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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nine feedlot cattle showed clinical signs consistent with those expected in thromboembolic meningoencephalitis. These signs included pyrexia, ataxia, posterior paresis, paralysis and coma. Brown necrotic foci with haemorrhagic borders were observed in the brains of three animals that had died. In these foci vasculitis, thrombosis, infarction and neutrophil infiltration were observed during microscopical examination. Haemophilus somnus was isolated in pure culture from the brains.
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PMID:Thromboembolic meningoencephalitis diagnosed in Natal. 402 Aug 20

A case of coma due to Wernicke's encephalopathy complicated by respiratory failure is described. Ventilation and thiamine administration lead to recovery, although Korsakoff's psychosis and ataxia persisted. A review of similar cases of coma emphasizes the absence of diagnostic features, but that if structural disease is excluded the presence of pupillary and ocular signs may support a diagnosis of Wernicke's encephalopathy. The response to thiamine may be diagnostic as in 8 of these patients who received it, but the long-term morbidity remains high.
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PMID:Reversible coma in Wernicke's encephalopathy. 402 93

A family with hemiplegic migraine has been documented for a period of over forty years. From this study and the literature we conclude that (1) migraine is a cause of recurrent coma which may be associated with life-threatening cerebral hemisphere oedema; (2) hyperpyrexia with CSF pleocytosis occurs in hemiplegic migraine, which may thus simulate viral meningoencephalitis; and (3) cerebral angiography is hazardous in hemiplegic migraine and may exacerbate coma and cerebral oedema. In the family reported, cerebellar ataxia was present during recovery from attacks of hemiplegic migraine and affected patients ultimately suffered from persistent ataxia with radiological cerebellar atrophy. This syndrome thus constitutes a distinct form of late-onset autosomal dominant cerebellar ataxia and also of familial periodic ataxia. The status of 'cerebellar migraine' is reviewed.
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PMID:Migraine coma. Meningitic migraine with cerebral oedema associated with a new form of autosomal dominant cerebellar ataxia. 404 74

In some of the brains of head injury, shearing of axons and vessels caused by direct impact is seen widely in the white matter. This type of injury is designated by neuropathologists as shear injury or diffuse damage of impact type. Macroscopic lesions adjacent to the superior cerebeller peduncle and lesions of the corpus callosum are commonly seen in the brains with severe shearing injuries and the former is detected by CT scan as a high density at the quadrigeminal cistern, and this indicates occurrence of a severe shearing injury. Among 600 patients with head injuries, we managed 23 cases with pure shearing injury. These cases are classified into three groups according to the duration of coma. In the fulminant type (7 cases) the patients had severe brainstem signs including impairment of vital signs and died immediately after the injury. In the severe type (8 cases) the patients were decerebrated with normal pupillary response on admission and were severely disabled (i.e. tremor, truncal ataxia, dementia). In the moderate type (8 cases), the patients had only disturbance of consciousness for a long period, and recovered almost to the pre-injury state. Follow-up CT scan showed enlargement of the ventricles and sulci.
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PMID:[Pure shearing injury--clinical signs and symptoms, diagnosis, prognosis and review of the literature]. 408 53

An experimental infection was induced in mice by intravenous and intraperitoneal inoculation with Oidiodendron kalrai. The infected mice developed a complex neurological syndrome consisting of hyperirritability, jumping, circling, and ataxia, followed by coma and death or by apparent recovery. Visible lesions accompanied by inflammatory reaction and fungal elements were seen only in kidneys, but organisms were also identified in and isolated from the liver, spleen, lungs, and brain. Cortisone alone or in combination with streptomycin rendered the mice highly susceptible to infection with O. kalrai, and lesions were found in the brains as well as in the kidneys of these mice. Treatment of infected mice with streptomycin alone increased the severity and duration of the neurological syndrome, but such treatment did not increase the mortality rate.
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PMID:Pathogenicity and neurological effects of Oidiodendron kalrai for mice. 568 32

Neurological involvement occurred in every one of a series of 30 patients with an insulinoma. The episodic nature of the hypoglycaemia caused symptoms and signs to fluctuate and often led to delay in diagnosis (mean length of history was 3 years). The commonest feature at first presentation was confusion (20 instances), but as the illness evolved, coma (16 instances) and convulsions (8 instances) became more frequent. Objective weakness was found in 7 patients, with 3 examples of hemiparesis and 2 each of paraparesis and monoparesis; in all, the weakness resolved over a period of 1 hr to 3 days when normoglycaemia was maintained. Other neurological features included subjective visual disturbances, headache, dysarthria and ataxia. 220 patients with an insulinoma from 7 series in the literature were reviewed. The high incidence of neurological features was confirmed, with confusion (152 cases), coma (82 cases) and convulsions (58 cases) predominating. Visual disturbances were common, though not accurately quantified in some series. Objective evidence of weakness on the other hand was reported in only 6 of the 222 patients. Other less common symptoms included headache (18 instances) and peripheral paraesthesiae (14 instances). In the 7 series reviewed, as in our own, it was found that in any one patient, each episode of hypoglycaemia was accompanied by the same symptom complex. The presence of an insulinoma should be considered in any patient with unusual, or inexplicable neurological features, particularly when they are intermittent. The diagnosis can be confirmed by demonstrating an inappropriately high circulating insulin level, for the ambient blood glucose concentration.
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PMID:Neurological aspects of insulinomas. 609 Oct 78

Marek's disease virus (MDV)3 is a highly oncogenic herpesvirus that usually causes visceral lymphomas and lymphoid infiltration of the peripheral nerves in chickens. A relatively rare encephalitic condition, first found in farm flocks and referred to as transient paralysis (TP), is also caused by MDV(1). TP symptoms occur 9 to 11 days after MDV inoculation and range from mild ataxia to profound coma. Most birds recover by 24 to 72 hr after onset of symptoms, although severely affected birds may die within the same time period. Previous studies in this laboratory (2) showed that susceptibility to TP is a recessive trait controlled by major histocompatibility complex (MHC) genes (i.e., B complex genes of chickens). Inbred line G-B1 chickens (B13/B13) are resistant to TP, whereas chickens from related inbred lines G-B2 (B6/B6) and G-B3 (B15/B15) are highly susceptible. In this study chickens were immunosuppressed by neonatal cyclophosphamide (CY) treatment or surgical bursectomy (BX) to determine the possible role of antibodies in the pathogenesis of TP.
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PMID:Suppression of humoral immunity in chickens prevents transient paralysis caused by a herpesvirus. 630 Feb 37

From the clinical point of view, the nervous system effects of alcohol are the most important when work-related problems are considered. Alcohol is a primary, descending, central nervous system depressant that causes a familiar dose-dependent progression of acute intoxication from euphoria to ataxia, stupor, and ultimately coma. Chronic effects of alcohol on the nervous system are more difficult to diagnose. Particularly an insidiously developing alcoholic psychoorganic syndrome is a very difficult problem in occupational health. The interactions of low-level, chronic exposure to solvents and heavy drinking are interesting but, unfortunately, poorly understood. Withdrawal phenomena ranging from common hangover to tremulousness, cerebral convulsions, and delirium can also severely disturb normal worklife. The multitude of factors which regulate drinking behavior among the working population provides a challenge for investigators in the field of occupational health. More research should be focused on alcohol diseases and their effects on work, the effects of work on alcohol consumption, and the interactions of alcohol and compounds present in the work environment. The first step towards these problems is the development of valid methods for the early detection of heavy drinkers among the working population.
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PMID:Alcohol, work and the nervous system. 639 13

Sodium valproate was administered to 38 patients, admitted to our unit in the last 18 months, and chosen because they had: (1) poor control of their seizures; (2) therapeutic concentrations in their plasma of at least two major antiepileptic drugs. In 8 of them, a therapeutic dosage of VPA caused modifications of the state of consciousness ranging from coma to drowsiness and stupor. These patients also showed gastrointestinal disturbances, asterixis, ataxia, tremor and a worsening of EEG abnormalities. The side effects of the drug were constantly associated with increased concentration of blood ammonia. Better penetration of ammonia into the CNS of patients undergoing frequent seizures and possibly having imperfectly functioning biological barriers, could explain our observations. In view of the unusually high percentage of patients suffering from serious VPA side effects, it is probably advisable to carefully monitor ammonemia in the first few days of VPA therapy in every patient treated with multiple anticonvulsants.
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PMID:Hyperammonemia and valproate-induced alterations of the state of consciousness. A report of 8 cases. 642 61

Six epileptic patients are described to whom the addition of Valproic Acid (VPA) to a previously unsatisfactory antiepileptic treatment caused a toxic encephalopathy. This was characterized by alterations of the state of consciousness in all patients a few days after the beninning of the treatment with VPA. These ranged from a marked drowsiness to coma and were often associated with gastrointestinal and neurological (ataxia, asterixis) symptoms. In all cases very high blood ammonia values were found and the EEGs showed a diffuse slowing down of the activity. After the discontinuation of the drug the toxic symptoms quickly ceased and ammonia values returned to the normal values. It is hypothesized that the interference of VPA on the metabolism of ammonia could play an important role in the pathogenesis of the VPA-induced toxic encephalopathy.
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PMID:[Alterations of the state of consciousness induced by valproic acid: 6 case reports]. 643 99


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