 49-year-old mother and her 28-year-old son with autosomal dominantly inherited bulbar spinal muscular atrophy (AD-BSMA). They showed progressive bulbar paresis, muscle wasting and weakness dominant in the proximal groups of limb muscles, and finger tremor. Onset of illness was in adult life. In laboratory examinations, elevated creatine kinase in serum and neurogenic changes either in EMG or muscle biopsy were noted. The son had neither gynecomastia nor abnormal sexual hormone levels which were observed in the sex-linked recessive bulbar spinal muscular atrophy (SR-BSMA). Elongation due to the CAG repeats at the androgen receptor gene of the X chromosome in SR-BSMA was not detected. In conclusion, it is clear that AD-BSMA is different from SR-BSMA on the basis of clinical and genetical aspects.
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PMID:[A mother and her son with autosomal dominant bulbar spinal muscular atrophy]. 130 Feb 63

Two women had a syndrome of progressive parkinsonism with ipsilateral rigidity, mild resting tremor, paresis, hyperreflexia, and an extensor plantar response. Symptoms had started 24 and 3 months after a surgical procedure in the affected limb. Neuroimaging studies were unhelpful. Both the parkinsonian features and the pyramidal tract signs responded well to dopaminergic drug treatment. We propose that the syndrome be called "idiopathic hemiparetic parkinsonism".
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PMID:Idiopathic hemiparetic parkinsonism, a syndrome distinct from idiopathic parkinsonism. 135 57

We prospectively examined 11 patients with magnetic resonance imaging-documented infarction in the paramedian thalamopeduncular region, which is supplied by the superior mesencephalic and posterior thalamosubthalamic arteries. Variations in the size and rostral-caudal extent of infarction correlated with the following three clinical patterns: (1) With unilateral paramedian mesencephalic infarction, an ipsilateral third nerve paresis was accompanied by mild contralateral hemiparesis or hemiataxia. Contralateral ptosis and impaired upgaze were observed in two patients; one of them showed additional damage to the posterior commissure. (2) With bilateral infarction in the thalamopeduncular junction, involving the mesencephalic reticular formation, supranuclear vertical gaze defects were accompanied by impaired consciousness or memory, and mild aphasia in some patients. Persistent amnesia was observed only when the dominant anterior nucleus or mamillothalamic tract was damaged. (3) With larger thalamopeduncular infarcts, partial or complete third nerve paresis was combined with supranuclear gaze disturbance and delayed contralateral tremor. An unusual gaze disorder, a variant of the vertical "one-and-a-half syndrome," occurred with a small strategically placed lesion at the thalamopeduncular junction, best explained by selective damage to supranuclear pathways or partial nuclear involvement. The primary cause of these infarctions was embolism to the basilar apex or local atheroma at the origin of the posterior cerebral artery.
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PMID:Paramedian thalamopeduncular infarction: clinical syndromes and magnetic resonance imaging. 151 Mar 56

A mutant strain of Han-Wistar rat carries an autosomal recessive gene producing spastic paresis which is characterized by ataxia, tremor and hind limb rigidity. Brains of affected rats and unaffected littermate controls were transected at the mesencephalon into rostral and caudal portions (the caudal portion contained the cerebellum and brainstem). Poly(A)+ mRNA was isolated from pooled rostral or caudal portions and injected into Xenopus oocytes. The oocytes were voltage-clamped and exposed to 1 mM L-glutamate, 500 microM kainate, 500 microM quisqualate, 200 microM N-methyl-D-aspartate (NMDA) or 1 mM gamma-aminobutyric acid (GABA). Oocytes injected with mRNA isolated from the caudal portions of the affected rat brains exhibited statistically significant increases in glutamate and kainate peak current responses compared to oocytes injected with mRNA from other brain samples. No differences were noted in the responses of the groups when exposed to quisqualate, NMDA or GABA. Cerebellar and brain stem mRNA were also isolated separately in different groups of mutants and unaffected littermates. Only oocytes injected with cerebellar mRNA from mutants displayed statistically significant increases in responses to glutamate and kainate. In parallel morphological studies changes in the cerebellum of mutants were also observed. These consisted of a loss of Purkinje cells and an asymmetrical disarrangement of the granule cell layer of cerebellar cortex. Taken together, the physiological and morphological results suggest that alterations in glutamate/kainate receptors in the cerebellum are phenotypic manifestations of the Han-Wistar mutation. The results are consistent with the hypothesis that this mutant rat might serve as a model of glutamate/kainate excitotoxicity in the brain.
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PMID:Altered excitatory amino acid function and morphology of the cerebellum of the spastic Han-Wistar rat. 168 5

In 108 patients referred for caloric testing, head-shaking nystagmus (HSN) was noted in 37 electronystagmography (ENG) recordings. A canal paresis was found in 31 patients and a sensorineural or mixed hearing loss in one or both ears was found in 45 patients. Both HSN and canal paresis were insensitive predictors of either hearing loss or of each other. HSN was less sensitive as well as less specific than canal paresis for hearing loss. These data suggest that HSN is not as powerful a test as canal paresis in detecting lesions of the 8th nerve.
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PMID:Head-shaking nystagmus: associations with canal paresis and hearing loss. 258 66


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