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PubMed1985

Description and analysis of the myotonolytic effects of phenytoin in the decerebrate cat: implications for potential utility of phenytoin in spastic disorders.

Phenytoin (DPH) was evaluated for its capacity to reduce several motor manifestations of decerebrate rigidity in the cat. In doses of the order of 40 to 50 mg/kg i.v., DPH diminished the force necessary to collapse the hyperextended limbs; at about half this dose range, the drug reduced gamma-motoneuron discharges; at still lower doses the drug profoundly depressed mechanical and electromyographic responses evoked by stretch from both forelimb and hindlimb extensor muscles. Serum levels of DPH associated with substantial reduction in electrical and mechanical manifestations of the extensor hypertonus were of the same order conventionally encountered when the drug is administered to humans for acute seizure management. The data are supportive of a centrally and peripherally mediated muscle relaxing effect of the drug in states where muscle spindle involvement is a contributing factor, and may help to explain further the utility of DPH in the treatment of spasticity.

Animals↗
PubMed1981

Decerebrate rigidity produced in cats by focal stereotactic radiofrequency lesions.

A method of producing decerebrate rigidity in cats by means of a radio frequency current was developed. Adequate control of the extent an shape of the lesions necessitated a preliminary investigation of the relationship between the intensity and duration of current, the size of the lesion, and the tissue impedance before and after destruction; this was performed on guinea pigs. The mesencephalic reticulum in cats was identified by depth microelectrode recording and electrical stimulation. Unilateral, midline, and combined stereotactic radiofrequency lesions were made. The anatomical location, the pathological characteristics, and the physiological significance of the lesions with regard to the production of decerebrate rigidity and of the other clinical reactions of the animals are discussed.

Animals↗
PubMed1991

Abnormal MRI signal in the rigid form of Huntington's disease.

Eighteen patients with Huntington's disease (HD) were examined with MRI. Eleven had the common hyperkinetic form, seven had the rigid variant. All seven patients with rigid HD had increased signal intensity in the neostriatum in intermediate and T2-weighted images. Only one hyperkinetic HD had similar findings. In all the other cases, signal abnormalities were questionable or absent. Histological differences that account for differences in signal intensity may therefore lie in the caudate nucleus and putamen. Age of onset may be important, since the rigid patients were younger. Follow up studies may help in understanding these signal differences.

Adolescent↗
PubMed1993

Neuroleptic malignant syndrome and clozapine.

Clozapine is an atypical neuroleptic drug that was initially thought not to cause neuroleptic malignant syndrome (NMS). We report a case of NMS associated with clozapine as a single agent that developed in a patient with no prior history of NMS. In contrast to other reported cases of NMS with clozapine monotherapy in which rigidity was reported to be absent, our patient had classic NMS with lead-pipe rigidity. NMS should be included in the differential diagnosis of a febrile patient with a history of any neuroleptic treatment, including clozapine.

Adult↗
PubMedDate not supplied

Pathophysiology of muscle tone.

Pathophysiology of muscle tone is discussed on the basis of recent knowledge about motor system organization. Decerebrate rigidity, "pyramidal" spasticity and extrapyramidal rigidity served as models of muscle tone alterations in lateral and ventral motor system lesions.

Brain↗
PubMed2002

Discrimination of morphine- and haloperidol-induced muscular rigidity and akinesia/catalepsy in simple tests in rats.

The present study was conducted to establish a simple method for measuring muscular rigidity in rats, which could be used for screening and is able to discriminate between rigidity and akinesia/catalepsy. Therefore, we treated rats with morphine (30 mg/kg i.p.), since large doses of morphine lead to muscular rigidity and akinesia. We measured muscular rigidity with a new method by determining the resistance of the hindlimb to passive flexion in the 'balance test' and also checked haloperidol (3 mg/kg i.p.) treated rats for muscular rigidity. Furthermore, catalepsy was also tested after administration of each of these drugs. Then, the influence of D(1)-like and D(2)-like dopamine receptor stimulation on muscular rigidity and catalepsy was studied. Therefore, the partial D(1) agonist SKF 38393 (3 and 8 mg/kg s.c.), the D(2)/D(1) agonist pergolide (0.25 and 0.5 mg/kg i.p.) and the dopamine precursor L-DOPA (50 and 100 mg/kg i.p.) were administered up to 30 min before muscular rigidity was measured in morphine-treated rats. The results showed that morphine, but not haloperidol led to muscular rigidity, whereas both drugs led to positive scores in the catalepsy test. The dopaminergic drugs partly antagonized the morphine-induced muscular rigidity in the doses applied, but not the catalepsy. Apparently, rigidity, akinesia/catalepsy produced by morphine can be discriminated from that produced by haloperidol in simple and quick tests.

Analgesics, Opioid↗
PubMed2003

Clinical manifestations of Parkinson's disease and parkinsonism.

The most common disorder in a patient presenting to a movement disorder clinic will be parkinsonism. The challenge is to provide the patient with the most accurate diagnosis and prognosis possible. The assumption at the time of initial presentation of the clinical diagnosis of Parkinson's disease is often wrong (20-25%). Waiting to see the pattern of progression, and response to medication provides invaluable additional information. This manuscript summarizes the clinical manifestations of Parkinson's disease and the main akinetic-rigid syndromes (progressive supranuclear palsy, multiple system atrophy, cortical-basal ganglionic degeneration, and dementia with Lewy bodies) that make up the differential diagnosis.

Basal Ganglia Diseases↗
PubMed1997

Posteroventral pallidotomy in movement disorders.

Since 1992 there has been renewed interest in pallidotomy now that the limitations and adverse effects of long-term dopaminergic therapy have become more apparent and more difficult to control in patients with advanced Parkinson's disease. The authors describe the effect of pallidotomy in 19 patients, sixteen of whom had advanced Parkinson's disease with painful dystonia and/or response fluctuations with severe akinesia while in "off" and dyskinesias while in "on". One patient had cortico-basal degeneration with rigidity, one patient had secondary dystonia and one had dystonic posturing due to Wilson's disease. Fifteen patients underwent unilateral pallidotomy, four patients had a staged bilateral procedure. Follow-up ranged from 3 to 42 months (mean 18 months). All patients with peak-dose dyskinesias and/or dystonia had marked reduction of symptoms, including the cases of Wilson's disease and secondary dystonia. The akinesia and rigidity scores of Parkinson-patients in "off" were greatly reduced, mainly but not only on the contralateral side. Evaluation by the patients showed remarkable improvement of symptoms in 79%, leading to substantially improved functional abilities in 68%. In this series the decrease in dopamine-response fluctuations, dystonia, hypokinesia and rigidity with functional improvement as judged by examiners and patients reflect a significant regain of independence.

Adolescent↗
PubMed1984

Behavioral effects of morphine, levorphanol, dextrorphan and naloxone in the frog Rana pipiens.

Systemic morphine induces explosive motor behavior and generalized muscular rigidity in frogs. Naloxone does not reverse either of these effects of morphine but at high doses causes muscular flaccidity and unresponsiveness to stimulation. Intraspinal morphine induces rigidity, but not explosive motor behavior, and this action is blocked by naloxone. Behavioral effects are seen rarely after intraspinal levorphanol (rigidity) and never after intraspinal dextrorphan or naloxone. In contrast to systemic morphine and naloxone, systemic levorphanol and dextrorphan are lethal to frogs at high doses.

Animals↗
PubMed1993

Significance of parkinsonian manifestations in essential tremor.

Parkinsonian features, notably resting tremor may be seen in some essential tremor patients but the significance of those is unknown. The reported risk of parkinsonism in essential tremor patients varies from being unchanged to 35 times higher than expected. We studied 9 patients with essential tremor who had autopsies. In 6 of the 9 (66%) resting tremor was noted and in 3 (33%) cases fully developed parkinsonism was noted. The parkinsonism was consequent to neuroleptic usage in 2 and to basal ganglia status lacunaris and cribrosus in one case but no consistent abnormalities were noted in 3 essential tremor only and 3 essential tremor plus resting tremor cases. We conclude that resting tremor is an age-related natural evolution in some essential tremor patients. We recommend that the additional diagnosis of parkinsonism in the essential tremor be made only when resting tremor, bradykinesia and rigidity are all evident. The risk of ideopathic Parkinson's disease in essential tremor cases is similar to the general population.

Aged↗
PubMed1980

Parental factors associated with rigidity in Huntington's disease.

The discriminatory power of ten factors has been explored in relation to the presence or absence of muscular rigidity in patients with Huntington's disease. The sex and neurological sign of an affected parent were the only two significant determinants of rigidity or choreoathetosis in offspring. It was shown, using the Mantel-Haenszel method of adjusting for confounding variables that the risk of a patient displaying rigidity (and thereby having a graver prognosis) is five times as great for those with rigid parents as it is for those with non-rigid parents. Additionally, the risk of a patient displaying rigidity is more than three times as great for those with affected fathers as it is for those with affected mothers. Some implications of these findings are discussed.

Age Factors↗
PubMed2001

Symptomatic characteristics of parkinsonism and the width of substantia nigra pars compacta on MRI according to ischemic changes in the putamen and cerebral white matter: implications for the diagnosis of vascular parkinsonism.

To investigate the significance of vascular lesions as a cause of secondary parkinsonism, we analyzed the symptomatic characteristics, the width of the substantia nigra pars compacta (SNpc) on MRI and the responsiveness to L-dopa in 227 parkinsonian cases, excluding those with drug-induced parkinsonism and neurodegenerative diseases other than idiopathic Parkinson's disease (IPD). They were classified into those without a significant infarct in the basal ganglia (n = 144), those with status lacunaris in the putamen (SLP; n = 66) and those with confluent white matter hyperintensity signals (CWMH; n = 17). The 4- to 6-Hz tremor and cogwheel rigidity were significantly more frequent in cases without significant infarct (69%) than those with SLP (50%) and those with CWMH (12%; p < 0.05). Among cases with 4- to 6-Hz tremor and cogwheel rigidity, the frequency of patients with a reduced SNpc width and L-dopa responders did not significantly differ between those with SLP (73 and 83%, respectively) and those without significant infarct (83 and 86%, respectively), suggesting that the diagnosis for most of these cases would be probable IPD. In contrast, among cases without 4- to 6-Hz tremor and cogwheel rigidity, those with a reduced SNpc width or L-dopa responders were significantly less frequent among cases with SLP (25 and 38%, respectively) than among those without significant infarct (75 and 71%, respectively; p < 0.05). Patients with neither 4- to 6-Hz tremor and cogwheel rigidity nor reduction in the SNpc width, for whom the probable diagnosis was vascular parkinsonism (VP), were significantly more frequent in cases with SLP (26%) and with CWMH (40%) than those without significant infarct (8%), accounting for 10.6% of the total parkinsonian cases. These findings suggest that parkinsonian cases with SLP or CWMH consist of not only cases with vascular-lesion-related VP but also IPD in which vascular lesions are not directly related to parkinsonism. Absence of 4- to 6-Hz tremor, cogwheel rigidity and the reduction in the SNpc width could be indicators for differentiating VP from IPD.

Aged↗
PubMed1986

On the mechanisms of the development of tolerance to the muscular rigidity produced by morphine in rats.

The development of tolerance to the muscular rigidity produced by morphine was studied in rats. Saline-pretreated controls given a test dose of morphine (20 mg/kg i.p.) showed a pronounced rigidity recorded as tonic activity in the electromyogram. Rats treated for 11 days with morphine and withdrawn for 36-40 h showed differences in the development of tolerance: about half of the animals showed a rigidity after the test dose of morphine that was not significantly less than in the controls and were akinetic (A group). The other rats showed a strong decrease in the rigidity and the occurrence of stereotyped (S) licking and/or gnawing in presence of akinetic or hyperkinetic (K) behaviour (AS/KS group), suggesting signs of dopaminergic activation. The rigidity was considerably decreased in both groups after 20 days' treatment. In a further series of experiments, haloperidol (0.2 mg/kg i.p.) was used in order to block the dopaminergic activation and to estimate the real degree of the tolerance to the rigidity without any dopaminergic interference. Haloperidol enhanced the rigidity in the A group. However, the level in the AS/KS group remained considerably lower than in the A group. The results suggest that rigidity, which is assumed to be due to an action of morphine in the striatum, can be antagonized by another process leading to dopaminergic activation in the striatum. Nevertheless, there occurs some real tolerance to this effect. The rapid alternations of rigidity and the signs of dopaminergic activation observed in the animals of the AS/KS group might be due to rapid shifts in the predominance of various DA-innervated structures.

Animals↗
PubMed2001

Quantification of the UPDRS Rigidity Scale.

In the clinical setting, parkinsonian rigidity is assessed using subjective rating scales such as that of the Unified Parkinson's Disease Rating System (UPDRS). However, such scales are susceptible to problems of sensitivity and reliability. Here, we evaluate the reliability and validity of a device designed to quantify parkinsonian rigidity at the elbow and the wrist. The method essentially quantifies the clinical examination and employs small sensors to monitor forces and angular displacements imposed by the clinician onto the limb segment distal to the joint being evaluated. Force and displacement data are used to calculate elastic and viscous stiffnesses and their vectorial sum, mechanical impedance. Interexaminer agreement of measures of mechanical impedance in subjects with Parkinson's disease was comparable to that of clinical UPDRS scores. Examiners tended to overrate rigidity on the UPDRS scale during reinforcement manoeuvres. Mechanical impedance was nonlinearly related to UPDRS ratings of rigidity at the elbow and wrist; characterization of such relationships allows interpretation of impedance measurements in terms of the clinical rating scales.

Biomechanical Phenomena↗
PubMed1998

[Valproic acid relieved marked rigidity in three patients with end-stage parkinsonism].

We applied valproic acid (VPA) on the rigidity of three parkinsonian patients, two with Parkinson disease and one with striatonigral degeneration. They were all at Hoehn and Yahr's stage V and showed marked rigidity. In these patients, effect of L-DOPA had become limited or increasing the dosage of L-DOPA was difficult because of its side effects. Parkinsonian symptoms were assessed by using motor score of Unified Parkinson's Disease Rating Scale. The degree of rigidity in these three patients was markedly decreased with 300-600 mg/day of VPA. The blood level of VPA ranged from 24.8 to 66.5 micrograms/ml, which was relatively low compared with the effective blood level as an anti-epileptic agent. Parkinsonian symptoms other than rigidity, and the increased deep tendon reflexes which were present in the patient with striatonigral degeneration were not affected by VPA. Reduction of L-DOPA intensified rigidity again which had been under control. Trials of VPA on parkinsonism have been reported from two groups (Price PA, et al. 1978; Nutt J, et al. 1979), neither of which has observed any benefit of VPA. The difference of their results and ours seems to depend on the stage of patients; their patients had mild to moderate symptoms, whereas ours were in the end stage with marked rigidity. Since the effect of VPA upon parkinsonism is limited to rigidity, the end-stage patients whose care is difficult due to severe rigidity may obtain the best benefit of VPA. VPA is considered to take effect by activating gamma-aminobutyric acid (GABA) system. Because GABA is a common inhibitory neurotransmitter distributed in the wide areas of the central nervous system, it is difficult to locate the action site of VPA with regard to the amelioration of rigidity. The stretch reflex loop in the spinal cord does not seem to be the action site because no change was noted in deep tendon reflex. GABAergic striatal efferent neurons do not seem to be the sole action site either, because parkinsonian symptoms were not affected except for rigidity. The vestibular nucleus which receives strong GABAergic afferents from cerebellar Purkinje cells is an efficient tonus regulator. Since suppression of the function of the nucleus is known to reduce rigidity, it is at least a candidate for the action site of VPA. But there is no direct evidence for this matter. The exact action site of VPA remains to be elucidated.

Aged↗
PubMed2000

Instrumentally detected changes in motor functioning in patients with low levels of antipsychotic dopamine D2 blockade.

Extrapyramidal side-effects (EPSE) of antipsychotic medication are related to the occupancy of dopamine D2 receptors and there appears to be a threshold of D2 occupancy below which clinically EPSE are unlikely to occur. It is unclear whether there are motor changes produced by 'subthreshold' levels of D2 occupancy that are not detectable by clinical examination. This study was designed to investigate whether a number of electromechanical instrumental techniques could detect 'subthreshold' motor changes and whether these changes correlate with dopamine D2 occupancy as measured by [11C]-raclopride PET scan. Twenty medication naïve patients were studied before and during treatment with low dose haloperidol. Instrumental techniques detected an asymmetrical worsening in motor function with drug treatment despite the failure of the group to experience significant EPSE. These changes did not correlate with D2 occupancy and measurements of rigidity, tremor, and bradykinesia did not closely inter-correlate.

Adult↗
PubMed1990

Striatal and nigral neuron subpopulations in rigid Huntington's disease: implications for the functional anatomy of chorea and rigidity-akinesia.

Neuropeptide immunohistochemistry was used to test several hypotheses of the anatomical bases of chorea and rigidity-akinesia. To test the hypothesis that elevated concentration of striatal somatostatin causes chorea, we visually compared the density of striatal neurons containing somatostatin and neuropeptide Y in brains affected by choreic or rigid-akinetic Huntington's disease (HD). The density of these neurons was elevated in both rigid-akinetic and choreic HD specimens with an apparently normal total number of these neurons, indicating that elevated somatostatin concentration, by itself, does not lead to chorea. We tested the hypothesis that rigid-akinetic HD results from deficient dopaminergic nigrostriatal neurotransmission by examining tyrosine hydroxylase-immunoreactive (TH-IR) neurons in the substantia nigra. In rigid-akinetic HD brains, there was no obvious reduction of nigral TH-IR neurons, indicating that rigid-akinetic HD is probably not due to loss of nigral dopaminergic neurons. Finally, we also examined the status of striatal projection neurons and found near total loss of all striatal neurons projecting to the lateral globus pallidus, medial globus pallidus, and substantia nigra in brains affected by rigid-akinetic HD in contrast to the preservation of neurons projecting to the medial globus pallidus in choreic HD. These results are consistent with the hypothesis that chorea results from preferential loss of striatal neurons projecting to the lateral globus pallidus and that rigid-akinetic HD is a consequence of the additional loss of striatal neurons projecting to the medial segment of the pallidum.

Adult↗