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)

Patients with renal failure may manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. After the institution of adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. These central nervous system disorders are referred to as uremic encephalopathy. The dialytic treatment of end-stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system; dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation, and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. There are at least three different forms of dialysis encephalopathy: sporadic, epidemic; and that associated with renal disease in children. In addition to the foregoing neurologic diseases which are specifically related to uremia and/or dialysis, a number of other neurologic disorders occur with increased frequency in patients with end-stage renal disease on chronic hemodialysis. These include subdural hematoma, electrolyte disorders, vitamin deficiencies, drug intoxication, hypertensive encephalopathy, and acute trace element intoxication. Renal transplantation is associated with a variety of central nervous system infections, reticulum cell sarcoma, and central pontine myelinosis. The present manuscript will review the clinical, structural, and biochemical components of those neurologic disorders which are peculiar to the uremic state and its treatment with dialysis.
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PMID:Uremic encephalopathies: clinical, biochemical, and experimental features. 675 30

Asterixis was observed in five parkinsonian patients who were taking levodopa. A prospective study revealed that 4 of 55 consecutive patients had asterixis. Liver and metabolic functions were normal in all patients. Asterixis always occurred as part of a toxic confusional state superimposed on a parkinsonian state associated with some dementia. Insomnia, hallucinosis, and myoclonus were also prominent in the affected patients. Because of this association with other signs of chronic drug toxicity and its reversal with drug withdrawal, the asterixis seemed to be drug-related.
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PMID:Drug-induced asterixis in Parkinson disease. 720 Feb 12

We retrospectively reviewed clinical and neurophysiological data of 6 epileptic patients who developed negative myoclonus and stupor a few days after introduction of valproate (VPA). Prompt remission of clinical signs and symptoms followed valproate withdrawal. We attempted to elucidate the pathophysiological mechanism of VPA-induced stupor and provide further polygraphic and backaveraging EEG documentation of negative myoclonus. During VPA-induced stupor electroencephalograms revealed posterior background slowing in all patients. Interictal epileptiform discharges were present in 3 patients. In all 6 patients close examination using simultaneous video-polygraphic recording showed negative myoclonus which was not time-related to lateralized spike discharges. In 2 of 3 patients with no spikes on conventional EEG who underwent backaveraged EEG recordings we detected a large (5 microV) cortical positive-negative wave time-locked (30-40 msec) with the postural modification of the contralateral wrist. This cortical potential was similar to that observed in patients with asterixis secondary to metabolic or toxic encephalopathies. In one patient i.v. administration of 10 mg diazepam did not modify this cortical potential and did not reverse the clinical manifestations. In all patients the only abnormal laboratory finding was an increased level of venous ammonemia. Our findings are against an epileptic origin of VPA encephalopathy and provide further argument in favour of a cortical non-epileptic mechanism mediating negative myoclonus. Benzodiazepines should be avoided in the management of this condition.
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PMID:Negative myoclonus during valproate-related stupor. Neurophysiological evidence of a cortical non-epileptic origin. 753 70

Meperidine neurotoxicity, characterized by recurrent convulsions, myoclonus, and asterixis, was diagnosed in an organ transplant recipient. Aside from cyclosporine toxicity, the literature regarding neurologic complications of transplantation contains limited reference to the neurotoxicity of therapy. The case reported illustrates how pharmacokinetic factors might render transplant patients particularly vulnerable to the neurotoxic side effects of certain medications, such as meperidine.
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PMID:Meperidine neurotoxicity after organ transplantation. 800 42

As a clinical diagnostic approach, the evoked potential has been used to differentiate movement disorders, especially myoclonic movements, Giant somatosensory evoked potentials (SEPs) and long-loop reflex to electrical stimulation of the peripheral nerve are commonly employed in the evaluation of patients with myoclonus. Recently, abnormality in a specific component of SEP frontal N30 has been reported in focal dystonia. Jerk locked back averaging has been applied to cortical reflex myoclonus, minipolymyoclonus, cortical tremor, simple tics, chorea-acanthocytosis, Huntington's chorea, etc. Silent period locked averaging is also used for asterixis. With these new electrophysiological techniques, evaluation of functional mechanisms in movement disorders may be expected, with fruitful results.
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PMID:[Clinical diagnosis of movement disorders--evoked potentials]. 827 66

We have described several kinds of involuntary movements occurring in metabolic encephalopathies. They are often associated with slowing of electroencephalographic basic activities and with loss of consciousness. Laboratory studies disclose the cause of the encephalopathies. Asterixis, first reported in hepatic encephalopathy, is produced by EMG silence during voluntary contraction. Myoclonus is associated with a short excessive EMG discharges. Tremor is caused by grouping EMG discharges. Some other kinds of involuntary movements are seen in metabolic encephalopathies. Clinical features of hepatic, uremic, hypoxic, and hypoglycemic encephalopathies are briefly described.
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PMID:[Dyskinesia in metabolic encephalopathy]. 827 69

Myoclonus appears to be generated by a brief transient activation of a focal region of motor cortex. Activation of a focal region of motor cortex can also give rise to a transient depression of function. If a subject, or patient, is trying to produce movement, this depression would lead to a brief lapse in muscle activation that would be interpreted as either asterixis or negative myoclonus. Both positive events and negative events can occur either individually or together. The physiological substrate in the cortex appears to be different for the two phenomena, and the pharmacology may differ as well.
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PMID:Transcranial magnetic stimulation. Negative effects. 884 63

Negative myoclonus (NM) is a motor phenomenon characterized by involuntary jerky movements due to a brief, sudden interruption of muscular activity. This motor disturbance can be observed in a variety of clinical conditions, that can range from physiological NM, occurring when falling asleep or after prolonged exercise, to asterixis, a form of NM observed in patients with toxic-metabolic encephalopathies or with focal brain lesions, or, as a paroxysmal phenomenon, labelled as epileptic negative myoclonus, in epileptic patients. Neurophysiological investigations are essential to diagnose NM and to distinguish it from other motor disorders, such as tremor or positive myoclonus. Furthermore, neurophysiological findings can provide useful information supporting a subcortical or cortical origin of NM. In cortical NM, recent data suggest a role of cortical active inhibitory areas in the generation of this motor phenomenon.
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PMID:Negative myoclonus. 889 93

The treatment of myoclonus is mainly based on the pathophysiological origin of the neuronal discharges producing the jerks. Myoclonus of cortical origin responds best to treatment. Drugs commonly used to treat epilepsy are usually capable of controlling action and stimuli-sensitive cortical myoclonus. Piracetam (6-20 g/day), clonazepam (2-12 mg/day), sodium valproate (1,200-3,000 mg/day), and primidone (500-1,000 mg/day) are the most useful ones, often given in combination. Myoclonus of non-cortical origin, i.e. reticular reflex myoclonus or spinal myoclonus, may respond to serotoninergic drugs and clonazepam, but there is much less scientific documentation and rationale behind the therapeutic approach to these different forms, and hence greater variability in the response. No specific drug treatment is yet available for negative myoclonus (Asterixis and postural lapses).
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PMID:Therapy of myoclonus. 889 99

Involuntary movements are an infrequent complication of treatment with phenytoin and include tremor, asterixis, myoclonus, parkinsonism, and dyskinesias. The mechanism by which phenytoin exerts its actions is unclear. Phenytoin has been observed to exert variable effects on dopamine metabolites and also may induce changes in serotonergic activity. In this report, we discuss the available experimental evidence concerning the possible mechanisms of involuntary movements induced by phenytoin. We describe a case of postural myoclonus during treatment with phenytoin.
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PMID:Postural myoclonus induced by phenytoin. 893 94


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