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)

Several fentanyl analogs (Bagley et al., 1989, J. Med. Chem. 32, 663) were compared to fentanyl and morphine for their effects on respiratory depression as determined by arterial blood gas (pH, pCO2 and pO2) measurements. Fentanyl (0.1 mg/kg), morphine (10 mg/kg), #16 (1-phenethyl-4-[N-(pyridin-2-yl)-N-(methoxymethylcarbonyl)amino] piperidine, 1 mg/kg), #17 (1-phenethyl-4-[N-(pyridin-2-yl) -N-(2-furoyl)amino]piperidine, 0.5 mg/kg) and #29 (1-phenethyl-4-[N- (pyrimidin-2-yl)-N-(methoxy-methylcarbonyl) amino]piperidine, 10 mg/kg) produced significant respiratory depression in rats. Pretreatment with the mu1-opioid receptor selective antagonist, naloxonazine (10 mg/kg), blocked the respiratory effect of fentanyl and its analogs, but not that of morphine. The results suggest that the mu1-opioid receptor plays an important role in the respiratory effects of fentanyl and its analogs. Hence, the mechanism of fentanyl-induced respiratory depression appears to be distinct from that produced by morphine. The most likely explanation for this difference is the possible contribution of muscle rigidity and catalepsy to the observed changes in blood gas parameters caused by the fentanyl analogs, while the respiratory depression of morphine, measured by these same parameters, appears to be independent of its effect on muscle rigidity.
Eur J Pharmacol 1996 Sep 26
PMID:Evidence for mu1-opioid receptor involvement in fentanyl-mediated respiratory depression. 889 2

A case of rhabomyolysis with attendant severe acute renal failure, arisen in a 59-year-old male treated with haloperidol-decanoate, is presented. The patient has been affected by paranoia schizophrenia since childhood, and he was treated with electroshock and successively with neuroleptics p.o. Four years before our observation, a therapy with haloperidol decanoate (50 mg i.m. monthly) was started. After some time, catatonic like episodes appeared, which got more and more frequent, until they appeared weekly. In occasion of the last of them, he was admitted to our hospital. At the objective examination he presented psychomotory arrest, perspiration, mytacism, severe muscle rigidity, moderate oedems to lower limbs. Laboratory findings showed a pattern consistent with rabdomyolysis and severe renal failure. After that haloperidol decanoate was stopped and rehydration and intensive diuretic therapy was started, the clinical and laboratory pattern went normal, persisting however a light creatinine increase. Probably the rhabdomyolysis was induced by the haloperidol decanoate, and renal failure by secondary severe hyvolemia. This case comes into the so-called neuroleptic malignant syndrome which can rarely arise in patients treated with antipsycotic agents and which causes high mortality, particularly when there are rhabdomyolysis and acute renal failure.
Recenti Prog Med 1996 Sep
PMID:[Rhabdomyolysis and acute renal failure caused by haloperidol-decanoate (neuroleptic malignant syndrome)]. 905 57

The traditional view of opioids held that the individual opioid agonists shared the same mechanism of action, differing only in their potency and pharmacokinetic properties. However, recent advances in opioid receptor pharmacology have made this view obsolete. Distinguishing features of the synthetic opioid agonists are related, at least in part, to variation in affinity and intrinsic efficacy at multiple opioid receptors. Respiratory depression is the opioid adverse effect most feared by anaesthesiologists. Specific kappa-receptor agonists produce analgesia with little or no respiratory depression. There are a number of commercially available kappa-receptor partial agonist drugs, the so-called agonist-antagonist or nalorphine-like opioids, which appear to have a limited effect on breathing. Within the series of fentanyl analogues there are differences in behaviour towards particular opioid receptors and there is evidence for subtle differences in respiratory depressant effects. Pethidine (meperidine) causes histamine release and myocardial depression, while the fentanyl analogues do not. Pethidine has atropine-like effects on heart rate, while fentanyl analogues reduce heart rate by a vagomimetic action. Severe bradycardia or even asystole is possible with fentanyl analogues, especially in conjunction with the vagal stimulating effects of laryngoscopy. Fentanyl analogues often produce minor reductions in blood pressure, and occasionally severe hypotension by centrally mediated reduction in systemic vascular resistance. Muscle rigidity and myoclonic movement occurs frequently during induction of anaesthesia with larger doses of opioids. Fentanyl and alfentanil have been reported to produce localised temporal lobe electrical seizure activity in patients with complex partial epilepsy. There are probably fewer biliary effects with agonist-antagonist opioids than the agonist opioids. The mechanism of adverse effects after spinal administration is distinctly different for morphine, which is very water soluble, compared with more lipid-soluble opioids. The systemic absorption of morphine after intrathecal or epidural administration is very slow, resulting in long duration of analgesia and low plasma concentrations, while lipid-soluble opioids are rapidly absorbed into the circulation and redistributed to the brain. The serotonin syndrome may result from coadministration of pethidine, dextromethorphan, pentazocine or tramadol with monoamine oxidase inhibitors (MAOIs) or selective serotonin (5-hydroxytryptamine; 5-HT) reuptake inhibitors (SSRIs). There are clinically important interactions between opioids and hypnosedatives, resulting in synergistic effects on sedation, breathing and blood pressure.
Drug Saf 1998 Sep
PMID:Adverse effects of opioid agonists and agonist-antagonists in anaesthesia. 974 65

The skeletal muscle ryanodine receptor (RYR1) is a calcium release channel that mediates efflux of calcium ions from the sarcoplasmic reticulum into the myoplasm during excitation-contraction coupling. Mutations in the RYR1 gene have been detected in about 50% of the patients suffering from malignant hyperthermia (MH), but evidence is accumulating that other genetic defects can also lead to MH in humans. MH is a life-threatening disorder induced by exposure to volatile anesthetics and/or the muscle relaxans succinylcholin during surgical procedures in affected patients. MH leads to skeletal muscle rigidity, hypermetabolism and rapid rise in body temperature. MH is also known in pigs where it is triggered by stress and therefore often referred to as porcine stress syndrome. The existence of an animal model has greatly faciliated the elucidation of the basis for the human disease. This review describes recent advances in the understanding of the physiological action of ryanodine receptors and new insights regarding the relation between different RYR1 mutations and distinct phenotypical appearances.
Int J Mol Med 1998 Sep
PMID:Ryanodine receptors and their role in genetic diseases (review). 985 1

Hyperthermia, skeletal muscle rigidity, rhabdomyolysis, acidosis and multiple system insufficiency characterize malignant hyperthermia. Anaesthetic malignant hyperthermia follows halogenated volatile agents and/or depolarizing muscle relaxants utilization. Diagnosis is based on in vitro muscle contracture in response to halothane and/or caffeine exposure. Neuroleptic malignant syndrome affects patients taking neuroleptic drugs; clinical findings include hyperthermia, extrapyramidal rigidity, acidosis, neurovegetative instability and neurological signs. We report three neuroleptic malignant syndrome patients with positive muscle contracture tests which shows that muscle from neuroleptic malignant syndrome patients may in some instances show alterations similar to those of anaesthetic malignant hyperthermia.
Arq Neuropsiquiatr 2000 Sep
PMID:[Malignant hyperthermia susceptibility in 3 patients with malignant neuroleptic syndrome]. 1097 14

The aim of the present study was to examine a potential beneficial effect of the blockade of metabotropic glutamate receptor subtype 5 (mGluR5) by the selective non-competitive antagonist, 2-methyl-6-(phenylethynyl)pyridine (MPEP), in models of parkinsonian symptoms in rats. Haloperidol, 0.25, 0.5 and 1mg/kg ip, was used to induce hypolocomotion, catalepsy and muscle rigidity, respectively. The locomotor activity was estimated by an open-field test, the catalepsy -- by a 9-cm cork test. The muscle rigidity was measured as an increased resistance of a hind leg to passive extension and flexion at the ankle joint. Additionally, increases in the electromyographic activity were recorded in the gastrocnemius and tibialis anterior muscles. MPEP (1.0-10mg/kg ip) inhibited the muscle rigidity, electromyographic activity, hypolocomotion and catalepsy induced by haloperidol. MPEP administered alone (5mg/kg ip) did not induce catalepsy, nor did it influence the muscle tone or locomotor activity in rats. The present results suggest that blockade of mGluR5 receptors may be important to amelioration of both parkinsonian akinesia and muscle rigidity.
Neuropharmacology 2001 Sep
PMID:Blockade of the metabotropic glutamate receptor subtype 5 (mGluR5) produces antiparkinsonian-like effects in rats. 1154 61

An 86-year old man presented with a 7-year history of gait disturbance. He was admitted to our hospital on April 2000 because he was experiencing difficulty eating due to progression of dropped head syndrome. Upon standing and sitting, remarkable dropped head and kyphosis were observed. When lying, the patient was able to stretch his neck, and he could stand and walk with the aid of a walker. Rigidity and resting tremor were present predominantly in the lower limbs. Parkinson's disease was diagnosed therefore L-dopa and Cabergoline were administered. Parkinsonism and dropped head syndrome improved in response to treatment. Cases involving dropped head syndrome due to Parkinson's disease are reportedly improved by L-dopa, but exasperated by dopamine agonists. The mechanism of dropped head is thought to be an imbalance in the tonus of the anterior and posterior neck muscles. Dropped head in the present case may have been a complication of Parkinson's disease since it improved in response to L-dopa.
Nihon Ronen Igakkai Zasshi 2001 Sep
PMID:[A case of elderly onset Parkinson's disease complicated by dropped head syndrome]. 1160 21

A potent heteronymous excitation of quadriceps motoneurones via common peroneal group II afferents has recently been demonstrated in normal subjects. The aim of this study was to investigate whether this group II excitation contributes to rigidity in Parkinson's disease. The early and late facilitations of the quadriceps H reflex elicited by a conditioning volley to the common peroneal nerve (CPN) at twice motor threshold, attributed to non-monosynaptic group I and group II excitations, respectively, were investigated. The comparison was drawn between results obtained in 20 "de novo" patients with Parkinson's disease (hemiparkinsonian, 17; bilateral, three) and 20 age-matched normal subjects. There was no statistically significant effect of "group" (patients/controls), "duration", "global severity" [Unified Parkinson's Disease Rating Scale (UPDRS)] or "side" (unilaterally versus bilaterally affected) factors on either group I or group II facilitations. To further the analysis, the factors of status (affected or non-affected limb), akinesia (lower limb akinesia score) and rigidity (lower limb rigidity score) were entered in a general linear model to explain the variations of the quadriceps H reflex facilitation. Rigidity was the only factor useful in predicting the value of the group II facilitation of the quadriceps H reflex (P < 0.007). Group I and group II facilitation was then compared between the rigid, non-rigid and control lower limbs [multivariate analysis of variance (MANOVA)]. Results are represented as mean +/- SEM (standard error of the mean). Group II facilitation was enhanced in the rigid lower limb of unilaterally affected patients (153.2 +/- 7% of control H reflex) compared with non-rigid lower limbs (124 +/- 4% of control H reflex; P < 0.007) or control lower limbs (126.1 +/- 4.1%; P < 0.01). There was no difference between the non-rigid lower limbs of the unilaterally affected patients and the control lower limbs, but a difference was observed between the rigid lower limbs of unilaterally less affected and bilaterally more affected patients (153.2 +/- 7% and 123.8 +/- 7.5% of control H reflex, respectively; P < 0.04). These results suggest a facilitation of the transmission in the interneuronal pathway activated by group II afferents in rigid lower limb of de novo hemiparkinsonian patients, probably resulting from a change in their descending monoaminergic inhibitory control.
Brain 2002 Sep
PMID:Transmission of group II heteronymous pathways is enhanced in rigid lower limb of de novo patients with Parkinson's disease. 1218 57

The aim of the present study was to find out whether the metabotropic receptor 1 (mGluR1) and group II mGluRs, localized in the striatum, are involved in antiparkinsonian-like effects in rats. Haloperidol (1 mg/kg ip) induced parkinsonian-like muscle rigidity, measured as an increased resistance of a rat's hind foot to passive flexion and extension at the ankle joint. (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA; 0.5-15 microg/0.5 microl), a potent and selective mGluR1 antagonist, or (2R,4R)-4-aminopyrrolidine-2,4-dicarboxylate (2R,4R-APDC; 7.5-15 microg/0.5 microl), a selective group II agonist, was injected bilaterally into the striatum of haloperidol-treated animals. AIDA in doses of 7.5-15 microg/0.5 microl diminished the haloperidol-induced muscle rigidity. In contrast, 2R,4R-APDC injections were ineffective. The present results may suggest that the blockade of striatal mGluR1, but not the stimulation of group II mGluRs, may ameliorate parkinsonian muscle rigidity.
Brain Res 2002 Sep 20
PMID:The striatum as a target for anti-rigor effects of an antagonist of mGluR1, but not an agonist of group II metabotropic glutamate receptors. 1223 Dec 32

Drug-induced hyperthermia is one condition that anesthesiologists may meet even though it is uncommon, it is life threatening. We report 3 cases of patients at Siriraj Hospital, Mahidol University who developed drug-induced hyperthermia and rhabdomyolysis from different mechanisms. In two of them, the diagnosis was suspected malignant hyperthermia. Rigidity, hyperthermia and tachyarrhythmia developed just after inhalation induction (halothane and sevoflurane) and intubation with succinylcholine. The other case was the result of amphetamine abuse. He also had received both succinylcholine and inhalation agent (isoflurane) but no obvious signs or symptoms were detected during anesthesia. He developed a gradual increase in fever over 13 hours post operation and complained of muscle pain (with leg muscle cramps). All of them showed a marked increase in muscle enzymes and had rhabdomyolysis. As a result of early detection and early manangement, these three patients survived without any permanent damage to vital organs. We conclude that Thai anesthesiologists should be more aware and alert to drug-induced hyperthermia especially as nowadays many teenagers abuse stimulant drugs and "triggering" drugs as antidepressant or serotonin reuptake inhibitors are prescribed more frequently. Early detection and management will decrease morbidity and mortality.
J Med Assoc Thai 2002 Sep
PMID:Drug-induced hyperthermia and rhabdomyolysis during the perioperative period: report of three patients. 1245 25


<< Previous 1 2 3 4 5 6 7 Next >>