Cases reported "Muscle Rigidity"

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1/3. Severe muscular rigidity at birth: malignant hyperthermia syndrome?

    A case of severe muscular rigidity in a premature male infant born by Caesarean Section under general anaesthesia is described. A probable diagnosis of malignant hyperthermia was supported by the clinical symptoms of muscular rigidity and cyanosis, a creatinine phosphokinase of 24,630 I.U. (Normal 0--100) and a urinary myoglobin of 248 mg/l (normal 6--35). The muscle tone and laboratory values slowly returned to normal over a period of days. Anaesthetic management for a ventriculoperitoneal shunt performed at seven weeks of age included pre and postoperative treatment with dantrolene. No crisis occurred at this time. The parents, who have normal CPK and a negative family history, were advised to treat the child as if he had malignant hyperthermia until such time as a definitive diagnosis can be made.
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2/3. syndrome of continuous muscle fiber activity. Case report with 11-year follow-up.

    A 16-year-old male patient who presented with muscle stiffness and dysphonia is described. electromyography revealed continuous motor activity that was unaffected by peripheral nerve block or general anaesthesia, but was abolished by curare. The patient had a marked improvement after using phenytoin. The follow-up 11-years later corroborates with the proposed benignity of this syndrome, in spite of being dependent on medication.
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keywords = anaesthesia
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3/3. Opisthotonos following propofol: a nonepileptic perspective and treatment strategy.

    In this report of opisthotonos during recovery from propofol anaesthesia, we relate clinical observations with scientific considerations, and propose a strategy for treatment of this rare side effect. Following a brief operative procedure, a healthy 29-yr-old woman developed recurrent opisthotonos while recovering from anaesthesia with alfentanil, propofol, and nitrous oxide. In contrast to accumulating reports, the patient remained conscious during each episode of back extension and retrocollis. The preservation of consciousness and similarities to strychnine-induced opisthotonos suggest to us that the mechanism may have a brainstem and spinal origin. Recent investigations show that propofol potentiates the inhibitory transmitters glycine and gamma-aminobutyric acid (GABA) which would enhance spinal inhibition during anaesthesia. Postanaesthetic opisthotonos, however, may be due to a propofol-induced tolerance to inhibitory transmitters. This rebound phenomenon would lead to an acute, enduring refractoriness in inhibitory pathways of the brainstem and spinal cord, resulting in increased activity of extensor motoneurons. We recommend a therapeutic strategy that restores inhibition by glycine and GABA at multiple sites; the preferred therapeutic agents would be diazepam and physostigmine. The episodes are usually short-lived, but two of the reviewed 17 patients developed recurrent retrocollis for four and 23 days following antiepileptic drug therapy. Since high doses of phenytoin and carbamazepine can result in opisthotonos, we recommend that anticonvulsants be reserved for postanaesthetic patients with electroencephalographic evidence of seizure activity.
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keywords = anaesthesia
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