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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↗
PubMed1989

Optimal indices for testing parkinsonian rigidity.

We assessed parkinsonian rigidity objectively at the wrist to determine the optimal angular velocity and displacement for detecting abnormality. The wrist was moved passively with a torque motor and the average work done for one complete cycle was computed. This objective rigidity score (ORS) was compared with a clinical rigidity score (CRS). ORS was more pronounced at faster movement velocities in parkinsonian patients, whereas in normal subjects there was only a modest increase in the score. Angular velocities of 140 to 190 degrees/second and displacements of +/- 25 to +/- 30 degrees were most sensitive for detecting parkinsonian rigidity and had good correlation with the CRS.

Adult↗
PubMed1984

Characteristic alterations in responses to imposed wrist displacements in parkinsonian rigidity and dystonia musculorum deformans.

The amplitude and temporal modulation of the segmented EMG activity in flexor carpi radialis, evoked by imposed angular wrist extension, was studied with respect to the level of pre-existing background activity in rigid parkinsonian (PK) and dystonia musculorum deformans (DMD) patients. The interdependence of the evoked M1 and M2-3 segments on pre-existing background EMG activity and initial velocity of imposed displacement was established previously for a normal population. Individual responses of 21 parkinsonian and 12 dystonic patients were compared to the established normal "response volume". The augmented magnitude of the M2-3 segment in rigid PK patients, which correlates to the measure of rigidity, could not be accounted for by the low level of pre-existing EMG activity. Therefore, increased descending facilitation does not impinge directly on alpha motoneurons. Paradoxical excitation in the shortened muscle and resetting of tonic tremor of the stretched muscle by the imposed wrist extension are two other demonstrated abnormalities which may also contribute to PK rigidity. In contrast, DMD patients demonstrated normal amplitude modulation of the M1 and M2-3 segments, but exhibited a disturbance of normal temporal mechanisms that result in constant duration of the M1 and M2-3 responses with imposed force step loads.

Adult↗
PubMed2000

Lumbar segmental rigidity: can its identification with facet injections and stretching exercises be useful?

OBJECTIVES: To describe a method for observing lumbar segmental rigidity and to show how motion measurements and pain/disability questionnaires can be used to evaluate outcomes of combined facet injections and stretching exercises. DESIGN: Preliminary 2-part study: (1) presentation of a technique for, identifying lumbar segmental rigidity based on physical observation of the spine's lateral bending; and (2) repeated measures of motion and pain/disability self-report in a chronic lumbar spinal disorder cohort, performed before and after treatment with combined facet injections and stretching exercises. SETTING: An outpatient tertiary rehabilitation facility providing interdisciplinary functional restoration for chronic disabling work-related spinal disorders. PATIENTS: Chronically disabled patients with lumbar spinal disorder (n = 39; mean age, 41yr; 82% male) with segmental rigidity at 1 or more levels on physical examination. Subjects averaged 20 months of disability, and 51% had preinjection spine surgery (average, 1.7 procedures involving up to 3 spinal segments). Thirty-nine percent of the cohort had a fusion at levels 1 or 2. INTERVENTIONS: Bilateral facet injections were administered under fluoroscopy to all patients, and 2 or 3 levels were performed in 93% of cases (range, levels 1-4). Patients were instructed in an unsupervised stretching program and were reassessed 2 to 4 weeks later. After an intensive supervised resistance exercise training program as part of interdisciplinary functional restoration, a third set of motion, pain, and disability measures were collected. MAIN OUTCOME MEASURES: Changes in true lumbar sagittal and coronal motion (T12-S1), measured with inclinometers, and pain/disability self-report were compared statistically. RESULTS: Patients' mobility improved significantly (p < .01-.0001) across all 4 motions. A large majority (71%-97%) of individuals improved on motion. According to self-reports made over the postinjection period, most patients improved their disability (83%) and pain intensity (63%) ratings. CONCLUSIONS: A simple physical examination technique for assessing lumbar spine segmental rigidity was used in this preliminary study to select patients and levels for combined facet injection and stretching exercise, with resultant improvements in mobility and self-reported pain/disability that may extend beyond the pharmacologic duration of the corticosteroid. The efficacy of either the facet injection or stretching components alone in achieving objective mobility improvements cannot be determined from the present study, but warrants future investigation.

Adult↗
PubMed2002

The effect of Trager therapy on the level of evoked stretch responses in patients with Parkinson's disease and rigidity.

OBJECTIVE: To quantify changes of evoked stretch responses (ESR) in the most rigid arm of patients with Parkinson's disease (PD) after Trager therapy. METHODS: Gentle rocking motion associated with this type of manual therapy was imparted to the upper limbs and body of 30 patients for 20 minutes. A pretest and 2 posttests (at 1 and 11 minutes after the treatment, respectively) were performed, consisting of electromyographic (EMG) recordings of the flexor carpi radialis and extensor digitorum communis while the patient's wrist was passively flexed and extended with an amplitude of 60 degrees and a frequency of 1 Hz. Patients received the treatment on the most rigid side of their bodies (ipsi-group) or on the contralateral side (contra-group). Half of patients in each group received the treatment while lying supine on a massage table (ipsi- and contra-supine) or sitting in a chair (ipsi- and contra-sitting). RESULTS: In general, the level of ESR were reduced by 36% immediately after treatment and remained 32% lower than pretest values 11 minutes after treatment (F = 41.45, P <.05). Patients who received the treatment lying supine benefited from a 42% reduction of ESR (F = 4.07, P <.05). The side on which the treatment was performed did not significantly influence the outcome of the treatment (F = 0.50, P >.05). However, post hoc analysis of the triple interaction (test x side x position) indicated that the sitting position was much less efficient for sustained contralateral effect (P >.05). CONCLUSIONS: Results from the present study strongly suggest that it is possible to modify the level of ESR by using Trager therapy. This stretch reflex inhibition may induce a reduction of the muscle rigidity seen in these patients. The present results may eventually lead to the development of a specific complementary therapy for patients with Parkinson's disease and rigidity.

Adult↗
PubMed1993

Neurochemical substrates of rigidity and chorea in Huntington's disease.

Huntington's disease is a progressive degenerative neurological disorder which produces a characteristic movement disorder termed chorea. Although chorea is associated with dysfunction of the basal ganglia, the underlying mechanisms by which dyskinesias such as chorea are produced, are poorly understood. Recent studies in primates have led to experimental models of chorea with postulated involvement of specific neural pathways. In the present study we attempted to determine the validity of the experimental models by measuring concentrations of gamma-aminobutyric acid (GABA), glutamate, substance P and met-enkephalin in the basal ganglia of Huntington's disease patients who manifested either chorea or rigidity/bradykinesia within 6 months of death. We also characterized changes in the Huntington's disease patients according to pathological grade, since this may be a confounding factor. We analysed post-mortem brain tissue from 12 controls, and 11 grade 3 and 12 grade 4 Huntington's disease patients. The grade 3 and 4 cases consisted of eight adult-onset choreic, nine adult-onset rigid and six juvenile-onset rigid patients. We also analysed the putamen and globus pallidus from 11 grade 2 adult onset choreic Huntington's disease patients. A model of chorea based on experimental studies in primates proposes that a loss of striatal GABAergic inhibitory projections to the globus pallidus externa leads to increased activity of the inhibitory globus pallidus externa GABAergic neurons which project to the subthalamic nucleus. It is believed that the loss of GABAergic inputs to the globus pallidus externa precedes a loss of GABAergic input to the globus pallidus interna, which occurs later in the disease and is associated with the development of rigidity and bradykinesia. In the choreic Huntington's disease patients whom we studied, there was a greater loss of GABA in the globus pallidus externa than in the globus pallidus interna, and the globus pallidus interna: globus pallidus externa GABA ratio was significantly increased compared with rigid patients. There were also increases in GABA in the subthalamic nucleus in the choreic patients, although this did not reach significance. A differential loss of met-enkephalin in the globus pallidus externa compared with substance P loss in the globus pallidus interna was not observed in either the choreic patients with advanced disease or the grade II patients. There was a significant increase in GABA concentrations in the ventroanterior nucleus of the thalamus in the choreic patients compared with rigid/bradykinetic patients.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1989

Fentanyl-induced muscle rigidity in unanesthetized and ketamine- or thiopental-anesthetized rats.

This study was undertaken to search for an alternative experimental model in the evaluation of fentanyl-induced muscle rigidity. Unanesthetized, spontaneously ventilating Sprague-Dawley rats, and rats anesthetized with either ketamine or thiopental whose ventilation was mechanically controlled, were studied. Intravenous administration of fentanyl (25, 50, or 100 micrograms/kg) caused an increase in electromyographic (EMG) activity in both unanesthetized and ketamine-anesthetized, but not in thiopental-anesthetized, animals. Muscle rigidity was more prominently manifested in the gastrocnemius muscle, when compared with the rectus abdominis muscle. Hypoxemia was exhibited during the course of rigidity by both spontaneously ventilating and ketamine-anesthetized rats, but not by thiopental-anesthetized animals. In addition, unanesthetized, spontaneously ventilating rats developed hypercarbia and respiratory acidosis. The authors suggest that, in addition to using unanesthetized animals, EMG activity in the gastrocnemius muscle of rats anesthetized with ketamine in whom ventilation is controlled may provide an alternative approach in the evaluation of fentanyl-induced muscle rigidity.

Anesthesia↗
PubMed1989

Dexmedetomidine, acting through central alpha-2 adrenoceptors, prevents opiate-induced muscle rigidity in the rat.

The highly-selective alpha-2 adrenergic agonist dexmedetomidine (D-MED) is capable of inducing muscle flaccidity and anesthesia in rats and dogs. Intense generalized muscle rigidity is an undesirable side effect of potent opiate agonists. Although the neurochemistry of opiate-induced rigidity has yet to be fully elucidated, recent work suggests a role for a central adrenergic mechanism. In the present study, the authors determined if treatment with D-MED prevents the muscle rigidity caused by high-dose alfentanil anesthesia in the rat. Animals (n = 42) were treated intraperitoneally with one of the following six regimens: 1) L-MED (the inactive L-isomer of medetomidine), 30 micrograms/kg; 2) D-MED, 10 micrograms/kg; 3) D-MED, 30 micrograms/kg; 4) D-MED [30 micrograms/kg] and the central-acting alpha-2 antagonist, idazoxan [10 mg/kg]; 5) D-MED [30 micrograms/kg] and the peripheral-acting alpha-2 antagonist DG-5128 [10 mg/kg], or; 6) saline. Baseline electromyographic activity was recorded from the gastrocnemius muscle before and after drug treatment. Each rat was then injected with alfentanil (ALF, 0.5 mg/kg sc). ALF injection resulted in a marked increase in hindlimb EMG activity in the L-MED treatment group which was indistinguishable from that seen in animals treated with saline. In contrast, D-MED prevented alfentanil-induced muscle rigidity in a dose-dependent fashion. The small EMG values obtained in the high-dose D-MED group were comparable with those recorded in earlier studies from control animals not given any opiate. The high-dose D-MED animals were flaccid, akinetic, and lacked a startle response during the entire experimental period.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
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↗
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↗
PubMed1989

Chest wall rigidity during fentanyl- and midazolam-fentanyl induction: ventilatory and haemodynamic effects.

In a double-blind randomised study, we examined if pretreatment with small doses of midazolam, given before anaesthesia induction with fentanyl, influences the occurrence of fentanyl-induced thoracic rigidity (FITR). At the same time, the effect of rigidity on the cardiovascular and respiratory system was assessed. Sixteen patients undergoing coronary artery bypass surgery were divided into two groups. The midazolam group (M) received 0.075 mg/kg midazolam i.v. and the placebo group (P) NaCl 0.9% 3 min before the start of fentanyl induction. During the induction period, FITR was assessed clinically on a 3-point scale. Haemodynamic and respiratory variables were collected before anaesthesia induction, at the end of the fentanyl infusion and 3 min after intubation. The incidence of FITR was high in both groups: 63% in Group M and 75% in Group P (n.s.); however, its severity was less in Group M. The appearance of rigidity affected the cardiovascular and the respiratory system: central venous and pulmonary capillary wedge pressures showed a sharp increase in patients with FITR accompanied by CO2 retention, due to an inability to ventilate these patients adequately. We conclude that small doses of midazolam do not prevent, but may attenuate, FITR and that the appearance of rigidity causes alterations of haemodynamic and respiratory variables during induction.

Clinical Trials as Topic↗
PubMed1986

A new class of potent centrally acting muscle relaxants: pharmacology of oxazolidinones in rat decerebrate rigidity.

The severity of anaemic decerebrate rigidity was quantitatively determined by measuring the frequency of electromyographic potentials in the rat. Some oxazolidinones markedly reduced the severity of this decerebrate rigidity in a dose-dependent manner, (4S,5R)-4-(2-methylpropyl)-3- [3-(perhydroazepin-1-yl)propyl]-5-phenyl-1,3-oxazolidin-2-on e (MLV-6976) being the most potent. In addition to the oxazolidinones, an aminoalcohol derivative, (1RS,2SR)-5-methyl-1-phenyl-2-(3-piperidinopropylamino )hexan-1-ol (MLV-5860) also reduced the rat decerebrate rigidity. In the oxazolidinone series, the optical isomers with absolute configuration (S) at the 4-position were more potent than the corresponding (4R)-isomers, while there was no significant difference in their LD50 values. Normal rats and mice receiving MLV-6976 at doses which reduced decerebrate rigidity showed no behavioural changes, impairment of motor coordination only appearing at extremely high doses. MLV-6976 and its derivatives did not affect spinal reflex potentials in cats. MLV-6976 reduced the severity of harmaline-induced tremor in mice in a dose-dependent manner, but slightly augmented tremorine-induced tremor. The frequency of the spike discharges induced by iontophoretically applied glutamate was reduced by MLV-6976 in a dose-dependent manner in rat cortical neurones. The amplitude of miniature endplate potentials of the rat diaphragm was decreased by MLV-6976 only at concentrations greater than 0.1 mM. It is concluded that MLV-6976 acts on the brainstem or/and higher levels of the brain rather than on the spinal cord or the peripheral nervous system to reduce the excessive activities of the nervous system.

Animals↗
PubMed1992

Stretch reflex of quadriceps femoris and its relation to rigidity in Parkinson's disease.

Much evidence suggests that parkinsonian rigidity is due to hyperactivity of a reflex arc. While tendon jerk and H reflex are not modified in Parkinson's disease (PD), the long-latency component of stretch reflex (LLR) shows an increased size in PD. It has been proposed that this modification could account for rigidity. We studied in 14 PD patients and 8 normal subjects the stretch reflex of the quadriceps femoris. The muscle was stretched by a torque motor in two experimental sets: at rest and with voluntary background activity. Latency, duration and size of the reflex were compared in two groups; correlation between size of the reflex and rigidity was investigated. A lower threshold for the reflex was found in PD patients in trials at rest, and LLR showed increased size and duration in trials with background activity. No clear relationships between these data and rigidity were demonstrated.

Adult↗
PubMed1993

Time course of postanoxic akinetic-rigid and dystonic syndromes.

Twelve previously normal patients with anoxic brain damage due to various causes are described. The mean age at anoxia was 27.4 years. Six patients, in their fourth decade or older, developed an early akinetic-rigid syndrome; the mean interval between anoxia and akinetic-rigid syndrome was 3.1 months (range, less than 1 week to 12 months). Four of these six patients also developed dystonia, usually after some months. Six other patients, all children or young adults, developed a pure dystonic syndrome; the mean interval between anoxia and dystonia was 9.7 months (range, 1 week to 36 months). Dystonia was generalized and progressed over a mean period of 21.9 months (range, 3 to 96 months). Severe bulbar involvement was common. Age determined whether an akinetic-rigid or a dystonic syndrome developed in our patients and those reported in the literature. Many, but not all, patients had lesions on brain imaging (or at autopsy). In those with visible lesions in the basal ganglia, those with dystonia tended to have damage in putamen, while those with an akinetic-rigid syndrome tended to have damage in the globus pallidus. There were exceptions.

Adolescent↗
PubMed1995

Botulinum toxin A for spasticity, muscle spasms, and rigidity.

We studied the effects of botulinum toxin A in 12 patients with spasticity and in eight patients with rigidity. The study design was a double-blind, placebo-controlled crossover trial with botulinum toxin A versus saline. Using the Ashworth Scale for spasticity and the Unified Parkinson's Disease Rating Scale for rigidity, we gave the patients a tone grade before and 2 weeks after treatment. Improvement in tone by two grades or more was considered clinically significant. In the spasticity group, botulinum toxin A reduced the tone of all patients significantly, improved functionality and nursing care in eight of 12 patients, and alleviated painful spasms in five of five patients. In the rigidity group, muscle tone was decreased in seven of eight patients, functionality improved in four of seven, and joint and muscle pain decreased in four of five. We conclude that botulinum toxin A is effective against the disabling effects of spasticity and rigidity. The treatment was well tolerated.

Adolescent↗
PubMed1992

Alfentanil-induced rigidity in newborn infants.

The authors evaluated whether alfentanil could be given before treatment procedures in critically ill mechanically ventilated neonates without adverse effects. Alfentanil (mean dose 11.7 micrograms/kg, range 9-15) was given intravenously to 20 mechanically ventilated critically ill newborn infants (mean birth weight 2510 g, range 1490-3990) during the first 3 days of life before treatment procedures. Heart rate, arterial blood pressure, transcutaneous partial pressure of O2, respiratory rate, and general activity were observed continuously from 10 min before the administration of alfentanil until 1 h after it. Plasma alfentanil concentrations were measured in 15 subjects. The pharmacokinetics of alfentanil varied greatly among the subjects. The hemodynamic changes were not clinically significant, and the most important side effect was muscle rigidity. Nine infants had mild or moderate rigidity, which had little or no effect on ventilation. Four infants had severe rigidity and jerking comparable to convulsive activity, transiently impairing ventilation and oxygenation for approximately 5-10 min. Increased inspired oxygen and increased pressure by manual ventilation were needed to prevent hypoxemia. Electroencephalographic recordings for three infants during alfentanil administration showed no evidence of increased seizure activity. We conclude that alfentanil should not be used for newborn infants without simultaneous muscle relaxation because of the danger of rigidity.

Alfentanil↗
PubMed1999

Rigid spine syndrome. Two case-reports.

UNLABELLED: Rigid spine syndrome is characterized by massive spinal rigidity, usually most marked in the cervical region. Stiffness of the peripheral joints is sometimes present. We report two cases. Patient 1 was a 12-year-old boy diagnosed at three years of age with Duchenne's muscular dystrophy because of delayed onset of walking. Contracture of the Achilles tendons, flexion contracture of the elbows, and loss of motion of the cervical spine were the main findings during the current evaluation. Radiographs of the affected joints were normal. An electrocardiogram showed an incomplete left bundle branch block. Muscle enzyme activities were moderately elevated. A myopathic pattern was seen on the electromyogram. A muscle biopsy showed muscle fiber atrophy with peri- and endomysial fibrosis. Patient 2 was a 39-year-old man with a five-year history of isolated rigidity of the cervical spine thought to be due to a spondylarthropathy. Extension was the only movement possible at the cervical spine. The peripheral joints showed no motion range limitation. Findings were normal from radiographs of the spine and sacroiliac joints, an erythrocyte sedimentation rate determination, an electromyogram, and muscle enzyme activity assays. A muscle biopsy showed muscle fiber atrophy with peri- and endomysial fibrosis. DISCUSSION: Rigid spine syndrome is rare in rheumatological practice and can simulate a number of other muscle and joint diseases. Peri- and endomysial fibrosis may be strongly suggestive, although nonpathognomonic. Involvement of the heart governs the prognosis.

Adult↗
PubMed1989

[Fentanyl versus sufentanil basic anesthesia. Hypnotic effect, muscle rigidity and efficacy of competitive muscle relaxants].

As induction agents for cardioanesthesia, sufentanil (S) and fentanyl (F) are usually employed in combination with nondepolarizing muscle relaxants. We investigated potential interactions of these opioids with the relaxant component, paying special regard to the role of muscular rigidity and opioid-induced alterations of hemodynamics. Narcotic anesthesia was induced randomly in 45 coronary artery bypass patients with either F (20 micrograms/kg) or S (4 micrograms/kg). After 6 min, neuromuscular blockade was initiated within each group randomly with either vecuronium (V) or pancuronium (P) (0.01 mg/kg each). During opiate administration, the times for cessation of spontaneous respiration and loss of responsiveness to verbal and tactile stimuli were measured. The degree of opiate-induced muscular rigidity, simultaneous changes in arterial paCO2, cardiac indices (CI) prior to opioid and relaxant administration, onset and recovery from neuromuscular blockade (by electromyographic train-of-four registration), and motor response to laryngoscopy and intubation were recorded. The onset of spontaneous apnea (TK = time to breathing upon command only) and unresponsiveness (TM = time to controlled mask ventilation) was significantly faster with S than with F. Muscular rigidity was moderate in 25% of patients and severe in 35%-40%, during the administration of both narcotics. No significant differences between S and F were observed. During ventilation by face mask, patients with clinically apparent rigidity showed a statistically significant mean increase in paCO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics↗