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Query: UMLS:C0027066 (myoclonus)
 4,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Post-hypoxic intention myoclonus is a specific myoclonic syndrome in which central serotonergic tone may be deficient. Tryptophan and 5-hydroxytryptophan administration to patients with post-hypoxic intention myoclonus increases pre-existing low levels of 5-hydroxyindoleacetic acid levels in the cerebrospinal bluid, and also suppresses myoclonus. Serotonin precursor administration does not help all patients with myoclonus and may actually worsen some myoclonic syndromes, including those secondary to lipid storage diseases. Treatments that alter serotonin metabolism can also produce myoclonus in experimental animals but their relevance to myoclonic syndromes in humans remains uncertain.
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PMID:Serotonergic mechanisms in myoclonus. 29 Jul 59

5-Hydroxytryptophan (5-HTP) induces a characteristic behavioural syndrome of altered motor activity with muscle jerking in guinea pigs. Myoclonic jerking occurs synchronously in forelimbs and hindlimbs and is associated with a stereotyped electromyographic (EMG) pattern of a burst of activity lasting 40-50 msec in active muscles, followed by silence lasting 50-70 msec, followed by a further variable period of muscle activity. Such myoclonus may be induced also by the administration of L-tryptophan plus a monamine oxidase inhibitor (MAOI), or by agents acting as serotonin (5-HT) receptor agonists. The 5-HTP-induced syndrome is antagonised by a central decarboxylase inhibitor (NSD-1035) and by agents which block 5-HT receptors (methysergide and cyproheptadine). 5-HTP-induced jerking is abolished below the level of a spinal cord transection, but persists in decerebrate animals. No electroencephalographic (EEG) changes are seen preceding the muscle jerks. The clinical significance of this animal model of myoclonus is discussed.
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PMID:5-hydroxytryptophan-induced myoclonus in guinea pigs. A physiological and pharmacological investigations. 30 85

Clonazepam (5-(2-chlorophenyl)-1,3-dihydro-7-nitro 2H-1,4 benzodiazepin-2-one) (2 mg/kg) reduced a p,p'-DDT-induced myoclonus in mice by 50%. This antimyoclonic action of clonazepam was counteracted by the serotonin (5-HT) receptor blockers methysergide, metergoline and cinnanserin and potentiated by the 5-HT uptake inhibitors fluoxetine and chlorimipramine. Clonazepam (4 mg/kg) reduced plasma tryptophan by 27%, but had no effect on brain tryptopham, 5-HT, 5-hydroxyindoleacetic acid, 5-HT synthesis and 3H-5-HT receptor binding. Clonazepam (10(-5) M) inhibited brain synaptosomal 3H-5-HT uptake by 23% and increased 3H-5-HT release by 24%. However, 2-8 mg/kg of clonazepam administered intraperitoneally had no effect on 5-HT uptake or release. gamma-Aminobutyric acid (GABA) agonists (muscimol, acetylenic GABA, amino-oxyacetic acid) and the GABA antagonists bicuculline and isoniazid had no effect on p,p'-DDT-induced myoclonus. Furthermore, bicuculline did not counteract the antimyoclonic effect of clonazepam. We suggest that the antimyoclonic action of clonazepam is mediated by enhancement of serotonergic rather than GABAergic neurotransmission.
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PMID:Antimyoclonic action of clonazepam: the role of serotonin. 52 Apr 16

While the 5-HT precursors tryptophan and 1-5-HTP cause an increase in serum prolactin concentration, a combination of 1-5-HTP with a peripheral decarboxylase inhibitor was found to reduce the serum prolactin concentration. This combination seemed to behave like a DA agonist. This effect is not produced by the decarboxylase inhibitor per se. A possible explanation is that 5-HTP is converted to 5-HT in CA-ergic neurons, that 5-HT supersedes the CA from the stores, and that some of the CA reach the synaptic cleft and stimulate CA receptors. Another possible explanation is that 5-HTP decarboxylase is centrally inhibited as well, and that an effect of 5-HTP itself is involved here. In view of the observations made it is doubtful whether the therapeutic effect of 5-HTP combined with a peripheral decarboxylase inhibitor in depressions and myoclonus can in fact be atributed to activation of central serotonergic systems.
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PMID:An unexpected effect of L-5 hydroxytryptophan-ethyl-ester combined with a peripheral decarboxylase inhibitor on human serum prolactin. 108 2

Animal data indicate that serotonin (5-HT) is a major neurotransmitter involved in the control of numerous central nervous system functions including mood, aggression, pain, anxiety, sleep, memory, eating behavior, addictive behavior, temperature control, endocrine regulation, and motor behavior. Moreover, there is evidence that abnormalities of 5-HT functions are related to the pathophysiology of diverse neurological conditions including Parkinson's disease, tardive dyskinesia, akathisia, dystonia, Huntington's disease, familial tremor, restless legs syndrome, myoclonus, Gilles de la Tourette's syndrome, multiple sclerosis, sleep disorders, and dementia. The psychiatric disorders of schizophrenia, mania, depression, aggressive and self-injurious behavior, obsessive compulsive disorder, seasonal affective disorder, substance abuse, hypersexuality, anxiety disorders, bulimia, childhood hyperactivity, and behavioral disorders in geriatric patients have been linked to impaired central 5-HT functions. Tryptophan, the natural amino acid precursor in 5-HT biosynthesis, increases 5-HT synthesis in the brain and, therefore, may stimulate 5-HT release and function. Since it is a natural constituent of the diet, tryptophan should have low toxicity and produce few side effects. Based on these advantages, dietary tryptophan supplementation has been used in the management of neuropsychiatric disorders with variable success. This review summarizes current clinical use of tryptophan supplementation in neuropsychiatric disorders.
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PMID:L-tryptophan in neuropsychiatric disorders: a review. 130 30

This work focuses on the neurophysiological features in a patient with action myoclonus and mental deterioration following methylbromide intoxication. The patient is a 28-year-old man, without respiratory distress or exposure to other toxics. Myoclonus improved with polytherapy (clonazepam, 5-HT, carbidopa, GABA). The neurophysiological and neuropsychological evidence in this patient suggests a possible double site of action of methylbromide at cortical and subcortical levels.
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PMID:Methylbromide intoxication: a case report. 137 51

To study the regulation of 5-HT1A receptors in the brainstem, the region most relevant to the serotonin syndrome and to serotonin-responsive human myoclonic disorders, we chronically treated rats with various 5-HT1A agonists and labeled 5-HT1A sites with [3H]8-OH-DPAT. Daily injection for 30 consecutive days of 10 mg/kg ip 8-OH-DPAT (pre- and post-synaptic 5-HT1A agonist) significantly decreased 8-OH-DPAT-evoked flat body posture, forelimb myoclonus, and hypothermia compared to chronic vehicle injection. There was no cross tolerance to 8-OH-DPAT in rats chronically injected with ipsapirone or buspirone (presynaptic 5-HT1A agonists). However, none of the 5HT1A agonists significantly altered Bmax of brainstem 5-HT1A binding sites. Chronic injection with other drugs such as 1-propranolol, (+/-) pindolol and spiperone (5-HT1A and 5-HT2 antagonists), methysergide (5-HT1 and 5-HT2 antagonist), and agonists and antagonists at various other 5-HT receptors also had no effect on binding parameters. These data demonstrate lack of cross-tolerance between pre- and post-synaptically acting 5-HT1A agonists and absence of down-regulation of presynaptic 5-HT1A sites at doses which induced tolerance of 5-HT1A-mediated behaviors of the serotonin syndrome. They suggest changes in the post-synaptic cell rather than the receptor recognition site as the mechanism of tolerance.
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PMID:Brainstem 5-hydroxytrytamine1A binding sites are not down-regulated by agonists which induce tolerance in the rat: myoclonus and other serotonergic behaviors. 138 64

The effects of a serotonin (5-HT) receptor agonist, 5-methoxy-N,N-dimethyltryptamine (5-MeODMT), on epileptic photosensitivity were studied in the lateral geniculate-kindled cat. 5-MeODMT at 4 mg/kg significantly suppressed photically induced myoclonus, but not paroxysmal EEG activity, at 0.5-1 h after injection. This antiepileptic effect was seen in association with the appearance of behavioral signs similar to those seen in the 5-HT syndrome. The present data provide further evidence that 5-HT plays an important role in photosensitive epilepsy, and suggest that the inhibitory effect of 5-MeODMT on photosensitivity results from its agonist action at 5-HT1 receptors.
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PMID:Behavioral and electroencephalographic effects of a serotonin receptor agonist (5-methoxy-N,N-dimethyltryptamine) in a feline model of photosensitive epilepsy. 140 49

We used saturation radioligand binding to measure nine types of serotonin receptors in 13 neuroblastomas from children. 5-HT1E and 5-HT3 sites were found in neuroblastomas with receptor density and affinity similar to human or rat brain. No 5-HT1A, 5-HT1B, 5-HT1C, 5-HT1D, 5-HT2, or 5-HT uptake sites were found in any of the tumors, although all were detected in human or rat brain. These data demonstrate that human neuroblastomas possess 5-HT receptors found in human brain and relevant to human myoclonus. We speculate that 5-HT receptors in human neural crest-derived tumors may have clinical and neurobiological significance.
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PMID:Serotonin receptors in human neuroblastoma: a possible biologic tumor marker. 153 97

A study was made of 36 EEGs chosen in terms of the principle of combination in them of two elements: (1) a focus of paroxysmal activity; (2) electrophysiological correlates of myoclonus whose stem origin was not questioned. The appearance of myoclonic and paroxysmal patterns distribution on the scalp was reproduced with the aid of color pictograms. It has been discovered that the stem myoclonic activity is largely grouped around the paroxysmal one; within the limits of the anterolateral quadrant of the scalp surface, one can see a tendency toward a compact recording of the stem myoclonic and authentic paroxysmal patterns. In cases where the paroxysmal activity is in the anterotemporal focus, the proximity of the points of the recording from the scalp of the stem myoclonic and paroxysmal patterns may appear maximal. As the latter ones get detectable during recording, the myoclonic patterns play the role of their satellites (rather than coincidents). This can serve a prerequisite for ascertaining local deficiency of 5-HT during observation on the EEG of compact-grouping myoclonic phenomena recorded within the limits of one anterolateral quadrant of the scalp surface.
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PMID:[Use of a topographic analysis of the myoclonic activity recorded from the scalp for detection of functional disorders of the serotoninergic systems]. 166 6


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