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)

In two cases of chronic schizophrenia complicated by diabetes mellitus, the concomitant use of the neuroleptica and oral antidiabetics was attended by the appearance of symptoms simulative of syndrome malin, i.e. hyperpyrexia, tachycardia, blood pressure instability, disturbances of consciousness, muscle rigidity, tremor, dysphagia, salivation and urinary incontinence. In one of these cases, the patient, a 47-year-old man, died 10 days later. In the other case, a 62-year-old woman, almost all the symptoms subsided after 14 days, and oral dyskinesia persisted for only one additional month. In both cases, hypoglycemia due to oral antidiabetics was not seen. In Case 2, a combined regimen of oral antidiabetics and neuroleptica was later resumed. Again, a similar set of symptoms as seen initially were noted, along with an elevation of the serum CPK level. Parenterally administered biperiden proved to be highly effective in the control of the symptoms. The pathogenetic mechanism of these symptoms might possibly be explained as potentiation of the action of the neuroleptica by oral antidiabetics.
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PMID:"Syndrome malin"-like symptoms probably due to interaction between neuroleptica and oral antidiabetic agents. 65 48

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

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

A report is made of a 65-year-old male who died of a malignant hyperthermia of 42 degrees C. Symptoms included muscle rigidity at the termination of operation for neck-clipping of an aneurysm of the anterior communicating artery. Latent myopathy was observed in skeletal muscle, and a bleeding focus was present in the left anterior region of the hypothalamus, coinciding with the temperature regulation center. The mechanism of onset of this disease is still poorly understood, but it seems that this disease occurred due to synergic effects of the hypothalamic hemorrhage and the pre-existing myopathy. The serum CPK level at the time of death was abnormally high (250 U), and 3.4% of isozyme CPK1 was detected. The serum myoglobin was 204, 850 ng/ml, a markedly high level, and myoglobinuric nephrosis was present as a result.
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PMID:Malignant hyperthermia. 711 2

To determine whether the incidence of masseter muscle rigidity is affected by the anaesthetic induction sequence, we prospectively studied for ten months the anaesthetic course in 5,641 infants and children who received muscle relaxation to facilitate tracheal intubation. The anaesthetic induction sequence consisted of intravenous sodium thiopentone (STP) 5 mg.kg-1 alone, halothane induction alone 1-4%, or halothane followed by STP. Inhalational inductions with halothane included nitrous oxide and oxygen. Tracheal intubation was facilitated by either intravenous succinylcholine (Sch) at least 1.5 mg.kg-1 or by a non-depolarizing muscle relaxant. The induction sequence and all episodes of MMR were recorded. Ninety percent of the patients received Sch and 10% received a non-depolarising agent. Of those who received Sch, 88% (5,064 patients) were anaesthetised with STP and 12% (607 patients) were anaesthetised with halothane alone or halothane followed by STP. Masseter muscle rigidity was defined clinically by the transient inability to distract the mandible from the maxilla such that the mouth could not be opened or could only be opened with force. No children anaesthetised with STP followed by Sch developed MMR. One child (0.9%) developed MMR after halothane and Sch and two developed MMR after halothane, STP and Sch (0.4%). The incidence of MMR after Sch was less with STP than with halothane alone or with halothane and STP (P < 0.025). The peak CPK values in the three children who developed MMR were 17,580 IU.L-1 after halothane and Sch, and 7,280 IU.-1 and 3,273 IU.-1 after halothane, STP and Sch. There was no evidence of MH reactions in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The incidence of masseter muscle rigidity after succinylcholine in infants and children. 791 8

Neuroleptic malignant syndrome is a potentially fatal syndrome that can occur in patients taking neuroleptics or other psychotropic drugs. It is characterized by muscle rigidity, hyperthermia, altered mentation, autonomic dysfunction, increased CPK and leukocytosis. A primary factor in NMS may be a decrease in functioning of dopaminergic neurons. Treatment usually consists of discontinuation of the neuroleptic drug, drug therapy with bromocriptine and dantrolene and supportive measures. The key to successful medical and nursing management is aggressive supportive care with a focus on preventing complications. With the frequency of administration of neuroleptic drugs, neuroscience nurses should be aware of this potentially lethal complication of neuroleptic therapy.
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PMID:Neuroleptic malignant syndrome: a dangerous complication of neuroleptic therapy. 844 78

We report a 60-yr-old woman with schizophrenia, who manifested a neuroleptic malignant (NM)-like syndrome after acute organophosphate poisoning (OPP). She attempted suicide by ingesting 40% emulsions of DMTP (S-2,3-dihydro-5-methoxy-2-oxo-1,3,4-thiadizol-3-yl-methyl O,O-dimethyl phosphorodithioate) 100 ml. On admission, she was unconscious and demonstrated convulsions, depressed respiratory movements, miosis and profuse salivation. Plasma cholinesterase concentration (842 IU.L-1) was very low and OPP was diagnosed. She was treated with gastric lavage, atropine and pralidoxime (PAM). By the seventh day after admission, symptoms of OPP disappeared and serum ChE had recovered to a sub-normal level. On the 13th day, she demonstrated coma, high fever (41.0 degrees C) and lead-pipe rigidity. Serum CPK was increased (1631 IU.L-1). Dantrolene sodium iv was administered for three days. Body temperature began to decrease in 24 hr, and her consciousness, muscle rigidity and other neurological symptoms returned to normal by the 16th day after admission. She was discharged from the hospital without sequelae 55 days after admission. We conclude that OPP can predispose to an NM-like syndrome and that dantrolene may be effective in the management.
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PMID:Neuroleptic malignant-like syndrome: a complication of acute organophosphate poisoning. 859 Apr 92

Excessive stimulation of serotonin 5HT1A receptors causes a syndrome of serotonin excess that consists of shivering, muscle rigidity, salivation, confusion, agitation and hyperthermia. The most common cause of this syndrome is an interaction between a monoamine oxidase inhibitor (MAOI) and a specific serotonin reuptake inhibitor. Venlafaxine is a new antidepressant agent that inhibits the reuptake of serotonin and norepinephrine. We report a venlafaxine-MAOI interaction that resulted in the serotonin syndrome in a 23-y-old male who was taking tranylcypromine for depression. He had been well until the morning of presentation when he took 1/2 tab of venlafaxine. Within 2 h he became confused with jerking movements of his extremities, tremors and rigidity. He was brought directly to a hospital where he was found to be agitated and confused with shivering, myoclonic jerks, rigidity, salivation and diaphoresis. His pupils were 7 mm and sluggishly reactive to light. Vital signs were: blood pressure 120/67 mm Hg, heart rate 127/min, respiratory rate 28/min, and temperature 97 F. After 180 mg of diazepam i.v. he remained tremulous with muscle rigidity and clenched jaws. He was intubated for airway protection and because of hypoventilation, and was paralyzed to control muscle rigidity. His subsequent course was remarkable for non-immune thrombocytopenia which resolved. The patient's maximal temperature was 101.2 F and his CPK remained < 500 units/L with no other evidence of rhabdomyolysis. His mental status normalized and he was transferred to a psychiatry ward. This patient survived without sequelae due to the aggressive sedation and neuromuscular paralysis.
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PMID:Serotonin syndrome from venlafaxine-tranylcypromine interaction. 888 41

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

A young male schizophrenic presented with neuroleptic malignant syndrome (NMS). Risperidone was the probable precipitating agent. Rigidity and elevated CPK levels poorly responded to bromocriptine, but showed good response to dantrolene. The role of specific treatment and the differential response of the symptom clusters are discussed.
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PMID:Risperidone-induced neuroleptic malignant syndrome : a case report. 2140 18


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