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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

Side effects of orally administered bismuthic salts have been known for many years. Many systems are involved, including the digestive and urinary. The authors discuss a recently discovered effect on the central nervous system, termed "bismuth encephalopathy". In the light of the medical literature reviewed, two original aspects are stressed: the clinical symptoms are stereotyped and completely reversible, and the distribution of the disease is almost epidemic, being limited in time and space. The prodromes include confusion, asthenia, slowing of mental functions and disturbance of gait. The clinical picture is dominated by four major symptoms: confusion (again), ataxia, dysarthria and, above all, myoclonic jerks. In conclusion, various pathogenetic hypotheses are considered. The purpose of this study is to enable the general practitioner to detect the development of this condition early in treatment with oral bismuthic salts. Withdrawal of the medication always results in normalization of the patient's condition.
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PMID:[Encephalopathy during oral treatment with bismuth salts]. 98 34

The clinical safety of lamotrigine (LTG), assessed in four completed randomized, double-blind, placebo-controlled crossover trials and an interim analysis of 27 12-month open studies, is discussed. LTG was added to existing antiepileptic drugs (AEDs) of adult patients with refractory epilepsy, using a twice-daily regimen. In the pooled data from the four double-blind studies (n = 92), the incidence of adverse experiences with LTG and placebo did not differ significantly. Two patients were withdrawn on LTG due to adverse experiences (one rash, one nausea and vomiting). In the open studies (pooled data; n = 572) the most commonly reported adverse experiences were dizziness, diplopia, somnolence, headache, ataxia, and asthenia (10-14% incidence). Forty-nine patients (8.6%) were withdrawn with adverse events, most commonly for rash (2.3%). No patients were withdrawn from any of the studies with physical, neurological, or ECG abnormalities thought attributable to LTG treatment. Laboratory measures, vital signs, and weight did not show any consistent changes of clinical significance, and no significant changes in plasma concentrations of concomitant AEDs after the addition of LTG were observed.
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PMID:Human safety of lamotrigine. 183 76

Idiopathic hypoparathyroidism was diagnosed in five young to middle-aged cats of mixed breeding. Three of the cats were male and two were female. Historic signs included lethargy (n = 5), anorexia (n = 5), muscle tremors (n = 4), weakness (n = 4), generalized seizures (n = 3), ataxia (n = 3), mental dullness or disorientation (n = 3), panting (n = 2), pruritus (n = 1), ptyalism (n = 1) and dysphagia (n = 1). Weakness (n = 4), dehydration (n = 2), cataracts (n = 2), hypothermia (n = 1), and bradycardia (n = 1) were found on physical examination. Results of electrocardiography revealed a prolonged Q-T interval in two cats. Results of initial laboratory tests revealed profound hypocalcemia and severe hyperphosphatemia with normal renal function. The diagnosis of hypoparathyroidism was made on the basis of the history, clinical signs, and results serum biochemical testing (i.e., severe hypocalcemia and hyperphosphatemia); in two cats, the diagnosis was also confirmed by histologic examination of parathyroid glands. Initial treatment included intravenous administration of 10% calcium gluconate and oral administration of large loading doses of calcium and vitamin D (dihydrotachysterol). Successful long-term management with dihydrotachysterol and calcium was achieved in all cats. The final dosage of dihydrotachysterol required to maintain normocalcemia in the five cats ranged from 0.004 to 0.04 mg/kg/day (mean = 0.015 mg/kg/day). Long-term calcium supplementation was given to three of the cats in dosages ranging from 29 to 53 mg/kg/day (mean = 42 mg/kg/day) of elemental calcium. One cat died after 28 months of therapy from widely metastatic hemangiosarcoma; the other three cats are still alive and well after 5 to 37 months of treatment.
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PMID:Idiopathic hypoparathyroidism in five cats. 202 14

The authors report the case of a 14-year-old boy who presented with shunted growth and low weight gain, asthenia with fatiguability on effort, clinical signs of myopathy, ataxia, epilepsy, deafness, loss of visual acuity and reduced intellectual capacities. Muscle biopsy revealed numerous ragged-red fibres and mitochondrial anomalies at ultrastructural examination. Cerebral biopsy showed spongiform changes. Both muscular and cerebral biopsies showed vascular lesions: swollen endothelial cells. Mitochondria increased in number with concentric whorls of cristae were observed in pericytes and smooth muscle cells. This mitochondrial vasculopathy could explain the neurological symptoms.
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PMID:[Muscle and brain biopsy in a case of mitochondrial encephalomyopathy. Demonstration of a mitochondrial vasculopathy]. 238 1

Weakness, lethargy, ataxia, lateral recumbency, limb paddling, tremors, salivation, and diarrhea were observed in newborn pigs on a commercial swine farm. Many pigs became moribund and died. All had been treated with an aerosol wound spray containing 2.5% chlorpyrifos. A controlled study was undertaken to determine whether the aerosol spray was the cause of these clinical signs. Pigs exposed to aerosol spray containing 2.5% chlorpyrifos at 3 hours (n = 4) and 6 hours (n = 3) after birth developed clinical signs similar to those on the farm; none survived. Pigs exposed at 24 hours (n = 5) after birth developed clinical signs consistent with those that had developed in pigs on the farm; 3 died and 2 survived. Of 3 pigs exposed to the same spray at 36 hours after birth, 1 developed tremors 7.5 hours later and diarrhea 9 hours later, then returned to normal.
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PMID:Toxicosis in newborn pigs associated with cutaneous application of an aerosol spray containing chlorpyrifos. 244 44

Only a few cases of carcinomatous neuropathy with tonic pupils have been reported. In the present paper we described a 53-year-old woman with subacute sensory neuropathy who had presented with bilateral tonic pupils. She noticed numbness over the medial aspect of the left thigh in March, 1988, and then developed dysesthesia over the left forearm and hand, mild weakness of left upper and lower extremities and urinary disturbance. Neurological symptoms were subacutely progressive and she was bed-ridden in May. She was admitted to our hospital in June, 1988. On examination, she had body-weight loss of 6 kg during the last six months and general status was otherwise unremarkable. She had anisocoria; the left pupil was larger in daylight than the right, while smaller in dim light. The left pupil scarcely reacted to light, but promptly constricted to near vision. The right pupil constricted normally to light and near vision. An instillation of 0.0625% pilocarpine solution showed supersensitive response of both pupils. An instillation of 1.25% epinephrine solution demonstrated mild dilation of both pupils. Thus, it was conceivable that she had postganglionic ciliary nerve damage characteristic of tonic pupil as well as the lesion of sympathetic nerve innervating pupillary dilator. She had severe sensory ataxia and pseudoathetosis of the hands. Weakness was mild to moderate in extremities. Almost all deep tendon reflexes were absent. All modalities of sensation, particularly on deep sense, were severely involved with sea-level-type distribution below Th7, and over C2 to C3 regions on the left side.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Subacute sensory neuropathy manifestated by tonic pupils associated with small cell carcinoma of the lung]. 255 97

We describe seven adults who had ataxia and severe sensory-nervous-system dysfunction after daily high-level pyridoxine (vitamin B6) consumption. Four were severely disabled; all improved after withdrawal. Weakness was not a feature of this condition, and the central nervous system was clinically spared. Although consumption of large doses of pyridoxine has gained wide public acceptance, this report indicates that it can cause sensory neuropathy or neuronopathy syndromes and that safe guidelines should be established for the use of this widely abused vitamin.
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PMID:Sensory neuropathy from pyridoxine abuse. A new megavitamin syndrome. 630 47

The clinical symptoms of cerebellar dysfunction are reviewed in relation to modern concepts of cerebellar physiology. Special attention is given to their topodiagnostical significance. Hypotonia, hyporeflexia, asthenia, delayed onset and offset as well as slowing of voluntary movement, ataxia, dysmetria, tremor and myoclonus result from damage of the lateral cerebellar hemispheres and the dentate nucleus. Three different key patterns of postural ataxia result from lesions of the anterior lobe, the vermal part of the vestibular cerebellum and dysfunction of cerebellar afferences respectively. The long latency response (M3) is significantly prolonged in patients with anterior lobe atrophy. Oculomotor symptoms mainly result from either lesions of the cerebellar flocculus, causing dysfunction of retinal-image stabilization or from damage to the dorsal vermis (VI and VII) and the fastigial nuclei, resulting in saccadic dysmetria.
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PMID:Clinical symptoms of cerebellar dysfunction and their topodiagnostical significance. 671 11

Lamotrigine is an antiepileptic agent which blocks voltage-dependent sodium channels, thereby preventing excitatory neurotransmitter release. Clinical evidence indicates that lamotrigine is effective against partial and secondarily generalised tonic-clonic seizures, as well as idiopathic (primary) generalised epilepsy. As monotherapy, lamotrigine 100 to 300 mg/day has similar medium term (30 to 48 weeks) efficacy to carbamazepine 300 to 1400 mg/day and phenytoin 300 mg/day against partial onset seizures and idiopathic generalised tonic-clonic seizures in adults with newly diagnosed epilepsy, and appears to be better tolerated than the older agents. As adjunctive therapy, lamotrigine (50 to 500 mg/day) has shown efficacy in short term ( < or = 6-months) placebo-controlled studies in adults with refractory partial epilepsy, reducing total seizure frequency (by < or = 60%) and producing improvement ( > or = 50% reduction in seizure frequency) in < or = 67% of patients. Both simple and complex partial seizures and secondarily generalised tonic-clonic seizures are reduced by lamotrigine, with generalised seizures (particularly absence seizures, atonic seizures and Lennox-Gastaut syndrome) tending to be more responsive than partial seizures. This reduction in seizure frequency is sustained on long term ( < or = 3 years) therapy and is reportedly accompanied by an improvement in psychological well-being. In children with refractory multiple seizure types, lamotrigine ( < or = 15 mg/kg/day; 400 mg/day) has proved effective as add-on therapy, with approximately equal to 40% of patients showing > or = 50% reductions in seizure frequency and approximately equal to 10 % achieving abolition of seizures after 3 months' treatment. Generalised seizures, including atypical and typical absence seizures, atonic and tonic seizures and Lennox-Gastaut syndrome are most responsive. The most common adverse events associated with lamotrigine are primarily neurological, gastrointestinal and dermatological. Maculopapular or erythematous skin rash, occasionally severe, occurs in approximately equal to 10% of patients and is the most common cause of treatment withdrawal. The risk of rash can, however, be minimised through adoption of a low, slow dosage titration schedule on initiating therapy. As monotherapy, lamotrigine produces less drowsiness than carbamazepine or phenytoin, and less asthenia and ataxia than phenytoin. Clinical experience would therefore suggest that lamotrigine is a particularly effective and generally well tolerated broad-spectrum agent for adjunctive treatment of both partial epilepsy and idiopathic generalised epilepsy in adults and children. Initial indications point to the drug filling an increasingly important future role in the monotherapy of newly diagnosed epilepsy.
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PMID:Lamotrigine. An update of its pharmacology and therapeutic use in epilepsy. 853 54


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