Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026837 (muscle rigidity)
 1,077 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of neuroleptic malignant syndrome (NMS) in a 23 year old male patient is reported. The symptoms were hyperthermia, muscle rigidity, change in mental status, sinus tachycardia, creatinine phosphokinase elevation and myoglobinuria. The patient suffered from severe muscle pain and compromised respiratory function. Treatment was cessation of neuroleptic medication and institution of intensive medical care focusing on symptomatic treatment. One week after admission clinical status and laboratory findings were normalized and the patient was readmitted to a psychiatric hospital. The neuroleptic medication of the reported patient had been olanzapine during seven months at a dose of 25 mg daily. The day before onset of NMS the pharmacological treatment was supplemented by 100 mg of clozapine. The cause of onset of NMS in this case is discussed. Clozapine, an atypical neuroleptic, is known to have reduced potential to cause NMS and in such cases without extrapyramidal symptoms. Olanzapine, however, has not yet been reported to cause NMS. Alternatively the cause of onset of NMS in this patient could be explained by the combination treatment and possible synergistic effect of the two antipsychotic drugs. Further research in this field is needed.
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PMID:[Neuroleptic malignant syndrome after treatment with olanzapine]. 1008 53

Tremor is the most common initial symptom and one of the cardinal features of Parkinson's disease. Mild tremor causes only minimal disability, but severe tremor causes more significant disability and distress for the patient than rigidity and/or bradykinesia. Anticholinergic agents, levodopa/DCI and dopamine agonists are most common and beneficial in parkinsonian tremor, but efficacies of these medications are variable among patients. Rigidity and bradykinesia are more responsive to levodopa/DCI therapy than tremor. Clozapine is an atypical neuroleptic agent, not on the market in Japan, and has been reported to decrease or ameliorate parkinsonian tremor through the studies of open label and double blind crossover as a new drug for parkinsonian tremor.
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PMID:[Pharmacological treatment of parkinsonian tremor]. 1106 52

Clozapine has recently been found to be associated with neuroleptic malignant syndrome (NMS) after long-term treatment. Here, I report on a 34-year-old Taiwanese woman who had been diagnosed with schizophrenic disorder 17 years previously. She had received clozapine 250 mg/day monotherapy for 7 years. She had sudden onset of NMS signs with high fever, profuse diaphoresis, severe muscular rigidity, elevated creatine phosphokinase level and consciousness disturbance. Brain computed tomography, blood culture and cerebral spinal fluid studies were negative. She had no muscle rigidity and fever after treatment with normal saline 1500 ml/day and diazepam 30 mg/day for 8 days. On day 15, a rechallenge with clozapine was done with caution because the patient was experiencing auditory hallucinations and delusions of persecution. The dose was slowly increased to 250 mg/day over 18 days. She had no active psychotic symptoms or NMS again in the following year. I reported this case to remind readers of the possibility of induced NMS with long-term use of clozapine and successful clozapine rechallenge.
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PMID:Neuroleptic malignant syndrome associated with long-term clozapine treatment: report of a case and results of a clozapine rechallenge. 1160 Nov 95

In view of a possible role of serotonin (5-hydroxytryptamine, 5-HT) and dopamine (DA) in neuroleptic-induced muscle rigidity and catalepsy, the present study is designed to investigate the neurochemical and extrapyramidal effects of atypical antipsychotic/neuroleptic drug i.e., Clozapine (CZP) on the metabolism of serotonin and dopamine particularly in the caudate (a region of the brain involved in the control of movement), accumbens and rest of the rat brain. Interaperitoneal (i.p) injections of CZP at doses of 5.0 & 10 mg/kg decreased significantly (p<0.01) locomotor activity in familiar (home cage) environment. CZP produced a significant (P<0.01) cataleptic response only at doses of 10 mg/kg used. Maximal cataleptic effects in rats occurred at high doses of CZP. Acute administration of CZP significantly (p<0.01) decreased levels of NA in accumbens at all the doses used. Significant increases (p<0.01) in the levels of NA observed in rest of the brain only at moderate dose (5 mg/kg) of CZP. Results showed significant (p<0.01) increases in the levels of caudate DA following the administration of CZP at 10 mg/kg. However administration of CZP at all the doses produced similar significant (p<0.01) increases in the levels of HVA in all the regions of the rat brain. Overall insignificant effects of CZP occurred on brain regional TRP. However, plasma TRP significantly (p<0.01) increased at 2.5 mg/kg dose of CZP. Administration of CZP at doses of 2.5 and 10 mg/kg significantly (p<0.01) decreased 5-HT levels in the rest of the brain. Administration of CZP produced insignificant (p>0.05) effects on 5-HIAA levels in the caudate and accumbens regions but CZP at doses of 2.5 and 5 mg/kg significantly (p<0.01) decreased 5-HIAA levels in the rest of the brain. Neurochemical and extrapyramidal effects of atypical antipsychotic (clozapine) are discussed in relation to a potential therapeutic profile in rats.
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PMID:Neurochemical and extra pyramidal effects of atypical neuroleptic clozapine in rats. 1641 38