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

In October 1976 an epidemic of 120 cases of paralytic shellfish poisoning was recorded in western Europe. Analysis of the 23 cases seen in Swizterland shows the following data; paresthesia of mouth and lips (100%); cerebellar syndrome (86%) with giddiness, ataxia, dysmetry and floating sensation; paresia or paralysis (62%); digestive symptoms (14%); no death. The mean incubation time is 3 hs 30 min; mean duration of the symptoms is 2 days. Half of the patients complain of asthenia and moderate memory disturbance lasting up to 3 weeks. The severity of the illness is in relation to the amount of ingested neurotoxin. The epidemiologic study shows that all European cases were due to consumption of mussels from the Atlantic coast of Spain.
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PMID:["Paralytic shellfish poisoning" (author's transl)]. 83 60

Inflammatory processes were provoked in 35 rats by subcutaneous implantation of sterile cotton-wool pads and treated five days by means of various antiphlogistic substances. The action of sodium salicylate (administered alone or in conjunction with gamma-globulin or with glucose) proved similar to that of prednisolone which was given as control substance. Human gamma-globulin exhibited neither anti-inflammatory nor pro-inflammatory effects. Experiments with twelve rabbits revealed that the pyretogenic potential of sodium nucleinate, one per cent (0.01 g/kg body weight) was stronger than that of animal charcoal or peptone. Yet, the two latter substances may be used, as well. The antipyretic effect of sodium salicylate was not as intensive but just as reliable as that of aminophenazone, when both preparations were applied to rabbits with induced fever. Concomitant administration of glucose is recommended to prevent development of undesired side-effects, such as giddiness or ataxia.
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PMID:[Antiphlogistic and antipyretic effect of sodium salicylate in rats and rabbits]. 616 73

Herniation of the hindbrain occurs when the lowest parts of the cerebellum and sometimes part of the medulla are moved downwards through the foramen magnum, a pressure difference acting across the foramen magnum moulding the tissues into a plug. It is suggested that the clinical course in both adults and babies with spina bifida may be explained by the hindbrain hernia acting as a valve.The term 'Chiari Type I deformity' is commonly used for an abnormality in which the tonsils and lowermost parts of the cerebellar hemispheres are prolapsed through a normal foramen magnum. Acute herniation may occur as a result of space-occupying lesions. Chronic herniation may be morphologically identical although it tends to be more severe. Sometimes it will produce few symptoms which often may be delayed so that the original causative lesion may not be apparent. Causes include bone softening, tumour, or previous meningitis. Birth injury is probably the commonest cause of the deformity, which presents clinically in adults.In infants with severe forms of spina bifida a hindbrain herniation is present. This abnormality may be called 'Chiari Type II deformity' or Arnold-Chiari deformity and is an intra-uterine abnormality in which the fourth ventricle and medulla are grotesquely herniated before they are properly developed and the foramen magnum is enlarged.The commonest clinical presentation of Chiari Type I deformity is syringomyelia, which is usually not diagnosed until adult life. Other presentations include syringobulbia, headache, oscillopsia, attacks of giddiness, lower cranial nerve palsies, and ataxia. Particularly characteristic are cough headache and cough syncope. Syringomyelia and syringobulbia in particular may be irreversible by the time they are diagnosed. Nevertheless, surgical decompression may be successful in relieving symptoms of headache, cough syncope, and long-tract compression; most cases of syringomyelia show some improvement and in others progression of the disease is arrested. Operative techniques for hindbrain herniation are discussed.Chiari Type II deformity is probably responsible for the progression of hydrocephalus after birth in the majority of babies with spina bifida. Measurement of pressure in the cerebrospinal fluid above and below the foramen magnum shows that intermittent pressure difference is commonly present at times of neurological deterioration. Surgical decompression of the hernia in adults allows correction of the valvular effect, which may be monitored by pressure measurements. In babies the associated hydrocephalus is usually so gross that it requires separate treatment, but pressure monitoring may be of value in assessing the state of the disease.
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PMID:Chronic herniation of the hindbrain. 701 51

Methyl chloride is encountered in the chemical industry as a methylating agent in the production of butyl rubber, tetramethyl lead, and other products as well as a blowing agent for some polystyrene foams. It is a potent CNS depressant whose principal route of absorption is by inhalation, although it can be absorbed through the skin. Symptoms of the neurotoxicity include headache, drowsiness, giddiness, ataxia, convulsion, and coma. This review focuses on the human case reports of acute and chronic exposures as well as some of the more important inhalation studies conducted with animals. The chemical and physical properties and the more important industrial uses are also discussed.
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PMID:Neurotoxicity of methyl chloride. 703 27

A rare case of extracerebral dural cavernous angioma sited near the sigmoid sinus is reported. This 60 yr old male patient gave history of episodic ataxia of left sided limbs experienced twice on same day and occasional giddiness. Examination did not reveal any findings. A mass was diagnosed on CT Scan following which angiography was carried out. The features matched with those of a meningioma. Retro-sigmoid craniectomy was performed. Occipital artery was coagulated. Tumor was dissected out. Post-operative course of the patient was uneventful. Histopathology revealed that the mass was a cavernous haemangioma.
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PMID:Dural cavernous haemangioma of posterior cranial fossa. 799 2

Between 1983 and 1990 a total of 74 freestyle mountaineers and 88 mountaineers with skis attempted to climb Mount Agri (Ararat). From the freestyle group two mountaineers were affected by acclimatisation disorder at 3200 m and seven at 4200 m above sea level. Acute mountain sickness (AMS) affected four mountaineers at 4200 m, eight at 4700 m, two at 5000 m and two at 5165 m, while 49 reached the summit. Only one of the mountaineers with skis was affected by AMS (at 4200 m), while all the others reached the summit. The symptoms of acclimatisation disorder and AMS, according to their degree of frequency, were headache, weakness, dyspnoea and palpitation, anorexia, nausea, vomiting, giddiness, ataxia and insomnia. Pulse rates varied between 115 and 124/min, and breathing between 30 and 38/min.
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PMID:Cases of acute mountain sickness on Mount Agri. 803 91

There have been several reports describing that immunoadsorption therapy improves the neurologic involvement in Fisher's syndrome (FS). However, few studies have assessed the usefulness of immunoadsorption therapy in view of the removal ability of anti-GQ(1b) antibody, which may function the development of FS. We examined the ability of immunoadsorbents for the anti-GQ(1b) antibody in a patient with FS. A 28-year-old woman developed diplopia and giddiness following a cough, fever and diarrhea. On admission (day 22), neurologic examination showed bilateral moderate oculomotor paralysis and bilateral complete abducens paralysis. She had areflexia, numbness of middle and ring fingers on the left and mild ataxic gait. Her serum had IgG anti-GQ(1b) and anti-GD(1b) antibodies. We examined the absorption of anti-ganglioside antibodies onto a polyvinyl alcohol gel (PVA), a phenylalanine-linked PVA (PH-350) and a tryptophan-linked PVA (TR-350) by the batchwise adsorption method. TR-350 absorbed the autoantibodies, but the removal ability of autoantibody by PVA and PH-350 was not proved. The FS patient was treated with TR-350 (days 29, 34 and 43) and PH-350 (day 39). Anti-GQ(1b) and anti-GD(1b) antibodies were significantly removed by the TR-350, in accordance with the results of the in vivo study. There was little loss of albumin as compared with the immunoglobulins and complements. The numbness and ataxia disappeared on day 44. The diplopia disappeared on day 106. TR-350 would be better than PH-350 in the treatment of FS by immunoadsorption therapy.
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PMID:[Immunoadsorption therapy on Fisher's syndrome--removal ability of anti-ganglioside antibodies by tryptophan-linked immunoadsorbent]. 866 31

INTRODUCTION. Acute intermittent familial ataxia is a rare disorder with autosomal dominant inheritance and unknown etiology which usually in childhood or adolescence. CASE 1. A 33-years-old woman who suffered from giddiness, gait ataxia, dysarthria and somnolence episodes. These episodes lasted between 4 and 72 hours. They generally occurred within a framework of emotional or physical stress. The following tests were performed: hemogram and biochemistry, blood and urine toxicology, immunological tests, cerebrospinal-fluid study, electrocardiogram, electroencephalogram, trunk and visual evocated potentials, cerebral computed tomography and cerebral magnetic resonance imaging. None of them gave significative results. CASE 2. A 12-years-old boy, son of the previous woman, who suffered from somnolence, gait ataxia and dysarthria with acute beginning. The same tests than in the above case were performed together with metabolic studies. There were no pathological findings in this case, either. The symptoms disappeared gradually in 6 days. His familial history led to a diagnosis of acute intermittent familial ataxia. A year later he suffered from a similar disorder and he was immediately treated with acetazolamide. The symptoms disappeared in 2 hours. CONCLUSIONS. Acute intermittent familial ataxia is a disorder of difficult identification. It can be easily confused with other periodical ones, because its diagnosis has to be based on the clinical findings and on the familial history. For this purpose, a therapeutic test with acetazolamide can be useful, since in most cases a spectacular clinical improvement has been observed.
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PMID:[Acute intermittent familial ataxia: report of a new family]. 868 Nov 77

Acute peripheral neuropathy caused by a disulfiram overdose is very rare and there is no report of it leading to vocal fold palsy. A 49-year-old woman was transferred to our department because of quadriparesis, lancinating pain, sensory loss, and paresthesia of the distal limbs. One month previously, she had taken a single high dose of disulfiram (130 tablets of ALCOHOL STOP TAB, Shin-Poong Pharm. Co., Ansan, Korea) in a suicide attempt. She was not an alcoholic. For the first few days after ingestion, she was in a confused state and had mild to moderate ataxia and giddiness. She noticed hoarseness and distally accentuated motor and sensory dysfunction after she had recovered from this state. A nerve conduction study was consistent with severe sensorimotor axonal polyneuropathy. Laryngeal electromyography (thyroarytenoid muscle) showed ample denervation potentials. Laryngoscopy revealed asymmetric vocal fold movements during phonation. Her vocal change and weakness began to improve spontaneously about 3 weeks after transfer. This was a case of acute palsy of the recurrent laryngeal nerve and superimposed severe acute sensorimotor axonal polyneuropathy caused by high-dose disulfiram intoxication.
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PMID:Acute vocal fold palsy after acute disulfiram intoxication. 1802 25

Methyl iodide is a monohalomethane and with a chemical formula CH(3)I. Acute exposures to methyl iodide have frequently occurred in the workplace. Predominantly, neuropsychiatric symptoms of acute exposure to monohalomethanes consist of headache, nausea, vomiting, drowsiness, dizziness, giddiness, diarrhea, confusion, ataxia, slurred speech, paralysis, convulsions, delirium, coma, and death. We report two cases who presented to our emergency services after accidental exposure to methyl iodide for a short duration. These case reports highlighted concurrence of frankly psychotic features and acute confusional state in workers vulnerable to industrial exposure to toxic chemicals. Understanding the mechanism of neuro-toxicity will perhaps throw some light on co-existence of both psychiatric and neurological symptoms. Awareness of these toxic effects at vulnerable work places will lead to timely and appropriate interventions. Importance of safety precautions and education of both workers and supervisors cannot be overemphasized here.
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PMID:Neuropsychiatric manifestations of methyl iodide. 2311 6


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