1/19. Beneficial effects of serotonin precursors in postanoxic action myoclonus.In two patients with postanoxic action myoclonus, L-tryptophan or a monoamine oxidase inhibitor induced a moderate improvement, but L-5-hydroxytryptophan had greater therapeutic effect. methysergide, a potent blocker of serotonin receptors, consistently induced a marked deterioration in myoclonus. Pretreatment cerebrospinal fluid 5-hydroxyindoleacetic acid levels were reduced significantly in both patients. These findings suggest that postanoxic action myoclonus likely is associated with insufficient serotonergic activity in the central nervous system. Data are inadequate to determine whether this apparent insufficiency reflects structural changes in 5HT-containing raphe nuclei due to a direct anoxic damage to these structures of functional changes caused by a secondary reduction in the activity of intact serotonergic neurons.- - - - - - - - - - ranking = 1keywords = serotonin (Clic here for more details about this article) |
2/19. reflex reticular myoclonus: relationship to some brainstem pathophysiological mechanisms.Two patients with reflex reticular myoclonus [RRM] were tested electrophysiologically and pharmacologically. In one of the cases the underlying disease was chronic Lyme borreliosis. In the other, the RRM attacks may have been associated with procarbazine therapy applied for Hodgkin's disease. No cortical lesion could be demonstrated either clinically or electrophysiologically [EEG, averaged EEg preceeding the jerks, SSEP]. An EMG analysis of the jerks revealed the shortest latency in the muscles innervated by the accessory nerve. The latencies became longer in a more rostral muscle [masseter], as well as in a more caudal one, the muscles innervated by the facial nerve were spared. it is presumed that the complete movement pattern of the myoclonus residues in the jerk generating structure. RRM in the described cases differs from the startle by sparing the facial nerve and from the papio papio baboon non-epileptic myoclonus by the activating effect of physostigmine. A partial therapeutic effect was achieved with a serotonine precursor, but a GABAergic therapy proved to be the most effective.- - - - - - - - - - ranking = 0.2keywords = serotonin (Clic here for more details about this article) |
3/19. Pathological findings in a case of hypoxic myoclonus treated with 5-hydroxytryptophan and a decarboxylase inhibitor.A 72-year-old woman suffered a respiratory arrest following intoxication with barbiturates. Her examination 27 months after the anoxic incident revealed involuntary jerks of trunk and limb muscles triggered by willed movements. On a regimen of 1 g L-5-HTP and 100 mg l-alpha-methyldopa hydrazine (carbidopa), action myoclonus disappeared completely. This medication had to be discontinued because of a regressive hysterical reaction. Two months later, she was found unconscious; resuscitation efforts were unsuccessful. autopsy showed death was caused by choking on food. Coronal slices of the cerebral hemispheres and transverse section of the brainstem and cerebellum revealed no lesion. No evidence of hypoxic damage could be demonstrated in the cerebral cortex, hippocampus, striatum, pallidum, subthalamus, thalamus, or other diencephalic structures. In the caudal half of the midbrain tegmentum, a marked astrocytic reaction of some duration was encountered in the lateral parts of the supratrochlearis nucleus, the lateral subnucleus of the mesencephalic gray, and the immediately adjacent cuneiform and subcuneiform nuclei. In the former nucleus, sites of presumed nerve cell disintegration were found, but the neuronal populations of this nucleus and of the other raphe nuclei were well maintained. The other brainstem structures and the cerebellum were normal. Our neuropathological findings suggest that hypoxic myoclonus (a) does not seem to be explained by demonstrable neuronal loss in motor structures, such as cerebellum, thalamus, or basal ganglia and (b) does not appear to be causally related to a detectable reduction in the serotonin-containing neurons of the brain but rather to a functional derangement of anatomically intact serotonergic pathways originating perhaps from other, as yet unidentified, damaged neuronal structures.- - - - - - - - - - ranking = 0.2keywords = serotonin (Clic here for more details about this article) |
4/19. Clinical, biochemical, and pharmacological observation in a patient with postasphyxic myoclonus: association to serotonin hyperactivity.Posthypoxic action myoclonus is usually associated with impaired serotonin (5-HT) neurotransmission but in some patients 5-HT precursors aggravate and 5-HT blockers improve action myoclonus. We studied a 65-year-old man who presented with action myoclonus following a prolonged episode of moderate hypoxia and severe hypercarbia. The myoclonus increased with 5-hydroxytryptophan (5-HTP) 1,200 mg/day plus carbidopa 300 mg/day and sodium salt of valproic acid (SVA) 800 mg/day, and improved with 1 mg of clonazepam (CNZ) in an intravenous bolus. Biochemical analysis of the cerebrospinal fluid (CSF) prior to any drug therapy did not reveal abnormalities in the levels of homovanillic acid (HVA) and methoxyhydroxyphenylglycol (MHPG) but 5-hydroxyindoleacetic acid (5-HIAA) levels were elevated in comparison with controls (33 versus 21 ng/ml). SVA therapy produced a moderate increase and 5-HTP plus carbidopa a threefold elevation of 5-HIAA in CSF and marked aggravation of action myoclonus. methysergide (3 mg/day) totally suppressed myoclonus and decreased CSF 5-HIAA to undetectable levels. methysergide also reduced CSF tryptophan to 40% of baseline levels. Discontinuation of methysergide and substitution by placebo was followed by reappearance of myoclonus. A partial and incomplete spontaneous remission of symptoms took place 7 months after the asphyxic episode. Action myoclonus and enhanced 5-HT neurotransmission may be present in patients in which acidosis reverses the effects of hypoxia on 5-HT neurotransmission.- - - - - - - - - - ranking = 1keywords = serotonin (Clic here for more details about this article) |
5/19. Serotonergic mechanisms in myoclonus.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.- - - - - - - - - - ranking = 0.2keywords = serotonin (Clic here for more details about this article) |
6/19. The effect of intravenous L-5-HTP in the myoclonic encephalopathy of infants.A 7 year old girl suffering from myoclonic encephalopathy of infants (MEI) underwent acute treatment by slow intravenous L-5-hydroxytrypthophan (L-5-HTP). The authors found a clear clinical physiological improvement of myoclonic symptoms at rest and during action, but the opsoclonus remained unchanged. The authors suggest that, at least in this case of MEI, the myoclonus was serotonin responsive, as already reported in action or intention and stimulus sensitive myoclonus.- - - - - - - - - - ranking = 0.2keywords = serotonin (Clic here for more details about this article) |
7/19. Post-hypoxic intention myoclonus treated with 5-hydroxy-tryptophan and an extracerebral decarboxylase inhibitor.Post-hypoxic intention myoclonus successfully treated by long-term administration of the combination of 5-hydroxytryptophan and carbidopa is described. Persistent euphoria and diarrhoea were essential side effects. methysergide (12 mg/day) blocked the therapeutic effect, indicating a specific serotoninergic function of precursor loading with 5-hydroxytryptophan. Tryptophan (8 g/day) had no effect on the myoclonus suggesting a reduced tryptophan hydroxylase activity. plasma concentrations of 5-hydroxytryptophan in the range of 10--30 micromoles per liter were obtained during maintenance therapy with 900 mg 5-hydroxytryptophan per day in combination with 150 mg carbidopa per day.- - - - - - - - - - ranking = 0.2keywords = serotonin (Clic here for more details about this article) |
8/19. Hereditary branchial myoclonus with spastic paraparesis and cerebellar ataxia: a new autosomal dominant disorder.We report a family with branchial myoclonus, spastic paraparesis, and cerebellar ataxia in which six members were affected in two generations and the inheritance appeared to be autosomal dominant. Age at onset ranged from 40 to 50 years. Rhythmic myoclonus involving the palate, pharynx, larynx, and face was followed by truncal ataxia and spastic paraparesis in most patients. CT and MRI revealed mild atrophy of the cerebral and cerebellar cortex and severe atrophy of the medulla and spinal cord. The pons appeared normal and the olives not hypertrophic. CSF studies revealed severe reduction of the serotonin metabolite 5-hydroxyindoleacetic acid. Treatment with 5-hydroxytryptophan and carbidopa at highest tolerated dose mildly improved ataxia but did not modify the myoclonus. Treatment with anticholinergics, benzodiazepines, phenytoin, valproate, carbamazepine, and baclofen was unsuccessful. The clinical symptoms were progressive, leading to death or severe disability 5 to 10 years after the onset of the disease.- - - - - - - - - - ranking = 0.2keywords = serotonin (Clic here for more details about this article) |
9/19. Is monoamine oxidase inhibitor induced myoclonus serotoninergically mediated?In the present study a single case observation of myoclonus during sleep-wave transition was monitored in a depressed patient treated with the monoamine oxidase inhibitor, phenelzine. The myoclonus had a rhythm of 1 c/second and lasted for two years, the duration of phenelzine treatment. myoclonus appeared neither during wakefulness nor during sleep, but at wake-sleep-wake transitions. This "switch" myoclonus was associated with phasic muscle hyperactivity during REM sleep. methysergide a 5-HT suppressor, decreased the switch myoclonus frequency and the REM muscle hyperactivity, indicating serotoninergic involvement in the mechanism of phenelzine induced myoclonus.- - - - - - - - - - ranking = 1keywords = serotonin (Clic here for more details about this article) |
10/19. Myoclonic seizures after abrupt withdrawal from phenelzine and alprazolam.monoamine oxidase inhibitors (MAOIs) are being used more frequently in the treatment of various psychiatric and neurological disorders. Although adverse effects of MAOI treatment are widely known, withdrawal symptoms are less well known. They include nausea, sweating, palpitations, nightmares, and psychosis. Withdrawal reactions from combination therapy with an MAOI and another agent are seldom described. Reported here is the occurrence of myoclonic seizures after the abrupt discontinuation of phenelzine and alprazolam. Alterations in the GABA and serotonin neurotransmitter systems as a result of withdrawal of the MAOI and the benzodiazepine may account for the seizures.- - - - - - - - - - ranking = 0.2keywords = serotonin (Clic here for more details about this article) |
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