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)

Hyponatremia is a significant complication of treatment with serotonin selective reuptake inhibitors (SSRI). We describe a case of a 53-year-old woman that was started on fluoxetine 20 mg/day for depression. Nine days later, the patient started with weakness, nausea, progressing to confusion, inappetence and vomit. Three hours later she became unresponsive and had a generalized seizure. She was brought to our emergency service. On admission, the patient was normovolemic, without focal motor deficits, but had mild generalized muscle rigidity and Babinski's sign bilaterally. Serum sodium was 105 mmol/L, serum osmolality, 220 mmol/L, and urinary osmolality, 400 mmol/L. The other laboratory exams, chest X-ray, cerebrospinal fluid and cranium tomography were normal. She was found to have fluoxetine-induced SIADH and it was discontinued. We started the hyponatremia correction and, in 5 days, the mental status of the patient gradually returned to a normal baseline, paralleling the resolution of her hyponatremia, without recurrence. Hyponatremia and SIADH should be considered if a patient experiences deterioration in his or her clinical condition while taking SSRI. The use of SSRI antidepressants should be remembered in the differential diagnosis of drug-induced hyponatremia.
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PMID:Severe hyponatremia and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with fluoxetine: case report. 1662 73

A 32-year-old man underwent subtotal thyroidectomy for Basedow's disease under general anesthesia. Preoperatively, the free thyroxine (fT4) and free triiodothyronine (fT3) levels were suppressed and thyroid stimulating hormone level was elevated with administration of iodine and propylthiouracil. Heart rate was 52 beats x min(-1) in sinus rhythm. General anesthesia was induced with fentanyl, propofol and vecuronium, and maintained with nitrous oxide, oxygen and sevoflurane. Systolic blood pressure was controlled within 100 and 130 mmHg. Rectal temperature was 36.5 degrees C after anesthesia induction, gradually rising at a range of 0.4 and 0.7 degrees C per hour, up to 38.6 degrees C four hours after the operation. Arterial blood gas showed bicarbonate 17.1 mEq x l(-1) and base excess -8.1 mmol x l(-1). The metabolic acidosis with normal anion gap lasted during and after the operation. We cooled his body with cold acetyl linger fluid and cooling mattress, and administered sodium bicarbonate. Heart rate increased to 96 beats x min(-1) before the end of operation. Subtotal thyroidectomy was finished in 5 hours 16 minutes. The amount of blood loss was 950 ml. Postoperatively, the serum fT4 and fT3 were suppressed. The serum creatine kinase and lactate dehydrogenase levels increased slightly. He did not show muscle rigidity and neurological disorders. We suspect that he has developed thyroid storm-like symptoms such as hyperthermia and tachycardia induced by subtotal thyroidectomy. Metabolic acidosis might be the result of distal tubular acidosis, which rarely accompanies Basedow's disease. Arterial blood gas analysis and urinalysis should be performed, preoperatively.
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PMID:[Hyperthermia and metabolic acidosis during subtotal thyroidectomy for a patient with Basedow's disease]. 1864 49

We describe a child who developed a malignant hyperthermia-like syndrome after exposure to succinylcholine and halothane. Many features of a typical malignant hyperthermia episode were present, including tachydysrhythmia, tachypnea, and fever in association with metabolic acidosis, hyperCKemia, myglobinemia, and rapid recovery without residual effects upon administration of dantrolene, sodium bicarbonate, and active cooling. Muscle rigidity, hypercarbia, and hyperkalemia were not observed. The patient was found to be heterozygous for a mutation in the carnitine palmitoyltransferase II gene (CPT2) encoding an arginine to cysteine substitution at amino acid 503 (R503C) with reduced activity of the enzyme.
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PMID:Malignant hyperthermia-like syndrome and carnitine palmitoyltransferase II deficiency with heterozygous R503C mutation. 1976 33

Parkinsonism is an extrapyramidal disorder characterised by tremor, muscle rigidity, bradykinesia and postural instability. The most common cause of parkinsonism is idiopathic Parkinson disease. Another common cause is drug-induced parkinsonism. Various drugs can cause parkinsonian symptoms. Many patients exhibiting these side-effects are mistakenly treated with dopaminergic medication. We present two patients with drug-induced parkinsonism induced by sodium valproate and cinnarizine, respectively. The symptoms disappeared after they stopped taking this medication.
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PMID:[Parkinsonism due to the medication]. 1990 Mar 8

We report the case of a 29-year-old man, who could not remember some words of Kanji and showed emotional instability. Magnetic resonance imaging (MRI) scan of his brain appeared normal. Cerebrospinal fluid (CSF) analysis showed lymphocytic pleocytosis. An electroencephalogram (EEG) showed slow activities in both frontal regions of the brain. He was diagnosed as acute encephalitis. On his fourth hospital day, he was found to be catatonic and showed mutism, akinetism, and catalepsy. On the ninth day, he showed hyperpyrexia, muscle rigidity, difficulty in swallowing, respiratory insufficiency, and rhabdomyolysis (creatine phosphokinase (CK), 3038 IU/l). He was diagnosed as malignant catatonia. Intravenous administration of acyclovir, high-dose methylprednisolone, antibiotics, diazepam, and dantrolene sodium was not effective. After initiating oral administration of olanzapine, his condition improved.
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PMID:[Patient with encephalitis presenting with olanzapine-responsive malignant catatonia]. 2053 83

Neroleptic malignant syndrome (NMS) is a serious side effect of antipsychotic medications. The risk factors for NMS are the patient's physiologic conditions such as dehydration, malnutrition, stress, and additional administration of sedative drugs including haloperidol. We report a case of 62-year-old schizophrenic man with bowel obstruction due to rectal cancer. Colostomy under general anesthesia was scheduled, and he had not taken oral medication. After intravenous injection of haloperidol for sedation, muscle rigidity, high fever, and an elevated serum level of creatine phosphokinase were observed. He was diagnosed as NMS, and sodium dantrolene was administered. After the improvement of NMS, colostomy was done. Dehydration and malnutrition of the patient were severe at the time of operation, and the possibility of NMS developing due to stress was thought to be very high. We administered sodium dantrolene to prevent NMS after the operation, and the management for prevention of NMS is discussed.
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PMID:[Perioperative management of neuroleptic malignant syndrome in a schizophrenic patient scheduled to undergo operation for bowel obstruction]. 2148 9

Neuroleptic malignant syndrome (NMS) is a physiologic phenomenon that has been associated with the use of both first- and second-generation antipsychotics resultant to their ability to block dopamine blockade in the basal ganglia and hypothalamic regions of the brain. The typical reaction involves the presentation of muscle rigidity, changes in mental status, temperature elevation, labile blood pressure, and elevations in creatinine kinase and white blood cell counts. The reaction is most often reported early in the course of therapy but is well documented to have the potential to occur at any point in time. Untreated NMS can be fatal, often from secondary causes such as deep venous thrombosis and pulmonary embolism. Treatment involves immediate discontinuation of the offending agent, supportive therapy of clinical symptoms, and may include the use of the skeletal muscle relaxant, dantrolene sodium, or the dopaminergic agents bromocriptine or amantadine. In this case, we present a patient who developed symptoms of NMS during the cross-taper and conversion from quetiapine to clozapine. The patient was treated for NMS; however, his clinical diagnosis was never able to be definitively determined as he was initially evaluated for septicemia and later treated for suspected bacterial infection with antibiotics, and clozapine-associated side effects cannot be ruled-out as a contributing source to the clinical presentation. The estimated Naranjo Scale score for this case report is 3.
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PMID:Suspected neuroleptic malignant syndrome during quetiapine-clozapine cross-titration. 2150 95

We report a case of malignant catatonia initially diagnosed as neuroleptic malignant syndrome (NMS) that responded successfully to diazepam administration. A 29-year-old man with mental retardation was admitted to our hospital because of high fever, muscle pain, and consciousness disturbance. Fifteen days before admission, he had developed muscle pain and weakness in his legs. He presented with fever, tachycardia, tachypnea, elevated blood pressure, excessive sweating, and neurological findings of lethargy and severe muscle rigidity in the neck and extremities. Laboratory findings included elevated serum creatine phosphokinase (CPK) level. His clinical features and the laboratory test results fulfilled the diagnostic criteria for NMS. He was treated for NMS with dantrolene sodium and bromocriptine mesylate for 2 weeks; however, there was no improvement. Therefore, treatment was changed to diazepam administration because of suspected malignant catatonia. One week after initiation of diazepam administration, his symptoms gradually improved, and the serum CPK level normalized. The diagnosis of malignant catatonia was confirmed because treatment with diazepam was dramatically effective, whereas the initial treatment for NMS was not beneficial. The clinical presentation of malignant catatonia is similar to that of NMS. Indeed, some authors have described NMS as a variant of malignant catatonia. If treatment is refractory in cases of NMS, malignant catatonia may be suspected, and changing treatment to diazepam administration may be useful.
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PMID:[Diazepam-responsive malignant catatonia in a patient with an initial clinical diagnosis of neuroleptic malignant syndrome: a case report]. 2151 31

Malignant hyperthermia (MH) is an uncommon, life-threatening pharmacogenetic disorder of the skeletal muscle. It presents as a hypermetabolic response in susceptible individuals to potent volatile anesthetics with/without depolarizing muscle relaxants; in rare cases, to stress from exertion or heat stress. Susceptibility to malignant hyperthermia (MHS) is inherited as an autosomally dominant trait with variable expression and incomplete penetrance. It is known that the pathophysiology of MH is related to an uncontrolled rise of myoplasmic calcium, which activates biochemical processes resulting in hypermetabolism of the skeletal muscle. In most cases, defects in the ryanodine receptor are responsible for the functional changes of calcium regulation in MH, and more than 300 mutations have been identified in the RYR1 gene, located on chromosome 19q13.1. The classic signs of MH include increase of end-tidal carbon dioxide, tachycardia, skeletal muscle rigidity, tachycardia, hyperthermia and acidosis. Up to now, muscle contracture test is regarded as the gold standard for the diagnosis of MHS though molecular genetic test is used, on a limited basis so far to diagnose MHS. The mortality of MH is dramatically decreased from 70-80% to less than 5%, due to an introduction of dantrolene sodium for treatment of MH, early detection of MH episode using capnography, and the introduction of diagnostic testing for MHS. This review summarizes the clinically essential and important knowledge of MH, and presents new developments in the field.
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PMID:Malignant hyperthermia. 2319 31

An 80-year-old woman with Parkinson's disease was scheduled for open heart surgery to repair thoracic aortic aneurysm. Parkinson's symptoms were normally treated using oral levodopa (200 mg), selegiline-hydrochloride (5 mg), bromocriptine-mesilate (2 mg), and amantadine-hydrochloride (200 mg) daily. On the day before surgery, levodopa 50mg was infused intravenously. Another 25 mg of levodopa was infused immediately after surgery. Twenty hours later, the patient developed tremors, heyperventilation, but no obvious muscle rigidity. Two days after surgery, the patient exhibited high fever, hydropoiesis, elevated creatine kinase, and a rise in blood leukocytes. She was diagnosed with neuroleptic malignant syndrome. She was intubated, and received dantrolene sodium. Symptoms of neuroleptic malignant syndrome disappeared on the fourth postoperative day. The stress of open heart surgery, specifically extracorporeal circulation and concomitant dilution of levodopa, triggered neuroleptic malignant syndrome in this patient. Parkinson's patients require higher doses of levodopa prior to surgery to compensate and prevent neuroleptic malignant syndrome after surgery.
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PMID:[Case of neuroleptic malignant syndrome following open heart surgery for thoracic aortic aneurysm with parkinson's disease]. 2449 82


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