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)

Cardiopulmonary arrest is a test of the brain's tolerance to global ischemia. New insights into the pathophysiology of global ischemia have led to the potential use of early prophylactic anticonvulsants, hypothermia, barbiturate coma, glucose manipulations, calcium-blocking agents, and hemodilution. A wide spectrum of neurologic sequelae may follow global ischemia, ranging from brain death, vegetative states, and impairment of higher intellectual function to syndromes of amnesia and cortical blindness, post-anoxic myoclonus, delayed leukoencephalopathy, and spinal stroke. The distinctive features of these sequelae and their pathophysiologic aspects are discussed. Special attention is given to brain death and prognostication.
Ann Intern Med 1985 Dec
PMID:Cardiopulmonary arrest. Pathophysiology and neurologic complications. 390 62

Two patients with a diagnosis of olivo-ponto-cerebellar atrophy developed cortical reflex myoclonus to visual (flash) and somaesthetic stimuli. Oral treatment with levodopacarbidopa (1000/100 mg) or subcutaneous administration of apomorphine (1 mg) abolished the visually-triggered myoclonus, without modifying reflex myoclonus to electrical or tactile stimulation. Intravenous administration of lisuride (0.1 mg) produced a marked reduction in both types of reflex myoclonus. These results indicate a selective inhibitory effect of dopamine agonist drugs on visual reflex myoclonus of cortical origin.
J Neurol Neurosurg Psychiatry 1985 Dec
PMID:Dopamine agonists suppress visual-cortical reflex myoclonus. 393 1

A 55-year-old man is presented who developed severe multifocal myoclonus and tonic clonic seizures in his early thirties, and progressive limb weakness in his mid forties, when a ragged red fibre myopathy was diagnosed. He went on to develop a distal motor neuropathy and respiratory failure. Respiratory function tests indicated respiratory failure secondary to respiratory muscle weakness and a central hypoventilation syndrome. CT scan revealed brain stem atrophy and brain stem evoked responses were abnormal. A sural nerve biopsy showed severe axonal degeneration. Cytochrome difference spectra and polarographic studies on isolated intact muscle mitochondria were normal. This study reports the association of respiratory failure and sleep apnoea with Fukuhara's syndrome and presents biochemical data suggesting that the mitochondrial respiratory chain may be intact in some patients with this syndrome.
J Neurol Sci 1985 Dec
PMID:Mitochondrial myoneuropathy with respiratory failure and myoclonic epilepsy. A case report with biochemical studies. 393 3

Tryptamine (1-320 mg/kg) evoked only slight muscle jerking in naive guinea-pigs but, in animals pretreated with pargyline (75 mg/kg; 1 hr previously), tryptamine induced a dose-dependent (6-160 mg/kg) myoclonus. The myoclonus induced by tryptamine (40 mg/kg) plus pargyline (75 mg/kg) was differentially inhibited by the indoleamine receptor antagonists, methergoline (5 mg/kg) which was more potent than methysergide (10 mg/kg), mianserin (10 mg/kg) which was more potent that cyproheptadine (10 mg/kg) and propranolol (20 mg/kg) which was more potent than cinanserin (10 mg/kg). This rank order of potency differed from that observed for the order of potency of these drugs in inhibiting the myoclonus induced by L-5-hydroxytryptophan (5HTP) plus carbidopa in guinea-pigs (Luscombe, Jenner and Marsden, Neuropharmacology, 1981), perhaps indicating involvement of pharmacologically distinct indoleamine receptors. Manipulation of presynaptic function of 5-hydroxytryptamine (5HT) by tryptophan hydroxylase inhibition with p-chlorophenylalanine to produce depletion of cerebral 5HT, or by an L-tryptophan load to elevate 5HT in brain, suggested that the functional integrity of serotonergic neurones is required for the expression of myoclonus induced by tryptamine plus pargyline. A range of blockers of 5HT re-uptake did not alter the jerking produced by tryptamine (40 mg/kg) in guinea pigs pretreated with pargyline (75 mg/kg; 1 hr previously), or the threshold myoclonus induced by a smaller dose of tryptamine (10 mg/kg; plus pargyline 75 mg/kg). It is suggested that myoclonus induced by tryptamine in guinea pigs pretreated with pargyline involves activation of post-synaptic indoleamine receptors by tryptamine by a mechanism which requires intact presynaptic function of 5HT.
Neuropharmacology 1982 Dec
PMID:Tryptamine-induced myoclonus in guinea-pigs pretreated with a monoamine oxidase inhibitor indicates pre- and post-synaptic actions of tryptamine upon central indoleamine systems. 613 Apr 89

The action of lorazepam was studied in photosensitive baboons. Animals were either naturally very photosensitive or rendered photosensitive by a previous injection of allylglycine. Intravenous administration of varying doses, from 0.05 to 0.5 mg/kg, of lorazepam blocked the myoclonus induced by intermittent light stimulation in all the animals. However, in the naturally photosensitive baboon the injection of lorazepam favoured the appearance of spontaneous myoclonus with no important EEG modification. This myoclonus is different from that induced by intermittent light stimulation, which is always preceded by spike-wave cortical discharges. Lorazepam-induced myoclonus appears during the period when the animal is not photosensitive and its origin is probably in the medulla or in the brain stem.
Electroencephalogr Clin Neurophysiol 1981 Dec
PMID:Opposite effects of lorazepam on two kinds of myoclonus in the photosensitive Papio papio. 617 64

Since p,p'-DDT-induced myoclonus is ameliorated by serotonin agonists and aggravated by serotonin antagonists, the effect of p,p'-DDT on serotonin metabolism in rat brain was examined. p,p'-DDT (600 mg/kg intragastrically) elevated plasma tryptophan as well as tryptophan and 5-hydroxyindoleacetic acid concentrations in all seven regional areas of the brain assayed. Serotonin levels were elevated only in the midbrain and cerebellum of p,p'-DDT-treated rats. p,p'-DDT increased serotonin turnover in the medulla and midbrain. p,p'-DDT had no effect on the transport of 5-hydroxyindoleacetic acid out of the central nervous system, serotonin uptake and release from nerve terminals, or serotonin receptor binding in the brain. The findings in this study do not support a brain serotonin deficiency hypothesis as the explanation for the response of p,p'-DDT-induced myoclonus to serotonin agonists.
Neurotoxicology 1981 Dec
PMID:p,p'-DDT-induced alterations in brain serotonin metabolism. 617 20

The degenerative type of progressive myoclonus epilepsy (PME) is a hereditary disease with grand mal seizures, stimulus sensitive myoclonus, characteristic EEG and mental deterioration in the late stage. GABAergic antiepileptic drugs are the most effective ones in this disease, with an unknown etiology. In this study, the GABA concentration in the CSF of 15 PME patients was measured and compared with values of sex- and age-matched epileptic controls. It was correlated with the concentrations of 5HIAA and HVA in the CSF, which were determined earlier from the same patients. The GABA concentration in the PME patients was statistically significantly decreased, to about 75% of that of the epileptic controls. It correlated with HVA and 5HIAA concentrations in the PME patients, but not in the epileptic controls. It is unknown whether these findings are related to the primary cause of PME or whether they are only secondary, owing to a loss of respective neurons or synapses.
Acta Neurol Scand 1982 Dec
PMID:Decrease of GABA in the cerebrospinal fluid of patients with progressive myoclonus epilepsy and its correlation with the decrease of 5HIAA and HVA. 618 74

Onset of confusion with myoclonus occurred in a 55-year-old patient hospitalized for infectious endocarditis and under intravenous dopamine. The speculative responsibility of dopamine in the occurrence of this myoclonic encephalopathy is discussed. Indeed, although dopamine does not cross the blood-brain barrier, inflammation of the wall of the cerebral vessels (immunologic vasculitis) may have enabled dopamine to reach the central nervous system.
Sem Hop 1982 Dec 16
PMID:[Myoclonal encephalopathy due to dopamine]. 629 75

We describe three patients with mitochondrial myopathy, dementia, loss of vision and hearing, seizure disorder with myoclonus, intermittent headaches of a vascular type, visual hallucinations, cerebellar dysfunction, and lactic acidosis. Muscle biopsies in all patients and liver biopsy in one revealed abnormal mitochondria. The disorder may be due to a deficiency of mitochondrial NADH-CoQ dehydrogenase.
Neurology 1983 Dec
PMID:Mitochondrial myopathy and encephalopathy: three cases--a deficiency of NADH-CoQ dehydrogenase? 641 59

One hundred patients were analyzed sequentially regarding to the presence of periodic movements in sleep (PMS) or nocturnal myoclonus. The criteria for considering PMS was the presence of 5 or more myoclonic movements per hour of sleep. The 18 patients included in the PMS category were compared with the remaining 82. Those with PMS had tendency to be older than the others. The movements were observed in stage 2 and less commonly in stages 3, 1, 4 and REM. Patients with PMS had generally higher number of arousals and K complexes. There was no difference between both groups regarding sex, history complaints, sleep efficiency, total sleep time, time in each stage and final diagnosis.
Arq Neuropsiquiatr 1984 Dec
PMID:[Polygraphic aspects of periodic movements in sleep]. 653 49


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