Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
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

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

Neuroleptic malignant syndrome (NMS) is a rare but potentially lethal form of drug-induced hyperthermia characterised by mental status changes, muscle rigidity, hyperthermia and autonomic dysfunction. Increased awareness and early recognition will lead to prompt management. The diagnosis of NMS presents a challenge because several medical conditions generate similar symptoms. The presentation and course of NMS can be quite variable ranging from a stormy and potentially fatal course to a relatively benign and self-limiting course. The most important aspect of treatment is prevention. This includes reducing risk factors (e.g. dehydration, agitation and exhaustion), early recognition of suspected cases and prompt discontinuation of the offending agent. All patients with psychosis should be monitored daily for dehydration and elevated temperature, have vital signs checked and agitation should be watched for. Antipsychotics should be used conservatively with gradual titration of doses. The management of NMS should be based on a hierarchy of symptom severity. Following an episode of NMS, the patient should be reassessed for further treatment with antipsychotics and rechallenge should not be attempted at least 2 weeks following resolution of symptoms of NMS. The patient and family should be educated about the episode and consent for further medication use obtained after a clear explanation of the risk-benefit analysis.
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PMID:Neuroleptic malignant syndrome. Recognition, prevention and management. 967 59

A 74-year-old man with depressive symptoms was admitted to a psychiatric hospital due to insomnia, loss of appetite, exhaustion, and agitation. Medical treatment was initiated at a daily dose of 20 mg paroxetine and 1.2 mg alprazolam. On the 10th day of paroxetine and alprazolam treatment, the patient exhibited marked psychomotor retardation, disorientation, and severe muscle rigidity with tremors. The patient had a fever (38.2 degrees C), fluctuating blood pressure (between 165/90 and 130/70 mg mm Hg), and severe extrapyramidal symptoms. Laboratory tests showed an elevation of creatine phosphokinase (2218 IU/L), aspartate aminotransferase (134 IU/L), alanine aminotransferase (78 IU/L), and BUN (27.9 mg/ml) levels. The patient received bromocriptine and diazepam to treat his symptoms. 7 days later, the fever disappeared and the patient's serum CPK levels were normalized (175 IU/L). This patient presented with symptoms of neuroleptic malignant syndrome (NMS), thus demonstrating that NMS-like symptoms can occur after combined paroxetine and alprazolam treatment. The adverse drug reaction score obtained by the Naranjo algorithm was 6 in our case, indicating a probable relationship between the patient's NMS-like adverse symptoms and the combined treatment used in this case. The involvement of physiologic and environmental aspects specific to this patient was suspected. Several risk factors for NMS should be noted in elderly depressive patients whose symptoms often include dehydration, agitation, malnutrition, and exhaustion. Careful therapeutic intervention is necessary in cases involving elderly patients who suffer from depression.
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PMID:Possible neuroleptic malignant syndrome related to concomitant treatment with paroxetine and alprazolam. 1672 68