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At least 19 recordsLinked to original sources
PubMedDate not supplied

The effects of thiopental sodium on fentanyl-induced muscle rigidity in a human model.

STUDY OBJECTIVE: To describe a safe human model in which to study the treatment of fentanyl-induced muscle rigidity and report on the efficacy of thiopental sodium for this purpose. DESIGN: Randomized, observer-blinded comparison of regimens. SETTING: Inpatient surgery at a university-affiliated teaching hospital. PATIENTS: Thirty patients scheduled for elective surgery in whom the administration of high-dose fentanyl was felt to be appropriate and who experienced severe muscle rigidity in the chest, abdomen, and upper extremities after the fentanyl was administered. INTERVENTIONS: One arm was isolated from circulation with a blood pressure (BP) cuff inflated to 100 mmHg above systolic blood pressure (SBP), after which fentanyl 25 to 50 micrograms/kg was administered intravenously (IV) at a rate of 1 mg/min in the contralateral arm. If severe muscle rigidity became apparent in three muscle groups (the chest, abdomen, and arms), patients were either (1) observed for 3.5 minutes without further intervention, (2) given thiopental sodium 1.5 mg/kg IV, followed 120 seconds later by succinylcholine 1 mg/kg IV, or (3) given succinylcholine 1 mg/kg IV, followed 120 seconds later by thiopental sodium 1.5 mg/kg IV. MEASUREMENTS AND MAIN RESULTS: A single observer, blinded to the technique, evaluated and recorded the degree of muscle rigidity present in the chest wall, abdomen, and upper extremities (one isolated from the circulation by a tourniquet) 90 seconds and 3.5 minutes after the onset of muscle rigidity in the control group and 90 seconds after the administration of either thiopental sodium or succinylcholine in the two experimental groups. The observer was the same individual in all instances. The muscle rigidity associated with the administration of high-dose fentanyl was clinically attenuated by the administration of thiopental sodium, especially in the extremities. Succinylcholine was more effective than thiopental sodium in producing muscle flaccidity in all muscle groups not isolated by a tourniquet. In no case did the muscle rigidity compromise our ability to oxygenate the patient adequately. CONCLUSIONS: Thiopental sodium does blunt the degree of muscle rigidity induced by high-dose fentanyl, though not as effectively as does succinylcholine. One can safely isolate an extremity prior to the administration of high-dose fentanyl and a muscle relaxant, intubate the trachea, and ventilate a patient, while retaining the ability to study the effect of centrally acting drugs on fentanyl-induced rigidity in the isolated extremity.

Fentanyl↗
PubMedDate not supplied

Fentanyl-induced muscle rigidity as affected by pretreatment with amantadine hydrochloride.

STUDY OBJECTIVE: To determine whether the degree of muscle rigidity in humans caused by the administration of high-dose fentanyl is affected by pretreatment with amantadine hydrochloride, a drug that stimulates the release of dopamine in the basal ganglia. DESIGN: Randomized, observer-blinded comparison of regimes. SETTING: Inpatient surgery at a university-affiliated teaching hospital. PATIENTS: Sixteen patients scheduled for elective surgery in whom the administration of high-dose fentanyl was felt to be appropriate. INTERVENTIONS: Eight patients in the control group were given diazepam 5 mg orally 1 hour prior to induction of anesthesia. Eight patients in an experimental group were given the same dose of diazepam and also were treated with amantadine 1 g orally in divided doses over a period of 25 hours prior to their scheduled surgery. At the time of surgery, all patients were given fentanyl 50 micrograms/kg intravenously at a rate of 1 mg/min and were clinically evaluated for the degree of muscle rigidity of the chest wall, abdomen, and extremities. MEASUREMENTS AND MAIN RESULTS: A single observer, blinded to the technique, evaluated and recorded the degree of muscle rigidity present in the chest wall, abdomen, and upper extremities immediately after administration of the fentanyl and 3 minutes later. The observer was the same individual in all instances. In no case did the muscle rigidity compromise our ability to adequately oxygenate the patient. CONCLUSIONS: Muscle rigidity associated with the administration of high-dose fentanyl is not attenuated by prior administration of amantadine in the dose range studied.

Abdominal Muscles↗
PubMed1992

Raised resting energy expenditure in Parkinson's disease and its relationship to muscle rigidity.

1. Resting energy expenditure was measured, by indirect calorimetry, in 12 patients with Parkinson's disease and in eight healthy age-matched control subjects. In the patients with Parkinson's disease measurements were made in both the untreated state and after an injection of the dopamine agonist apomorphine (treated state). In each state muscle rigidity was recorded. 2. Resting energy expenditure was higher in patients with Parkinson's disease in both the treated and untreated states than in the control subjects. Of the patients with Parkinson's disease, seven showed no difference in resting energy expenditure between the two treatment states, whereas four showed markedly increased resting energy expenditure in the untreated state. The change in resting energy expenditure in the untreated state, as compared with the treated state, was significantly related to the development of muscle rigidity in the untreated state. 3. In Parkinson's disease, even in optimally treated patients, resting energy expenditure is raised and this may contribute to the weight loss seen in this disease. Severe muscle rigidity occurring during untreated periods results in a further increase in resting energy expenditure.

Apomorphine↗
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↗
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↗
PubMedDate not supplied

[Syndrome of the superior oblique muscle rigidity: clinico-anatomical aspects and results of treatment of 8 patients].

Tenectomy of the superior oblique muscle resulted in complete disappearance of Brown's syndrome in 7 out of 8 children operated on. In view of this, it can be a method of choice in treatment of the syndrome. There was the first clinical case of an additional abnormal attachment of the superior oblique muscle tendon to the sclera. In another patient an abnormal marked vascularization of the tendon identified histologically had the appearance of a muscular structure at the site of the tendon seen at the operation.

Age Factors↗
PubMed1977

Prolonged muscle rigidity following administration of succinylcholine.

Succinylcholine should be avoided in any patient with known myotonia because of the possibility of an abnormal rigid response. In addition, the possibility of undiagnosed myotonia should be considered in any myopathic patient. While not all myotonic responses are associated with malignant hyperthermia, the anesthetic should be discontinued immediately and the patient should be closely observed for elevation of temperature.

Child↗
PubMed1992

[Effect of small doses of L-dopa on synergic tonic reaction in patients with childhood cerebral palsy].

As many as 8 patients aged 8-19 years suffering from infantile cerebral paralysis (ICP) with torsion dystonia, akinetic, rigid, spastic and hypotonically atactic syndromes were examined for the maximum amplitude of EMG activity of the musculus tibialis anterior in voluntary rear flexion of the foot and in Strümpell's tibial synkinesia before treatment and after intake of small doses of L-DOPA (nakom, 62 mg/day). It has been established that the amplitude of voluntary EMG activity and the rate of impulse transmission in efferents of the tibial nerve remained practically unchanged during treatment; in all the cases, the synergic EMG activity, discharges of EMG and prolonged activity decreased; the scope of active movements in the talocrural joint increased by 10-20 degrees. The greatest decrease of synergic EMG activity (by 40%) was recorded in patients with rigid muscle tone, the mean in patients with spastic and spastic -dystonic (by 25-33%), the least one (17%) in muscle hypotonia. It is assumed that voluntary and synergic automatic movements have varying neuromediator supply. The effect of L-DOPA is realized via changes in the function of suprasegmental brain structures regulating polysynaptic postural reflexes with primary action on extensors. The effects of the subcortical nuclei, stem and cerebellar systems are made possible by dopamine neuromediation to a different measure.

Adolescent↗
PubMed1991

Structure-activity studies of neurotensin on muscular rigidity and tremors induced by 6-hydroxydopamine lesions in the posterolateral hypothalamus of the rat.

It has previously been reported that intracerebroventricular administration of neurotensin (30 micrograms) reduced muscular rigidity and tremors, induced by a neurochemical lesion with 6-hydroxydopamine in the posterolateral hypothalamus of rats. In the present study, the effects of two fragments (NT1-10 and NT8-13) and two analogues ([D-Tyr11]-NT and [Ala11]-NT) of neurotensin on the grasping time (index of muscle rigidity) and tremors in 6-hydroxydopamine-lesioned rats are reported. Intracerebroventricular administration with 120 micrograms of NT1-10 and [Ala11]-NT had no effect on the muscle rigidity and tremors induced by the neurochemical lesion. The administration of NT8-13 60 micrograms) significantly attenuated both behavioural responses. The analogue [D-Tyr11]-NT produced a much greater attenuation of the muscle rigidity and tremors. The dose of 1.8 micrograms of [D-Tyr11]-NT significantly reduced the grasping time, while the number of tremors was attenuated with the threshold dose of 0.9 micrograms. Together, these results suggest that the effects of neurotensin on muscle rigidity and tremors, induced by pretreatment with 6-hydroxydopamine injected into the posterolateral hypothalamus, were not caused by non-specific effects but largely depended on the carboxy terminal of the peptide. The tyrosine residue in position 11 of the molecule plays a critical role in the action of neurotensin, as shown with the high potency and duration of action of the analogue [D-Tyr11]-NT. As previously suggested, the greater effect with [D-Tyr11]-NT may be due to greater resistance of the analogue to enzymatic degradation because of the incorporation of the D-Tyr amino acid, in position 11 of neurotensin.

Animals↗