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PubMedDate not supplied

Pretreatment with sedative-hypnotics, but not with nondepolarizing muscle relaxants, attenuates alfentanil-induced muscle rigidity.

STUDY OBJECTIVE: To evaluate and compare the efficacy of various pretreatment agents to attenuate or prevent opioid-induced muscle rigidity using a well-established, previously described clinical protocol. DESIGN: Prospective, controlled, single-blind, partially randomized study. SETTING: Large medical center. PATIENTS: ASA physical status I-III patients undergoing elective surgical procedures of at least 3 hours' duration. INTERVENTIONS: The effect of pretreatment with nondepolarizing muscle relaxants (atracurium 40 micrograms/kg or metocurine 50 micrograms/kg), benzodiazepine agonists (diazepam 5 mg or midazolam 2.5 mg), or thiopental sodium 1 mg/kg on the increased muscle tone produced by alfentanil 175 micrograms/kg was compared with a control group (given no pretreatment). MEASUREMENTS AND MAIN RESULTS: Rigidity was assessed quantitatively by measuring the electromyographic activity of five muscle groups (biceps, intercostals, abdominals, quadriceps, and gastrocnemius). Rigidity also was rated qualitatively by attempts to initiate and maintain mask ventilation, attempts to flex an extremity, and the occurrence of myoclonic movements. Pretreatment with the two nondepolarizing muscle relaxants had no effect on the severe muscle rigidity produced by high-dose alfentanil. Whereas thiopental was only mildly effective, the benzodiazepines midazolam and diazepam significantly attenuated alfentanil rigidity (p < 0.05). CONCLUSION: This study suggests that benzodiazepine pretreatment is frequently, but not always, effective in preventing opioid-induced muscle rigidity.

Abdominal Muscles↗
PubMed1999

Raclopride and chlorpromazine, but not clozapine, increase muscle rigidity in the rat: relationship with D2 dopamine receptor occupancy.

The aim of the present study was to investigate the relationship between effects on muscle tone and D2 receptor occupancy of two typical antipsychotic drugs, raclopride and chlorpromazine, and the atypical drug, clozapine. Increased muscle tone (i.e., muscle rigidity), was measured as increases in tonic electromyographic (EMG) activity of the antagonistic muscles of the rat hind limb. D2 dopamine receptor occupancy was assessed in the striatum and substantia nigra, areas involved in the regulation of muscle tone. Raclopride and chlorpromazine produced dose-dependent increases in EMG activity associated with D2 occupancy of 68%-80% in the striatum and 67%-76% in the nigra. No significant increases in EMG were observed with clozapine which showed low D2 occupancy. The results are consistent with those from human studies showing extrapyramidal side effects were associated with striatal D2 occupancy of > 70%.

Animals↗
PubMed1986

Masseter muscle rigidity and malignant hyperthermia susceptibility.

Seventy-seven patients who developed masseter muscle rigidity (MMR) after receiving succinylcholine to facilitate tracheal intubation were evaluated for malignant hyperthermia (MH) susceptibility by in vitro halothane and caffeine contracture tests. Thirty-nine patients were diagnosed as MH-susceptible. Neither age, sex, nor type of surgery or anesthesia distinguished MH-susceptible from nonsusceptible patients. Two susceptible and two nonsusceptible patients had evidence of a myopathy. Fifty-two patients had serum creatine phosphokinase (CPK) levels measured in the perioperative period. Although all values were above normal, CPK values equal to or greater than 20,000 IU within 24 hr of trismus (in the absence of myopathy) were observed in six of 30 patients diagnosed as MH-susceptible, but were found in none of the nonsusceptible patients. Considering the high percentage of patients exhibiting MMR that are indeed susceptible to MH (approximately 50%) compared to estimates of MH in the population as a whole (approximately 0.005%), MMR should be considered a presumptive sign of MH. Perioperative CPK values greater than 20,000 IU are highly suggestive of MH susceptibility. Patients exhibiting MMR should be evaluated for MH susceptibility and myopathies. Succinylcholine should be avoided for subsequent anesthetics in patients with a history of MMR.

Caffeine↗
PubMedDate not supplied

Effects of naloxone and neuroleptic drugs on muscle rigidity and heart rate of the nervous Pointer dog.

Muscle rigidity, a persistent physiological characteristic of the nervous Pointer dog, is not only attenuated by the major neuroleptic drugs, haloperidol and pimozide but also by naloxone. In addition, naloxone administration results in a modest but significant increase in heart rate of these subjects. The data obtained in this study add support for the concept that an abnormality in central nervous system dopaminergic function is involved in the genesis of abnormal behavior of this animal model.

Animals↗
PubMed2006

Repeat episodes of severe muscle rigidity in a child receiving sevoflurane.

We report on a patient who developed two episodes of severe muscle rigidity, increased endtidal CO2 and increased creatine phosphate kinase associated with sevoflurane anesthesia. Dysrhythmias and hyperthermia were not observed and dantrolene was not administered. Genetic testing for the 17 known mutations associated with malignant hyperthermia (MH) was negative. Although we cannot rule out MH or other neuromuscular diseases we suggest that this rare event may be a direct effect of sevoflurane.

Abnormalities, Multiple↗
PubMed1993

Antagonist effects of beta-funaltrexamine and naloxonazine on alfentanil-induced antinociception and muscle rigidity in the rat.

Alfentanil is a potent and short-acting mu opioid agonist that produces both antinociceptive effects and muscle rigidity. In the present study, the susceptibility of alfentanil-induced antinociception and rigidity to antagonism by the selective mu antagonist beta-funaltrexamine and the selective mu-1 antagonist naloxonazine was examined. Alfentanil (37.7-150.0 micrograms/kg) produced a dose-dependent increase both in antinociception as measured by the warm-water tail-dip assay and in rigidity as measured by electromyographic recording of the gastrocnemius muscle. Both beta-funaltrexamine (10.0 and 20.0 mg/kg) and naloxonazine (7.5 and 15.0 mg/kg) produced dose-dependent and parallel rightward shifts in the alfentanil dose-effect curves for both antinociception and rigidity. Furthermore, the alfentanil dose-effect curves for antinociception and rigidity were shifted to the right to a similar degree by any given pretreatment. These results suggest that alfentanil-induced antinociception in the warm-water tail-dip test and rigidity are mediated by pharmacologically similar populations of opioid receptors. More specifically, these results suggest that mu-1 opioid receptors mediate both alfentanil-induced antinociception and rigidity.

Alfentanil↗
PubMed1991

Brain sites mediating opiate-induced muscle rigidity in the rat: methylnaloxonium mapping study.

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.

Alfentanil↗
PubMedDate not supplied

[Neuroleptic malignant syndrome in a patient with polyneuropathy: mechanism of muscle rigidity and elevated serum creatine kinase levels].

A 49-year-old man was admitted with the chief complaints of muscle weakness and gait disturbance. His neurological examination was compatible with peripheral neuropathy, and laboratory tests revealed IgA monoclonal gammopathy, increased protein content in the cerebrospinal fluid (CSF) without pleocytosis, and slow motor and sensory nerve conduction velocity. He was diagnosed as having chronic inflammatory demyelinating polyneuropathy with IgA monoclonal gammopathy of undetermined significance. The patient was treated with steroid, and plasmapheresis. He became so restless that antidepressant and haloperidol were administered. Then, he became unresponsive, and developed high fever, sweating, tachycardia, and tremor. Examination of CSF showed increased 3-methoxy-4-hydroxy-phenylglycol and decreased homovanillic acid. He was diagnosed as having neuroleptic malignant syndrome (NMS). However, his muscle tonus was still flaccid in his lower extremities that had been suffered from chronic polyneuropathy. Interestingly, his serum creatine kinase (CK) content was only slightly elevated. We suppose that the pathophysiological location of NMS might be primarily central, and that muscle rigidity and elevation of serum CK might not occur, if the peripheral nerves were completely impaired.

Creatine Kinase↗
PubMed1994

Masseter muscle rigidity and malignant hyperthermia susceptibility in pediatric patients. An update on management and diagnosis.

BACKGROUND: Controversy exists regarding the definition of masseter muscle rigidity (MMR) and anesthetic management after MMR. This study reports current anesthetic management after MMR, estimates the incidence of clinical malignant hyperthermia (MH) in patients with MMR, and is the first to evaluate the coincidence of MMR with malignant hyperthermia susceptibility (MHS) according to the 1987 North American Malignant Hyperthermia Group protocol. METHODS: Practicing anesthesiologists referred pediatric patients for biopsy between 1986 and 1991 based on evidence of MMR after succinylcholine (1975-1991). The clinical scenario was described as MMR alone or MMR followed by signs of MH, including arterial CO2 tension > 50 mmHg, arterial pH < or = 7.25, and base deficit > 8. Patients had caffeine-halothane muscle contracture testing to determine MHS. RESULTS: Seventy patients (50 boys and 20 girls) were evaluated. Eighty-three percent (58 of 70) of anesthetics were halothane-succinylcholine. In 68% (48 of 70) of cases, the anesthetic was discontinued, whereas anesthesia was continued with nontriggering agents in 11% (8 of 70) and with triggering agents in 13% (9 of 70). Fifty-nine percent (41 of 70) of patients were diagnosed as MHS by muscle biopsy. In 7% (5 of 70) of patients, clinical MH developed within 10 min of MMR. CONCLUSIONS: This study, by using the current North American Malignant Hyperthermia Group protocol, reaffirms the high incidence (59%, 41 of 70) of MHS associated with MMR as confirmed by muscle biopsy. Of the MHS patients, 5 developed signs of clinical MH. Most anesthesiologists in this study, when confronted with MMR, discontinued anesthesia. Because of the potential lethality of MH and the > 50% concordance between MMR and MHS, the most conservative course of action after MMR is to discontinue the anesthetic and observe the patient for clinical evidence of MH. An acceptable alternative, depending on the urgency of the surgery, would be to continue anesthesia with nontriggering agents for MH, with appropriate monitoring.

Adolescent↗
PubMed1999

L-701,324, a selective antagonist at the glycine site of the NMDA receptor, counteracts haloperidol-induced muscle rigidity in rats.

RATIONALE: It has recently been suggested that the overactivity of glutamatergic neurotransmission may contribute to the pathophysiology of Parkinson's disease. Therefore, a search for new compounds which block glutamatergic receptors and show antiparkinsonian properties in animal models of this disease seems to be justified. OBJECTIVE: The aim of this study was to determine whether L-701,324 [7-chloro-4-hydroxy-3(3-phenoxy) phenylquinoline-2-(H)-one], a selective and full antagonist at the glycine site of the NMDA receptor, counteracts parkinsonian-like muscle rigidity and catalepsy induced by haloperidol in rats. METHODS: The muscle tone was measured as the resistance developed to passive flexion and extension of the hind limb. Electromyographic (EMG) activity was additionally recorded in the gastrocnemius and tibialis anterior muscles. RESULTS: L-701,324 (2.5-40 mg/kg IP) dose-dependently decreased the muscle tone enhanced by haloperidol (1-5 mg/kg IP). Likewise, the haloperidol-enhanced resting EMG activity and the EMG reflex response to passive movements were diminished by lower and almost abolished by higher doses of L-701,324. However, up to a dose of 20 mg/kg IP, L-701,324 did not influence haloperidol (0.5 mg/kg IP)-induced catalepsy. Moreover, L-701,324 (1.25-5 mg/kg IP) given alone or together with haloperidol (0.5-1 mg/kg IP) disturbed rotarod performance. Gross observation of behaviour indicated that rats injected with L-701,324 in doses equal to or higher than 5 mg/kg, alone or in combination with haloperidol, were markedly ataxic, i.e. rats showed signs of disturbed balance and loss of control over their hind limbs. CONCLUSIONS: The present study suggests that L-701,324 exhibits a beneficial action in the animal model of parkinsonian rigidity, but not that of parkinsonian akinesia. Nonetheless, this compound is not devoid of motor side-effects.

Animals↗
PubMedDate not supplied

Muscle rigidity induced by the opioid analgesic tramadol, but not by the non-opioid flupirtine.

The influence of high doses of two analgesic drugs, tramadol and flupirtine on the electromyographic activity in the gastrocnemius soleus muscles was examined. Tramadol (100-200 mg/kg po) dose-dependently induced a tonic electromyographic activity, which is generally accepted as a model of the opiate-induced muscle rigidity. That effect was antagonized by intraperitoneal injection of naloxone (0.8 mg/kg ip). On the other hand, flupirtine even in the high doses (100-200 mg/kg po) did not induce any tonic electromyographic activity. The obtained results confirm an opiate-like action of tramadol, but not that of flupirtine, on the muscle tension.

Administration, Oral↗
PubMed2000

Three cases with different presentation of fentanyl-induced muscle rigidity--a rare problem in intensive care of neonates.

We report about two newborns with sudden onset of inability of mechanical ventilation due to transient chest wall rigidity after fentanyl i.v. bolus of 2 and 4 microg/kg, respectively, resulting in severe hypoxemia and secondary bradycardia. A third case developed a rigidity of the tongue after fentanyl bolus, which created some unusual difficulties in bypassing the tongue for insertion an endotracheal tube. Because of common usage of this agent for analgesia we direct attention to the possibility of fentanyl-induced muscle rigidity. We underline the necessity of a slow bolus injection to prevent this dangerous adverse effect and we recommend the administration of naloxone and/or muscle relaxants as therapy in conjunction with mechanical ventilation.

Analgesics, Opioid↗
PubMed1990

Malignant hyperthermia susceptibility in adult patients with masseter muscle rigidity.

We sought to determine the incidence of malignant hyperthermia (MH) susceptibility in adult patients with a previous episode of masseter muscle rigidity (MMR). The medical records and in vitro contracture test results of all patients over 15 years of age tested for MH because of previous MMR from 1985 to 1988 were reviewed. The number of children (age less than 16 yr) tested for MH because of previous MMR was also determined for the same four-year period, for comparison of coincidence rates. Six of 24 adult patients (25 per cent) were proved MH-susceptible by in vitro contracture testing. No clinical sign associated with the episode of MMR was predictive of MH-susceptibility. Two of six MH-susceptible patients developed acute MH following MMR. In the same four-year period, 75 children were tested for MH-susceptibility because of previous MMR; 44 (59 per cent) had a positive in vitro contracture test. We conclude that the coincidence of MMR and MH-susceptibility is lower in adults than children. Episodes of acute MH do occur after MMR, but the onset of MH may be delayed. Conservative management of MMR in adult patients is recommended.

Adult↗
PubMedDate not supplied

[Effect of polysynaptic flexion reflex on monosynaptic reflexes of calf muscles prior to and following intramuscular injection of ethylbenzatropine in drug-induced muscle rigidity].

In patients with drug-induced parkinsonism and in healthy subjects the effect of stimulation of low-threshold skin fibres of sural nerve producing the polysynaptic flexion reflex of the short head of the biceps femoris muscle on the monosynaptic H reflex of calf muscles was studied before and after administration of ethylbenzatropine. In healthy subjects stimulation of low-threshold skin nerve was followed by facilitation of H reflex in the time of 70 to 200 msec. from the conditioning stimulation to the test stimulation. After one single intramuscular dose of ethylbenzatropine this late facilitating effect disappeared. In patients with drug-induced parkinsonism stimulation of afferent fibres of flexion reflex failed to cause late facilitation of H reflex and one dose of ethylbenzatropine brought no changes. During systematic administration of the drug an evident tendency for facilitation of H reflex was observed, similarly as in healthy subjects. The results obtained in healthy subjects and in patients with drug-induced parkinsonism are explained as evidence of inhibitory action of noradrenaline in certain chains of spinal interneurons, since noradrenaline release in the spinal cord is determined by the striatal equilibrium between the cholinergic and dopaminergic systems. The corrective action of ethylbenzatropine would depend on its central action on certain spinal chains of interneurons determining transmission of impulses from dermal afferent nerves to alpha motoneurons.

H-Reflex↗