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)

1. Neuroleptic drugs (antipsychotics) produce numerous side effects which include serious extrapyramidal symptoms consisting of akathisia, dystonia, neuroleptic malignant syndrome, parkinsonian reactions such as postural abnormality, tremor, akinesia or bradykinesia, rigidity, and tardive dyskinesia. 2. Among the complications of neuroleptic chemotherapy, the most serious and potentially fatal complication is malignant syndrome, which is characterized by extreme hyperthermia, "lead pipe" skeletal muscle rigidity causing dyspnea, dysphagia, and rhabdomyolysis, autonomic instability, fluctuating consciousness, leukocytosis, and elevated creatine phosphokinase. 3. Neuroleptic malignant syndrome should be differentiated from malignant hyperthermia, lethal catatonia, and other pathological states producing some of these same symptoms. 4. In addition to neuroleptics, malignant syndrome has been caused by thymoleptics (antidepressants), metoclopramide (antiemetic), metoclopramide combined with cimetidine, tetrabenazine, overdosage of benzodiazepine, phenelzine, dothiepin and alcohol, and amphetamine. 5. Factors leading to and/or facilitating the emergence of neuroleptic malignant syndromes are reportedly organic brain syndrome, dehydration, exhaustion, external heat load, excessive sympathetic discharge, use of long acting neuroleptics, high doses of neuroleptics, rapid dose titration with neuroleptics, abrupt discontinuation of antiparkinsonism agents, and concurrent lithium therapy. 6. Although, the pathogenesis of neuroleptic malignant syndrome is not understood completely, a blockade of dopaminergic receptors in the hypothalamus, spinal cord and striatum, an alteration of dopaminergic-serotonergic transmission in the body, an enhanced synthesis and action of prostaglandin E1 and E2, and a modification of calcium-mediated signal transduction in the body have been suggested. 7. The treatment of malignant syndrome includes immediate withdrawal of neuroleptic drugs, i.v. infusion of dantrolene, and oral administration of bromocriptine; or alternatively i.v. infusion of dantrolene and the combination of levodopa-carbidopa. 8. Other measures to enhance the therapeutic effectiveness of the aforementioned regimens are to include the use of anticholinergic drugs such as benztropine to enhance the effectiveness of bromocriptine, of lorazepam if catatonic symptoms persist, or of electroconvulsive therapy (ECT) if psychotic symptoms persist. 9. These treatments, however, must be "active" rather than "passive", in order to avert fatalities and/or unfortunate sequelae from this iatrogenic and incompletely understood disease.
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PMID:Pathogenesis and treatment of neuroleptic malignant syndrome. 197 19

Lethal catatonia, a syndrome described several decades before the advent of neuroleptic drugs, has been regarded by many investigators as clinically similar to, and perhaps indistinguishable from, neuroleptic malignant syndrome. However, published case reports of the two syndromes indicate differences in mode of onset, signs and symptoms, and outcome. Lethal catatonia often begins with extreme psychotic excitement, which, if persistent, can lead to fever, exhaustion, and death. Neuroleptic malignant syndrome begins with severe extrapyramidally induced muscle rigidity. Because lethal catatonia often requires neuroleptic treatment and neuroleptic malignant syndrome necessitates immediate cessation of neuroleptics, their early clinical differentiation is important.
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PMID:Clinical differentiation between lethal catatonia and neuroleptic malignant syndrome. 260 93

1. A reversible disturbance of basal ganglia function was produced in monkeys by the intramuscular administration of reserpine.2. Pallidal discharge was then compared with that recorded in the same animals during movement performance and following passive manipulation of the limbs.3. Akinesia, loss of postural support of the trunk, head and neck and absent postural reflexes were the predominant motor abnormalities produced by reserpine administration.4. Occasionally, postural tremor and catatonia were apparent. Rigidity and resting tremor were absent.5. Recordings made in the pallidum during the presence of akinesia revealed a marked reduction in natural neuronal discharge.6. Some pallidal neurones that remained active were driven in an uncharacteristic manner by peripherally generated afferent inputs from wide territories and by a variety of peripheral stimuli.7. The findings suggest the hypothesis that the akinesia in these animals was due to the diminished pallidal activity, and that pallidal discharge is normally a prerequisite for the performance of spontaneous motor activity. Pallidal neuronal firing may provide a background excitability to motor regions involved in the maintenance and elaboration of natural motor activity.
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PMID:The effects of reserpine on motor activity and pallidal discharge in monkeys: implications for the genesis of akinesia. 741 43

Lethal catatonia is often regarded as clinically similar to, and perhaps indistinguishable from, neuroleptic malignant syndrome. However, the two syndromes reveal differences in the mode of onset, signs and symptoms, and outcome. Lethal catatonia often begins with extreme psychotic excitement, which, if persistent, can lead to fever, exhaustion, and death. Neuroleptic malignant syndrome begins with severe extrapyramidally induced muscle rigidity. Early clinical differentiation is important, because lethal catatonia often requires neuroleptic treatment, and neuroleptic malignant syndrome necessitates immediate cessation of neuroleptics.
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PMID:[Clinical differentiation between lethal catatonia and neuroleptic malignant syndrome: a case report]. 765 87

The combined effects of amphetamine (AMPH) and 3-nitropropionic acid (3-NPA) were investigated to determine how the energy depletion proposed to be produced by AMPH interacts with an inhibitor of mitochondrial respiration to produce striatal neurotoxicity. Neither two doses (2 h apart) of 3.75 mg/kg AMPH alone nor a single dose of 30 mg/kg 3-NPA i.p. produced neurotoxicity in the striatum or lowered striatal dopamine content in rat. Administration of 40 mg/kg of 3-NPA alone almost invariably produced either lethality or did not produce neurotoxicity in the striatum of surviving animals. However, 30 mg/kg of 3-NPA administered along with 2 doses of 3.75 mg/kg AMPH to 47 animals produced striatal damage in the 31 survivors with 15 of the surviving rats showing muscle rigidity/catatonia for several days after dosing, along with decreased food consumption. Thirteen of these 15 rats showed degeneration of axons and cell bodies in the medial caudate-putamen with minimal damage to the globus pallidus. However, two rats exhibited hindlimb paralysis and signs of axonal and neuronal soma degeneration in the thalamus and cerebellar nuclei as well as striatum. Sixteen of the rats given both AMPH and 3-NPA exhibited only torpidity and loss of muscle tone 1-3 h after dosing. Such rats showed no signs of neuronal cell degeneration in the striatum, but did show significant dopamine depletions (60% of control) and reductions in tyrosine hydroxylase immunoreactivity at 14 days postexposure. The mitochondrial dysfunction produced by 3-NPA combined with activation of neuronal pathways by AMPH may have predisposed terminals, axons and cell bodies in striatum to degeneration.
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PMID:Parenterally administered 3-nitropropionic acid and amphetamine can combine to produce damage to terminals and cell bodies in the striatum. 881 96

A 39-year-old man with schizophrenia developed severe catatonia, hyperthermia, muscle rigidity, tachycardia, leukocytosis, and elevated muscle enzyme levels while receiving zotepine therapy. Neuroleptic malignant syndrome (NMS) was diagnosed. After withdrawal of zotepine therapy, transfer to a neurologic intensive care unit, provision of supportive care, and administration of adjunctive bromocriptine therapy, the patient's fever and catatonia subsided. Biochemical irregularities spontaneously returned to normal with no complications. Antipsychotic therapy was restarted with risperidone 12 days after the patient's NMS resolved. After more than 1 year of follow-up, he experienced no adverse events. A recent decrease in mortality from NMS is related to increased awareness of this disorder, but not to treatment with specific agents. Clinicians need to recognize NMS early; although rare, it is a potentially fatal complication of antipsychotic treatment.
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PMID:Zotepine-induced catatonia as a precursor in the progression to neuroleptic malignant syndrome. 1620 9

The neuroleptic malignant syndrome (NMS) is a rare, but potentially lethal side effect of conventional and atypical antipsychotic drugs. We present a 62 years old male patient who was admitted to our institution because of sudden onset of mild hyperthermia, muscle rigidity, stupor, leucocytosis and massive rhabdomyolysis after 30 years uneventful treatment with clozapine. The medication with clozapine was suspended because of the suspicion of NMS. When the acute symptoms were abated, the treatment with clozapine was resumed again after 14 days. The very next day, the patient suffered again from raised body core temperature, leucocytosis, elevated serum creatine kinase and new catatonia. The therapy with clozapine was stopped definitively and benzodiazepines were administered assuming a relapse of an alleviated, probably reconvening NMS. Under the treatment with benzodiazepines the patient was free of symptoms even after 1 month. To our knowledge, the latency of 30 years between the beginning of the treatment with clozapine and the onset of NMS is the longest period in the literature. According to our case, the differential diagnosis of NMS is not always trivial and is therefore discussed.
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PMID:[Neuroleptic malignant syndrome after 30 years treatment with clozapine: a rarely seen differential diagnosis on intensive care units]. 1649 63

Neuroleptic malignant syndrome (NMS) is a rare disorder seen most often in patients exposed to antipsychotic medications. This syndrome is generally manifested by hyperthermia, muscle rigidity, autonomic instability, altered mental status, tremors, elevated serum creatinine phosphokinase and leucocytosis. It was first described by Delay during the 1960s. It is considered a medical emergency and is fatal if not promptly addressed. It is clinically relevant not only to psychiatrists but all clinicians since patients taking neuroleptics are seen by physicians from virtually every specialty. Relevant studies report a mortality rate of 10-20%. Conditions that share some features of NMS but have different treatment regimens include serotonergic syndrome, lethal catatonia, malignant hyperthermia, infections and various heat disorders. The importance of recognition and prompt intervention can not be overemphasized. Fever is a predominant symptom in NMS. The authors present an unusual case of NMS in a schizophrenic patient without fever who had been on aripiprazole. To date, there are only three possible reported cases of NMS related to aripiprazole. This case report serves to remind clinicians of the essential features in the diagnosis and management of NMS.
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PMID:A case report of neuroleptic malignant syndrome without fever in a patient given aripiprazole. 1701 30

The typical symptoms and signs of neuroleptic malignant syndrome (NMS) consist of fever muscle rigidity (stiffness, myoclonus, rod-like), alterations of consciousness (confusion, agitation, aggression, or catatonia), autonomic nervous system disturbances (i.e., hypertension, tachycardia, tachypnea, profuse sweating, and urine incontinence), abnormal blood tests such as low serum electrolytes, elevated serum creatinine phosphokinase (CPK) level, and leukocytosis. Muscle rigidity is often associated with myonecrosis, myoglobinuria, and elevated serum CPK. The mortality among NMS cases is in the 10 to 70% range depending on the severity of the symptoms and time of therapeutic approach. Mandatory therapy should include removal of causative agents, correction of body fluid and electrolytes, administration of benzodiazepine, clonazepam and bromocriptine (dopamine agonist), proved life-saving medications. The authors reported herein six cases with unusual clinical features of NMS. Four of them had been on antipsychotic for a year before becoming anorexic, dehydrated, agitated, and violent with paranoid delusion. One instance with underlying delirium tremens developed NMS after receiving haloperidol (30 mg IV) in addition to diazepam (200 mg IV) within 24 hours. Another patient was found to suffer from severe NMS after receiving bupropion (Dopamine inhibitor antidepressant) 300 mg/day. All patients displayed cardinal signs and symptoms of NMS in addition to dehydration and pallor. They were treated in the psychiatric ward and recovered rapidly from NMS after receiving clonazepam and bromocriptine and removal of the offending agents.
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PMID:Neuroleptic malignant syndrome: a review and report of six cases. 1721 72

An 18-year-old woman was treated with neuroleptic analgesia using fentanyl, morphine, droperidol and haloperidol for general anesthesia and pain control for her knee operation. Postoperatively, she showed emotional unstableness, following dyspnea, tachycardia, fever, hyperhydrosis, muscle rigidity and myoclonus like involuntary movement. She received infusion of 140 mg dantrolene in total under suspicion of having neuroleptic malignant syndrome, but her symptoms improved slightly. After being transferred to our hospital, she exhibited immobility, mutism, rigidity, and catalepsy, and she was suspected of having lethal catatonia. Infusion of diazepam 10 mg resulted in dramatical improvement of her symptoms. Differential diagnosis between neuroleptic malignant syndrome and catatonia is difficult; however, a first line therapy is differential diagnosis. Thus, physician should consider catatonia when treating neuroleptic malignant like syndrome.
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PMID:[Case with difficulty in differentiating between transient neuroleptic malignant syndrome and catatonia after neuroleptic analgesia]. 2016 67


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