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At least 1,153 records · Page 64Linked to original sources
PubMed1983

Differential effects of limbic versus striatal dopamine loss on motoric function.

Bilateral 6-hydroxydopamine injections into either the ventral tegmental area, or the substantia nigra pars compacta in rats, produced severe losses of dopamine in the nucleus accumbens-olfactory tubercle and striatum respectively. After 1 and 3 months postoperation, the depletion of limbic dopamine was associated with reduced spontaneous locomotor activity, which was enhanced by apomorphine (0.125 mg/kg), but not amphetamine (1.0 mg/kg). The severe loss of striatal dopamine had no persistent effect on spontaneous or D-amphetamine-induced locomotor activity, but did produce a persistent augmentation of rigidity. Although there was considerable recovery, both lesions chronically increased catalepsy scores. The results of this study suggested that limbic dopamine deficits may be important in initiation of movement; whereas, striatal dopamine deficits may contribute more to the rigidity aspects of Parkinsonism.

Animals↗
PubMed1986

Treatment of neuroleptic malignant syndrome with electroconvulsive therapy.

A case of neuroleptic malignant syndrome unresponsive to supportive medical therapy was successfully treated by electroconvulsive therapy. Electroconvulsive therapy may offer a safe and rapidly effective intervention in cases of neuroleptic malignant syndrome complicated by high fever and severe muscular rigidity which do not improve with supportive care.

Electroconvulsive Therapy↗
PubMed1989

Effect of L-dopa on dementia-related rigidity.

L-dopa 100 mg plus benserazide 25 mg versus placebo were given 3 times daily to 14 consecutive patients with dementia and rigidity. The treatment was crossed over to the alternative therapy after a 7-day period. Despite a mean 60% raise in CSF-HVA during L-dopa administration, no patient responded to the treatment. These data suggest that dementia-associated rigidity differs, at least, pharmacologically from parkinsonian rigidity.

Aged↗
PubMed2002

Worry and heart rate variables: autonomic rigidity under challenge.

[Borkovec, T. D. (1994). Worrying: perspectives on theory, assessment and treatment (pp. 5-34). West Sussex: Wiley] proposes that the cognitive activity of worry restricts autonomic nervous system activity, producing autonomic rigidity. Autonomic rigidity affects both sympathetic nervous system [Behav. Res. Ther. 28 (1990) 69.] and parasympathetic nervous system activity [Behav. Ther. 26 (1995)457.]. Three experiments investigated the relationship between worry and autonomic system activity as indexed by heart activity measures. In the first experiment, we measured average heart rate when worriers were required to perform a public speaking task. No difference was found in heart rate between worriers and controls. The second and third experiments measured average heart rate and heart period variability (HPV) in worriers and controls during relaxation, non-stressful cognitive tasks, worried thinking, and aversive imagery conditions. There was no support for the autonomic rigidity view as worriers did not respond differently to non-worriers. These findings challenge the view that autonomic rigidity applies generally to worry.

Adolescent↗
PubMed1992

Quantifying drug-induced changes in parkinsonian rigidity using an instrumental measure of activated stiffness.

We review the literature on quantifying parkinsonian rigidity and present data from 124 subjects to demonstrate the clinical utility of activated stiffness to model rigidity. This method eliminates many of the confounding variables associated with the subjective assessment of rigidity. This 5-min computer-assisted procedure was highly reliable and sensitive to pharmacologic influences that produce and reduce parkinsonian rigidity.

Adult↗
PubMed1983

Fentanyl-O2-N2O rigidity and pulmonary compliance.

Induction of anesthesia with fentanyl has been associated with such extreme rigidity as to cause failure of bag-and-mask ventilation. The etiology of this failure has not been investigated. Therefore, fentanyl-induced rigidity was studied in 5 control patients to establish the dose at which ventilation became impossible and in 5 patients with tracheostomies to investigate changes in pulmonary compliance. Anesthesia was induced with 3 micrograms/kg/min fentanyl to a total of 30 micrograms/kg. In control patients, failure to maintain bag-and-mask ventilation occurred at a mean fentanyl dose of 17 micrograms/kg. In patients with tracheostomies, compliance decreased 16% below baseline levels with fentanyl-100% O2 and an additional 22% with 60% N2O, returning to baseline levels after paralysis. It is concluded that the site of the cause of inability to maintain bag-and-mask ventilation after fentanyl lies above the trachea, specifically at the glottis. Glottic rigidity causes glottic closure and upper airway obstruction.

Adult↗
PubMed1983

The role of the substantia nigra in motility of the rat. Muscular rigidity, body asymmetry and catalepsy after injection of morphine into the nigra.

Unilateral injection of morphine (1.0, 2.5 or 5.0 micrograms/0.5 microliter) into the substantia nigra pars reticulata produced, in a dose-dependent way, tonic activity in the electromyogram (EMG) recorded from the ipsilateral gastrocnemius-soleus muscle of unanaesthetized rats. The effect produced by 5 micrograms of morphine was antagonized by co-administration of 5 micrograms of naloxone. Bilateral injection of morphine (5 micrograms each side) also produced a tonic activity in the EMG and catalepsy, but no asymmetry of posture. Unilateral injection of morphine (5 micrograms) into the substantia nigra pars compacta produced contralateral turning and/or stereotypy, but no tonic activity in the EMG. Naloxone (5 micrograms), when injected into the substantia nigra failed to produce any tonic activity in the EMG or any catalepsy. Larger doses of naloxone (10 or 20 micrograms) produced slight to moderate tonic activity in the EMG when injected into the pars reticulata. Injections of saline (0.5 microliter) into either the reticulata or compacta were ineffective. Bilateral lesions of the caudate nucleus with kainic acid (1 microgram each side) did not prevent the development either of the tonic activity in the EMG or of the catalepsy, which were both produced by unilateral injection of morphine (5 micrograms) into the pars reticulata. These results suggest that opioid mechanisms in the nigra might play a role in the regulation of posture and muscle tone and participate in the expression of motor functions controlled by the striatum (and probably also by the nucleus accumbens).

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↗
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↗
PubMed1993

Automated method for the measurement of fentanyl-induced muscular rigidity.

An automated method is described that can accurately and reliably measure weight displacement resulting from hindlimb extension due to muscular rigidity following opioid administration in rats. IV administration of fentanyl (0.035 mg/kg) immediately induced rigidity. Rigidity was dose dependently reversed by the alpha 2-agonist clonidine with an ED50 value equal to 0.011 mg/kg IV. Second, rigidity was restored following administration of the alpha 2-antagonist idazoxan (0.3 mg/kg, IV) thereby confirming an alpha 2-mediated mechanism of action. Previously, reversal of fentanyl-induced muscular rigidity was measured by subjective rating criteria not suitable for quantitative potency comparisons. The new automated rigidity model provides a simple yet precise measurement of the ability of alpha 2-agonists to attenuate opioid-induced muscular rigidity in rats.

Adrenergic alpha-2 Receptor Antagonists↗