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)

A 46-year-old man developed neuroleptic malignant syndrome with acute myoglobinuric renal failure after the discontinuation of sulpiride and maprotiline treatment. He showed the characteristic features of hyperpyrexia, altered consciousness, muscle rigidity, and autonomic dysfunction. Laboratory data showed lysis of skeletal muscle cells and renal impairment. Muscle biopsy revealed necrosis and regenerative changes in muscle fibers. Renal biopsy showed focal tubulitis and interstitial infiltration of small inflammatory cells. The combination of sulpiride and maprotiline has not previously been reported to be the cause of neuroleptic malignant syndrome and acute myoglobinuric renal failure.
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PMID:A case of neuroleptic malignant syndrome with acute renal failure after the discontinuation of sulpiride and maprotiline. 194 57

Abecarnil (ZK 112119; isopropyl-6-benzyloxy-4-methoxymethyl-beta-carboxylate) is a metabolically stable beta-carboline derivative with potent anxiolytic and few sedative and ataxic effects in rodents. The anticonvulsant and muscle relaxant actions of abecarnil have been evaluated in mice, rats, gerbils and baboons. Abecarnil raised the threshold for tonic electroconvulsions in mice after corneal but not after auricular application, had no effect on maximal electroshock-induced tonic convulsions triggered by either method, protected mice against the tonic hindlimb extension in PTZ-, picrotoxin- and 3-mercaptopropionate-induced seizures and blocked clonus after PTZ, DMCM (methyl-4-ethyl-6,7-dimethoxy-9H-pyrido-(3,4-b)-indol-3-carboxylate) and 3-mercaptopropionate. Abecarnil had no effect on convulsions induced by bicuculline and strychnine. Furthermore, abecarnil blocked kindled seizures after chronic administration of PTZ and FG 7142 (beta-carboline-3-carboxylic acid methylamide) and protected mice and rats against limbic convulsions induced by pilocarpine. Severity and afterdischarge duration of amygdala-kindled seizures were reduced in rats treated with abecarnil. Abecarnil also antagonized selectively convulsions induced by i.c.v. administration of kainate, but not those triggered by N-methyl-D-aspartate or quisqualate. In genetic models of reflex epilepsy, abecarnil was effective against sound-induced convulsions in DBA/2 mice, against air blast-induced generalized seizures in gerbils and against myoclonus in baboons Papio papio. The anticonvulsant effect of abecornil in a PTZ seizure model in mice was potentiated by ethosuximide, whereas no significant potentiation was found with diazepam, clonazepam, diphenylhydantoin, carbamazepine and phenobarbital. Electromyographic monitoring in a etorphine model of muscle rigidity in rats showed no or little muscle relaxant effect of abecarnil.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Anticonvulsant action of the beta-carboline abecarnil: studies in rodents and baboon, Papio papio. 197 Mar 62

1. Neuroleptic drugs (antipsychotics) produce numerous side effects which include serious extrapyramidal symptoms consisting of akathisia, dystonia, neuroleptic malignant syndrome, parkinsonian reactions such as postural abnormality, tremor, akinesia or bradykinesia, rigidity, and tardive dyskinesia. 2. Among the complications of neuroleptic chemotherapy, the most serious and potentially fatal complication is malignant syndrome, which is characterized by extreme hyperthermia, "lead pipe" skeletal muscle rigidity causing dyspnea, dysphagia, and rhabdomyolysis, autonomic instability, fluctuating consciousness, leukocytosis, and elevated creatine phosphokinase. 3. Neuroleptic malignant syndrome should be differentiated from malignant hyperthermia, lethal catatonia, and other pathological states producing some of these same symptoms. 4. In addition to neuroleptics, malignant syndrome has been caused by thymoleptics (antidepressants), metoclopramide (antiemetic), metoclopramide combined with cimetidine, tetrabenazine, overdosage of benzodiazepine, phenelzine, dothiepin and alcohol, and amphetamine. 5. Factors leading to and/or facilitating the emergence of neuroleptic malignant syndromes are reportedly organic brain syndrome, dehydration, exhaustion, external heat load, excessive sympathetic discharge, use of long acting neuroleptics, high doses of neuroleptics, rapid dose titration with neuroleptics, abrupt discontinuation of antiparkinsonism agents, and concurrent lithium therapy. 6. Although, the pathogenesis of neuroleptic malignant syndrome is not understood completely, a blockade of dopaminergic receptors in the hypothalamus, spinal cord and striatum, an alteration of dopaminergic-serotonergic transmission in the body, an enhanced synthesis and action of prostaglandin E1 and E2, and a modification of calcium-mediated signal transduction in the body have been suggested. 7. The treatment of malignant syndrome includes immediate withdrawal of neuroleptic drugs, i.v. infusion of dantrolene, and oral administration of bromocriptine; or alternatively i.v. infusion of dantrolene and the combination of levodopa-carbidopa. 8. Other measures to enhance the therapeutic effectiveness of the aforementioned regimens are to include the use of anticholinergic drugs such as benztropine to enhance the effectiveness of bromocriptine, of lorazepam if catatonic symptoms persist, or of electroconvulsive therapy (ECT) if psychotic symptoms persist. 9. These treatments, however, must be "active" rather than "passive", in order to avert fatalities and/or unfortunate sequelae from this iatrogenic and incompletely understood disease.
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PMID:Pathogenesis and treatment of neuroleptic malignant syndrome. 197 19

The effects of inosine (INO) on substrate metabolism and rigor formation in ischemic myocardium were examined in isolated rabbit hearts. Metabolite content was assessed in tissue extracts by chemical analysis and in the whole heart by 13C and 31P nuclear magnetic resonance spectroscopy. In ischemic hearts metabolizing either [3-13C]pyruvate or [1-13C]glucose, 1 mM INO increased both total and 13C-labeled alanine content; lactate content was unaffected. At 3 minutes of ischemia, tissue alanine was 1.81 +/- 0.11 microM/g wet wt (mean +/- SEM) in hearts perfused with pyruvate+INO versus 1.23 +/- 0.15 microM/g wet wt in hearts perfused with pyruvate alone (p less than 0.05). INO reduced tissue glycogen during ischemia in pyruvate-perfused hearts. Tissue alanine content in ischemic hearts that were supplied glucose+INO (1.29 +/- 0.13 microM/g wet wt) was greater than in ischemic hearts supplied glucose alone (0.65 +/- 0.14 microM/g wet wt). Alanine was found to originate from pyruvate and was a glycolytic end product in glucose-perfused hearts. INO raised the [3-13C]alanine/[3-13C]lactate ratio in ischemic, intact hearts (glucose = 0.24 +/- 0.07 versus glucose+INO = 0.60 +/- 0.09; pyruvate = 0.49 +/- 0.08 versus pyruvate+INO = 0.89 +/- 0.08). At 7 minutes of ischemia, ATP content fell to 70 +/- 3% with glucose+INO versus 58 +/- 5% with glucose alone. Rigor (stone heart) was delayed from 14.7 +/- 1.3 to 23.2 +/- 1.6 minutes with INO. INO did not change ATP content in ischemic hearts that were supplied pyruvate but delayed rigor (pyruvate = 9.9 +/- 1.2 minutes; pyruvate+INO = 15.6 +/- 1.0 minutes), possibly at the expense of glycogen. Supplemental glucose improved the effectiveness of INO with pyruvate to preserve ATP (pyruvate+glucose = 42 +/- 6%; pyruvate+glucose+INO = 72 +/- 6%) and further delayed rigor (pyruvate+glucose = 13.3 +/- 1.5 minutes; pyruvate+glucose+INO = 20.3 +/- 1.8 minutes). Glucose metabolism supported improved energetic and contractile states in ischemic hearts treated with INO. Thus, cardioprotection of the ischemic heart by INO was associated with preservation of functional integrity and improved energy production due to increased glycolytic activity. Activation of glycolysis in the presence of INO was accommodated by augmented alanine production without the additional accumulation of lactate.
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PMID:Effects of inosine on glycolysis and contracture during myocardial ischemia. 199 56

Neuroleptic malignant syndrome is a rare but potentially life-threatening reaction to neuroleptic drugs. The syndrome develops rapidly, and may occur at the initiation of neuroleptic therapy or after long-term use; its pathogenesis is unclear. The signs and symptoms associated with the syndrome are hyperpyrexia, extreme muscle rigidity, an altered level of consciousness, and autonomic dysfunction. We describe a case of neuroleptic malignant syndrome in a patient who had Escherichia coli urosepsis caused by thioridazine.
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PMID:Neuroleptic malignant syndrome and Escherichia coli urosepsis. 200 33

The occurrence of the rare but potentially fatal neuroleptic malignant syndrome must be considered by the surgeon treating a patient who develops hyperthermia, mental abnormalities, autonomic instability, and muscle rigidity after exposure to phenothiazines or other neuroleptic drugs. The dopamine agonist bromocriptine appears to be the treatment of choice in adults and seemed to be effective and well tolerated in our patient. Although the syndrome cannot be prevented, recognition is crucial, since effective general and specific therapy is available. Differentiating neuroleptic malignant syndrome from malignant hyperthermia allows early appropriate treatment with bromocriptine.
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PMID:Neuroleptic malignant syndrome: occurrence in a child after reconstructive surgery. 201 9

A 27 year-old female in 39th week gestation with schizophrenia underwent an emergency Cesarean section using general anesthesia. A diagnosis of schizophrenia was made two years previously, since then oral anti-psychotic drugs such as chlorpromazine had been given to her. In June 1989 she suddenly became excited and generalized muscle rigidity was observed without any triggering episodes. Her excitement was so marked that we had to administer intramuscular levomepromazine 75 mg and diazepam 10 mg to her, but they failed to sedate her adequately. Emergency Cesarean section was scheduled to overcome this situation. Spinal or epidural anesthesia was not indicated because of her vigorous excitement, and anesthesia was induced with thiopental 350 mg and succinylcholine 40 mg. Induction-delivery time was 12 minutes. Pentazocine 30 mg in combination with nitrous oxide was given for the maintenance of anesthesia. Plasma levomepromazine levels were 46.9 ng.ml-1 in the mother and 11.3 ng.ml-1 in the umbilical vein, respectively. The baby's Apgar score was 9 and 1 min and 9 at 5 min after the delivery. The baby developed slight generalized tremor until next day, probably due to effect of levomepromazine given before the Cesarean section. The patient was discharged without any cardiorespiratory trouble and her baby has been doing well so far.
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PMID:[An emergency cesarean section using general anesthesia for a patient with schizophrenia]. 202 Jan 5

Imaging techniques for renal obstruction remain in a continual state of flux. An improved data base has been developed for renal ultrasonography, permitting a more precise evaluation of hydronephrosis. Rigidity with regard to an algorithm for renal obstruction is not recommended because it would be fixed at a point in time and dependent upon the equipment and expertise of a given institution. In all likelihood ultrasonography will continue to be used as the primary screening tool. A role for the intravenous urogram remains, especially in the acute presentation of renal obstruction. It is interesting to note that the initial description of the percutaneous nephrostomy tube was as a diagnostic technique in patients who had long-standing ureteropelvic junction obstruction. Prediction of recoverability of the kidneys was not possible without relieving the obstruction and assessing the ability of the postobstructive kidney to function. Recoverability of renal function cannot be assessed on a short-term basis but takes time. Up to 8 weeks is necessary before the kidney has established its new baseline level of function. The percutaneous nephrostomy has become an integral tool for the interventional radiologist and is used in treatment. Indeed, its treatment role is important, and even today we must be careful not to assess the kidneys' functional status after placement of the nephrostomy tube without allowing the renal unit sufficient time for recovery. The future undoubtedly will bring further tremendous changes in our assessment of renal obstruction. It is important that radiologists position themselves at the forefront of these developments.
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PMID:Contemporary concepts in imaging urinary tract obstruction. 202 4

Previous work has demonstrated that direct injections of methylnaloxonium (MN), a hydrophilic quaternary opiate antagonist, in the area of the nucleus raphe pontis (RPn) significantly attenuated alfentanil-induced muscle rigidity in the rat. To extend these observations and to explore further the regions important for opiate-induced rigidity, rats were implanted with chronic guide cannulae aimed at discrete brain sites with an emphasis on the region from the periaqueductal grey (PAG) to the RPn. Each animal was pretreated by a blinded observer with an intracerebral injection of MN (125 ng total dose) or saline, and electromyographic (EMG) activity was recorded from the gastrocnemius muscle. Alfentanil (ALF; 500 micrograms/kg) was then administered subcutaneously and the magnitude of tonic EMG activity was assessed as a measure of hindlimb rigidity. The administration of MN into the pontine raphe nucleus (RPn) and also into the more lateral nucleus reticularis tegmenti pontis significantly attenuated ALF rigidity compared with saline-pretreated controls. Within the midbrain, MN selectively reversed rigidity when injected into the periaqueductal grey (PAG). The dorsal PAG appeared to be a more important site than the ventral PAG. There was no significant effect on ALF rigidity of MN injections into brain regions between the ventral PAG and the RPn while MN injections into the deep layers of the superior colliculus, lateral to the dorsal PAG, partially attenuated ALF rigidity. In contrast, rigidity was not consistently reversed after MN injections into the basal ganglia, the dorsal superior colliculus, or the region of the decussation of the dorsal tegmentum. This study provides strong evidence that nuclei of the reticular formation, specifically the PAG, raphe pontis, and reticularis tegmenti pontis that are known to play a role in other opioid-mediated behaviors, are important in opiate-induced muscle rigidity in the rat. These results could have implications for the prevention of this undesirable effect of high-dose opiate administration.
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PMID:Brain sites mediating opiate-induced muscle rigidity in the rat: methylnaloxonium mapping study. 203 35

The neurobiological aspects of human neural transplants are far from being understood. We have approached their study by means of a multidisciplinary working team. Nine patients with Parkinson's disease were subjected to open brain surgery for grafting of autologous adrenal medulla. Not all patients improved. Those patients that did so showed different patterns of improvement. Rigidity was the sign most relieved in this group of patients. Electroencephalographic changes were attributable to surgical manipulation. High-performance liquid chromatographic quantification of catecholaminergic metabolites did not correlate with post-grafting outcome. Biopterin levels showed a significant increment after surgery. More interdisciplinary studies ought to be done on neural transplants.
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PMID:Multidisciplinary analysis of the effectiveness of autologous neural transplant (adrenal medulla) as treatment of Parkinson's disease. 208 Mar 46


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