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PubMed1980

Severe muscular rigidity at birth: malignant hyperthermia syndrome?

A case of severe muscular rigidity in a premature male infant born by Caesarean Section under general anaesthesia is described. A probable diagnosis of malignant hyperthermia was supported by the clinical symptoms of muscular rigidity and cyanosis, a creatinine phosphokinase of 24,630 I.U. (Normal 0--100) and a urinary myoglobin of 248 mg/l (normal 6--35). The muscle tone and laboratory values slowly returned to normal over a period of days. Anaesthetic management for a ventriculoperitoneal shunt performed at seven weeks of age included pre and postoperative treatment with dantrolene. No crisis occurred at this time. The parents, who have normal CPK and a negative family history, were advised to treat the child as if he had malignant hyperthermia until such time as a definitive diagnosis can be made.

Anesthesia, General↗

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↗

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↗

PubMed1986

The role of striatal cholinergic mechanisms for the development of limb rigidity: an electromyographic study in rats.

The muscarinic cholinergic agonist bethanechol (0.25-1.0 micrograms) injected bilaterally into various parts of the rat neostriatum induced a tonic electromyogram (EMG) activity in the gastrocnemius muscle which is considered to be a measure of limb rigidity. This tonic EMG activity was found to be dose-dependent and muscarine-specific since it could be blocked by coadministration of the muscarinic antagonist N-methylscopolamine (1.0 micrograms). Tonic EMG activity of comparable amount was observed after injections of bethanechol (1.0 microgram) into all regions of the neostriatum but not into the globus pallidus, thalamus, zona incerta or cortex. The tonic EMG activity induced by intrastriatal injection of bethanechol (1.0 microgram) was abolished by a subsequent injection of the GABAmimetic drug muscimol (25 ng) into the posterior part of the substantia nigra pars reticulata suggesting that bethanechol-induced limb rigidity is mediated via impairment of GABAergic transmission within the substantia nigra pars reticulata.

Animals↗

PubMed1995

Parkinson's disease rigidity: EMG in a small hand muscle at "rest".

The presence of excessive EMG at "rest" might be an important factor in the genesis of Parkinson's disease (PD) rigidity, and we studied it in the first dorsal interosseous muscle (FDI) of 8 idiopathic PD patients. We had 8 age- and sex-matched normal controls. In the PD group, the average area of the surface EMG at "rest" correlated significantly with the clinical evaluation of rigidity and remained abnormally enhanced for 10-15 min after a command to "relax." Later, it tended to decline, but its entity was still much greater than in controls. The EMG "at rest" consisted of unwilled motor unit (MU) firing. A larger MU number was recruited in patients than in controls at "rest." MU rate coding was similar in both groups. Eventually, patients could get periods of EMG silence which, however, were interrupted by short EMG bursts, even if there was no muscle stretch. These bursts were interpreted as residual fragments of the original excessive EMG at "rest." MUs first recruited during such bursts showed high, but not total, overlapping with those first recruited by a gentle voluntary contraction or by a weak transcranial magnetic stimulus to motor cortex. We conclude that EMG activity at "rest" was made up of the discharge of low-threshold MUs, with a recruitment order similar to that resulting from descending cortico-spinal volleys. However, we cannot exclude other possible input sources to the alpha-motoneurones at "rest."

Aged↗

PubMed1976

Parkinsonian akinesia, rigidity and tremor in the monkey. Histopathological and neuropharmacological study.

Parkinsonian postural tremor and rigidity most likely involve the disruption of the dopaminergic (DA) nigrostriatal mechanisms and the corresponding rubro-olivo-cerebello-rubral loop without excluding the involvement of related dentato-rubral and dentato-thalamic nervous fascicles. The integrity of the magnocellular division of the red nucleus and of the rubrotegmentospinal pathway, however, is apparently essential for the expression of rigidity. Akinesia most likely results from the bilateral involvement of brain stem catecholaminergic (CA) mechanisms including the DA nigrostriatal pathways. Finally the integrity of the pallidothalamic fibers seems to represent an essential feature for the improvement of these motor disorders by DA agonists, suggesting that certain of these agents, such as apomorphine, exert their main effects through the neostriatal DA receptors.

Animals↗

PubMed1986

Separation of the tremorous and muscular rigidity components of the ethanol withdrawal syndrome in the rat.

The alcohol withdrawal syndrome consists of a kinetic tremor, the tremorous component, and a peculiar abnormality of tone called asterixis, the muscular rigidity component. The severity of the ethanol withdrawal syndrome in the rat is generally assessed by the severity of the tremors. 3-Hydroxybutyrate suppresses the tremorous component but not the muscular rigidity component of the ethanol withdrawal syndrome, thus effectively differentiating the two components in the rat.

3-Hydroxybutyric Acid↗

PubMed1982

A mechanographic method for measurement of muscle tone in the conscious rat. The calf muscle stretch response in reserpine-induced rigidity.

A simple mechanographic method for the measurement of muscle tone in awake rats is presented. It utilizes principles corresponding to those in clinical assessment of tone and it has been applied to an animal model of Parkinson's disease: the reserpine-treated rat. The rat was restrained by a plastic cylinder and by metal cuffs at the ankles. The hind feet were repeatedly dorsiflexed by an electromechanical manipulator and the resulting calf muscle tension was indirectly measured with a strain-gauge system. The relative contributions to the stretch response from the different muscle groups acting on the ankle joint in the awake and untreated rat and during reserpine-induced rigidity are described. Very little active tension was found in the untreated rat. After treatment with reserpine, continuous activation of the muscle was found in EMG recordings and there was a sharp increase in the tension recorded during stretch. The static response to the increased isometric stretch was augmented. An additional, tonic response to ramp stretch was elicited at all stretch velocities. There was no evidence for phasic responses to rapid stretch in reserpine-induced rigidity. The amplitude of the myomechanogram was thus found to be independent of the ramp stretch velocity. Subsequent injection of apomorphine abolished the increased stretch response. It is demonstrated that changes in muscle tone could be followed during drug treatment and that the method can be used in investigations of the pathophysiological mechanisms behind the disorders of muscle tone.

Animals↗

PubMed1988

Reconsideration of the concept of enhanced static fusimotor drive in rigidity in patients with Parkinson's disease.

The electromyographic responses elicited in the first dorsal interosseus muscle by small muscle stretches or by electrical stimulation of the median nerve were investigated in parkinsonian patients and in age-matched healthy subjects. Stimuli were applied during a steady level of contraction in the intrinsic hand muscle. This ensured comparable levels of excitability in the alpha-motoneurone pool in patients and normals. It was found that the normal short-latency stretch reflex was almost absent in rigid patients, while responses to electrical stimulation of low-threshold nerve fibres were of equal size in both groups. This result suggests that there is a change in fusimotor control of muscle spindles in Parkinson's rigidity without alteration of the central gain of the Ia-transmitted stretch reflex.

Electric Stimulation↗

PubMed1989

Involvement of the substantia innominata/ventral pallidum complex in transmitting forelimb muscular rigidity evoked from the nucleus accumbens in rats.

In the present study it was investigated whether muscular rigidity elicited from the nucleus accumbens could be transmitted via the substantia innominata/ventral pallidum (SI/VP) complex. For this purpose rats were equipped with cannulae aimed at the nucleus accumbens and/or the SI/VP, and with electrodes in the triceps muscle of the forelimb. In the first set of experiments it was found that the GABA agonist muscimol (10-25 ng/0.5 microliters) dose-dependently increased tonic EMG activity upon injection into the SI/VP region. The GABA antagonist bicuculline (50 ng/0.5 microliters) antagonized the effects of muscimol (25 ng/0.5 microliters). In the second set of experiments it appeared that the increase in tonic EMG activity induced by haloperidol (1000 ng/0.5 microliters) injected into the nucleus accumbens was antagonized by subsequent injection of bicuculline (25 ng/0.5 microliters) into the SI/VP complex. These data suggest that the SI/VP complex may be one station through which the muscular rigidity elicited from the nucleus accumbens is transmitted to lower brain structures.

Animals↗

PubMed1990

Involvement of coerulospinal noradrenergic pathway in fentanyl-induced muscular rigidity in rats.

Unilateral, site-specific microinjection of fentanyl (2.5 micrograms/50 nl) into the locus coeruleus (LC) in Sprague-Dawley rats anesthetized with ketamine evoked a significant increase in the electromyographic activity recorded from both caudal lateral extensor and gastrocnemius muscles. This correlate of opiate-induced muscular rigidity was appreciably antagonized by a pretreatment with the specific alpha 1-adrenoceptor blocker, prazosin (250 micrograms/kg, i.v.). On the other hand, an equimolar dose (0.65 mumol/kg) of the specific alpha 2-adrenoceptor blocker, yohimbine (0.23 mg/kg, i.v.) failed to prevent the occurrence of fentanyl-induced EMG activation. We suggest that the coerulospinal noradrenergic pathway may be directly involved in the elicitation of muscular rigidity by fentanyl, possibly via alpha 1-adrenoceptors in the spinal cord.

Adrenergic Fibers↗

PubMed1993

Antagonization of fentanyl-induced muscular rigidity by denervation of the coerulospinal noradrenergic pathway in the rat.

The present study examined the effect of denervating the coerulospinal noradrenergic pathway on the muscular rigidity elicited by fentanyl in Sprague-Dawley rats anesthetized with ketamine. We demonstrated that the dopamine-beta-hydroxylase-positive nerve terminals arborizing on spinal motoneurons that innervate the sacrococcygeus dorsi lateralis (SCDL) muscle were significantly eliminated by DSP4 treatment. Unilateral microinjection of fentanyl (2.5 micrograms/50 nl) into the locus coeruleus of these animals also failed to evoke discernible increase in the electromyographic activity recorded from the SCDL muscle. These results lend further support for our previous finding that the coerulospinal noradrenergic neurotransmission is critically involved in fentanyl-induced muscular rigidity.

Animals↗

PubMed1994

Involvement of G(o) alpha subtype of guanine nucleotide-binding regulatory protein at the locus coeruleus in fentanyl-induced muscular rigidity in the rat.

Previous work from our laboratory suggested that locus coeruleus (LC) and the coerulospinal noradrenergic pathway are intimately related to the elicitation of muscular rigidity by fentanyl. The present study attempted to identify the subtype of guanine nucleotide-binding regulatory protein that may participate in this process, using Sprague-Dawley rats anesthetized with ketamine and under mechanical ventilation. Immunofluorescent staining with a polyclonal antiserum directed against a 39-kDa protein that corresponds to the alpha subunit of G(o) revealed the presence of G(o) alpha immunoreactivity in neurons of the LC. Bilateral microinjection of the same G(o) alpha antiserum into the LC also significantly blunted the enhanced electromyographic activity recorded from the sacrococcygeus dorsalis lateralis muscle induced by intravenous administration of fentanyl (100 micrograms/kg). These results suggest that G(o) alpha protein at the LC may participate in the signal transduction process that underlies muscular rigidity induced by high-dose fentanyl.

Animals↗

PubMed1991

Hypokinesia, rigidity, and tremor induced by hypothalamic 6-OHDA lesions in the rat.

Bilateral administration of 6-hydroxydopamine in the medial fore-brain bundle at the level of the posterolateral hypothalamus in rats resulted in hypokinesia, muscular rigidity and tremor as determined by various behavioral assessment procedures. These neurological signs were accompanied by marked decreases in the concentrations of dopamine and its main metabolites dihydroxyphenylacetic acid and homovanillic acid in both striatum and nucleus accumbens. Administration of apomorphine (1 mg/kg) or L-Dopa (60 mg/kg) reversed or totally abolished the hypokinesia, rigidity and tremor in lesioned animals. Together, the present findings demonstrate that bilateral intrahypothalamic administration of 6-OHDA results in the appearance of the three cardinal symptoms of Parkinson's disease in rats. This model should prove to be valuable for both the study of the neuropathological processes underlying the neurological signs of this disease and the screening of potential antiparkinson agents.

3,4-Dihydroxyphenylacetic Acid↗

PubMed2004

Neonatal chest wall rigidity following the use of remifentanil for cesarean delivery in a patient with autoimmune hepatitis and thrombocytopenia.

Remifentanil is a useful adjunct in general anesthesia for high-risk obstetric patients. It provides effective blunting of the rapid hemodynamic changes that may be associated with airway manipulation and surgical stimulation. There have been no previous reports of opioid-related rigidity in the neonate delivered by a parturient receiving intraoperative remifentanil. We present a case of short-lived neonatal rigidity and respiratory depression following remifentanil administration during cesarean section to a parturient with autoimmune hepatitis complicated by cirrhosis, esophageal varices and thrombocytopenia.

Adult↗

PubMed1999

Identification of axial rigidity during locomotion in Parkinson disease.

OBJECTIVES: To identify coordination changes and stability in the movements of the trunk during locomotion in Parkinson disease (PD) as a function of walking velocity. STUDY DESIGN: Comparison of treadmill locomotion with an opto-electronic tracking device. PATIENTS: Newly diagnosed patients with PD (n = 27) and a group of healthy control subjects (n = 11). RESULTS: Coordination between transversal pelvic and thoracic rotations showed significantly smaller changes in mean relative phase (p < .0001) and lower variability in relative phase (p < .0001) in the PD group. No significant differences were found in stride duration and variability in stride duration. CONCLUSIONS: The relative phase data contradict traditional notions of increased variability in motor control in PD and pinpoint the importance of the trunk in identifying axial rigidity. This discrepancy may be due to lack of control for walking velocity in earlier studies. It is concluded that systematic manipulation of walking velocity can identify coordination deficits and rigidity in trunk movement. This coordination of trunk movement can also be a sensitive measure for (early) diagnosis and the assessment of movement and pharmacological therapy in PD.

Acceleration↗

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↗

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↗