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PubMed2001

(S)-4C3HPG, a mixed group I mGlu receptor antagonist and a group II agonist, administered intrastriatally, counteracts parkinsonian-like muscle rigidity in rats.

The aim of the present study was to determine whether S-4-carboxy-3-hydroxyphenylglycine (S)-4C3HPG, a mixed group I glutamate metabotropic receptor antagonist and a group II agonist, attenuated parkinsonian-like muscle rigidity in rats. Muscle tone was examined using a combined mechano and electromyographic method, which measured simultaneously the muscle resistance (MMG) of the rat's hind foot to passive extension and flexion in the ankle joint and the electromyographic activity (EMG) of the antagonistic muscles of that joint: gastrocnemius and tibialis anterior. Muscle rigidity was induced by pretreatment with haloperidol (1 mg/kg i.p.). (S)-4C3HPG injected in doses of 5 and 15 microg/0.5 microl bilaterally, into the rostral region of the striatum, decreased both the haloperidol-induced muscle rigidity (MMG) and the enhanced electromyographic activity (EMG). The present results suggest that blockade of mGluR1 receptors and/or activation of mGluR2 ones, localized in the rostral part of the striatum, may be responsible for the anti-parkinsonian effect of (S)-4C3HPG.

Animals↗
PubMed1996

Neuroleptic malignant syndrome: two cases without muscle rigidity.

OBJECTIVE: Two patients with neuroleptic malignant syndrome without muscle rigidity are described. CLINICAL PICTURE: Both patients developed fever and altered consciousness while taking neuroleptic but did not develop muscle rigidity; the symptoms subsided when the neuroleptic was stopped but recurred when it was given again. TREATMENT: The neuroleptic was stopped; one patient received supportive treatment and the other received bromocriptine. OUTCOME: One patient died while the other survived. CONCLUSION: The pathophysiology is proposed as a combination of involvement of the central thermoregulatory, neuroregulatory and autonomic nervous systems, and the peripheral skeletal muscle. It supports the concept of a spectrum of clinical severity of neuroleptic malignant syndrome.

Adult↗
PubMed1995

Masseter muscle rigidity associated with glycine1306-to-alanine mutation in the adult muscle sodium channel alpha-subunit gene.

BACKGROUND: Succinylcholine-induced masseter muscle rigidity (MMR) is a potentially life-threatening complication of anesthesia and is closely correlated with the heterogeneous disorder malignant hyperthermia (MH) susceptibility. MMR also is identified with a variety of neuromuscular disorders, including the myotonias, that are associated with abnormal in vitro contracture test (IVCT) results. Recently, mutations in the adult skeletal muscle sodium channel alpha-subunit gene (SCN4A) have been shown to cause generalized nondystrophic myotonias, some of which are associated with mild nonspecific symptoms. The purpose of the current investigation was to begin to evaluate the molecular genetic relationship between known mutations in the SCN4A gene, MMR, and the results of the IVCT used to diagnose MH-susceptibility. METHODS: A single extended pedigree of 16 individuals was ascertained through a proband who experienced MMR and whole-body rigidity after succinylcholine administration. Subsequently, four individuals were shown to have a mild form of myotonia on clinical and laboratory examination. IVCT was carried out according to standardized protocols. Mutations in the SCN4A gene were sought in exons 22 and 24 using single-strand conformational analyses. Variability in the SCN4A gene sequence was confirmed by direct DNA sequence analyses. RESULTS: Four individuals with myotonia were shown to carry a guanine-to-cytosine mutation at nucleotide position 3917 of the reported SCN4A sequence. This DNA mutation was coinherited with MMR and an abnormal IVCT result in this family. Previous studies have demonstrated that the glycine1306-to-alanine substitution is associated with a mild clinical syndrome referred to as myotonia fluctuans. CONCLUSIONS: The current report provides direct evidence that succinylcholine-induced MMR, whole-body rigidity, and an abnormal IVCT result are associated with a mutation in the SCN4A gene.

Alanine↗
PubMed1998

Muscle rigidity induced by fluphenazine in rats is antagonized by L-DOPA, an antiparkinsonian drug.

The aim of the present study was to find out whether the classic neuroleptic fluphenazine is a good model compound for inducing parkinsonian-like muscle rigidity in rats. The muscle tone was measured as resistance developed by the rat's hind foot to passive flexion and extension. Fluphenazine in doses of 0.4-3.0 mg/kg i.p. induced a dose-dependent increase in the hind foot resistance to passive movements. The muscle rigidity induced by fluphenazine 1.5 mg/kg i.p.) was counteracted in a dose-dependent manner by the main antiparkinsonian drug L-DOPA (25-75 mg/kg i.p.). The present results suggest that the fluphenazine-induced muscle rigidity may be a useful model of parkinsonian rigidity.

Animals↗
PubMed1987

Ketanserin pretreatment reverses alfentanil-induced muscle rigidity.

Systemic pretreatment with ketanserin, a relatively specific type-2 serotonin receptor antagonist, significantly attenuated the muscle rigidity produced in rats by the potent short-acting opiate agonist alfentanil. Following placement of subcutaneous electrodes in each animal's left gastrocnemius muscle, rigidity was assessed by analyzing root-mean-square electromyographic activity. Intraperitoneal ketanserin administration at doses of 0.63 and 2.5 mg/kg prevented the alfentanil-induced increase in electromyographic activity compared with animals pretreated with saline. Chlordiazepoxide at doses up to 10 mg/kg failed to significantly influence the rigidity produced by alfentanil. Despite the absence of rigidity, animals that received ketanserin (greater than 0.31 mg/kg i.p.) followed by alfentanil were motionless, flaccid, and less responsive to external stimuli than were animals receiving alfentanil alone. Rats that received ketanserin and alfentanil exhibited less rearing and exploratory behavior at the end of the 60-min recording period than did animals that received ketanserin alone. These results, in combination with previous work, suggest that muscle rigidity, a clinically relevant side-effect of parenteral narcotic administration, may be partly mediated via serotonergic pathways. Pretreatment with type-2 serotonin antagonists may be clinically useful in attenuating opiate-induced rigidity, although further studies will be necessary to assess the interaction of possibly enhanced CNS, cardiovascular, and respiratory depression.

Adjuvants, Anesthesia↗
PubMed1997

Masseter muscle rigidity and nondepolarizing neuromuscular blocking agents.

Masseter muscle rigidity has been identified as a possible risk factor for malignant hyperthermia (MH) and is usually noted in children receiving intravenously administered succinylcholine chloride after mask induction with halothane. Nondepolarizing muscle relaxants are considered safe for persons susceptible to MH. In this article, we present a case of clinically recognized jaw rigidity in the absence of succinylcholine after administration of a non-depolarizing muscle relaxant that was reported to the Malignant Hyperthermia Association of the United States hot line. The patient had recurrent jaw rigidity during subsequent anesthesia when a different non-depolarizing muscle relaxant was given. The North American MH Registry was then reviewed for similar cases. Three cases of masseter muscle rigidity in the presence of nondepolarizing muscle relaxants were discovered. Two of the patients were not found to be susceptible to MH; however, the third patient had positive findings on muscle biopsy. These cases do not provide enough information to confirm the ability of nondepolarizing muscle relaxants to cause jaw rigidity in the absence of MH.

Adult↗
PubMed2006

The effects of olanzapine and fluphenazine on plasma cortisol, prolactin and muscle rigidity in schizophrenic patients: a double blind study.

Pharmacotherapy of schizophrenia is associated with the stressful side effects. Muscle rigidity causes distress, discomfort and poor compliance. The aim of the study was to determine the relationship between plasma hormones (cortisol and prolactin/PRL) and muscle rigidity in female schizophrenic patients treated with olanzapine or fluphenazine. In a randomized, double-blind 22-weeks study, 12 patients were treated with olanzapine (5-20 mg/day) and 10 patients received fluphenazine (6-21 mg/day). Treatment with olanzapine moderately decreased, while treatment with fluphenazine significantly increased plasma cortisol levels and muscle rigidity. The marked and moderate increase in plasma PRL levels were found in patients treated with fluphenazine and olanzapine, respectively. The results suggested that olanzapine induced moderate neuroendocrine effects and a reduction in rigidity as compared to fluphenazine treatment.

Adult↗
PubMed1989

Dexmedetomidine, acting through central alpha-2 adrenoceptors, prevents opiate-induced muscle rigidity in the rat.

The highly-selective alpha-2 adrenergic agonist dexmedetomidine (D-MED) is capable of inducing muscle flaccidity and anesthesia in rats and dogs. Intense generalized muscle rigidity is an undesirable side effect of potent opiate agonists. Although the neurochemistry of opiate-induced rigidity has yet to be fully elucidated, recent work suggests a role for a central adrenergic mechanism. In the present study, the authors determined if treatment with D-MED prevents the muscle rigidity caused by high-dose alfentanil anesthesia in the rat. Animals (n = 42) were treated intraperitoneally with one of the following six regimens: 1) L-MED (the inactive L-isomer of medetomidine), 30 micrograms/kg; 2) D-MED, 10 micrograms/kg; 3) D-MED, 30 micrograms/kg; 4) D-MED [30 micrograms/kg] and the central-acting alpha-2 antagonist, idazoxan [10 mg/kg]; 5) D-MED [30 micrograms/kg] and the peripheral-acting alpha-2 antagonist DG-5128 [10 mg/kg], or; 6) saline. Baseline electromyographic activity was recorded from the gastrocnemius muscle before and after drug treatment. Each rat was then injected with alfentanil (ALF, 0.5 mg/kg sc). ALF injection resulted in a marked increase in hindlimb EMG activity in the L-MED treatment group which was indistinguishable from that seen in animals treated with saline. In contrast, D-MED prevented alfentanil-induced muscle rigidity in a dose-dependent fashion. The small EMG values obtained in the high-dose D-MED group were comparable with those recorded in earlier studies from control animals not given any opiate. The high-dose D-MED animals were flaccid, akinetic, and lacked a startle response during the entire experimental period.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1987

The neostriatal inhibition of catalepsy, but not of muscle rigidity, evoked from the substantia nigra pars reticulata.

The effects of a bilateral blockade of neo- and palleostriatal GABAergic mechanisms on catalepsy and muscle rigidity resulting from picrotoxin injection into the substantia nigra pars reticulata (SNR) were studied. The catalepsy and rigidity were induced by a unilateral injection of 100 ng/0.5 microliter of picrotoxin. Bilateral injections of 250 ng/l microliter of picrotoxin into the intermediate-ventral parts of the caudato-putamen (CP) abolished the catalepsy but had no effect on the muscle rigidity induced by an intranigral injection of the drug. Bilateral injections of 250 ng/l microliter of picrotoxin into the globus pallidus (GP) did not influence the catalepsy and rigidity induced by the intranigral injection of the drug. The results indicate that the impulses, connected with the catalepsy evoked from the SNR seem to be transmitted back to the CP and blocked therein by inhibition of GABAergic synapses in its intermediate-ventral part. The impulses, connected with the muscle rigidity evoked from the SNR, presumably do not return to the striatum.

Animals↗
PubMed1994

The incidence of masseter muscle rigidity after succinylcholine in infants and children.

To determine whether the incidence of masseter muscle rigidity is affected by the anaesthetic induction sequence, we prospectively studied for ten months the anaesthetic course in 5,641 infants and children who received muscle relaxation to facilitate tracheal intubation. The anaesthetic induction sequence consisted of intravenous sodium thiopentone (STP) 5 mg.kg-1 alone, halothane induction alone 1-4%, or halothane followed by STP. Inhalational inductions with halothane included nitrous oxide and oxygen. Tracheal intubation was facilitated by either intravenous succinylcholine (Sch) at least 1.5 mg.kg-1 or by a non-depolarizing muscle relaxant. The induction sequence and all episodes of MMR were recorded. Ninety percent of the patients received Sch and 10% received a non-depolarising agent. Of those who received Sch, 88% (5,064 patients) were anaesthetised with STP and 12% (607 patients) were anaesthetised with halothane alone or halothane followed by STP. Masseter muscle rigidity was defined clinically by the transient inability to distract the mandible from the maxilla such that the mouth could not be opened or could only be opened with force. No children anaesthetised with STP followed by Sch developed MMR. One child (0.9%) developed MMR after halothane and Sch and two developed MMR after halothane, STP and Sch (0.4%). The incidence of MMR after Sch was less with STP than with halothane alone or with halothane and STP (P < 0.025). The peak CPK values in the three children who developed MMR were 17,580 IU.L-1 after halothane and Sch, and 7,280 IU.-1 and 3,273 IU.-1 after halothane, STP and Sch. There was no evidence of MH reactions in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed2000

The role of metabotropic glutamate receptor (mGluR) ligands in parkinsonian muscle rigidity.

It has been shown that the primary striatal dopaminergic hypofunction which is at the origin of Parkinson's disease, results in a secondary hyperactivity of glutamatergic neurotransmission. In the search for a therapy of Parkinson's disease, ionotropic, mainly NMDA, receptor antagonists were found to have moderately beneficial, yet also some undesirable side-effects. Therefore the present study was aimed at determining whether some metabotropic glutamate receptor (mGluR) ligands may have antiparkinsonian effects in the haloperidol-induced muscle rigidity. To this end three mGluR ligands were used: the potent and selective mGluR I antagonist (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA), the mixed group II agonist/ group I antagonist (S)-4-carboxy-3-hydroxyphenyl-glycine ((S)-4-C3HPG), and the potent group II agonist (+)-2-aminobicyclo[3.1.0.]hexane-2,6,-dicarboxylic acid (LY354740). Only LY354740 penetrated the brain from the periphery; for this reason other drugs were injected bilaterally into the rostral striatum or nucleus accumbens. The muscle tone was recorded by a mechanomyographic/electromyographic (MMG/EMG) method which measured the resistance of a rat's hind foot and the EMG reflex response of its muscles to passive movements. (S)-4C3HPG (5 and 15 microg/0.5 microl) and LY354740 (5 and 10mg/kg i.p.) diminished the muscle rigidity induced by haloperidol (1 mg/kg i.p.). AIDA (0.5-15 microg/0.5 microl) injected into the striatum was only slightly effective in the highest dose used. However, when injected into the nucleus accumbens AIDA (15microg/0.5microl) significantly and strongly counteracted the haloperidol-induced muscle rigidity. Our results suggest that stimulation of group II striatal mGluRs seems to play a major role in diminution of parkinsonian-like muscle rigidity. However, it seems that the antagonism of group I mGluRs located in the nucleus accumbens may also be of importance to the antiparkinsonian effect.

Animals↗
PubMed2003

Contribution of the serotonin 5-HT1A receptor agonism of 8-OH-DPAT and EMD 128130 to the regulation of haloperidol-induced muscle rigidity in rats.

The aim of the present study was to find out whether (+/-)-8-hydroxy-2(di-n-propylamino)tetralin (8-OH-DPAT), a prototypical 5-HT1A agonist, and (R)-(-)-2-[5-(4-fluorophenyl)-3-pyridylmethylaminomethyl]-chromane HCl (EMD 128130), a compound with serotonin 5-HT1A-agonist and dopamine D2-like antagonist properties, are able to attenuate the haloperidol-induced (1 mg/kg) muscle rigidity in rats. Muscle tone was examined using a combined mechano- and electromyographic (EMG) method that simultaneously measured the mechanical muscle resistance (MMG) of the rat's hind foot to passive movements in the ankle joint, and the EMG activity of two antagonist muscles. Both 8-OH-DPAT (0.125-0.5 mg/kg i.p.) and EMD 128130 (1-10 mg/kg i.p.) dose-dependently decreased the haloperidol-enhanced MMG to passive movements, as well as the tonic and the long-latency reflex EMG activities. Provided these results can be extrapolated to humans, the efficacy of EMD 128130 in relieving the haloperidol-induced muscle rigidity supports the concept that novel antipsychotics with 5-HT1A agonist and dopamine D2 antagonist activities should have a favourable extrapyramidal side-effect profile.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1989

Fentanyl-induced muscle rigidity in unanesthetized and ketamine- or thiopental-anesthetized rats.

This study was undertaken to search for an alternative experimental model in the evaluation of fentanyl-induced muscle rigidity. Unanesthetized, spontaneously ventilating Sprague-Dawley rats, and rats anesthetized with either ketamine or thiopental whose ventilation was mechanically controlled, were studied. Intravenous administration of fentanyl (25, 50, or 100 micrograms/kg) caused an increase in electromyographic (EMG) activity in both unanesthetized and ketamine-anesthetized, but not in thiopental-anesthetized, animals. Muscle rigidity was more prominently manifested in the gastrocnemius muscle, when compared with the rectus abdominis muscle. Hypoxemia was exhibited during the course of rigidity by both spontaneously ventilating and ketamine-anesthetized rats, but not by thiopental-anesthetized animals. In addition, unanesthetized, spontaneously ventilating rats developed hypercarbia and respiratory acidosis. The authors suggest that, in addition to using unanesthetized animals, EMG activity in the gastrocnemius muscle of rats anesthetized with ketamine in whom ventilation is controlled may provide an alternative approach in the evaluation of fentanyl-induced muscle rigidity.

Anesthesia↗
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↗
PubMed1988

Reversal of prolonged postoperative muscle rigidity by dantrolene: a case report.

The use of dantrolene to reverse severe unexplained postanaesthetic muscle rigidity in a previously "healthy" 13-year-old male is described. Anaesthesia was induced with thiopentone. After intubation with pancuronium, the patient had an entirely uneventful nitrous oxide, oxygen and halothane anaesthetic. Immediately following reversal of the relaxant, the patient developed generalized muscle tightness and rigidity involving the trunk and extremities. This was prolonged and severe enough to interfere with adequate ventilation. The patient also had a prolonged recovery from the anaesthetic. After ruling out malignant hyperthermia and some other causes of rigidity, a tentative diagnosis of myotonia was made. The symptoms responded to IV dantrolene in a total dose of 2.0 mg.kg-1. Further testing failed to establish a definite diagnosis. Dantrolene could be a useful drug in treating such unexplained muscle rigidity.

Adolescent↗
PubMed2004

[Masseter muscle rigidity after suxamethonium during induction and postoperative abortive malignant hyperthermia in a patient with esophageal achalasia].

A 38-year-old man diagnosed as esophageal achalasia developed masseter muscle rigidity after intravenous suxamethonium during anesthetic induction. Anesthesia was maintained with intravenous agents and epidural blockade, while the masseter muscle rigidity continued. After the surgery, his body temperature increased to 38.8 degrees C concomitantly with the appearance of myoglobinuria suggesting the occurrence of abortive malignant hyperthermia. These symptoms were dissolved by dantrolene administration. He was later proved to be negative with CICR test.

Adult↗
PubMed2002

Atropine reduces raclopride-induced muscle rigidity by acting in the ventral region of the striatum.

Parkinson-like extrapyramidal motor side effects associated with the use of antipsychotic drugs, such as increased muscle rigidity, are thought to result from blockade of striatal dopamine D2 receptors. While anticholinergic medications (muscarinic receptor antagonists) ameliorate extrapyramidal side effects, the mechanisms underlying their effectiveness remain unclear. We investigated the site of action of atropine, a non-selective muscarinic receptor antagonist, in reducing increased muscle rigidity, assessed as increases in tonic electromyographic (EMG) activity, induced by the selective dopamine D2 receptor antagonist, raclopride. Atropine significantly reduced raclopride-induced EMG increases in rat hindlimb muscles, when injected into the ventral striatum, but not the dorsal striatum or the substantia nigra. Atropine's site of action was localised to a small area of muscarinic receptors within the ventral part of the striatum, using quantitative autoradiography. These findings provide new information about the regulation of motor control by muscarinic receptor antagonists and additional evidence about the functional heterogeneity of the striatum.

Animals↗