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)

Myoclonus (myos: muscles and klonos: agitation. jerk) reflect some dysfunction of the central nervous system. Their multiform clinical presentations correlate to various physiopathological mechanisms and neuropharmacological substrates, still imprecisely known. The etiologies are quite numerous but it is important to distinguish from the physiologic forms epileptic, symptomatic, essential or segmental myoclonus. The treatment, largely depending of the underlying cause, mainly includes clonazepam and valproate.
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PMID:[Myoclonus]. 920 75

The pyrazoloacridine (PZA) analogue NSC366140 (PD115934) entered clinical trial based on unique preclinical characteristics including solid tumor selectivity in vitro, marked antitumor activity in vivo against murine solid tumors, selectivity against noncycling cells, and activity against multidrug-resistant tumor cells. After identification of the pre-clinical efficacy and an acceptable toxicity profile, a Phase I study of PZA was carried out. A total of 28 patients was entered and received a total of 67 treatment courses. The drug was administered via a 1-h infusion every 21 days. The starting dose was 30 mg/m2 with 2-fold dose escalations through 480 mg/m2. The next dose escalation was 50%, to 720 mg/m2. Grade I through grade IV toxicities were observed. Since no dose-limiting toxicities were observed at 480 mg/m2, and up to grade IV toxicities were observed at 720 mg/m2, an intermediate dose, 600 mg/m2, was evaluated. Dose-limiting toxicities at 720 mg/m2 were hematological (grade III and IV neutropenia) in four of six patients and neurological (up to grade III cerebral toxicities, including restlessness, dizziness, agitation/anxiety, personality changes, and nightmares, as well as myoclonus) in three of six patients treated. The pharmacokinetic parameters which helped predict these toxicities included area under the curve and peak plasma level. Pharmacokinetic studies showed interpatient variations in all parameters studied. The mean area under the curve levels of PZA at the highest two dose levels in patients were near the level detected in mice at their maximum tolerated total dose. The recommended starting dose for Phase II trials using this schedule is 600 mg/m2.
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PMID:Phase I clinical trial of pyrazoloacridine NSC366140 (PD115934). 981 48

The serotonin syndrome is a rare, but potentially fatal complication to treatment with serotonin reuptake inhibitors. Due to increasing prescription of these drugs the condition must be expected to occur more often. Symptoms include changes in mental status (confusion, agitation and restlessness), neuromuscular symptoms (shivering, ataxia, myoclonus and hyperreflexia) and autonomic dysfunction (fever, diaphoresis, hypertension and tachycardia). The syndrome is most often produced by concurrent use of two or more drugs that enhance serotonin neurotransmission. Monotherapy may also elicit the syndrome. We report the development of serotonin syndrome with a fatal outcome in a patient treated with paroxetin++. Interactions with alimemazin++, melperon++ and karbamazepin may have contributed to the outcome. The serotonin syndrome usually resolves within 24 hours when the suspected drugs are discontinued. However, there may be a dramatic progression of symptoms requiring intensive supportive care to prevent death.
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PMID:[Serotonin syndrome with fatal outcome caused by selective serotonin reuptake inhibitors]. 1038 11

A 50-year-old man was admitted to our hospital because of disorientation and nocturnal restlessness. The patient presented chronically progressive dementia. No myoclonus or periodic synchronous discharge (PSD) was found over time, with abnormal evidence in MRI-FLAIR (fluid-attenuated inversion recovery) images alone. Brain biopsy and prion protein gene analysis led to the final diagnosis of Creutzfeldt-Jakob disease (CJD) induced by the point mutation at codon 232 (Met to Arg). To date the cases of M232R mutation-induced CJD have been reported to present clinical symptoms and pathological evidences similar to sporadic CJD cases, and differential diagnosis between the types has been believed to be difficult. Our case suggests that some types of CJD induced by point mutation at codon 232 cannot be easily inferred from clinical findings.
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PMID:[A case of codon 232 mutation-induced Creutzfeldt-Jakob disease visualized by the MRI-FLAIR images with atypical clinical symptoms]. 1082 2

The serotonin(5-HT) syndrome(SS) is a condition of both the central and peripheral 5-HTergic hyperstimulation, characterized by a constellation of 5-HT-related side effects(confusion, agitation, restlessness, myoclonus, hyperreflexia, diaphoresis, shivering or tremor in the setting of the recent addition of 5-HTergic agents. The SS is produced most often by the concurrent use of monoamine oxidase inhibitors and other 5-HTergic agents. However, more recent reports suggest that the tricyclic antidepressant or selective serotonin reuptake inhibitor(SSRI) monotherapy induces the SS. Recently, for the operationalized assessment of both the presence and the severity of the core symptoms of the SS, Hegerl et al. developed the Serotonin Syndrome Scale(SSS) as a modification of the diagnostic criteria of the SS proposed by Sternbach. Since, in Japan, some novel 5-HTergic agents have been, and will be in use, recognition of the SS is quite important. Therefore, for clinical application of SSS, we prepared the Japanese-language version (JSSS).
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PMID:[The Japanese version of the serotonin syndrome scale (JSSS)]. 1087 22

Serotonin syndrome is an underreported complication of pharmacotherapy that has been relatively ignored in the medical literature. We discuss 2 recent cases seen at our institution and 39 cases described in the English-language literature since 1995. We found that patients with serotonin syndrome most often (74.3%) presented within 24 hours of medication initiation, overdose, or change in dosage. The most common presenting symptoms and signs were confusion, agitation, diaphoresis, tachycardia, myoclonus, and hyperreflexia. The prevalences of hypertension, coma/unresponsiveness, seizures, and death were not as prominent in our study as previously reported, perhaps reflecting earlier recognition and intervention. The most common therapeutic intervention was supportive care alone (48% of patients). The use of 5-hydroxytryptamine (5-HT) antagonists such as cyproheptadine, however, has become more common and might reduce the duration of symptoms. Only 1 death occurred, and most patients (57.5%) had complete resolution of their symptoms within 24 hours of presentation. The increased use of serotonergic agents (alone and in combination) across multiple medical disciplines presents the possibility that the prevalence and clinical significance of this condition will rise in the future. Internists will need to be increasingly aware of and prepared for this pharmacologic complication. Prevention, early recognition of the clinical presentation, identification and removal of the offending agents, supportive care, and specific pharmacologic therapy are all important to the successful management of serotonin syndrome.
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PMID:Serotonin syndrome. Presentation of 2 cases and review of the literature. 1094 49

Selective serotonin reuptake inhibitor medications are considered relatively safe even in overdose. We report a massive overdose of sertraline with the highest serum sertraline concentration reported to date. Clinical features of this patient were confusion, agitation, myoclonus, hyperreflexia, fever, and creatine kinase elevation. This case may represent serotonin syndrome caused by sertraline overdose alone.
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PMID:Massive sertraline overdose. 1105 8

In humans, hydromorphone (HMOR) is metabolised principally by conjugation with glucuronic acid to form hydromorphone-3-glucuronide (H3G), a close structural analogue of morphine-3-glucuronide (M3G), the major metabolite of morphine. In a previous study we described the biochemical synthesis of H3G together with a preliminary evaluation of its pharmacology which revealed that it is a neuroexcitant in rats in a manner analogous to M3G. Thus the aims of the current study were to quantify the neuro-excitatory behaviours evoked by intracerebroventricular (icv) H3G in the rat and to define its potency relative to M3G. Groups of adult male Sprague-Dawley rats received icv injections (1 microL) of H3G (1 - 3 microg), M3G (2 - 7 microg) or vehicle via a stainless steel guide cannula that had been implanted stereotaxically seven days prior to drug administration. Behavioural excitation was monitored by scoring fifteen different behaviours (myoclonic jerks, chewing, wet-dog-shakes, rearing, tonic-clonic-convulsions, explosive motor behaviour, grooming, exploring, general activity, eating, staring, ataxia, righting reflex, body posture, touch evoked agitation) immediately prior to icv injection and at the following post-dosing times: 5, 15, 25, 35, 50, 65 and 80 min. H3G produced dose-dependent behavioural excitation in a manner analogous to that reported previously for M3G by our laboratory and reproduced herein. H3G was found to be approximately 2.5-fold more potent than M3G, such that the mean (+/- S.D.) ED50 values were 2.3 (+/- 0.1) microg and 6.1 (+/- 0.6) microg respectively. Thus, our data clearly imply that if H3G crosses the BBB with equivalent efficiency to M3G, then the myoclonus, allodynia and seizures observed in some patients dosed chronically with large systemic doses of HMOR, are almost certainly due to the accumulation of sufficient H3G in the central nervous system, to evoke behavioural excitation.
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PMID:Hydromorphone-3-glucuronide: a more potent neuro-excitant than its structural analogue, morphine-3-glucuronide. 1145 32

To define the incidence and type of neurological complications and associated factors, we reviewed 41 consecutive patients who had 45 procedures for liver transplantation. Encephalopathy occurred after 28 procedures (62%) with immediate onset and no significant recovery before death or re-transplantation in 11 (24%), slow recovery in eight (18%) and delayed onset (1-50 days, average 11) in six (13%). Intermittent confusion and agitation with full recovery followed three (6.6%), and focal and generalized seizures followed five (11%) procedures with multifocal myoclonus in two and status epilepticus in one; isolated focal seizures followed two and myoclonus or unclassified seizures, one each. All patients with seizures had encephalopathy. Three patients had neuropathy (2 generalised and 1 focal). Other complications included headache (2), tremors (2), fatigue (2), restlessness, nervousness, transient enuresis, intermittent dizziness, critical illness myopathy and detached retina. Brain imaging showed atrophy in three (6.6%) instances, intracerebral haemorrhage in two, multiple infarctions in one, and intracerebral and subarachnoid haemorrhage with infarction in one. Cerebrospinal fluid analysis showed increased protein in three, hemorrhage in one, and no abnormality in one patient. Of 12 patients (29%) who died before discharge, five in the first and three in the second week post-transplantation, 11 (92%) had encephalopathy post-operatively. Neurological complications after transplantation were associated with increased mortality. Post-operative hypomagnesaemia was associated with the development of nervous system complications. We did not identify any clear pre-operative predictors of development of post-operative neurological complications.
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PMID:Neurological complications in liver transplantation. 1201 80

Chlorambucil is an alkylating agent commonly used in veterinary oncology for conditions including lymphoma. Chlorambucil neurotoxicity has been well recognized in human patients. Onsets of central nervous system signs, such as myoclonus, tremors, muscular twitching, agitation, and tonic-clonic seizures, have been reported in humans and laboratory animals treated with chlorambucil. This case of a cat with intestinal lymphoma represents the first veterinary patient reported to have chlorambucil-induced neurotoxicity. Neurotoxicity should be considered a potential side effect of chlorambucil therapy in veterinary patients.
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PMID:Chlorambucil-induced myoclonus in a cat with lymphoma. 1275 2


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