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)

We immobilized individuals of four free-ranging felid species, leopard cat (Prionailurus bengalensis), clouded leopard (Neofelis nebulosa), Asiatic golden cat (Catopuma temminckii), and marbled cat (Pardofelis marmorata) with ketamine hydrochloride and xylazine hydrochloride (KH-XH) and with tiletamine hydrochloride and zolazepam hydrochloride (TH-ZH) between March 1998 and July 2002. Mean (+/-SD) dose of KH and XH was 26.51+/-5.71 mg/kg and 1.89+/-0.43 mg/kg, respectively (n=25), and mean dose of TH-ZH was 11.61+/-3.39 mg/kg (n=28). Dose was significantly correlated with induction time (P<0.001) and duration of anesthesia (P<0.05), but not with recovery time. There were significant differences between the drug combinations in time to induction (P<0.03) and time to anesthesia (P<0.01); recovery times were not significantly different. We conclude that immobilization of these felids with TH-ZH and KH-XH is effective and safe, but TH-ZH is preferred because of the smaller volume of drug necessary for sedation, faster time to induction, and absence of prolonged muscle rigidity during anesthesia.
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PMID:Comparative immobilization of wild felids in Thailand. 1546 29

Malignant hyperthermia is an autosomal dominant disorder which results in a severe reaction to anesthetic agents in approximately 0.0005 to 0.5% of patients exposed to general anesthesia. Malignant hyperthermia is characterized by severe muscle rigidity, myoglobunuria, high fever, tachycardia, and arrhythmia precipitated by depolarizing muscle relaxants (succinylcholine) and inhalational anesthetic agents (halothane). When MH occurs, the anesthetic agents must be discontinued immediately and dantrolene should be administered.
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PMID:[Current diagnosis and therapy of malignant hyperthermia]. 1577 67

An 18 month-old girl was diagnosed as ventricular septal defect (VSD) with mild aortic valve prolapse. She underwent a closure of VSD. Intra-and early postoperative course was uneventful. However, 20 hours after surgery, sudden bradycardia led to cardiac arrest and strong muscle rigidity was seen. Hyperkalemia and metabolic acidosis rapidly progressed and resuscitation was failed. Extracorporeal life support and continuous hemodialysis were initiated, but the patient died with multiple organ failure on 5th postoperative day. Her clinical course supported the diagnosis of delayed onset malignant hyperthermia. Histopathological findings of muscle biopsy were consistent with rhabdomyolysis, and immunopathological stains demonstrated changes as in a Duchenne type muscular dystrophy carrier. Delayed onset malignant hyperthermia is an extremely rare complication of general anesthesia. We should be aware of this lethal condition, which occurs with a certain time lag after surgery, especially when the patient has possible background of myopathy.
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PMID:[Delayed onset malignant hyperthermia after a closure of ventricular septal defect]. 1577 37

The neurodegenerative death of dopaminergic neurons of the pars compacta of the substantia nigra leads to the classical triad of resting tremor, muscle rigidity, and bradykinesia of Parkinson's disease. Parkinson's disease is a common disease of elderly patients requiring perioperative anaesthesia. Particular anaesthetic problems are neurological, respiratory, and cardiovascular. The clinical features and the interaction of common anaesthetics with the drug therapy of the patient present an anaesthetic challenge and directly influence perioperative morbidity and mortality.
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PMID:[Anaesthesia in patients with Parkinson's disease]. 1577 5

A healthy 5-year-old boy presented for arch bar placement under general anesthesia in an operating room in a dental school. The patient had previously undergone general anesthesia without complication, and no family history of anesthetic problems were reported. Halothane mask induction, intravenous catheter placement, and nasal intubation proceeded uneventfully without the aid of a muscle relaxant. Halfway through the procedure, signs and symptoms of malignant hyperthermia, including muscle rigidity, hypercarbia, tachypnea, and tachycardia were noted. Immediate treatment, including discontinuation of the triggering agent, dantrolene administration, and cooling measures were applied, and once stable, the child was transferred to Columbus Children's Hospital for further management. The patient experienced no postoperative complications. Further discussion regarding the pathophysiology and management of malignant hyperthermia is provided.
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PMID:A case report of malignant hyperthermia in a dental clinic operating room. 1585 46

Masseter muscle rigidity during general anesthesia is considered an early warning sign of a possible episode of malignant hyperthermia. The decision whether to continue or discontinue the procedure depends on the urgency of the surgery and severity of masseter muscle rigidity. Here, we describe a case of severe masseter muscle rigidity (jaw of steel) after succinylcholine (Sch) administration during general anesthetic management for rigid bronchoscopic removal of a tracheal foreign body. Anesthesia was continued uneventfully with propofol infusion while all facilities were available to detect and treat malignant hyperthermia.
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PMID:Succinylcholine-induced masseter muscle rigidity during bronchoscopic removal of a tracheal foreign body. 1589 86

Malignant hyperthermia (MH) is a rare genetic condition which may manifest for the first time during anaesthesia associated with a routine surgical procedure. Characterised initially by muscle rigidity, increased body temperature and metabolic acidosis, the syndrome may prove fatal unless prompt, effective treatment is administered. The sudden development of MH constitutes a medical emergency; hence it is essential that theatre practitioners are knowledgeable about the presenting symptoms and management of the condition.
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PMID:Malignant hyperthermia. 1617 7

Toxin-induced hyperthermic syndromes are important to consider in the differential diagnosis of patients presenting with fever and muscle rigidity. If untreated, toxin-induced hyperthermia may result in fatal hyperthermia with multisystem organ failure. All of these syndromes have at their center the disruption of normal thermogenic mechanisms, resulting in the activation of the hypothalamus and sympathetic nervous systems.The result of this thermogenic dysregulation is excess heat generation combined with impaired heat dissipation. Although many similarities exist among the clinical presentations and pathophysiologies of toxin-induced hyperthermic syndromes, important differences exist among their triggers and treatments. Serotonin syndrome typically occurs within hours of the addition ofa new serotonergic agent or the abuse of stimulants such as MDMA or methamphetamine. Treatment involves discontinuing the offending agent and administering either a central serotonergic antagonist, such as cyproheptadine or chlorpromazine, a benzodiazepine, or a combination of the two. NMS typically occurs over hours to days in a patient taking a neuroleptic agent; its recommended treatment is generally the combination of a central dopamine agonist, bromocriptine or L-dopa, and dantrolene. In those patients in whom it is difficult to differentiate between serotonin and neuroleptic malignant syndromes, the physical examination may be helpful:clonus and hyperreflexia are more suggestive of serotonin syndrome,whereas lead-pipe rigidity is suggestive of NMS. In patients in whom serotonin syndrome and NMS cannot be differentiated, benzodiazepines represent the safest therapeutic option. MH presents rapidly with jaw rigidity, hyperthermia, and hypercarbia. Although it almost always occurs in the setting of surgical anesthesia, cases have occurred in susceptible individuals during exertion. The treatment of MH involves the use of dantrolene. Future improvements in understanding the pathophysiology and clinical presentations of these syndromes will undoubtedly result in earlier recognition and better treatment strategies.
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PMID:Toxin-induced hyperthermic syndromes. 1622 63

In experimental and clinical studies, an objective assessment of peripheral muscle resistance represents one of the key elements in determining the efficacy of therapeutic manipulations (e.g. pharmacological, surgical) aimed to ameliorate clinical signs of spasticity and/or rigidity. In the present study, we characterize a newly developed limb flexion resistance meter which permits a semi-automated, computer-controlled measurement of peripheral muscle resistance (PMR) in the lower extremities during a forced flexion of the ankle in the awake rat. Ischemic paraplegia was induced in Sprague-Dawley rats by transient aortic occlusion (10 min) in combination with systemic hypotension (40 mm Hg). After ischemia the presence of spasticity component was determined by the presence of an exaggerated EMG activity recorded from gastrocnemius muscle after nociceptive or proprioceptive afferent activation and by velocity-dependent increase in muscle resistance. Rigidity was induced by high dose (30 mg/kg, i.p.) of morphine. Animals with defined ischemic spasticity or morphine-induced rigidity were then placed into a plastic restrainer and a hind paw attached by a tape to a metal plate driven by a computer-controlled stepping motor equipped with a resistance transducer. The resistance of the ankle to rotation was measured under several testing paradigms: (i) variable degree of ankle flexion (40 degrees, 50 degrees, and 60 degrees), (ii) variable speed/rate of ankle flexion (2, 3, and 4 sec), (iii) the effect of inhalation anesthesia, (iv) the effect of intrathecal baclofen, (v) the effect of dorsal L2-L5 rhizotomy, or (vi) systemic naloxone treatment. In animals with ischemic paraplegia an increased EMG response after peripheral nociceptive or proprioceptive activation was measured. In control animals average muscle resistance was 78 mN and was significantly increased in animals with ischemic spasticity (981-7900 mN). In ischemic-spastic animals a significant increase in measured muscle resistance was seen after increased velocity (4 > 3 > 2 sec) and the angle (40 degrees > 50 degrees > 60 degrees) of the ankle rotation. In spastic animals, deep halothane anesthesia, intrathecal baclofen or dorsal rhizotomy decreased muscle resistance to 39-80% of pretreatment values. Systemic treatment with morphine induced muscle rigidity and corresponding increase in muscle resistance. Morphine-induced increase in muscle resistance was independent on the velocity of the ankle rotation and was reversed by naloxone. These data show that by using this system it is possible to objectively measure the degree of peripheral muscle resistance. The use of this system may represent a simple and effective experimental tool in screening new pharmacological compounds and/or surgical manipulations targeted to modulate spasticity and/or rigidity after a variety of neurological disorders such as spinal cord traumatic or ischemic injury, multiple sclerosis, cerebral palsy, or Parkinson's disease.
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PMID:Measurement of peripheral muscle resistance in rats with chronic ischemia-induced paraplegia or morphine-induced rigidity using a semi-automated computer-controlled muscle resistance meter. 1630 23

Remifentanil is a potent mu-opioid receptor agonist and has some unique pharmacokinetic characteristics compared to other anilidopiperidine opioids (e.g. fentanyl, alfentanil, and sufentanil). As remifentanil is metabolised rapidly by nonspecific esterases that are widespread throughout the plasma and tissuses, its duration of action is very short. It is cleared very rapidly, and its clearance is not affected by renal and hepatic function. The context-sensitive half-time of remifentanil remains consistently short, even after administration for a long time. Consequently, emergence is quick even after anesthesia of long duration. As other piperidine opioids, remifentnil has some adverse effects such as respiratory depression, muscle rigidity, bradycardia, and nausea as well as vomiting. Because of the rapid dissipation of analgesic effect following remifentanil discontinuation, postoperative analgesia should be provided before or soon after anesthesia using longer-acting opioid analgesics, non-opioid analgesics, or local as well as regional anesthesia.
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PMID:[Remifentanil]. 1685 41


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