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)

Acute morphine induced a dose-dependent hypokinesia and rigidity, but only mild and non-dose-dependent catalepsy. AMT, injected 1/2 h after morphine, slightly potentiated catalepsy but not hypokinesia during 3 h after morphine; in contrast, rigidity was decreased. The behavioral changes induced by AMT were accelerated in onset and reached their usual development, although AMT toxicity and hypothermia were completely antagonized; thus, it would appear that AMT hypokinesia/catalepsy are not the consequence of toxicity. When morphine was injected 4 h after AMT, a mutual potentiation of the two drugs on hypokinesia and catalepsy was observed, although previous biochemical measurements had shown no effect of morphine on CA depletion under these conditions. Rigidity appeared to be antagonized. After 17 days of repeated injections, morphine no longer elicited hypokinesia and catalepsy, but no cross-tolerance developed to the AMT behavioral changes. A similar lack of cross-tolerance to the effects of AMT or haloperidol was observed when morphine tolerance was induced by pellet implantation. Catalepsy and hypokinesia developed in a much more pronounced way after two large i.p. doses than after small, multiple administration of AMT; this difference was accompanied by a significantly lower concentration of brain DA, but not NA in the former group. The hyperthermic response observed after a 40 mg/kg s.c. injection of morphine was reversed to hypothermia when the same dose was given 4 or 10 h after CA synthesis inhibition. Cocaine strongly antagonized AMT hypokinesia and catalepsy when given 8 1/2 h after AMT, and, although to a lesser extent, even when injected 12 1/2 h after AMT.
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PMID:AMT catalepsy and hypokinesia: interaction with morphine and cocaine. 98 53

Rhabomyolysis with myoglobinuria has been added relatively recently to the neurologic complications associated with the increased use of cocaine and the introduction of its alkaloid form (crack). This retrospective study reports our experience with 14 patients who presented with rhabdomyolysis after cocaine use in a municipal hospital over a 3-year period. Seven patients used "crack", 2 intravenous and 3 nasal insufflation. All patients but one had hyperthermia, 11 altered mental status, 8 tachycardia, and 4 muscle rigidity. Nine developed renal failure; 3 of these patients died. Two other patients died of cardiorespiratory arrest. Cocaine-related rhabdomyolysis has a high mortality. The observed association with hyperthermia and other central neurologic features resembles the neuroleptic malignant syndrome. Since chronic cocaine use may alter the availability of dopamine either through transmitter depletion or decrease in the number of dopamine receptors, a common pathogenetic mechanism is possible. However, other mechanisms, which are not mutually exclusive but rather frequently overlapping, may play an important role. These include agitation, hyperthermia, adrenergic overstimulation leading to vasoconstriction and ischemia or calcium release from the sarcoplasmic reticulum resulting in increased entry into the muscle cell leading to cell death; in addition, cocaine has direct toxic effect on the muscles.
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PMID:Rhabdomyolysis and hyperthermia after cocaine abuse: a variant of the neuroleptic malignant syndrome? 748 66