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)

Anesthetic-induced malignant hyperthermia in pigs and humans is characterized by muscle rigidity and rapid, often fatal, increases in body temperature. A defect in Ca2+ homeostasis has been suspected as underlying the disease, based on the preventive effect of dantrolene sodium, an agent thought to reduce Ca2+ levels in the cytoplasm. We describe here direct measurements of cytoplasmic ionized Ca2+ levels in lymphocytes from seven normal and 12 malignant hyperthermia-susceptible pigs, using the fluorescent indicator quin2. No differences in the concentration of cytoplasmic ionized Ca2+ were found in cells from malignant hyperthermia-susceptible pigs (160 +/- 10 nM) relative to the controls (150 +/- 10 nM). However, addition of halothane in vitro caused a significant increase (to 270 +/- 30 nM) in lymphocytes from malignant hyperthermia-susceptible pigs, but not from normal pigs (180 +/- 10 nM). The halothane-mediated increase in cytoplasmic ionized Ca2+ required extracellular Ca2+. It is suggested that general anesthetics such as halothane increase the permeability of the cell surface to Ca2+, and that this increase may, on its own or indirectly, increase the cytoplasmic level of ionized Ca2+ during a malignant hyperthermia crisis. The detection of a halothane-dependent increase in cytoplasmic ionized Ca2+ selectively in malignant hyperthermia-susceptible pigs could be the basis for a noninvasive test for malignant hyperthermia.
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PMID:Selective increase in cytoplasmic calcium by anesthetic in lymphocytes from malignant hyperthermia-susceptible pigs. 357 44

We report the case of a 4.9-year-old boy with congenital hydrocephalus and obstruction of his shunt who just after the induction of anaesthesia suddenly developed generalized muscle rigidity that made intubation impossible. Because of temporary mydriasis the situation could hardly be differentiated from acute cerebral herniation. The lack of any decrease in muscle tone after emergency trephination and drainage of the right lateral ventricle and the immediate improvement following intravenous dantrolene left no doubt about the diagnosis of malignant hyperthermia. The diagnosis was confirmed by the increase in serum creatine phosphokinase and the documentation of massive myoglobinuria. Reconstruction of the course of the first anaesthetic necessary for shunt implantation at the age of 62 days revealed that the same symptoms already had occurred. However, they then were not attributed to malignant hyperthermia but interpreted as symptoms of acute herniation. A detailed description of this first anaesthetic is given which again elucidates the problems associated with the abrupt onset of muscular hypertonus in a patient with neurologic disorder; moreover this may well be the first published case report of malignant hyperthermia at the age of just 2 months.
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PMID:[Symptoms of acute cerebral hernia following induction of anesthesia in hydrocephalus--malignant hyperthermia in reality]. 378 92

Seventy-seven patients who developed masseter muscle rigidity (MMR) after receiving succinylcholine to facilitate tracheal intubation were evaluated for malignant hyperthermia (MH) susceptibility by in vitro halothane and caffeine contracture tests. Thirty-nine patients were diagnosed as MH-susceptible. Neither age, sex, nor type of surgery or anesthesia distinguished MH-susceptible from nonsusceptible patients. Two susceptible and two nonsusceptible patients had evidence of a myopathy. Fifty-two patients had serum creatine phosphokinase (CPK) levels measured in the perioperative period. Although all values were above normal, CPK values equal to or greater than 20,000 IU within 24 hr of trismus (in the absence of myopathy) were observed in six of 30 patients diagnosed as MH-susceptible, but were found in none of the nonsusceptible patients. Considering the high percentage of patients exhibiting MMR that are indeed susceptible to MH (approximately 50%) compared to estimates of MH in the population as a whole (approximately 0.005%), MMR should be considered a presumptive sign of MH. Perioperative CPK values greater than 20,000 IU are highly suggestive of MH susceptibility. Patients exhibiting MMR should be evaluated for MH susceptibility and myopathies. Succinylcholine should be avoided for subsequent anesthetics in patients with a history of MMR.
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PMID:Masseter muscle rigidity and malignant hyperthermia susceptibility. 394 3

The safety of etomidate for induction of anesthesia in malignant hyperthermia-susceptible (MHS) pigs was evaluated in a two-phase experiment. Two litters of Purebred Poland China pigs, one MHS (n = 4) and the other malignant hyperthermia-resistant (MHR) (n = 4) were used. Phase I compared MHS vs MHR animals in terms of cardiovascular, metabolic, and skeletal muscle rigidity responses to etomidate and fentanyl anesthesia and to a subsequent malignant hyperthermia (MH) challenge with halothane-succinylcholine. When three of the four criteria for the diagnosis of MH occurred (rigidity, tachycardia, or increases in temperature or end-tidal CO2) in an animal, phase I was terminated. In phase II, only the MHS animals were used and experimental procedures were as in phase I except thiopental replaced etomidate. In phase I, evidence was inadequate to support the diagnosis of MH based upon responses of MHS pigs to the infusion of etomidate even though the infusion of etomidate in MHS pigs was associated with statistically significant increases in body temperature and plasma lactate levels above those observed in MHR pigs. Heart rate and bicarbonate levels were lower in MHS than in MHR pigs during etomidate infusion. With discontinuation of etomidate and a subsequent challenge with halothane-succinylcholine, all four pigs developed the MH syndrome within 15-30 min. Thiopental replacement of etomidate in the phase II experiment resulted in a twofold greater time (45-75 min) for halothane-succinylcholine to trigger MH in the susceptible pigs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Malignant hyperthermia: is etomidate safe? 398 91

A report is made of a 44-year-old female who died of malignant hyperthermia during general anesthesia for an operation of left subtrochanteric femoral fracture. Symptoms began with increases in heart rate and blood pressure after the introduction of anesthesia with halothane and were accelerated by the administration of succinylcholine, followed by muscle rigidity and high temperature. The typical wine red urine was observed. The oral temperature of 42 degrees C was recorded within 1 h after succinylcholine. The rectal temperature was 30 degrees C 22 h after death. Severe pulmonary edema and tubular necrosis of the kidney were found by postmortem examination. No latent myopathy was observed. The creatine phosphokinase levels in plasma obtained after the onset of malignant hyperthermia and at the time of autopsy were abnormally high and were 5632 and 34,854 mU/ml, respectively. Plasma myoglobin levels were 130,000 and 2.8 X 10(6) ng/ml, respectively.
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PMID:An autopsy case of malignant hyperthermia. 398 93

This study examines in vitro the contractures induced by halothane and succinylcholine in skeletal muscle taken as biopsy specimens from 42 patients referred to the authors' laboratory for diagnosis of malignant hyperthermia (MH) susceptibility. In addition, possible differences between the response of preparations from these same patients with and without a history of masseter muscle rigidity following succinylcholine (SCh) administration were determined to investigate the in vitro relationship of masseter muscle rigidity to MH. Halothane 3%-induced contractures in preparations from MH susceptibles were similar, whether the group had a history of masseter muscle rigidity (1.15 +/- 0.18 g; n = 10) or not (1.02 +/- 0.21 g; n = 14). Halothane did not induce significant contractures in those diagnosed as normals. Succinylcholine alone did not elicit contractures from preparations derived from MH susceptibles or nonsusceptibles. Succinylcholine induced significant contractures in all preparations preexposed to halothane. Preparations from MH-negative patients with a history of masseter muscle rigidity were rendered sensitive to halothane (contractures of 1.17 +/- 0.30 g; n = 4) when SCh was present. In contrast, halothane added in the presence of SCh did not induce contractures to the same extent in preparations from MH-negative patients without a history of masseter muscle rigidity. This is the first reported in vitro method by which to examine the clinically troublesome interaction between SCh and halothane. This approach also may prove to be important in further investigations of the relationship between masseter muscle rigidity and MH.
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PMID:In vitro interaction between halothane and succinylcholine in human skeletal muscle: implications for malignant hyperthermia and masseter muscle rigidity. 402 68

A non-lethal procedure for identifying pigs apt to develop malignant hyperthermia is described. Susceptible animals were exposed to a variety of anaesthetic and other agents and it was shown that thiopentone sodium and CT 1341 (Glaxo) afforded a measure of protection against the development of the syndrome. Pretreatment with procaine did not prevent the onset of the condition and the administration of procaine when muscle rigidity was present failed to prevent a fatal outcome. The syndrome was induced in susceptible animals by halothane, chloroform, and a combination of halothane with suxamethonium. The effects of cyclopropane in susceptible pigs could not be predicted, and other tests showed that suxamethonium alone would not induce muscle contracture. Pretreatment with lignocaine failed to prevent induction of the syndrome by halothane.We believe that the porcine syndrome may result from more than one defect and that in one particular type the most effective treatment is immediate cooling coupled with the administration of sodium bicarbonate.
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PMID:Further studies of porcine malignant hyperthermia. 501 6

A 51-year-old male patient with no history of musculo-skeletal or myopathic abnormalities, but suffering from manic-depressive psychosis, attempted suicide with an overdose of dolpersin hydrochloride (Mydocalm), dipenzepine hydrochloride (Noveril), meprobamate (Mepronox) and nitrazepam (Mogadon). He developed high fever, muscle rigidity, tachycardia, arrhythmias, hypotension and mottled cyanosis, symptoms well-known in persons with malignant hyperthermia, an autosomally inherited disease of skeletal muscle. There is also discussed the manifestation and the symptoms of an acute rhabdomyolysis. The diagnosis was confirmed by chemical pathological laboratory findings, including respiratory and metabolic acidosis, myoglobinaemia accompanied by myoglobin diuresis, and elevated creatine phosphokinase (CPK values up to 2790 U/l). Electron microscopic examination of muscle tissue revealed signs of myolysis and mitochondrial reactions with pleoconic hyperplasia. No inhalation anaesthetics or skeletal muscle relaxants, such as succinyl choline, were used in this case. Therefore, malignant hyperthermia might have been induced by a combination of drugs which were not known to induce this abnormal muscular reaction. However, the muscle relaxant effect of dolpersin hydrochloride may have acted as a possible inducer of the attack.
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PMID:[Possible malignant hyperthermia as reaction to an overdose of myotonolytic, antidepressive and sedative drugs (author's transl)]. 611 87

The neuroleptic malignant syndrome (NMS) is an uncommon and potentially lethal complication of therapy with neuroleptics characterized by pallor, hyperthermia, and extrapyramidal signs (Delay and Deniker, 1968). Malignant hyperthermia (MH) is a rare but often fatal complication of general anesthesia characterized by hyperpyrexia and muscle rigidity, but not related to neuroleptic therapy. For both syndromes, NMS and MH, a common pathophysiology has been considered (Meltzer, 1973; Itoh, 1977; Caroff, 1980). These two syndromes may also be clinically indistinguishable from "acute lethal catatonia" characterized by fever, muscular hypertonicity, and stupor, first described by Stauder in 1934. We now report a case in whom NMS appeared following neuroleptic treatment for a psychotic depressive syndrome. After remission from the NMS, the patient underwent general anesthesia nine times for electroconvulsive therapy (ECT) without ill effect. This case supports the theory of distinct pathogenic mechanisms for both NMS and MH.
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PMID:General anesthesia after neuroleptic malignant syndrome. 613 3

We report a patient with Duchenne muscular dystrophy who developed malignant hyperpyrexia during general anaesthesia. During anaesthesia bradycardia was followed by ventricular fibrillation, on which ventricular flutter supervened and a body temperature rise of 0.6 degrees C for 15 minutes, myoglobinuria and elevation of CPK level were observed. The caffeine sensitivity test of biopsied muscle fibers revealed an increase in sensitivity, although there was no sign of muscle rigidity during or after anaesthesia. Diagnosis of Duchenne muscular dystrophy was first established after the development of malignant hyperpyrexia in the present case as well as in previously reported cases. Determination of serum CPK is very important before general anaesthesia.
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PMID:Malignant hyperpyrexia and Duchenne muscular dystrophy: A case report. 621 75


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