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

Mipafox administered to rats daily for 35 days produced ataxia and a reduction in the level of dopamine in the corpus striatum. Treatment with Leptophos for the same period produced slight motor dysfunction and a small but significant reduction in the level of striatal dopamine. Fenitrothion neither produced motor dysfunction nor changed the level of striatal dopamine. The cholinesterase activity of corpus striatum was inhibited by all the compounds. The results suggest the possible involvement of striatal dopamine in the delayed neurotoxic effects of certain organophosphorus compounds.
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PMID:Role of striatal dopamine in delayed neurotoxic effects of organophosphorus compounds. 5 73

Clinical reports on 430 children with acute codeine intoxication are evaluated. Of 234 children who had taken more than 5 mg/kg body-weight, 8 had respiratroy arrest necessitating intubation and artificial ventilation; 2 of them died. In all other cases the intoxication produced one or more of the following symptoms: somnolence, ataxia, miosis, vomiting, rash, swelling, and itching of the skin, but no life-threatening side-effects. Close supervision of respiration is the main principle of management when more than 2 mg codeine/kg body-weight has been taken. Gastric voiding may be useful if done soon after ingestion. Charcoal and purgatives should be given in all cases.
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PMID:Codeine intoxication in childhood. 5 70

4 patients are described with ophthalmoplegia (Figs. 1 and 2) and ataxia with acute onset. Three of them showed only very slight symptoms of generalized polyneuritis. Measurement of sensory nerve conduction velocity (Fig. 4, Table 2) and determination of vibration sense by an electrical vibrator (Fig. 3) proved to be helpful for diagnosis. The ocular EMG revealed signs of peripheral denervation in 3 cases. Pathological changes of the somatosensory evoked potential (Fig. 5) which has been registered in one case, might give some speculation as to whether or not central nervous pathways are affected.
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PMID:Electrophysiological findings in the syndrome of acute ocular muscle palsy with ataxia (Fisher syndrome). 6 26

Four patients with Whipple's disease which had responded to antibiotic therapy, later developed neurologic disease identical to that seen in patients with Whipple's disease who died without treatment. Dementia, myoclonus, ataxia, and supranuclear ophthalmoplegia were the main neurologic features. Restarting antibiotics has been followed by stabilization of disease in all four. Two have improved. In three, the previously diagnosed and treated Whipple's disease was not considered as a possible cause of the neurologic disease until the symptoms and signs were far advanced. It is advisable to periodically evaluate all patients with Whipple's disease, even after successful treatment. Signs of neurologic disease should be considered a possible recurrence of Whipple's disease and antibiotics restarted.
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PMID:Neurologic disease in patients with treated Whipple's disease. 6 1

No chromosomal anomaly was found in 15 cases of typical Friedreich's ataxia and three cases of atypical recessive ataxia studied with Q and G banding techniques. No difference between frequency of chromosomes gaps or breakages was noted amongst patients with Friedreich's ataxia and controls.
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PMID:Friedreich's ataxia: observations with Q and G banding of human chromosomes. 6 12

The presence of alpha-2-macroglobulin (alpha-2-M) on the surface of peripheral blood lymphocytes from normal human subjects and from patients with chronic lymphatic leukaemia (CLL) and with ataxia-teleangectasia was studied by indirect immunofluorescence technique. Same experiments were done on purified subpopulations of normal blood peripheral lymphocytes (B and T). The percentage of alpha-2-M bearing lymphocytes is 17 +/- 6% as regard to normal subjects (Ig-bearing cells are 14%): in CLL the percentage of alpha-2-M bearing cells generally is significantly lower than that of Ig-bearing cells (IgM-IgD). On selected subpopulations, 90% of alpha-2-M bearing cells are present among non T-cells and only 5% among T-cells (probably due to not absolute purification). Blocking experiments using anti-Ig sera did not affect significantly the percentage of alpha-2-M bearing cells and using anti-alpha-2-M sera did not affect that of Ig-bearing cells. The percentage of E-rosette forming cells is not affected by pretreatment of peripheral lymphocytes with anti-Ig and/or anti-alpha-2-M sera. Hypothesis is set forth that alpha-2-M bearing cells could be a lymphocytes subpopulation made by a subgroup of B-cells and by K-cells, taking part in that immunoregulatory system in which collaborate many serum alpha-globulins and T-suppresor cells.
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PMID:[Presence of alpha-2-macroglobulin on the membrane of peripheral human blood lymphocytes : a new lymphocyte maker]. 6 74

Clinical and sural nerve biopsy findings are described in four hypothyroid patients with manifestations of a diffuse peripheral neuropathy. Clinical examination revealed distal sensory inpairment, complaints of burning and lancinating extremity pains, ataxia and a decrease of deep tendon reflexes with total ankle jerk loss. In one patient, signs of the peripheral neuropathy comprised the leading symptomatology of the underlying metabolic disorder. Light and electron microscopic investigations of the sural nerve biopsies revealed a marked reduction of myelinated fibers, affecting mainly the large myelinated axons. The histograms showed a pathological unimodal spectrum of myelinated fiber diameters. Dystrophic and degenerative changes in axons of all fiber classes and the presence of clusters of thinly myelinated small fibers suggest that neuroaxonal degeneration and incomplete regeneration may represent the major pathogenetic mechanism of the neuropathy in these hypothyroid patients.
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PMID:Polyneuropathy in hypothyroidism. Clinical and nerve biopsy study of 4 cases. 6 2

The author reports of 2 cases (sisters of 13 and 15 years old) with the Refsum syndrome. The disease had its onset at the age of 12 and 5 years with a progressive development and remissions. The clinical picture was characterized by a recurrent syndrome of polyradiculoneurites with a slight protein cellular dissociation in the CSF, an expressed sensitive ataxia with elements of cerebellar disorders, a drop in the acuity of sight, audition, intellectual level and a deformation of the talipes of the Friedreich type. In a single examination of fatty acids in the blood serum by the method of gas chromotography there were no data pointing to the existence of 3, 7, 11, 15-tetra metylhexadecone acids. On the basis of an immunological study the author discusses the role of autoimmune reactions in the pathogenesis of the diseases. A differential diagnosis was conducted between acanthocytosis and porphyria with recommendations in regard to treatment.
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PMID:[Clinical picture and pathogenesis of the Refsum syndrome]. 7 Sep 17

Phosfolan, chlorpyrifos, and stirophos when applied to white mice at sublethal doses did not induce any delayed neurotoxic effect. On the other hand, Leptophos and EPN when administered orally at sublethal or lethal levels clearly produced a delayed neurotoxic ataxia in treated mice. The five tested organophosphorus insecticides were compared for their ability to inhibit cholinesterase, neurotoxic esterases and monoamine oxidase. I50 values were estimated for each case. The results revealed that all five compounds were inhibitors of cholinesterase, but only Leptophos and EPN were shown to be potent inhibitors for both neurotoxic esterase and monoamine oxidase in the mouse brain. Additional particular properties of both Leptophos and EPN were found in their ability to cause delayed neurotoxic ataxia in chickens and sheep fed once on sublethal doses of these compounds. It is believed that the phosphonate ester configuration of EPN and Leptophos has a specific mode of toxic action which is mainly located at the central nervous system. It is also postulated that these delayed neurotoxic agents might inhibit postganglionic sympathetic neurons, thus resulting in chronic paralytic effects.
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PMID:Neurotoxicity of organophosphorus insecticides Leptophos and EPN. 7 68

Five patients experienced severe encephalopathy within hours of receiving their initial dose of cranial irradiation for the treatment of central-nervous-system leukaemia. Neurological findings included cranial-nerve palsies, seizures, ataxia, depressed consciousness, increased intracranial pressure, and signs of herniation. Symptoms developed within 3-30 hours of the first radiation treatment of 50-200 rad. Each patient had also received one or more injections of intrathecal chemotherapy before encephalopathy developed. The aetiology of this syndrome is uncertain but may involve transient cerebral oedema and/or an altered blood-brain barrier produced by the combination of intrathecal chemotherapy and cranial irradiation.
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PMID:Acute encephalopathy after initiation of cranial irradiation for meningeal leukaemia. 7 11


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