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)

A range of D1 receptor agonists were tested for their ability to facilitate limbic motor seizures induced by a subthreshold dose of the chemoconvulsant pilocarpine (100 mg/kg IP) in mice. ED50 values (mumol/kg) were calculated from log dose-probit analyses, giving relative proconvulsant potencies of SKF 82958 > CY 208-243 > SKF 77434 = SKF 75670 = SKF 80723 > SKF 38393. The compound SKF 82526, which poorly crosses the blood-brain barrier, did not lower the seizure threshold. Convulsions consisted of rearing and forepaw myoclonus, leading to status epilepticus at higher doses of the D1 agonists. No deaths were recorded. A maximum seizure incidence of 50% was obtained with SKF 75670, compared to 100% for the other compounds. Apart from SKF 82526, the D1 agonists all elicited behavioural signs of central D1 receptor stimulation, including motor restlessness, grooming and sniffing. There was no obvious relationship between the abilities of these D1 agonist drugs to promote epilepsy and their effects on unconditioned motor behaviour, or their affinities and efficacies at the striatal D1 receptor. It is concluded that a reduction of the seizure threshold is an inevitable consequence of central D1 receptor stimulation with existing D1 agonists.
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PMID:Seizure promotion by D1 agonists does not correlate with other dopaminergic properties. 810 96

Two instances of successful treatment of the rare ocular dyskinesia, opsoclonus, with chlormethiazole are reported. A 65-year-old woman had the opsoclonus-myoclonus syndrome associated with carcinoma of the breast; her myoclonia and opsoclonus did not respond to intravenous diazepam or phenytoin. Treatment with intravenous chlormethiazole resulted in rapid control of her myoclonic attacks, followed by slower but complete resolution of the opsoclonus. Following control of the acute symptoms the patient was transferred to an oral chlormethiazole maintenance dose which was further reduced and subsequently discontinued after 5 months, when the patient's overall clinical status had improved. A 53-year-old man with opsoclonia, myoclonia, ataxia and encephalopathy, not associated with neoplasia, was given immunosuppressor drugs to establish basal control, and oral chlormethiazole for symptomatic treatment. Almost immediately after the initial dose of chlormethiazole the patient became more orientated; he was sedated and the agitation and myoclonic fits were brought under control quite quickly. The opsoclonus responded progressively and was completely resolved after a few days. The initial oral dose of chlormethiazole was gradually reduced and was discontinued after 5-6 months. Chlormethiazole was well tolerated; it may have an important role in the management of the rare opsoclonus-myoclonus syndrome.
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PMID:Chlormethiazole in the management of the opsoclonus-myoclonus syndrome. 818 45

The serotonin syndrome, induced by serotoninergic agents, includes confusion, agitation, myoclonus, diaphoresis, tremor and diarrhea. The authors prospectively evaluated all these symptoms in 38 depressed inpatients fullfilling DSM-III-R criteria for major depression. Sixteen (42%) of 38 patients presented at least one symptom of serotonin syndrome. In 14 cases tremor and myoclonus occurred simultaneously, and 10 patients presented at the same time tremor plus myoclonus, diaphoresis and shivering. Except for 2 patients, symptoms were transient, lasted less than 1 week and disappeared with the pursuit of treatment.
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PMID:Prospective evaluation of the serotonin syndrome in depressed inpatients treated with clomipramine. 829 81

In animals the occurrence of a behavioural syndrome consisting of hyperactivity, stereotyped movements and increase of temperature has been induced by MAOIs, 5-HT precursors (L-tryptophan) and 5-HT reuptake inhibitors. Most of these manifestations were specifically blocked by a pretreatment with an inhibitor of serotonin synthesis. In humans, the association of myoclonus, diarrhea, confusion, hypomania, agitation, hyperreflexia, shivering, incoordination, fever and diaphoresis, when patients are treated with serotoninergic agents, could constitute a "serotonin syndrome". Such cases of serotonin syndrome were reported after treatments with L-tryptophan, MAOIs, serotonin reuptake inhibitors and tricyclics alone or in association. The authors prospectively evaluated all the "serotonin-related" symptoms in 38 depressed inpatients fulfilling DSM III-R criteria of major depression. 16 (42%) out of 38 patients presented at least one symptom of serotonin syndrome. In 14 cases tremor and myoclonus occurred simultaneously and 10 patients presented at the same time tremor, myoclonus, diaphoresis and shivering. Except for two patients, symptoms were transient, lasted less than one week and disappeared with the pursuit of the treatment. Most often, serotonin syndrome thus corresponds to a reaction induced by a combination of serotoninergic agents at high dosages. In very rare cases, a toxic and potentially fatal interaction can occur between MAOIs, tricyclics and selective serotonin reuptake inhibitors at therapeutic dosages. Serotonin syndrome also provides an heuristic model of the putative mode of action of antidepressants. Serotonin-related symptoms are the physical and objective expression of the antidepressant-induced increase in serotonin. The specificity of serotonin-related syndrome also needs to be discussed since most of the symptoms, such as tremor and diaphoresis, are not in all cases related to an increase in serotonin.
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PMID:[The serotonin syndrome: review of the literature and description of an original study]. 852 62

In advanced cancer patients close to death, delirium, multifocal myoclonus, and restlessness may occur. Multi-organ failure and related metabolic changes are mostly responsible for these symptoms. A pharmacologic approach to manage the delirium is necessary in the majority of cases. Benzodiazepines, neuroleptics, and barbiturates are the most common drugs used. In the case reported, propofol administered at very low doses provided good control of neuropsychiatric symptoms. After a loading dose of 20 mg, an infusion of 50-70 mg per hr was started. The patient died peacefully after 8 hr of propofol infusion, without requiring opioids. Propofol seems to be a promising drug in treating the terminal agitated state that can be associated with the dying process.
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PMID:Propofol in terminal care. 859 25

Serotonin syndrome, a condition with numerous clinical neurological manifestations, is the result of central serotonergic hyperstimulation. Features of the syndrome include mental status and behavioral changes (agitation, excitement, hypomania, obtundation), motor system involvement (myoclonus, hemiballismus, tremor, hyperreflexia, motor weakness, dysarthria, ataxia) and autonomic symptoms (fever, chills, diarrhea). Serotonin syndrome has been reported exclusively in patients on medications for psychiatric illness and Parkinsonism, despite the fact that the putative action of many antimigraine agents also involves the serotonin system. We herein report six patients with migraine who developed symptoms suggestive of the serotonin syndrome. Five were taking one or more serotomimetic agents for migraine prophylaxis (sertraline, paroxetine, lithium, imipramine, amitriptyline). In each case the symptoms and signs developed in close temporal proximity with use of a migraine abortive agent known to interact with serotonin receptors. In three instances the agent was subcutaneous sumatriptan and, in three, intravenous dihydroergotamine. In each instance the symptoms were transient and there was full recovery. With the ever increasing use of migraine medications active at serotonin receptor sites, cases of serotonin syndrome will likely occur more frequently. It is important that physicians treating migraine are aware of the serotonin syndrome and are able to recognize its varying presentations.
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PMID:Serotonin syndrome complicating migraine pharmacotherapy. 886 67

Terminal restlessness is a variant of delirium observed in some patients in their last days of life. Readily reversible causes of restlessness should be identified and treated. Benzodiazepines give effective palliation of this condition, and, unlike haloperidol and the phenothiazines, do not exacerbate the existing tendency to myoclonus and convulsions.
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PMID:Palliative care: an update on "terminal restlessness". 900 13

We describe a patient treated with trazodone, amitriptyline and lithium carbonate who developed anxiety, restlessness, tremor, myoclonus, hyperreflexia, diaphoresis, rigidity and hyperthermia. The constellation of findings was diagnostic of serotonin syndrome. Although doses of trazodone and amitriptyline were relatively low, serotonin syndrome developed in this patient. It is suggested that the combination with lithium facilitated the effect of central serotonergic responses mediated by trazodone and amitriptyline.
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PMID:A case of serotonin syndrome induced by concomitant treatment with low-dose trazodone and amitriptyline and lithium. 903 98

A 62-year-old man receiving subcutaneous fentanyl for the management of cancer pain developed generalized central excitation after an overdose of 5000 micrograms of fentanyl. The patient developed acute confusion, restlessness, generalized myoclonus, visual hallucinations, and hyperalgesia and tremors upon tactile stimulation of the arms or legs. These symptoms rapidly disappeared after the administration of 0.2 mg of naloxone. Within an hour the symptoms reappeared and once again, responded immediately after a second injection of 0.2 mg of naloxone. Our findings suggest that fentanyl overdose can occasionally present with general central irritability that responds to naloxone.
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PMID:Acute neuropsychiatric findings in a patient receiving fentanyl for cancer pain. 906 31

The selective pharmacology of the selective serotonin reuptake inhibitors (SSRIs) results in a lower potential for pharmacodynamic drug interactions relative to other antidepressants such as the tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs). However, the SSRIs have been implicated in the development of the serotonin syndrome--a potentially life-threatening complication of treatment with psychotropic drugs. The syndrome is produced most often by the concurrent use of two or more drugs that enhance central nervous system serotonin activity and often goes unrecognized because of the varied and nonspecific nature of its clinical features. The serotonin syndrome is characterized by alterations in cognition (disorientation, confusion), behavior (agitation, restlessness), autonomic nervous system function (fever, shivering, diaphoresis, diarrhea), and neuromuscular (ataxia, hyperreflexia, myoclonus) activity. The difference between this syndrome and the occurrence of adverse effects caused by serotonin reuptake inhibitors alone is the clustering of the signs and symptoms, their severity, and their duration. There are important pharmacokinetic interactions between SSRIs and other serotonergic drugs due principally to their effects on the cytochrome P450(CYP) isoenzymes, the potential for which varies widely amongst the SSRI group, which may increase the likelihood of a pharmacodynamic interaction. The exceptionally long washout period required after fluoxetine discontinuation may cause additional problems and/or inconvenience. Patients with serotonin syndrome usually respond to discontinuation of drug therapy and supportive care alone, but they may also require treatment with antiserotonergic agent such as cyproheptadine, methysergide, and/or propranolol. To reduce the occurrence, morbidity, and mortality of the serotonin syndrome, it must be both prevented by prudent pharmacotherapy and given prompt recognition when it is present.
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PMID:Selective serotonin reuptake inhibitor-induced serotonin syndrome: review. 916 67


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