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PubMed2002

Encephalomyelitis with rigidity complicating human immunodeficiency virus infection.

A 34-year-old man with human immunodeficiency virus type 1 (HIV-1) presented with axial rigidity, painful spasms, and delayed hemiparesis and dementia. Cerebrospinal fluid analysis showed no antiglutamic acid dehydrogenase antibodies but viral genome from Epstein-Barr virus was detected by polymerase chain reaction. Clinical features and possible viral aetiology of progressive encephalomyelitis with rigidity are briefly discussed.

Adult↗
PubMed1989

[Muscular rigidity caused by alfentanil: prevention].

We studied three groups of 30 patients each, undergoing minor orthopaedic surgery, anaesthetized with alfentanil (30 micrograms/kg bolus followed by an infusion of 0.3 micrograms/kg/min), thiopental 3 mg/kg and 70% N2O via facial mask. Patients in group I were treated, three minutes before induction, with vecuronium 0.02 mg/kg i.v., while those in group II were premedicated with diazepam 0.15 mg/kg i.m. 30-45 minutes before induction. Group III served as control. Muscular rigidity was evaluated clinically with a subjective score based on a scale of 0 (no rigidity) to 3 (severe rigidity). Diazepam did not give significant protection from muscular rigidity. Vecuronium administration did not significantly reduced the number of patients who became rigid, but significantly decreased the incidence of severe rigidity (p less than 0.005), the mean rigidity score (p less than 0.05) and the incidence of rigidity at the induction of anaesthesia (p less than 0.0005). We also observed a progressively increasing incidence of rigidity with increasing age (not significantly) and body weight (p less than 0.05 total rigidity, p less than 0.01 severe rigidity).

Adolescent↗
PubMedDate not supplied

The neurophysiologic basis of abnormal movements in basal ganglia disorders.

Recent anatomical and physiological studies have shed new light on the functional organization of the basal ganglia and the contributions of these structures to movement. While the striatum receives input from the entire neocortex, this information appears to remain segregated in the basal ganglia along lines established at the cortical level. There appears to be, in the broadest sense, a maintained segregation of information relevant to motor and "complex" functions. The concept of segregated parallel subcortical loops subserving "motor" and "complex" functions is discussed. Single cell studies in the basal ganglia of behaving animals have revealed specific relations of neuronal activity to movements of individual body parts and a relation to specific parameters of movement, particularly direction, amplitude, and velocity. The pathophysiologic basis of akinesia tremor, rigidity, and diskinesias is discussed in light of recent findings.

Animals↗
PubMed2000

Objective quantification of resting and activated parkinsonian rigidity: a comparison of angular impulse and work scores.

The clinical assessment of rigidity is influenced by a number of variables which limit the reproducibility of rating scores and the usefulness of comparisons between subjects. We evaluated an objective measure of rigidity which uses unpredictable but reproducible limb perturbations mimicking the waveform, rate, and amplitude of those used in the clinical examination; and evaluates total resistive force, thus avoiding assumptions about the relative influence of elastic, viscous, or inertial components of the measured resistive forces on the genesis of rigidity. We then used this measure to quantify the effects of an activation procedure on parkinsonian rigidity, because this forms an important but poorly understood part of the routine clinical examination. We studied 20 patients with a clinical diagnosis of Parkinson's disease and 10 age-matched control subjects. A torque motor was used to deliver reproducible, transient, sinusoidal perturbations varying between 1.0 and 1.5 Hz. To quantify rigidity, we calculated angular impulse scores, which reflect the relationship between change in total resistive torque and time. Angular impulse scores were compared with work scores, which have previously been found to correlate with clinical assessments of rigidity. All subjects were studied at rest and with activation. Angular impulse scores were more consistently correlated with rigidity and more clearly differentiated between patients and control subjects than work scores. Activation increased both clinical and objective rigidity scores; activated angular impulse scores ranged from approximately 100%-200% of resting values. When plotted against clinical rigidity scores, activated angular impulse scores lay on a continuum with resting values. We conclude that angular impulse is a valid objective measure of parkinsonian rigidity. Activation increases rigidity, but to varying degrees in different patients. To improve the sensitivity and reproducibility of clinical rigidity assessments, parkinsonian rating scales should include separate resting and activated scores.

Aged↗
PubMed1978

Impaired dopamine function and muscular rigidity induced by 6-aminonicotinamide in rats.

In corpus striatum, 6-aminonicotinamide (6-AN), 10 mg/kg i.p. lowered the concentration of dopamine and markedly reduced the disappearance of dopamine after synthesis inhibition with alpha-methyl-p-tyrosine. In the dopamine-rich part of the limbic system, the formation of DOPA after decarboxylase inhibition with 3-hydroxybenzylhydrazine was decreased. In diencephalon, 6-AN altered neither the steady-state level nor the utilization of noradrenaline. The data suggest that the muscular rigidity induced by 6-AN may be associated with disruption of dopaminergic transmission.

6-Aminonicotinamide↗
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↗
PubMed2007

Role of hyperactive cerebellum and motor cortex in Parkinson's disease.

Previous neuroimaging studies have found hyperactivation in the cerebellum and motor cortex and hypoactivation in the basal ganglia in patients with Parkinson's disease (PD) but the relationship between the two has not been established. This study examined whether cerebellar and motor cortex hyperactivation is a compensatory mechanism for hypoactivation in the basal ganglia or is a pathophysiological response that is related to the signs of the disease. Using a BOLD contrast fMRI paradigm PD patients and healthy controls performed automatic and cognitively controlled thumb pressing movements. Regions of interest analysis quantified the BOLD activation in motor areas, and correlations between the hyperactive and hypoactive regions were performed, along with correlations between the severity of upper limb rigidity and BOLD activation. There were three main findings. First, the putamen, supplementary motor area (SMA) and pre-SMA were hypoactive in PD patients. The left and right cerebellum and the contralateral motor cortex were hyperactive in PD patients. Second, PD patients had a significant negative correlation between the BOLD activation in the ipsilateral cerebellum and the contralateral putamen. The correlation between the putamen and motor cortex was not significant. Third, the BOLD activation in the motor cortex was positively correlated with the severity of upper limb rigidity, but the BOLD activation in the cerebellum was not correlated with rigidity. Further, the activation in the motor cortex was not correlated with upper extremity bradykinesia. These findings provide new evidence supporting the hypothesis that hyperactivation in the ipsilateral cerebellum is a compensatory mechanism for the defective basal ganglia. Our findings also provide the first evidence from neuroimaging that hyperactivation in the contralateral primary motor cortex is not a compensatory response but is directly related to upper limb rigidity.

Aged↗
PubMed2004

Long-term suppression of extrapyramidal motor symptoms with deep brain stimulation (DBS).

Deep Brain Stimulation (DBS) was investigated for the treatment of extrapyramidal motor symptoms. Both tremor and rigidity as well as akinesia are known to be permanently suppressed by applying a high-frequency current to different basal ganglia nuclei. Chronic DBS was performed in 113 patients using stereotactically implanted quadripolar electrodes in the ventrolateral thalamus (n = 43), the globus pallidus internus (n = 15), or the subthalamic nucleus (n = 55). Subcutaneous implantation of the generator occurred during a second procedure following correct positioning of the electrodes and confirmation of effectiveness by external stimulation. Patients were followed up using standardized rating scales before and after surgery. Deep Brain Stimulation significantly suppresses extrapyramidal symptoms such as tremor (p < 0.001), rigidity (p < 0.001), dyskinesia (p < 0.01), akinesia, and dystonia (p < 0.05). Permanent side effects were avoided by changing the stimulation parameters. Severe complications occurred in only two patients (n = 2, 1.8 %). DBS is a safe and effective long-term treatment for tremor, rigidity, dyskinesia, akinesia and dystonia.

Adult↗
PubMed1975

Myocardial oxygen consumption in isometric contraction of various strengths due to paired stimulation and quick-release.

In all of the experiments described, the oxygen consumption during isometric contraction was dependent solely upon the magnitude of active tension developed, and not on the rate of tension development or on the duration of contraction. There is a constant linear relationship between tension development and oxygen uptake. Any sudden interruption of active tension in the rising phase of the contraction terminates the energy utilization by the contractile system. These findings provide evidence to suggest that in isometric contraction of heart muscle, a rigid and constant coupling exists in the transformation of chemical energy to the mechanical tension.

Animals↗
PubMed2000

Assignment of a form of congenital muscular dystrophy with secondary merosin deficiency to chromosome 1q42.

We have previously reported an autosomal recessive form of congenital muscular dystrophy, characterized by proximal girdle weakness, generalized muscle hypertrophy, rigidity of the spine, and contractures of the tendo Achilles, in a consanguineous family from the United Arab Emirates. Early respiratory failure resulting from severe diaphragmatic involvement was present. Intellect and the results of brain imaging were normal. Serum creatine kinase levels were grossly elevated, and muscle-biopsy samples showed dystrophic changes. The expression of the laminin-alpha2 chain of merosin was reduced on several fibers, but linkage analysis excluded the LAMA2 locus on chromosome 6q22-23. Here, we report the results of genomewide linkage analysis of this family, by use of homozygosity mapping. In all four affected children, an identical homozygous region was identified on chromosome 1q42, spanning 6-15 cM between flanking markers D1S2860 and D1S2800. We have identified a second German family with two affected children having similar clinical and histopathological features; they are consistent with linkage to the same locus. The cumulative LOD score was 3.57 (straight theta=.00) at marker D1S213. This represents a novel locus for congenital muscular dystrophy. We suggest calling this disorder "CMD1B." The expression of three functional candidate genes in the CMD1B critical region was investigated, and no detectable changes in their level of expression were observed. The secondary reduction in laminin-alpha2 chain in these families suggests that the primary genetic defect resides in a gene coding for a protein involved in basal lamina assembly.

Antigens, CD↗
PubMed1986

The role of the nucleus raphe pontis and the caudate nucleus in alfentanil rigidity in the rat.

Attempts to eliminate or reduce the rigidity induced with high-dose narcotic anesthesia in the operating room have been only partially successful. Previous investigations of opioid receptor sites mediating this rigidity have implicated two central regions: the nucleus raphe pontis (NRP) within the reticular formation and the caudate nucleus (CN) within the basal ganglia. The present study used systemically administered alfentanil (ALF), a potent, short-acting fentanyl analog, and intracerebrally infused methylnaloxonium (MN), a quaternary derivative of naloxone, to elucidate further the functional role of the NRP and CN in rigidity. ALF (0.5 mg/kg s.c.) produced a reliable model of rigidity, as documented by gastrocnemius electromyography. The onset of this rigidity was within 60 s of ALF administration, with a total duration of approximately 40-50 min. Intracerebroventricular (i.c.v.) injections of 2.0 or 4.0 micrograms of MN 15 min prior to ALF treatment prevented rigidity, while 0.125 or 0.5 microgram had no significant effect on rigidity. MN injected directly into the NRP at doses as low as 0.125 microgram significantly antagonized ALF-induced rigidity, while injections of MN into the caudate nucleus at doses as high as 4.0 micrograms failed to antagonize ALF-induced rigidity. These observations demonstrate that injection of MN into the NRP is at least 16-fold more effective in blocking ALF-induced rigidity than MN injected into the ventricle and, more importantly, at least 32-fold more effective than MN injected into the CN. The results suggest that the NRP may be an important site for the neural control of muscular rigidity associated with high-dose narcotic administration.

Alfentanil↗
PubMed1996

[Axial (neck and trunk) rigidity in Parkinson's disease, striatonigral degeneration and progressive supranuclear palsy].

Our previous study showed that the alternating knee tilt test in supine position is a useful method to assess the trunk rigidity. We investigated the progression of axial (neck and trunk) rigidity in Parkinson's disease (PD), striatonigral degeneration (SND), and progressive supranuclear palsy (PSP) by using this method. We assessed rigidity on a scale of 0 (absent) to 3 (severe) on five parts of the body: neck, trunk, wrist, elbow and knee in 57 patients with PD, 13 patients with SND and 18 patients with PSP. In PD patients, the degree of neck and trunk rigidity correlated well with the duration of disease and the staging scale. There was neck rigidity in 27% of PD patients with unilateral involvement of the limbs, but the trunk tonus was normal in them. There was rigidity in the neck and trunk of all PD patients with bilateral involvement of the limbs. When the limb rigidity was predominant on one side, the trunk rigidity was predominant on the opposite side. In SND patients, the degree of neck and trunk rigidity roughly correlated with the duration of disease and the staging scale. In SND patients with unilateral involvement of the limbs, tonus of the neck and trunk was normal. In SND patients with bilateral involvement of limbs, there was rigidity in both the neck and the trunk. In PSP patients, the degree of neck rigidity correlated well with the duration of disease and the staging scale, but the degree of rigidity in the trunk and limb remained relatively mild even at the advanced stage. Accordingly, in PSP patients there was a dissociation of the degree of neck rigidity from that of trunk and limb rigidity. In conclusion, the assessment of axial (neck and trunk) rigidity may be useful for the clinical diagnosis of parkinsonism and the staging scale scoring.

Adult↗