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At least 631 records · Page 35Linked to original sources
PubMed2004

Clawed toes deformity due to spasticity of the extensor digitorum muscle. A case report.

Spasticity is a characteristic and early component of the lesions of the pyramidal tract of demyelinising diseases such as multiple sclerosis, and is included in the chief neurological scales to evaluate this disease. We report the case of a woman with a clawed toes deformity caused by spasticity of the extensor digitorum (longus and brevis) muscles.

Journal Article↗
PubMed2001

The effect of quadriceps femoris muscle strengthening exercises on spasticity in children with cerebral palsy.

BACKGROUND AND PURPOSE: The Bobath neurodevelopmental treatment approach advised against the use of resistive exercise, as proponents felt that increased effort would increase spasticity. The purpose of this study was to test the premise that the performance of exercises with maximum efforts will increase spasticity in people with cerebral palsy (CP). Spasticity, in the present study, was defined as a velocity-dependent hyperexcitability of the muscle stretch reflex. SUBJECTS: Twenty-four subjects with the spastic diplegic form of CP (mean age=11.4 years, SD=3.0, range=7-17) and 12 subjects without known neurological impairments (mean age=11.6 years, SD=3.5, range=7-17) were assessed. METHODS: Knee muscle spasticity was assessed bilaterally using the pendulum test to elicit a stretch reflex immediately before and after 3 different forms of right quadriceps femoris muscle exercise (isometric, isotonic, and isokinetic) during a single bout of exercise training. Pendulum test outcome measures were: (1) first swing excursion, (2) number of lower leg oscillations, and (3) duration of the oscillations. RESULTS: There were no changes in spasticity following exercise between the 2 groups of subjects. DISCUSSION AND CONCLUSION: These results do not support the premise that exercises with maximum efforts increase spasticity in people with CP.

Adolescent↗
PubMed1996

Acoustic and electrical activities during voluntary isometric contraction of biceps brachii muscles in patients with spastic cerebral palsy.

This study was designed to compare electromyogram (EMG) and acoustic myogram (AMG) recordings of biceps brachii muscles in patients with spastic cerebral palsy (CP). The maximal voluntary contraction (MVC) in the CP group was approximately one half of that of the normal group even after being normalized by the muscle cross-sectional area (CSA) (18.6 - 5.9 kNm/m2 in CP, 37.3 +/- 2.9 kNm/m2 in normal). Both CP and normal groups demonstrated a progressive increase in the root mean squared values per unit muscle CSA in the EMG (RMSEMG/CSA) as well as in the AMG (RMSAMG/CSA) with increasing force up to 50% MVC. The increasing magnitude of the RMSEMG/CSA with force was not significantly different between two subject groups. However, all the levels of force resulted in significantly smaller RMSAMG/CSA in the CP group compared to the normal group. The ratios of RMSAMG to RMSEMG in the CP group (0.75 +/- 0.03 m/s2/mV) were significantly smaller than those in the normal group (1.37 +/- 0.07 m/s2/mV) at force levels above 30% MVC. These results suggest that motor disabilities in CP patients are caused not only by primary neural impairment but also by secondary deterioration in muscular contractile properties, probably resulting from muscle fiber atrophy. This appears to be more selective in fast twitch fibers.

Acoustics↗
PubMed1985

Intrinsic laryngeal muscle activity in a spastic dysphonia patient.

EMG activity from four intrinsic laryngeal muscles (thyroarytenoid, posterior cricoarytenoid, interarytenoid, and cricothyroid) was obtained from one female spastic dysphonia patient while she performed a variety of speech and nonspeech tasks. These tasks were performed before and during a period of temporary unilateral laryngeal muscle paralysis. In the nonparalyzed condition, adductory muscle activity showed intermittent sudden increases that coincided with momentary voice arrests. These muscle patterns and accompanying voice interruptions were not present either when speech was produced in falsetto register or at anytime during the paralysis condition. The data suggest that individuals with this type of spastic dysphonia have normal morphology of recurrent laryngeal nerves and intrinsic laryngeal muscles, which means that the triggering mechanism(s) for spastic dysphonia symptoms must be located at some point neurologically upstream from the larynx.

Combined Modality Therapy↗
PubMed1971

Hamstrings stretch reflex in human spasticity.

In 16 patients with spastic paralysis the hamstrings stretch reflex was found to increase as the velocity of stretch increased, and generally to subside after movement ceased. These effects are attributable to the dynamic property of the primary spindle ending. The stretch reflex commonly appeared in only the last third of the stretching movement and was maximal as the knee became fully extended. This is consistent with the static properties of the primary and secondary spindle endings, and accounts for the absence of the clasp-knife phenomenon in the spastic hamstrings. The difference in the nature of the stretch reflex in spastic flexor and extensor muscles is best explained by the differential reflex effects of group II afferent fibres which facilitate flexor motoneurones and inhibit extensor motoneurones.

Electromyography↗
PubMed1980

Neurophysiological evaluation of chronic spinal cord stimulation in patients with upper motor neuron disorders.

Spinal cord stimulation was found to be an effective method for improving motor performance in patients with upper motor neuron disorders. Electromyographic analysis of segmental and suprasegmental activity was performed in 11 patients who had used spinal cord stimulation for more than 12 months. Neurophysiological analysis of electromyographic findings revealed improvement of volitional motor control and a reduction of spasticity in the examined muscles of the lower limbs in all patients.

Adult↗
PubMedDate not supplied

[The potentials of manual therapy in the neuromotor correction of the statokinetic disorders in infantile cerebral palsy].

It is shown that manual therapy to abolish functional cervical and lumbar blocks is beneficial in reducing spasticity of the synergic muscles, biomechanic characteristics of the support and kinematic pace phases improve. Manual therapy in multimodality rehabilitation treatment of cerebral paralysis creates a functional base for neuromotor correction of a defective motor stereotype in these patients.

Adolescent↗
PubMed1987

Triceps spasticity in traumatic hemiplegia: diagnosis and treatment.

Three patients with adult-acquired hemiplegia are described with the unusual dynamic deformity of spasticity of the triceps muscle. This deformity produces motor imbalance with the triceps overpowering the elbow flexors, thus impeding volitional elbow flexion. The nature of the deformity was defined by electromyography of the muscle groups about the elbow, which demonstrated out-of-phase inhibitory electrical activity of the triceps muscle. Treatment consisted of V-Y lengthening of the triceps muscle to achieve agonist-antagonist motor balance. The operation improved hand placement for all three patients.

Adult↗
PubMed1993

Effect of the beta-carboline abecarnil on spinal reflexes in mice and on muscle tone in genetically spastic rats: a comparison with diazepam.

Abecarnil is a beta-carboline agonist at benzodiazepine receptors with potent anxiolytic activity but no muscle relaxant side effects in rodents. Clinical experience suggests that changes in the muscle tone induced by benzodiazepines are related to their effects on spinal reflexes. The authors therefore analyzed the effect of treatment with abecarnil on spinal monosynaptic (Hoffmann reflexes) and polysynaptic (flexor) reflexes in mice and the influence of abecarnil on muscle tone in genetically spastic rats. The i.v. administration of abecarnil in mice (dose range, 0.02-1 mg/kg) depressed flexor reflexes in a dose-dependent manner; Hoffmann reflexes remained unchanged. Administration of diazepam i.v. (0.01-1 mg/kg) also reduced flexor reflexes and had little or no effect on Hoffmann reflexes. In genetically spastic rats, i.v. administration of abecarnil (10-30 mg/kg) decreased the muscle tone in a dose- and time-dependent manner. A similar muscle relaxant effect was observed in such rats after i.v. administration of diazepam (0.1-0.8 mg/kg). By contrast, i.p. administration of abecarnil in mice did not influence spinal reflexes up to the dose of 1 mg/kg and, in genetically spastic rats, did not affect muscle tone up to the dose of 100 mg/kg. Administration of diazepam i.p. (1 mg/kg) depressed flexor reflexes in mice and over the range 0.2 to 5 mg/kg produced a dose- and time-dependent decrease of muscle tone in genetically spastic rats. The muscle relaxant effect of i.p. diazepam could be antagonized by i.p. administered abecarnil. These studies thus demonstrate that i.v. but not i.p. administration of abecarnil may result in muscle relaxant action in mice and in genetically spastic rats.

Animals↗
PubMed2000

[Ultrastructural study on the peripheral nerve and skeletal muscle of patients with spastic cerebral palsy].

OBJECTIVE: To explore pathological features of the peripheral nerve and skeletal muscle of patients with spastic cerebral palsy. METHODS: The peripheral nerve and skeletal muscle of 25 patients with spastic cerebral palsy were observed by gross examination during operation, and under microscope and electron microscope. RESULTS: Gross examination showed that peripheral nerve and skeletal muscle was normal during operation. Microscope showed that some skeletal muscle fibers degenerated, and the connective tissue proliferated. electronmicroscopically the damage of demyelination was extensive on the peripheral nerve; the pathological changes of Schwann's cell were sooner and more severe than axons; the pathological changes of myelinated nerve fiber were more obvious than the nonmyelinated nerve fiber; the lymphocyte were found around the microvasculature within the perineurium; the mitochondrion of skeletal muscle fiber increased in number, the sarcoplasmic reticulum and transverse tubule decreased and developed badly, the degenerative muscle fiber showed cell edema or the pathological changes of myofibril. All the peripheral nerve and skeletal muscle fiber affected had no repair and regeneration. CONCLUSIONS: The demyelination of the peripheral nerve of patients with spastic cerebral palsy is primary, and the skeletal muscle of patients with spastic cerebral palsy is secondary pathological change. The activity of nerve and muscle regeneration is bad.

Adolescent↗
PubMedDate not supplied

[Muscle tonus in rigidity and spasticity].

The results of the examination of the muscle tone by passive movement of the extremity at a low and high rate in patients with spasticity are discussed. In parkinsonism high resistance was noted to passive movements of the extremity at a low rate (with a period of oscillatory movement of 100 s and more) as well as in the first cycles of rapid sinusoidal movement (with a period of 1 s) if the extremity had been at rest for a lengthy period of time. In spasticity of other etiology, there was a gradual increase of the amplitude on the mechanomyogram in high rates of passive movements, which was evidently due to growth of stimulation in the stretch-reflex arc from cycle to cycle as the result of sumation with trace stimulation from the preceding cycles. The shape of the spectromechanomyogram, which is marked by a rise in the region of the high rates, is considered to be a sign of spasticity, whereas the size of this rise is accepted as a quantitative index of the spastic component of the muscle tone.

Electromyography↗