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PubMed1995

Inhibition by intrathecal prazosin but not yohimbine of fentanyl-induced muscular rigidity in the rat.

We evaluated the effect of intrathecally administered prazosin, alpha 1-adrenoceptor antagonist, or yohimbine, alpha 2-adrenoceptor antagonist, on fentanyl-induced muscular rigidity. Adult, male Sprague-Dawley rats were anesthetized with ketamine and were under mechanical ventilation. Fentanyl given intravenously (100 micrograms/kg) or microinjected into the bilateral locus coeruleus (LC) (2.5 microgram/50 nl) consistently evoked a significant increase in the electromyographic activity recorded from the sacrococcygeus dorsalis lateralis muscle. This implied muscular rigidity was appreciably antagonized by prior intrathecal (10 microliters) administration of prazosin (5 or 10 nmol), but not equimolar dose of yohimbine. These results suggest that the spinal alpha 1-adrenoceptors in the coerulospinal noradrenergic pathway play a key role in fentanyl-induced muscular rigidity.

Adrenergic alpha-Antagonists↗
PubMed2006

Abdominal pain with rigidity secondary to the anti-emetic drug metoclopramide.

We report a case of abdominal pain with rigidity, mimicking an acute abdomen, caused by metoclopramide, a common anti-emetic drug. Extrapyramidal symptoms are commonly reported side-effects of this medication. They generally include involuntary movements of limbs, torticollis, oculogyric crisis, rhythmic protrusion of tongue, trismus, or dystonic reactions resembling tetanus, etc. Abdominal rigidity due to this medication, resembling an acute abdomen, has not been reported previously. This case report illustrates the importance of considering medication side-effects when evaluating a patient with abdominal pain and rigidity.

Abdomen, Acute↗
PubMed2001

(S)-4C3HPG, a mixed group I mGlu receptor antagonist and a group II agonist, administered intrastriatally, counteracts parkinsonian-like muscle rigidity in rats.

The aim of the present study was to determine whether S-4-carboxy-3-hydroxyphenylglycine (S)-4C3HPG, a mixed group I glutamate metabotropic receptor antagonist and a group II agonist, attenuated parkinsonian-like muscle rigidity in rats. Muscle tone was examined using a combined mechano and electromyographic method, which measured simultaneously the muscle resistance (MMG) of the rat's hind foot to passive extension and flexion in the ankle joint and the electromyographic activity (EMG) of the antagonistic muscles of that joint: gastrocnemius and tibialis anterior. Muscle rigidity was induced by pretreatment with haloperidol (1 mg/kg i.p.). (S)-4C3HPG injected in doses of 5 and 15 microg/0.5 microl bilaterally, into the rostral region of the striatum, decreased both the haloperidol-induced muscle rigidity (MMG) and the enhanced electromyographic activity (EMG). The present results suggest that blockade of mGluR1 receptors and/or activation of mGluR2 ones, localized in the rostral part of the striatum, may be responsible for the anti-parkinsonian effect of (S)-4C3HPG.

Animals↗
PubMed1992

Raised resting energy expenditure in Parkinson's disease and its relationship to muscle rigidity.

1. Resting energy expenditure was measured, by indirect calorimetry, in 12 patients with Parkinson's disease and in eight healthy age-matched control subjects. In the patients with Parkinson's disease measurements were made in both the untreated state and after an injection of the dopamine agonist apomorphine (treated state). In each state muscle rigidity was recorded. 2. Resting energy expenditure was higher in patients with Parkinson's disease in both the treated and untreated states than in the control subjects. Of the patients with Parkinson's disease, seven showed no difference in resting energy expenditure between the two treatment states, whereas four showed markedly increased resting energy expenditure in the untreated state. The change in resting energy expenditure in the untreated state, as compared with the treated state, was significantly related to the development of muscle rigidity in the untreated state. 3. In Parkinson's disease, even in optimally treated patients, resting energy expenditure is raised and this may contribute to the weight loss seen in this disease. Severe muscle rigidity occurring during untreated periods results in a further increase in resting energy expenditure.

Apomorphine↗
PubMed2000

Three cases with different presentation of fentanyl-induced muscle rigidity--a rare problem in intensive care of neonates.

We report about two newborns with sudden onset of inability of mechanical ventilation due to transient chest wall rigidity after fentanyl i.v. bolus of 2 and 4 microg/kg, respectively, resulting in severe hypoxemia and secondary bradycardia. A third case developed a rigidity of the tongue after fentanyl bolus, which created some unusual difficulties in bypassing the tongue for insertion an endotracheal tube. Because of common usage of this agent for analgesia we direct attention to the possibility of fentanyl-induced muscle rigidity. We underline the necessity of a slow bolus injection to prevent this dangerous adverse effect and we recommend the administration of naloxone and/or muscle relaxants as therapy in conjunction with mechanical ventilation.

Analgesics, Opioid↗
PubMed2002

The diagnostic accuracy of Kernig's sign, Brudzinski's sign, and nuchal rigidity in adults with suspected meningitis.

To determine the diagnostic accuracy of Kernig's sign, Brudzinski's sign, and nuchal rigidity for meningitis, 297 adults with suspected meningitis were prospectively evaluated for the presence of these meningeal signs before lumbar puncture was done. Kernig's sign (sensitivity, 5%; likelihood ratio for a positive test result [LR(+)], 0.97), Brudzinski's sign (sensitivity, 5%; LR(+), 0.97), and nuchal rigidity (sensitivity, 30%; LR(+), 0.94) did not accurately discriminate between patients with meningitis (>/=6 white blood cells [WBCs]/mL of cerebrospinal fluid [CSF]) and patients without meningitis. The diagnostic accuracy of these signs was not significantly better in the subsets of patients with moderate meningeal inflammation (>/=100 WBCs/mL of CSF) or microbiological evidence of CSF infection. Only for 4 patients with severe meningeal inflammation (>/=1000 WBCs/mL of CSF) did nuchal rigidity show diagnostic value (sensitivity, 100%; negative predictive value, 100%). In the broad spectrum of adults with suspected meningitis, 3 classic meningeal signs did not have diagnostic value; better bedside diagnostic signs are needed.

Adolescent↗
PubMed1976

Progressive encephalomyelitis with rigidity.

Two cases of encephalomyelitis are described in which the major clinical manifestation was muscular rigidity and stimulus-sensitive muscular spasms. It is suggested, from pathological evidence, that this rigidity was of spinal origin, and that this disorder is a rare but recognizable entity. Comparison is made with previously reported cases of rigidity of spinal origin, including encephalitis lethargica, and with 'subacute myoclonic spinal neuronitis' and the 'stiff man syndrome.'

Adult↗
PubMed1989

Seizures during opioid anesthetic induction--are they opioid-induced rigidity?

The tape recorded EEGs of 127 patients anesthetized with large doses of opioids were retrospectively analyzed for evidence of opioid-induced seizures, and in particular, correlated with movements that occurred during induction and could be clinically interpreted as seizures. Bilateral EEG leads in patients receiving fentanyl (20), sufentanil (20), or alfentanil (87) were recorded. Forty-six of these patients from all opioid groups manifested intense rigidity, as assessed both clinically and by EMGs recorded from eight muscles in 69 of the patients receiving alfentanil. This intense rigidity often resembled seizures, in that the phenomenon entailed severe stiffness of both limbs and trunk, with an explosive onset of myoclonic limb movements, and associated vertical nystagmus. Electroencephalographic observations were extensive, entailing 69 h of paper recordings played back from the tapes, at paper speeds of 30 or 60 mm/s, with detailed annotations from the voice track. These paper recordings were examined in detail independently by three of the investigators, who were unaware of the clinical phenomena that had occurred. The only observed EEG activity that could have been interpreted as epileptiform consisted of small sharp waves related to muscle activity or other artifact. The EEG never indicated seizure activity during these drug-induced movements and rigidity. Reports of opioid-induced seizures are reviewed and a set of criteria is offered to help achieve future consistency and credibility in evaluating this phenomenon. The available evidence does not support the existence of opioid-induced seizures in the clinical setting.

Alfentanil↗
PubMed1995

Masseter muscle rigidity associated with glycine1306-to-alanine mutation in the adult muscle sodium channel alpha-subunit gene.

BACKGROUND: Succinylcholine-induced masseter muscle rigidity (MMR) is a potentially life-threatening complication of anesthesia and is closely correlated with the heterogeneous disorder malignant hyperthermia (MH) susceptibility. MMR also is identified with a variety of neuromuscular disorders, including the myotonias, that are associated with abnormal in vitro contracture test (IVCT) results. Recently, mutations in the adult skeletal muscle sodium channel alpha-subunit gene (SCN4A) have been shown to cause generalized nondystrophic myotonias, some of which are associated with mild nonspecific symptoms. The purpose of the current investigation was to begin to evaluate the molecular genetic relationship between known mutations in the SCN4A gene, MMR, and the results of the IVCT used to diagnose MH-susceptibility. METHODS: A single extended pedigree of 16 individuals was ascertained through a proband who experienced MMR and whole-body rigidity after succinylcholine administration. Subsequently, four individuals were shown to have a mild form of myotonia on clinical and laboratory examination. IVCT was carried out according to standardized protocols. Mutations in the SCN4A gene were sought in exons 22 and 24 using single-strand conformational analyses. Variability in the SCN4A gene sequence was confirmed by direct DNA sequence analyses. RESULTS: Four individuals with myotonia were shown to carry a guanine-to-cytosine mutation at nucleotide position 3917 of the reported SCN4A sequence. This DNA mutation was coinherited with MMR and an abnormal IVCT result in this family. Previous studies have demonstrated that the glycine1306-to-alanine substitution is associated with a mild clinical syndrome referred to as myotonia fluctuans. CONCLUSIONS: The current report provides direct evidence that succinylcholine-induced MMR, whole-body rigidity, and an abnormal IVCT result are associated with a mutation in the SCN4A gene.

Alanine↗
PubMed2005

Postural stability of Parkinson's disease patients is improved by decreasing rigidity.

Postural instability has a big impact on the quality of life of patients with Parkinson's disease (PD) as it often leads to an insecure stance and fall. We investigated if postural stability in these patients improves by decreasing rigidity with a dopaminergic agonist. In our study, we tested eight PD patients with no concomitant diseases. Their age was 61 +/- 2 years (mean +/- SE) and their Hoehn-Yahr score was 3 +/- 0.1. The patients were evaluated according to the Unified Parkinson's Disease Rating Scale for motor function (mUPDRS) and with stabilometric measurements of forward-backward and side-to-side body oscillations during free stance with eyes open. Both evaluations were performed in an "off "state and in an apomorphine-induced "on" state. As expected, the mUPDRS score was significantly decreased in the "on" state with posture being improved in six patients, gait in eight patients and postural stability in seven of eight patients. In addition, apomorphine caused a significant reduction of the relative amplitude of lower frequencies and an increase of the relative amplitude of higher frequencies of forward-backward body oscillations. The results of stabilometry and mUPDRS evaluations are in agreement with the effect of apomorphine on rigidity, indicating that postural stability of PD patients is improved by decreasing rigidity.

Antiparkinson Agents↗
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↗
PubMed1980

Two methods of measuring muscle tone applied in patients with decerebrate rigidity.

Two methods were used to measure muscle tone in patients with decerebrate rigidity. In the first method forces of square waveform were applied and the calculated compliance of the joint was used as an index of rigidity. Oscillatory transients were seen at the same frequency as the physiological tremor. The range of normal variation in compliance was large and the values measured in the patients flucuated markedly which limited the value of this index. In the second method, where forces of sinusoidal waveform were employed, the resonant frequency of the joint was measured and used as an index of rigidity. This index proved reliable and reproducible.

Adolescent↗
PubMed1980

A patient with reflex myoclonus and muscle rigidity: "jerking stiff-man syndrome".

A patient with progressive muscular rigidity associated with reflex myoclonus is described. The muscular rigidity was predominantly axial, and the myoclonic jerks affected axial and leg muscles. Jerks occurred either spontaneously, or in response to touch to the perioral region, or to stretch of head and neck muscles. Physiological investigations suggested that the myoclonus originated in the medulla and was mediated by fast-conducting pathways upwards through the brainstem and down the spinal cord. The relationship of this condition to other types of muscular rigidity with and without myoclonus is discussed.

Adult↗
PubMed1988

The rigid spine syndrome in two sisters.

Two half-sisters aged 14 and 18 years are described with a rigid spine syndrome as the cardinal clinical feature of an autosomal dominant neuromuscular disorder. Ten years previously, a diagnosis of multicore disease had been made from the clinical signs and muscle biopsy findings. Long term follow-up revealed a non-specific muscular dystrophy with axial predominance and a rigid spine in the younger girl; the older sister presented at the age of 18 with a rigid spine as the only myopathic sign. Computed tomography of the muscles showed severe involvement of the paraspinal musculature, in contrast with either less or no involvement of the other muscles.

Adolescent↗
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↗
PubMed1989

Pathophysiology of rigidity and akinesia in Parkinson's disease.

Although rigidity and akinesia are two of the cardinal features of Parkinson's disease, their exact pathophysiology remains uncertain. Mechanisms which may contribute to rigidity include accentuation of the long-latency component of the stretch reflex and enhanced fusimotor drive causing increased sensitivity of muscle spindles. Current evidence concerning the role of these factors in rigidity is reviewed. The relationship between akinesia, prolonged reaction times, and delay in initiation of internally generated movements in parkinsonian patients is discussed.

Humans↗
PubMed2004

Diabetes mellitus and progression of rigidity and gait disturbance in older persons.

BACKGROUND: Parkinsonian-like signs, including rigidity, gait disturbance, and bradykinesia, are common and progressive in old age and are associated with morbidity and mortality. Few risk factors for these signs have been identified. Diabetes mellitus, also a common chronic condition in old age and known to be associated with physical and neurologic disability, may be associated with parkinsonian-like signs. OBJECTIVE: To examine the relation of diabetes to four parkinsonian-like signs. METHODS: Participants were 822 older Catholic clergymen and women who were without clinically diagnosed Parkinson disease or dementia at baseline. For up to 9 years, they had uniform annual evaluations, which included a modified version of the motor portion of the Unified Parkinson's Disease Rating Scale, from which previously established measures of four specific parkinsonian-like signs were derived. Participants were evaluated for the presence of diabetes, based on direct medication inspection and history. RESULTS: Diabetes was present in 128 (15.6%) participants. In random effects models controlling for age, sex, and education, diabetes was associated with worsening rigidity (p < 0.01) and gait (p < 0.05), over an average of 5.6 years of follow-up, but not with change in bradykinesia or tremor. The presence of stroke did not substantially affect the association of diabetes with rigidity but reduced the association of diabetes with gait to a trend (p = 0.08). CONCLUSION: Diabetes may be a previously unrecognized risk factor for progression of parkinsonian-like signs in older persons.

Aged↗