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

Norepinephrine, epinephrine, dopamine, serotonin and their major catabolites were measured in 17 regions of the left hemisphere of two brains obtained from two brothers with Alzheimer's disease with very early onset. The clinical diagnosis was confirmed by histological examination of the right hemispheres and brain stems. The quantitative data were compared with our values in normal brains. In the patient suffering from the less severe dementia, there was a severe reduction of the serotonin concentration in all examined neocortical areas and its concentration was even below the detection limit in the nucleus amygdalis, hippocampus, caudate nucleus, putamen, globus pallidus and substantia nigra. In the other patient, who suffered from a more pronounced dementia with myoclonus, the serotonin concentration was below the detection limit in all examined structures. In contrast with these findings, the noradrenergic, adrenergic and dopaminergic systems appeared to be relatively unaffected by the disease process. Focusing our attention on the nuclei wherein the monoamine transmitter systems originate, it appeared that neuronal losses and neurofibrillary tangles clearly predominated in the substantia grisea subependymalis, the nucleus centralis superior and the nucleus raphe dorsalis, origin of the main serotonergic system. The serotonin deficiency sheds light on possible mechanisms of myoclonus in Alzheimer's disease.
 ...
PMID:Distribution of biogenic amines and their catabolites in brains from patients with Alzheimer's disease. 381 69

Administration of p,p'-DDT to rats produced myoclonus, but unlike previous studies in mice, this was not decreased by administration of clonazepam. Precursors of 5-hydroxytryptamine (5-HT) (L-tryptophan and L-5-HTP) reduced the intensity of myoclonus, but the 5-HT agonists, quipazine and Org 6582 did not. Antagonists of 5-HT (methergoline, methysergide and cinanserin) did not potentiate the myoclonus induced by p,p'-DDT. Drugs altering the function of dopamine and noradrenaline (apomorphine, clonidine or phenoxybenzamine) also had no effect on this myoclonus. Administration of monoamine oxidase inhibitors (MAOIs; pargyline, nialamide and tranylcypromine) markedly attenuated the myoclonus, an effect that could not be attributed to an action on any one monoamine system. No observable changes in cerebral biochemical parameters of 5-HT occurred at the onset of myoclonus, although tryptophan and 5-hydroxyindoleacetic acid (5-HIAA) in brain were increased following periods of prolonged myoclonus. Electrophysiological analysis of the myoclonus in the rat induced by p,p'-DDT revealed changes in EEG and EMG activity which suggested an origin for the myoclonus in the brainstem. Although this was similar to electrophysiological findings in some human patients with post-anoxic action myoclonus, the pharmacological studies suggest that the myoclonus induced by p,p'-DDT in the rat is not a suitable model for screening potential drugs to be used in the treatment of this disorder.
 ...
PMID:Myoclonus in the rat induced by p,p'-DDT and the role of altered monoamine function. 402 63

1 The effect of catechol on uptake and K+-stimulated release of gamma-aminobutyric acid (GABA), D-aspartate, noradrenaline and acetylcholine has been studied in slices of cerebral cortex and thalamus. 2 Low concentrations of catechol did not influence the uptake of any of the neurotransmitters in either brain area. 3 Noradrenaline release was unaffected by catechol. 4 Acetylcholine release from both cortical and thalamic slices was inhibited by high concentrations of catechol. This phenomenon is unlikely to be related to catechol-induced convulsions. 5 Catechol (100 microM) inhibited GABA release from cortical slices by 28%. However, at a concentration of 10 microM catechol enhanced the release of D-aspartate from thalamic slices by over 100%. 6 Potentiated release of excitatory amino acid transmitters may contribute to the enhanced excitability of thalamic cells which occurs during sensory myoclonus induced by low doses of catechol.
 ...
PMID:The effect of the convulsant agent, catechol, on neurotransmitter uptake and release in rat brain slices. 611 45

The GABA-withdrawal syndrome (GWS) is a model of local status epilepticus following the interruption of a chronic GABA infusion into the rat somatomotor cortex. GWS is characterized by focal epileptic electroencephalographic discharges and associated contralateral myoclonus. In neocortical slices obtained from GWS rats, most neurons recorded in the GABA-infused area are pyramidal neurons presenting bursting properties. The bursts are induced by white-matter stimulation and/or intracellular depolarizing current injection and correlate with a decrease of cellular sensitivity to GABA, caused by its prolonged infusion. This effect is related to a calcium influx that may reduce the GABAA receptor-mediated inward current and is responsible for the bursting properties. Here we present evidence for the involvement of calcium- and NMDA-induced currents in burst genesis. We also report modulatory effects of noradrenaline appearing as changes on firing patterns of bursting and nonbursting cells. Complementary histochemical data reveal the existence of a local noradrenergic hyperinnervation and an ectopic expression of tyrosine hydroxylase mRNAs in the epileptic zone.
 ...
PMID:The GABA-withdrawal syndrome: a model of local status epilepticus. 1070 10

The alkaloid ricinine isolated from the plant Ricinus communis, when administered to mice at high doses, induces clonic seizures accompanied by electroencephalographic alterations in the cerebral cortex and hippocampus. The lethal nature of ricinine-induced seizures is considered to be a good model for the study of the events that cause death during clonic seizures, particularly those related to respiratory spasms. The initial signs (pre-seizure period) were marked by exophthalmus and decreased locomotor behavior. Animals killed during the preseizure period presented an increased utilization rate (HVA/DA) of dopamine (DA), an increased concentration of noradrenaline (NA), and a decreased concentration of glutamate (Glu), glutamine (Gln), taurine (Tau), and serotonin (5-HT) in the cerebral cortex. The seizure period is characterized by the occurrence of hind limb myoclonus and respiratory spasms, which are followed by death. Alterations in the cerebral cortex concentration of these neurotransmitters persisted during the seizure period. These alterations are only partially observed in the hippocampus, mainly during the seizure period. The present results suggest that an increased release of Glu in the cerebral cortex can be implicated in the genesis of the ricinine-induced seizure and that it triggers many anticonvulsive mechanisms, like the release of Tau, DA, 5-HT, and NA.
 ...
PMID:Amino acid and monoamine alterations in the cerebral cortex and hippocampus of mice submitted to ricinine-induced seizures. 1206 66

The clinical and EEG data of a 49-year-old man with myoclonic and generalized tonic-clonic seizures resulting from early childhood encephalitis are described. He experienced no tonic-clonic seizure for 10 years before brief exposure first to 60 mg/day duloxetine and then to 20mg/day paroxetine for depressive symptoms. These drugs were separately prescribed at a 9-month interval, and after beginning each drug, the patient experienced tonic-clonic seizures of worsening intensity and myoclonus of increasing frequency. Clinical features correlated with subcontinuous, generalized spike-wave discharges on the EEG. Discontinuation of antidepressant treatment resulted in rapid disappearance of clinical and electrophysiological manifestations of myoclonic status. We suggest care must be taken when using serotonin-noradrenaline reuptake inhibitors (SNRIs) or selective serotonin reuptake inhibitors (SSRIs), as these drugs pose the risk of complications in the specific population of people with myoclonic seizures.
 ...
PMID:Antidepressant-associated myoclonic status in a patient with symptomatic generalized epilepsy: does risk occur with therapeutic doses? 1943 83

Many pharmacological agents may induce a variety of movement disorders, including dystonia, tremor, parkinsonism, myoclonus and dyskinesia, with an acute, subacute or more chronic time course. Motor symptoms may be isolated or part of a more extensive cerebral or systemic condition, such as the neuroleptic malignant syndrome or the serotonin syndrome. Drug-induced movement disorders share a number of features that should make them easy to identify, including a clear temporal relationship between medication initiation and symptom onset, a dose-effect, and, with the exception of tardive syndromes, complete resolution after discontinuation of the offending agent. Diagnosis relies on a thorough medication history. Medications commonly involved include dopamine receptor blockers, antidepressants and anti-epileptics, among many others. Mechanisms underlying drug-induced movement disorders involve blockade, facilitation or imbalance of dopamine, serotonin, noradrenaline and cholinergic neurotransmission in the basal ganglia. The present review focuses on drug-induced movement disorders that typically develop as an acute (hours to days) or subacute (days to weeks) event, including acute dystonic reactions, akathisia, drug-induced parkinsonism, neuroleptic malignant syndrome, serotonin syndrome, parkinsonism-hyperpyrexia syndrome, drug-induced tremor, drug-induced hyperkinesias and movement disorders associated with the use of recreational drugs.
...
PMID:Acute and subacute drug-induced movement disorders. 2426 59