Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027066 (myoclonus)
 4,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was done to investigate possible late central nervous system (CNS) complications of latent measles infection in hamsters. Signs of CNS disease, consisting of myoclonus and paralysis, occurred in some weanling hamsters inoculated intraperitoneally at 3 or 9 days of age with antithymocyte serum (ATS) and measles virus, but no late complications in adult life attributable to measles virus were seen. A single series of ATS injections plus an injection of measles virus resulted in sustained antibody formation postulated due to establishment of a latent viral infection, whereas similar treatment with normal rabbit serum plus virus caused no or minimal antibody response. The majority of hamsters receiving ATS as newborns and ATS plus virus as weanlings also did not produce antibody. This differential effect of ATS may be due to combined elimination of suppressor and helper cells in the latter ATS-treated group and of suppressor cells only in the former ATS-treated group. Cellular immunity could not be evaluated since lymphocytes from inoculated and uninoculated hamsters released equal and variable amounts of 51Cr for both infected and noninfected labeled, allogeneic hamster target cells.
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PMID:Complications and immunological studies of measles virus infection in antithymocyte-treated hamsters. 30 5

Progressive rubella panencephalitis is a very rare slow virus disease of the nervous system. The authors present a case, concerning a young man, aged 20 years, died 11 months after the onset of the disease. The following peculiarities of the case are emphasized: 1) the clinical symptomatology and the evolution (myoclonus, lack of cerebellar impairment) could suggest the diagnosis of SSPE; 2) the EEG recordings showed epileptiform abnormalities, long latency diffuse periodic complexes and--during interferon therapy and simultaneously with a temporary clinical improvement--the appearance of short latency anterior periodic complexes.
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PMID:Progressive rubella panencephalitis. Follow-up EEG study of a case. 129 90

Opsoclonus-myoclonus (OM) is a neurological disorder usually occurring in infancy, clinically manifested by various involuntary movements. The pathogenesis of OM is unknown, but since the disease often is associated with viral infection or with neuroblastoma, an immunologic basis for OM has been postulated. We have studied two children with OM whose serum contained antibodies directed against the 210 kDa neurofilament protein; these antibodies were not seen in the serum of 21 children with other neurological disorders. Neurofilament proteins, which are found only in neurons, may be of prime importance in neuronal function, especially during development of the nervous system. Our findings suggest that generation of antibodies to the neurofilament proteins can occur in patients with opsoclonus-myoclonus; the role of the anti-NF210K antibodies in the pathogenesis of OM, however, is uncertain.
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PMID:Anti-neurofilament protein antibodies in opsoclonus-myoclonus. 329 94

Changes in the spontaneous brain electrical activity and sleep organization were investigated in 5 mice strains during the evolution of experimental fixed rabies infection. Cortical electrodes were chronically implanted for continuous EEG recording and spectral analysis until death. Three evolutionary phases were individualized. The initial phase exhibited alterations of sleep stages, REM sleep disappearance, pseudoperiodic facial myoclonus and first clinical signs. The mature phase was characterized by a generalized EEG slowing (2-4 cycles/s). The terminal phase occurring with extinction of hippocampal rhythmic slow activity showed a flattening of cortical activity. The brain electrical activity ceased about 30 min before the cardiac arrest. Paroxysmal activities appeared during the course of the disease as bursts of rhythmic slow waves, pseudoperiodic spikes or occasionally ictal epileptic discharges. Spectral analysis revealed a progressive and characteristic clustering of the EEG frequency band power values. The spread of infection in the CNS was monitored by specific immunofluorescence studies which revealed the presence of rabies virus antigen in the pons, the cerebellum, the thalamus and the cortex during the initial phase. The pyramidal field of the hippocampus was infected during the mature phase but the gyrus dentatus was never infected even at the terminal phase. These studies show that particular neuronal functions are impaired during rabies virus infection suggesting that neuronal alterations may be involved in the pathogenic mechanisms leading to lethality.
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PMID:Electrophysiological and sleep alterations in experimental mouse rabies. 380 86

A case of rhythmic myoclonus affecting only the lower part of the body is described. This occurred as an acute self-limiting illness. The changes in the cerebrospinal fluid (CSF) suggested a viral infection. Clinical and electrophysiological findings indicated that the involuntary movements were arising at spinal level and were independent of suprasegmental influences. There are few previously reported cases of spinal myoclonus, all different in various respects from the present one, which is reminiscent of the results of experimental inoculation of virus into feline spinal cord.
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PMID:Spinal myoclonus. 444 6

A chronic progressive neurologic disease was observed and monitored for 18 months in a young, tamed Bengal tiger. Clinical, serologic, and neuropathologic evidence of canine distemper virus infection was seen. Clinical signs included convulsions, myoclonus, and slowly progressive ataxia. Marked increases in neutralizing antibodies against canine distemper virus were seen in the serum and cerebrospinal fluid. Neuropathologic findings were nonsuppurative meningoencephalomyelitis, with perivascular cuffing, demyelination, and inclusion bodies typical of canine distemper virus. It was concluded that, in light of this case and an earlier report of canine distemper in lion cubs, vaccination of this subgroup of carnivores with a killed vaccine may be beneficial if exposure to other animals susceptible to canine distemper is anticipated.
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PMID:Chronic encephalomyelitis caused by canine distemper virus in a Bengal tiger. 668 17

Subacute sclerosing panencephalitis (SSPE) is a persistent viral infection of the central nervous system due to a defective measles virus. Beginning with progressive cognitive malfunctioning, myoclonus and other less specific neurologic signs and symptoms, it usually evolves to a vegetative, decorticated state and death. Disease course and characteristics can be highly variable. Since the widespread measles vaccination in the Western countries started in the late seventies and early eighties, the incidence of SSPE has dropped significantly. Also adult onset is more frequently seen which changes the field of differential diagnosis. In this article 3 atypical cases of SSPE are described with peculiarities such as adult onset, pronounced extrapyramidal involvement, remission and prolonged disease course. Common features of the disease are emphasized to enable accurate diagnosis which is based on clinical features, presence of high titers of serum and cerebrospinal fluid (CSE) measles antibodies, MRI and EEG.
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PMID:Prolonged and atypical course in some cases of subacute sclerosing panencephalitis. 910 44

After two days of malaise, headache, nausea, and vomiting, a 26-year-old man suddenly developed opsoclonus and stance and gait ataxia, without myoclonus. Having excluded a paraneoplastic etiology, we assumed that the disorder was probably related to a viral infection. Spontaneous resolution occurred in about two months. Opsoclonus became flutter dysmetria and then resolved. Saccadic eye movement recording disclosed the occurrence of hypermetria, increased velocity, and delayed latency, which also resolved. In this patient, the correspondence between clinical and ocular motor abnormality courses suggests a transient cerebellar dysfunction as the possible pathophysiologic mechanism for opsoclonus.
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PMID:Opsoclonus in a patient with cerebellar dysfunction. 1060 72

To study clinical peculiarities of parainfectious opsoclonus-myoclonus syndrome (OMS) in children and to elaborate approaches to its pharmacotherapeutic correction, 20 children, including 12 girls and 8 boys, have been examined using neurological, neurophysiological, immunological and virological methods along with magnetic resonance tomography (MRT). Age-at-disease-onset was from 8 months to 3 years old. The development of neurological symptoms was related to a virus infection (55% of cases) or vaccination (15%). Marked disease seasonality (autumn, spring) was observed. In some cases, a possible role of infectious factor in the disease development was confirmed by virological and immunological studies. OMS was featured by the absence of specific brain MRT changes and low frequency of significant abnormalities of cerebrospinal fluid. A positive experience of the use of hormonal therapy and immunomodulators is presented.
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PMID:[Opsoclonus-myoclonus syndrome in children]. 1837 15

Opsoclonus-myoclonus-ataxia syndrome (OMS) is a rare neurological disorder of probably autoimmune origin. Most cases are associated with a remote neoplasm or a viral infection; however in some instances no underlying aetiology can be demonstrated. We report the presence of anti-glutamic acid decarboxylase antibodies (anti-GAD Abs) in the serum and CSF of a patient with idiopathic OMS. Treatment with intravenous immunoglobulin led to a remarkable clinical improvement with parallel reduction of anti-GAD titers. Anti-GAD Abs have been associated with several neurological syndromes. They could also be responsible for the clinical triad of OMS, by impairing GABAergic transmission in specific brainstem and cerebellar circuits. We propose that testing for anti-GAD Abs should be performed in OMS, especially when no other aetiological association can be demonstrated.
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PMID:Opsoclonus-myoclonus-ataxia syndrome with autoantibodies to glutamic acid decarboxylase. 1843 86


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