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PubMed1984

Huntington's disease: survival of large striatal neurons in the rigid variant.

A morphometric method was employed to investigate the relationship of rigidity and hyperkinesia to the degree of striatal and nigral nerve cell loss in one patient with the rigid variant of Huntington's disease and four patients with hyperkinetic chorea. Both striatal neuron populations, small and medium-sized neurons and large neurons, were affected in the patients with hyperkinetic chorea, whereas the large neurons were preserved in the patient with the rigid variant. The substantia nigra was slightly involved in each patient. The findings suggest that the rigid variant of Huntington's disease may reflect the unbalanced activity of residual, mostly large, striatal neurons, inhibiting the substantia nigra.

Aged↗
PubMed2003

A computer model of rigidity and related motor dysfunction in Parkinson's disease.

This work explores the involvement of spinal circuits in the generation of parkinsonian rigidity and related motor dysfunction. A computer model of spinal proprioceptive input processing, derived from previous work on spasticity modeling, was adapted to the simulation of parkinsonian rigidity. Model parameters were varied to generate simulations reproducing experimental data obtained using the pendulum test of the leg in 10 parkinsonian patients and 3 healthy subjects. Convenient reproductions of experimental traces in rigidity were obtained by the combination of a low reflex gain and a decrease in reflex threshold. These findings are consistent with studies reporting an increase of spinal interneuron excitability and proprioception deficits in Parkinson's disease (PD). Moreover, as the threshold parameter was much lowered, our model generated typical features of parkinsonian resting tremor, endorsing the hypothesis of a participation of a spinal oscillator in this disorder. Finally, tuning the reflex gain during simulations of rigidity resulted in the generation of active movement, opening some hypotheses on pathophysiology of motor dysfunction in PD, and notably, of akinesia. More generally, this work accredits the hypothesis of the involvement of an aperiodic, altered supra-spinal motor drive in PD, resulting in spinal dysfunction, through specific descending motor pathways. This may lead to a search for new (spinal) pharmacological targets in PD. It emphasizes further the value of computer modeling in understanding motor control in health and disease.

Computer Simulation↗
PubMed2001

SCH 58261, an A(2A) adenosine receptor antagonist, counteracts parkinsonian-like muscle rigidity in rats.

The aim of the present study was to find out whether blockade of adenosine A(2A) receptors by a selective antagonist, SCH 58261, influenced parkinsonian-like muscle rigidity. Muscle tone was examined using a combined mechano- and electromyographic method which simultaneously measured muscle resistance (MMG) of a rat hindfoot to passive extension and flexion in the ankle joint and electromyographic activity (EMG) of the antagonistic muscles of that joint: gastrocnemius and tibialis anterior. Muscle rigidity produced by reserpine (5 mg/kg + alpha-methyl-p-tyrosine, 250 mg/kg) was antagonized by SCH 58261 (0.1-5 mg/kg). SCH 58261 (5 mg/kg) also reduced reserpine-enhanced tonic and reflex EMG activities in both the gastrocnemius and the tibialis muscles. Moreover, SCH 58261 in doses of 1 and 5 mg/kg abolished muscle resistance induced by haloperidol (0.5 mg/kg). However, only the highest dose of SCH 58261 (5 mg/kg) decreased tonic EMG activity enhanced by haloperidol. Administration of L-DOPA (75 and 100 mg/kg) dose-dependently decreased the muscle resistance as well as tonic EMG activity evoked by haloperidol. Combined administration of SCH 58261 (0.1 mg/kg) and L-DOPA (50 mg/kg) in doses which did not affect the haloperidol-induced muscle rigidity produced a pronounced synergistic effect. The ability of SCH 58261 to diminish the parkinsonian-like muscle rigidity and to potentiate the effect of L-DOPA in this model seems to indicate a therapeutic value of this compound in the treatment of Parkinson's disease.

Adrenergic Uptake Inhibitors↗
PubMed1980

Depression of reserpine-induced muscular rigidity in rats after administration of lisuride into the spinal subarachnoid space.

Muscular rigidity was induced by reserpine (10 mg/kg) in rats and the tonic activity of the gastrocnemius muscle was recorded in the electromyogram. Systemic administration of lisuride, an ergoline, resulted in a dose-dependent depression of rigidity. To examine the spinal cord as a site of action for lisuride to depress reserpine-induced rigidity, a method for the chronic catheterization of the lumbar spinal subarachnoid space was used, which allowed the administration of drugs to reserpinized, intact rats without anaesthesia. Lisuride injected into the lumbar spinal subarachnoid space resulted in a longlasting depression of rigidity. These results suggest that the spinal cord is an important site of action of lisuride.

Animals↗
PubMed1981

Further characterization of opioid receptors in the striatum mediating muscular rigidity in rats.

In previous studies, we had found that opioid receptors in the striatum can mediate muscular rigidity which can be recorded as a tonic EMG activity in the gastrocnemius-soleus muscle of rats. We have now tried to evaluate the type of opioid receptors mediating the EMG activity. For this purpose, opioids regarded to be selective agonists at one type of opioid receptors were injected into the striatum of unanesthesized rats. Morphine, a micro-type agonist, in the dose of 40 nmol induced a pronounced EMG activity, while 10 to 40 nmol of [D-Ala2, D-Leu5] enkephalin, a delta-type agonist, led to no or little effect, respectively. beta-Endorphin, which reacts with the epsilon -type of receptors, was completely ineffective in doses of 3 or 15 nmol. The benzomorphan compound Mr 2033-Cl, which is a kappa-type agonist, induced a moderate activity in the dose of 15 nmol; 3 nmol were ineffective. beta-Casomorphin-4 was the most potent of the drugs studied in our system, since 9 nmol induced a pronounced rigidity, which was naloxone-reversible (2 mg/kg i.p.). The doses of these opioids effective in comparison with their known in vitro potencies suggest that the rigidity is mediated by a group of striatal opioid receptors, which has some similarity to the micro-type, but also shows some differences. In contrast, haloperidol, injected either into the striatum (30 nmol) or systemically (2 mg/kg i.p.), did not induce any EMG activity, suggesting that a decrease in dopaminergic neurotransmission is not the primary mechanism inducing the rigidity. beta-LPH62-77 and beta-LPH66-77 (15 nmol) intrastritally] were also completely inactive.

Animals↗
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↗
PubMed2003

Fentanyl-induced rigidity during emergence from general anesthesia potentiated by venlafexine.

PURPOSE: To present and discuss a case of opioid-induced rigidity with low-dose fentanyl during recovery from anesthesia. CLINICAL FEATURES: A 41-yr-old woman underwent laparotomy for total abdominal hysterectomy and bilateral salpingo- oophorectomy under general anesthesia. She received a total of 500 micro g of fentanyl by iv intermittent boluses during the three-hour anesthetic. During emergence from anesthesia, while intubated, the patient presented with rigidity. No changes in ventilatory parameters were measured during the episode. The only notable predisposing factor was treatment with venlafexine, an antidepressant that modifies serotonin and norepinephrine levels. She was successfully treated with iv naloxone 20 micro g. The rest of the postoperative period was uneventful. CONCLUSION: We observed an atypical case of opioid-induced rigidity in contrast to the classical syndrome, which presents at induction with high-dose opioids. This syndrome has many clinical presentations with neurologic and ventilatory signs of varying intensity. Early recognition of the syndrome and adequate treatment is crucial. If treated adequately, opioid-induced rigidity is self-limited with few complications.

Adult↗
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↗
PubMed1975

The evaluation of anti-parkinson drugs on reserpine-induced rigidity in rats.

The effect of anti-parkinson drugs on reserpine-induced rigidity was examined using a technique which measured rigidity by hind limb palpation. Centrally acting dopaminergic and anti-cholinergic drugs were able to antagonize reserpine-induced rigidity, whereas peripherally acting drugs had no effect. Results are discussed in terms of possible modes of action. Relative potencies of the drugs studied in this model were well correlated with the dose ranges of clinically established anti-parkinson drugs. It is concluded that measurement of reserpine-induced rigidity by hind limb palpation is a rapid and sensitive technique to evaluate potential anti-parkinson drugs.

Amantadine↗
PubMed1986

GABA mechanisms of ventromedial thalamic nucleus in morphine-induced muscle rigidity.

The aim of the study was to investigate the role of the ventromedial thalamic nucleus in the rigidity induced by morphine. Muscle rigidity was assessed using an electromyographic method (EMG) in non-anaesthesized rats with electrodes implanted unilaterally in the gastrocnemius soleus muscle. Subcutaneous (s.c.) injections of morphine in doses of 5, 10 or 20 mg/kg evoked tonic EMG activity in the gastrocnemius soleus muscle; this was estimated as muscle rigidity. Picrotoxin was injected bilaterally into the ventromedial nucleus in doses of 50-400 ng/0.5 microliter 30 min after morphine administration. Picrotoxin in doses of 200 and 400 ng attenuated the tonic EMG activity induced by morphine, 10 mg/kg s.c. Picrotoxin in a dose of 400 ng reduced the tonic activity induced by morphine, 20 mg/kg s.c. The results suggest that the thalamic ventromedial nucleus mediates the morphine-induced rigidity.

Animals↗
PubMed1989

Depression of decerebrate rigidity in the rat by antagonists of excitatory amino acids.

Effects of intravenous antagonists of excitatory amino acids on decerebrate rigidity in the rat were examined. Kynurenate, ketamine, (4S, 5R)-4-(2-methylpropyl)-3-[3-(perhydroazepin-1-yl)propyl]-5-phenyl- 1,3- oxazolidin-2-one hydrochloride (MLV-6976), (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclo-hepten-5,10-imine maleate (MK-801), 3-((/-)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) and DL-2-amino-7-phosphonoheptanoic acid (APH) reduced the severity of decerebrate rigidity in a dose-dependent manner, although there was a large variability in the effective doses. The blood pressure, which was determined simultaneously, did not show a uniform change in the presence of these antagonists. The time course of the change of the blood pressure did not coincide with that of decerebrate rigidity. These results suggest a possibility that the glutamatergic system may function, at least in part, in the onset of the decerebrate rigidity.

Amino Acids↗
PubMed1988

Localization of brainstem sites which mediate alfentanil-induced muscle rigidity in the rat.

Previous work has demonstrated that direct injections of methylnaloxonium (MN), a relatively lipophobic quaternary opiate antagonist, in the area of the nucleus raphe pontis (RPn) significantly attenuated alfentanil-induced rigidity. It was hypothesized that other hindbrain sites, particularly the other raphe nuclei, might play a role in this rigidity. Therefore, a study was performed in which 57 rats, divided into four groups, were implanted with chronic guide cannulae directed at brain sites anterior, lateral, or posterior to the RPn. After each animal was pretreated with intracerebral injections of MN, alfentanil (0.5 mg/kg) was administered subcutaneously. Electromyographic activity was recorded from the gastrocnemius muscle as a measure of hindlimb rigidity. Each animal was subsequently injected at 4 to 5 day intervals with MN two additional times at sites 1 and 2 mm deeper, respectively, than the initial injection. Data were thus obtained on animals treated with either MN or saline at 3 successive histologically identified sites which were either anterior, lateral or posterior to the RPn. The administration of MN into two specific sites in the region just lateral to the nucleus raphe pontis significantly [F(1,38) = 18.68 and 5.02 respectively, p less than 0.05] reversed the rigidity produced by systemic alfentanil administration. There was a weak effect of MN injections anterior to the RPn but this could not be localized to any one site. These results suggest that discrete brainstem regions involved in opiate action can be sensitively and selectively identified by direct intracranial injections of a lipophobic opiate antagonist.(ABSTRACT TRUNCATED AT 250 WORDS)

Alfentanil↗
PubMed1989

Asymmetry of neuroleptic-induced rigidity: development of quantitative methods and clinical correlates.

Twenty-six medicated schizophrenic patients and 14 normal controls underwent laboratory assessment for the presence and asymmetry of neuroleptic-induced rigidity to evaluate the sensitivity, reliability, and validity of a quantitative procedure. Measures of muscle stiffness were made in the upper extremities. Results indicated that 65% of the patients exhibited pathological rigidity. Moreover, 76% of these patients exhibited asymmetric rigidity, while the remaining 24% exhibited bilateral symptoms. Newly treated patients exhibited a greater laterality of rigidity toward the right side compared with patients who were on stable treatment regimens for at least 3 months. Since parkinsonism reflects dopamine receptor blockade by neuroleptic medication, probably in the striatum, we suggest that the lowered susceptibility of the right striatum to drug-induced parkinsonism supports the hypothesis that striatal dopaminergic activity may be asymmetric and more marked in the right striatum among recently treated patients.

Adult↗
PubMed1994

Antagonization of fentanyl-induced muscular rigidity by neurotensin at the locus coeruleus of the rat.

We evaluated the interaction between neurotensin (NT) and mu-opioid receptors at the locus coeruleus (LC), using fentanyl-induced muscular rigidity as our experimental index. Adult, male Sprague-Dawley rats anesthetized with ketamine (120 mg/kg, i.p., with 24 mg/kg/h i.v. infusion supplements) were used. Intravenous injection of fentanyl (100 micrograms/kg) consistently promoted a significant increase in the electromyographic activity recorded from the sacrococcygeus dorsalis lateralis muscle. This implied muscular rigidity was appreciably and dose-dependently antagonized by prior intracerebroventricular (i.c.v.) application of NT (15, 30 or 60 nmol/5 microliter). Microinjection of the tridecapeptide (300 or 600 pmol/100 nl) into the bilateral LC produced similar results. This suppressive effect of NT on fentanyl-induced muscular rigidity was antagonized by simultaneously administered NT antiserum (1:80), or partially blocked by its antagonist, (D-Trp11)-NT (300 pmol), but not by normal rabbit serum (1:80). These results suggest that NT may interact with the mu-opioid receptors at the LC, resulting in the suppression of fentanyl-induced muscular rigidity in the rat.

Animals↗
PubMed2006

A comparison of the effects of imposed extension and flexion movements on Parkinsonian rigidity.

OBJECTIVE: To test a hypothesis that Parkinsonian rigidity is more pronounced in imposed extension than flexion movement. METHODS: Twelve Parkinsonian subjects (both "Off" and "On" medication states) and seven control subjects participated in the protocol, in which a servomotor imposed wrist flexion and extension. Rigidity was quantitatively evaluated by the rectified torque integral with time, i.e., temporal score, and by the torque integral with joint angle, i.e., work score, for extension and flexion, respectively. RESULTS: In the "Off" state, the imposed extension induced a significantly higher resistance than did flexion. Dopaminergic medication significantly reduced the temporal score associated with imposed extension, and significantly decreased the work score of both movements. Compared with controls, the scores were higher for patients in the "On" state. CONCLUSIONS: Rigidity is more readily elicited in extension movement. The distinction is not evident in clinical practice, whereas it can be clearly revealed with the application of biomechanical analyses. SIGNIFICANCE: This distinction may prove to be a standard feature of rigidity. The procedures may be helpful in diagnosis and useful in evaluating new treatments and developing rehabilitation programs.

Aged↗
PubMed2005

Succinylcholine-induced masseter muscle rigidity during bronchoscopic removal of a tracheal foreign body.

Masseter muscle rigidity during general anesthesia is considered an early warning sign of a possible episode of malignant hyperthermia. The decision whether to continue or discontinue the procedure depends on the urgency of the surgery and severity of masseter muscle rigidity. Here, we describe a case of severe masseter muscle rigidity (jaw of steel) after succinylcholine (Sch) administration during general anesthetic management for rigid bronchoscopic removal of a tracheal foreign body. Anesthesia was continued uneventfully with propofol infusion while all facilities were available to detect and treat malignant hyperthermia.

Anesthesia, General↗
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↗
PubMed1999

Efficacy of pramipexole, a new dopamine receptor agonist, to relieve the parkinsonian-like muscle rigidity in rats.

The aim of the present study was to assess the efficacy of pramipexole (2-amino-4,5,6, 7-tetrahydro-6-propyl-amino-benzthiazole-dihydrochloride), a new dopamine D(2)/D(3) receptor agonist, to attenuate parkinsonian-like muscle rigidity in rats. Muscle tone was examined using a combined mechano- and electromyographic (EMG) method, which simultaneously measured the muscle resistance of a rat's hindlimb to passive extension and flexion at the ankle joint, and the EMG acitivity of the antagonistic muscles of that joint: gastrocnemius and tibialis anterior. Muscle rigidity was produced by reserpine (5 mg/kg) injected in combination with alpha-methyl-p-tyrosine (250 mg/kg) or by haloperidol (0.5 mg/kg). Pramipexole in doses of 0.5-5 mg/kg antagonized both reserpine+alpha-methyl-p-tyrosine- and haloperidol-induced muscle rigidity. Pramipexole also reduced reserpine-enhanced tonic and reflex EMG activities in the gastrocnemius muscle. The present results suggest that stimulation of the postsynaptic dopamine receptor may be chiefly responsible for the antiparkinsonian action of pramipexole. The ability of pramipexole to diminish the parkinsonian-like muscle rigidity seems to indicate a therapeutic value of this compound in the treatment of Parkinson's disease.

Animals↗