Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0026837 (muscle rigidity)
 1,077 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of metoclopramide-induced neuroleptic malignant syndrome with cerebrospinal fluid (CSF) lactic acidosis was reported. A 44-year-old Japanese woman noted tarry stool on July 2, 1988 and was treated with metoclopramide and cimetidine for nausea and vomiting. Hydroxyzine pamoate was also administered for insomnia at 3:10 am and she became comatose with muscle rigidity at 3:40-4:30 am on July 3. Tachycardia and high fever (39.5 degrees C) were evident at 8:00 am on July 4. She was transferred to the Kyushu University Hospital. On admission, serum creatine kinase was elevated to 1640 IU/1; MM fraction was 100%. She was diagnosed as malignant syndrome. Cerebrospinal fluid was normocellular with protein 38 mg/dl and glucose 122 mg/dl. Cerebrospinal fluid lactate increased markedly to 3.43 mmol/l, CSF pH was 7.264, HCO3- 14.4 mEq/l, indicating CSF metabolic acidosis. She became afebrile after the 10th hospital day, and gradually but completely recovered within a month. She was discharged on August 16, 1988. The anti-dopaminergic activity of metoclopramide was considered to be primarily responsible for the development of malignant syndrome in this case. Cerebrospinal fluid lactic acidosis seemed to reflect hyperpyrexia or malignant syndrome induced derangement of the brain metabolism.
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PMID:[A case of metoclopramide-induced neuroleptic malignant syndrome with cerebrospinal fluid lactic acidosis]. 188 79

The regulation of intracellular free calcium ions (Ca2+) in skeletal muscle at rest and during contraction depends on mechanisms such as Na(+)-Ca2+ exchangers, Ca(2+)-ATPases, and the voltage-sensitive ryanodine receptor. The susceptibility of these regulatory mechanisms to free-radical-mediated damage may be increased because of their location within the lipid membranes of sarcolemma, sarcoplasmic reticulum, and mitochondrion with resultant uncontrolled increases in myoplasmic Ca2+ concentration and cell death. The potentially fatal pharmacogenetic disorder, malignant hyperthermia (MH), is characterised by muscle rigidity, arrhythmias, lactic acidosis, and a rapid rise in body temperature. The sequence of events responsible for the MH syndrome remains uncertain, but it has been variously ascribed to faults in many of the Ca2+ regulatory mechanisms. In swine the condition is associated with a specific mutation in the ryanodine receptor, whereas in humans the syndrome is genetically heterogenous. Free-radical-mediated peroxidation of membrane lipids and proteins also results in the rapid efflux of Ca2+ from organelles, and the detection of products of free radical reactions in tissue from MH-susceptible individuals using electron spin resonance spectroscopy provides evidence for the involvement of free radicals in the MH syndrome.
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PMID:Free radicals and calcium homeostasis: relevance to malignant hyperthermia? 846 27

Thiafentanil oxalate, previously known as A-3080, is a synthetic opioid used for chemical immobilization of a variety of nondomestic hoofstock species. This study compared the combination of thiafentanil oxalate, medetomidine, and ketamine (TMK; 0.09 +/- 0.02 mg/kg, 0.01 +/- 0.003 mg/kg, and 1.36 +/- 0.33 mg/kg, respectively) with the combination of medetomidine and ketamine (MK; 0.09 +/- 0.02 mg/kg and 3.48 +/- 0.55 mg/kg, respectively) for anesthetization of 17 captive male axis deer (Axis axis) for vasectomy. Nine deer received TMK and eight deer received MK via projectile syringe during the months of January and February, 2005. Mean induction and arousal times, vital signs, and arterial blood gas values were monitored and compared. All animals received supplemental oxygen during the surgical procedure. Animals receiving TMK were reversed with naltrexone (100 mg/mg thiafentanil) and atipamazole (5 mg/mg medetomidine). Animals receiving MK were reversed with atipamazole (5 mg/mg medetomidine). Two MK animals and three TMK animals required supplementation with ketamine i.v. immediately upon handling. Six of the nine animals immobilized with TMK required intubation for positive-pressure ventilation. Two of these six animals also required isoflurane to maintain anesthesia. Mean induction time was 3.5 +/- 2.0 min in the TMK group, and 9.8 +/- 6.7 min in the MK group. Despite shorter mean induction times, animals anesthetized with TMK experienced unpredictable inductions, apnea, muscle rigidity, limb movement, and significant respiratory and metabolic lactic acidosis. MK resulted in smoother inductions, better respiratory function, and less adverse metabolic disturbances, and thus was considered superior to TMK for anesthesia in captive axis deer at the dosages tested.
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PMID:Anesthesia of male axis deer (Axis axis): evaluation of thiafentanil, medetomidine, and ketamine versus medetomidine and ketamine. 1731 36