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At least 541 records · Page 30Linked to original sources
PubMed1988

A new syndrome of axial muscle rigidity associated with etretinate therapy.

We report on three cases of a novel syndrome associated with treatment for psoriasis with the retinoid etretinate. The distinctive features of this syndrome include rigidity that is restricted to the axial muscles, impairment of neck extension greater than flexion, impairment of anteflexion at the waist, severe impairment of lateral flexion at both the waist and the neck, and, in one case, rigidity of proximal lower extremity muscles. Peripheral nerve block extinguished the lower extremity rigidity in one patient, and two patients had a favorable response to Sinemet. One patient had persistence of symptoms and findings 2 years after discontinuation of etretinate. The clinical features of this syndrome are consistent with an effect of etretinate on central, possible catecholaminergic neurons.

Adult↗
PubMed1989

Stability of the head in pitch (neck flexion-extension): studies in normal subjects and patients with axial rigidity.

The dynamic stability of the head in pitch during normal upright posture has been studied in normal subjects and patients with neurological disease affecting neck muscle tone by examining angular head acceleration responses to unpredictable linear motion of the trunk in the direction of surge. Within the frequency range of natural head movements the transfer function between head and trunk for both normal subjects and patients approximated a second-order linear differential equation involving inertia and coefficients of viscosity and elasticity. The degree of neck rigidity was determined by the damping ratio (viscosity:elasticity), which averaged .35 for normal subjects and ranged from 0.6 to 0.96 for patients with rigid syndromes. A patient with absent labyrinthine function and a "floppy" head had a damping ratio 0.18. The technique gives a numerical measurement of neck rigidity, which could be of value in characterising severity of disorder and response to therapy.

Adult↗
PubMed1997

Botulinum toxin A improves muscle spasms and rigidity in stiff-person syndrome.

We studied the effect of botulinum toxin A (BTA) on painful muscular spasms and rigidity in two bedridden patients with clinical, electrophysiologic, and immunologic evidence of stiff-person syndrome. We injected BTA or saline solution into several limb muscles with both the rater and patient blinded to the order of the injections. A physician, unaware of the treatment order, used an objective rating scale for rigidity and spasm frequency scale and independently assessed the treatment results. BTA administration significantly reduced rigidity and stopped the spasms in all limbs. Following BTA injection on one side, the spasm frequency decreased bilaterally possibly because of the spread of hematogenous toxin.

Botulinum Toxins, Type A↗
PubMed1985

Assessment of motor neuron excitability in parkinsonian rigidity by the F wave.

F-wave responses from abductor pollicis brevis muscle occurred more frequently, with a larger amplitude and longer duration in rigid parkinsonian patients than in age-matched normal controls. F-wave potentiation during voluntary contraction was impaired in parkinsonian patients. These findings suggest that spinal motor neuron excitability is enhanced in rigidity. F-wave amplitude was significantly correlated to the clinical evaluation of motor disability, so that the F wave may be regarded as a useful approach to quantitative evaluation of rigidity.

Aged↗
PubMed1986

The spectrum of the so-called rigid spine syndrome: nosological considerations and report of three female cases.

Three female cases of the "rigid spine" syndrome are reported and associated with different nosological entities. One patient was affected by congenital muscular dystrophy and one by a morphological pattern of fibre type disproportion with type I atrophy. The third patient showed very peculiar morphological changes on a muscle biopsy specimen resembling a vacuolar myopathy, which is rarely described in association with the rigid spine syndrome. The importance of an adequate investigation of the rigid spine syndrome and the recognition of the presence or absence of cardiomyopathy, if there is to be correct genetic counselling, is discussed.

Adolescent↗
PubMed1980

Opioid receptors in the caudate nucleus can mediate EMG-recorded rigidity in rats.

Systemic administrations of opioids are known to induce "catatonia" or "lead pipe rigidity" in rats. The relevance of the caudate nucleus in inducing rigidity was tested. For this purpose, several opioids (or saline) were injected into the head of the caudate nucleus ("intrastriatal" injection) through an implanted cannula, and the electromyographical activity (EMG) was recorded in the gastrocnemius-soleus muscle (GS). Morphine (7.5-3.0 microgram), injected unilaterally, induced a continuous EMG activity in the ipsilateral GS muscle. This effect could be antagonized by systemic administration of naloxone (1 or 2 mg/kg i.p.). D-ala2-met5-enkephalinamide (3 microgram) and levorphanol (22.5 microgram) induced an EMG activity, too, whereas an equimolar dose of dextrorphan was ineffective, indicating that this effect was stereospecific and mediated via opioid receptors in the caudate nucleus. The EMG activity observed after systemic morphine administration (15 mg/kg i.p.) was antagonized by intrastriatal injection of naloxone (5 microgram). From our results, it can be concluded that the striatum--at least the head of the caudate nucleus--plays an important role in mediating the rigidity observed after systemic administration of morphine and other opioids.

Animals↗
PubMed1984

Role of muscarinic cholinergic mechanisms in the substantia nigra pars reticulata in mediating muscular rigidity in rats.

Bethanechol chloride (5-25 micrograms), when injected into the substantia nigra pars reticulata (SNR) of rats, produced muscular rigidity in a dose-dependent way, and in addition, catalepsy and ipsilateral posture. The effects of bethanechol in the dose of 25 micrograms were prevented by co-administration of 10 micrograms scopolamine hydrochloride. Injections of 25 micrograms bethanechol or 10 micrograms scopolamine into the reticulata only slightly affected the muscular rigidity produced by 15 mg/kg i.p. morphine hydrochloride. The results suggest that muscarinic cholinergic mechanisms in the substantia nigra pars reticulata, although effective by themselves, affect by expression of at least one striatal functional alteration, the muscular rigidity, in a less effective way than GABAergic or endogenous opioid mechanisms do.

Animals↗
PubMed1995

Does reserpine induce parkinsonian rigidity?

The aim of the study was to find out whether the reserpine-induced rigidity is similar to that seen in parkinsonism. Simultaneous measurements of the muscle resistance of the hind foot to passive bending and stretching in the ankle joint, as well as of the electromyographic (EMG) activity of the gastrocnemius and tibialis anterior muscles of rats were carried out. Reserpine was injected in a dose of 10 mg/kg alone or with alpha-methyl-p-tyrosine (250 mg/kg) 1, 4 and 27.5 h before the measurements. Reserpine increased the muscle resistance of the rat's hind leg to passive movements. That effect was the strongest at 1-2 h after the injections, and diminished markedly afterwards. The rigidity was accompanied with an increase in the resting, as well as in the stretch-induced short- and long-latency EMG activity in the gastrocnemius muscle. However, the intensity of the latter symptom did not change for a long period of time, which seems to correlate with the striatal dopamine depletion. The results suggest that the reserpine-increased EMG activity is a good model of parkinsonian rigidity.

Adrenergic Uptake Inhibitors↗
PubMed2002

Local application of L- threo-hydroxyaspartate and malonate in rats in vivo induces rigidity and damages neurons of the substantia nigra, pars compacta.

In order to study neuronal death in Parkinson's disease, neurons of the substantia nigra, pars compacta in rats were exposed to elevated levels of glutamate and decreased levels of energy in vivo and consequences for behavior and neuronal morphology were studied. Thus, repeated local injections (9x) of the glutamate uptake inhibitor L- threo-hydroxyaspartate (L-THA; 833 microM in 0.3 microl) in the presence or absence of the succinate dehydrogenase inhibitor malonate (25 mM in 0.3 microl) were applied during three weeks. 24 h after injection, rigidity and catalepsy were measured, as well as, at the end of the three week period, locomotion, rearing and exploratory behavior. Thereafter, the cytoarchitecture of the substantia nigra, pars compacta of the brains of these rats was described. The L-THA plus malonate injected rats did not differ in their behavior from carrier injected rats, except for rigidity: their scores were higher than that of carrier and L-THA injected rats (P < 0.05), while L-THA injected rats did not differ from carrier injected controls. Observations on cresyl violet sections revealed, that, although many neurons with a shrunken nucleolus and faintly stained cytoplasm were present in both L-THA and L-THA plus malonate treated rats, the ventral edge of the substantia nigra, pars compacta containing modified cells was longer in L-THA plus malonate than in L-THA injected rats (P < 0.05). This indicates, that a minimum amount of damage to neurons in the ventral part of the substantia nigra, pars compacta might be required for the expression of rigidity.

Animals↗
PubMed1985

Muscular rigidity and delineation of a dopamine-specific neostriatal subregion: tonic EMG activity in rats.

In order to investigate the role of neostriatal dopamine receptors in muscular rigidity we have studied catalepsy and spontaneous muscle tone in rats receiving haloperidol injections into various parts of the neostriatum. It was found that low doses of haloperidol (250-750 ng/0.5 microliter) induced a tonic activity in the EMG of the gastrocnemius-soleus muscle when injected into the most rostral part of the neostriatum (A 8620-9650). This tonic EMG activity was found to be both dose-dependent and dopamine-specific: the haloperidol effect of 500 ng could be inhibited by 500 ng apomorphine. No muscular rigidity could be observed when haloperidol (500 ng/0.5 microliter) was injected further caudally into the neostriatum or into the medial part of the nucleus accumbens. With regard to the haloperidol-induced catalepsy as measured by means of the bar test, a similar distribution of effective and ineffective injection sites was observed; however, higher doses of haloperidol (1.5-2.5 micrograms/0.5 microliter) were required. Thus catalepsy and muscular rigidity were found to be closely related phenomena within the neostriatum. Finally, it is discussed how information relevant to tonic EMG activity is transmitted from the substantia nigra pars compacta to the superior colliculus and the ventromedial thalamus via the neostriatum and the substrate nigra pars reticulata.

Animals↗
PubMed1984

The role of the colliculus superior in the expression of muscular rigidity.

Muscular rigidity, recorded as tonic activity in the electromyogram of the gastrocnemius-soleus muscle in the rat was produced by bilateral injections of muscimol (37.5-75 ng) into the intermediate or deep layers of the colliculus superior. This effect of muscimol was not only dose-dependent but also gamma-aminobutyric acid (GABA)-specific since it could be prevented by coadministration of the GABA antagonist bicuculline methiodide. Injections of muscimol into either the superficial layers of the colliculus superior or the underlying reticular formation were without effect in this respect. These results indicate that the region containing the terminals of the nigrocollicular pathway is involved in the expression of muscular rigidity (recorded as a tonic EMG activity). Muscimol injections into the colliculus superior did not lead to catalepsy thus providing additional evidence for the notion that muscular rigidity and catalepsy are two separate phenomena which are in part mediated by different neuronal pathways.

Animals↗
PubMed1983

Motility, rigidity and turnover of dopamine in the striatum after administration of morphine to rats: a re-evaluation of their mechanisms.

Whether the delayed behavioural activation and the increase in dopamine (DA) turnover in the striatum reflect signs of rebound effects or of counter-regulatory processes directed against locomotor depression and/or muscular rigidity was studied in rats. Administration of a large dose of morphine (30 mg/kg i.p.) induced strong muscular rigidity, which was measured as tonic activity in the electromyogram (EMG). This effect was maximal after one hour and disappeared during the fourth hour. The locomotor activity, on the other hand, disappeared after 30 min and re-appeared during the fourth hour, followed by a locomotor stimulation with a maximum after 4.5 hr. Striatal lesions produced with kainic acid did not affect the complete locomotor depression (akinesia), except by slightly prolonging this effect, and did not influence the delayed locomotor stimulation. These lesions did not inhibit, but, on the contrary, enhanced the increase in striatal concentration of 3,4-dihydroxyphenylacetic acid (DOPAC). Injections of morphine (10 micrograms) into the substantia nigra led to an increase in the level of DOPAC in the ipsilateral, but not the contralateral striatum. These results, in conjunction with those of other authors, suggest that the increase in DA turnover in the striatum and the delayed locomotor stimulation ought to be regarded as actions of morphine on sites different from those mediating muscular rigidity.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

Pharmacological characteristics of tremor, rigidity and hypokinesia induced by reserpine in rat.

The experiments characterized the dose- and time-dependence of parkinsonian motor signs induced by reserpine in rats and a standardized system of manipulation of animals, evaluation of symptoms and analysis of data was devised. The assay procedure yielded no more than 0.5, 4.5 and 0.0% false positives with the evaluation of tremor, rigidity and hypokinesia, respectively. A dose-dependent and often complete blockade of all three signs was obtained with L-DOPA plus carbidopa (10:1) as well as with other classes of pharmacological agents that are used in the treatment of Parkinson's disease, i.e. direct or indirect dopamine (DA) agonists (amantadine, pergolide, lisuride) and inhibitors of monoamine oxidase (MAO) (clorgyline, pargyline, deprenyl, tranylcypromine). The inhibitor of the uptake of DA, nomifensine, and anticholinergics, 5-hydroxytryptamine (5-HT) antagonists, histamine antagonists and tricyclic antidepressants exerted little or no effect. The effects of putative agonists and antagonists at alpha 1- and alpha 2-adrenoceptors were also examined. Yohimbine blocked tremor and rigidity, but not hypokinesia, at 0.66 and 0.28 mg/kg, respectively. It is suggested that alpha-adrenergic mechanisms and, in particular, alpha 2-adrenoceptors, may be involved in reserpine-induced tremor and rigidity. Noradrenergic and dopaminergic systems can conceivably interact to progressively generate these different motor signs.

Animals↗
PubMed1989

Differential effects of prazosin and yohimbine on fentanyl-induced muscular rigidity in rats.

Whereas muscular rigidity is a well-known phenomenon that is related to anesthesia induced by large doses of narcotic drugs, the precise underlying mechanism(s) remain to be fully elucidated. This study investigated the possible role of noradrenergic neurotransmission and the participation of alpha-adrenoceptors in this phenomenon. Male Sprague-Dawley rats, under ketamine-induced anesthesia (120 mg/kg, i.p.) and with proper control of respiration, body temperature and end-tidal CO2 were used. Intravenous administration of fentanyl (100 micrograms/kg) consistently caused a significant increase in the electromyographic (EMG) activity, recorded from both gastrocnemius and abdominal rectus muscles. This implied muscular rigidity was markedly antagonized by pretreatment with the specific alpha 1-adrenoceptor blocker, prazosin (50 or 250 micrograms/kg, i.v.). This antagonism occurred in spite of a high level of fentanyl in the plasma, as determined by radioimmunoassay. The specific alpha 2-adrenoceptor blocker, yohimbine (1.15 or 2.3 mg/kg, i.v.), on the other hand, not only failed to prevent fentanyl-induced activation of the EMG, but actually potentiated the response. It is concluded that noradrenergic neurotransmission, possibly originating from the locus coeruleus, may participate in the elicitation of muscular rigidity by fentanyl. Furthermore, this process may involve an excitatory action through alpha 1-, and an inhibitory action through alpha 2-adrenoceptors, in the spinal cord.

Animals↗
PubMed1983

Aortic occlusion by a balloon catheter: a method to induce hind limb rigidity in rats.

Post-ischaemic spinal extensor or flexor rigidity can be induced in different species by clamping or ligature of the descending aorta after thoracotomy or laparotomy. A similar motor deficit can also be induced by an intraluminal aortic occlusion produced by inflation of a balloon attached to the tip of a catheter inserted via the femoral artery. This method is easy to perform and avoids all the possible complications of thoracotomy or laparotomy. In rats the occlusion time for obtaining the maximum percentage of animals exhibiting a permanent hind limb extensor (62.5%) or flexor (12.5%) rigidity was 15-16 minutes. A marked depression of hind limb sensory perception accompanied this rigidity but there were no urinary, bowel or skin disturbances. The unilateral femoral ligation following the catheterization did not induce a difference in muscle tone between both hind limbs. The present procedure which is simpler than other published procedures might thus serve as a useful animal model for spastic paraplegia.

Animals↗
PubMed1980

Seven cases of Huntington's disease in childhood and levodopa induced improvement in the hypokinetic--rigid form.

Seven cases of the infantile form of Huntington's disease--six boys and one girl--were observed in the space of six years. Six children showed the hypokinetic-rigid form of the disease. Results of clinical, speech evaluations, laboratory tests, EEG and LPEG corresponded with data in literature. Initial signs and symptoms were mild sensorimotor and behavioural disturbances. In five patients, all affected by the hypokinetic-rigid form, CSF HVA and 5HIAA were determined. CSF HVA levels were found to be significantly lowered in three patients. One child showed significant decrease of CSF 5HIAA. Levodopa, orally administrated to these five patients during 8 days to 6 weeks in dosages of 75 to 600 mg per day, induced in all a marked improvement of the hypokinesia and/or rigidity, speech and social behaviour. Two children developed slight choreatic movements and one child had to be withdrawn from the drug because of decrease of appetite.

Adolescent↗
PubMed1989

Involvement of locus coeruleus and noradrenergic neurotransmission in fentanyl-induced muscular rigidity in the rat.

Whereas muscular rigidity is a well-known side effect that is associated with high-dose fentanyl anesthesia, a paucity of information exists with regard to its underlying mechanism(s). We investigated in this study the possible engagement of locus coeruleus of the pons in this phenomenon, using male Sprague-Dawley rats anesthetized with ketamine. Under proper control of respiration, body temperature and end-tidal CO2, intravenous administration of fentanyl (50 or 100 micrograms/kg) consistently promoted an increase in electromyographic activity recorded from the gastrocnemius and abdominal rectus muscles. Such an induced muscular rigidity by the narcotic agent was significantly antagonized or even reduced by prior electrolytic lesions of the locus coeruleus or pretreatment with the alpha-adrenoceptor blocker, prazosin. Microinjection of fentanyl (2.5 micrograms/50 nl) directly into this pontine nucleus, on the other hand, elicited discernible electromyographic excitation. It is speculated that the induction of muscular rigidity by fentanyl may involve the coerulospinal noradrenergic fibers to the spinal motoneurons.

Adrenergic Fibers↗
PubMed1995

Involvement of potassium and calcium channels at the locus coeruleus in fentanyl-induced muscular rigidity in the rat.

Previous work from our laboratory suggested that Go alpha protein at the locus coeruleus (LC) may be involved in the signal transduction process that underlies muscular rigidity induced by fentanyl. The present study further evaluated the roles of K+ and L-type Ca2+ channels, gating of which is known to be associated with activation of Go alpha protein, in this process, using Sprague-Dawley rats anesthetized with ketamine. Bilateral microinjection into the LC of tetraethylammonium chloride (100 or 200 pmol), a K+ channel blocker, and S(-)-Bay K 8644 (0.5 nmol), a Ca2+ channel activator, produced significant antagonization of the EMG activation elicited by fentanyl (100 micrograms/kg, i.v.), as recorded from the sacrococcygeus dorsalis lateralis muscle. On the other hand, local application to the bilateral LC of diazoxide (10 or 20 nmol), an ATP-dependent K+ channel activator, and nifedipine (0.25 or 0.5 pmol), a L-type Ca2+ channel blocker, was ineffective in blunting fentanyl-induced muscular rigidity. These results suggest that activation of K+ channels and/or inhibition of L-type Ca2+ channels secondary to triggering of the Go alpha protein at the LC may underlie the signal transduction process in the mediation of fentanyl-induced muscular rigidity.

Animals↗