Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to evaluate the feasibility of reflex excitability measurement techniques in the partial measurement of spasticity related to cerebral stroke. Techniques involved the testing of the soleus H-reflex at specific ankle positions during passive dorsiflexing movements with and without background plantarflexing contractions; conditions attempted to simulate the terminal stance phase of gait. Testing of 12 stroke subjects, having cerebrovascular lesions related only to occlusion of the middle cerebral artery, demonstrated significantly (p < 0.01) less inhibition of the H-reflex during passive ankle dorsiflexion compared to 12 matched, healthy controls. However, evocation of the H-reflex during a low-level, voluntary plantarflexing contraction concomitant with passive dorsiflexion, did not reflect a statistical difference between the two groups. The two conditions were thought to each represent measures of faulty presynaptic inhibition as indicators of cerebral spasticity. A Chi-square calculation of sensitivity for the passive ankle movement without background plantarflexing contraction condition, was shown to significantly differentiate (p < 0.05) between the stroke and normal groups. A positive, but weak, correlation was found for stroke subjects between this reflex measure and the Ashworth clinical measure of spasticity (r = 0.49). Although stroke subjects exhibited increased joint stiffness when the full range of passive ankle dorsiflexion movement was considered, in comparison to the matched healthy control subjects, no significant increase in passive stiffness was found at the joint position of the reflex evocation. Size of the cerebral lesion, as determined from CT or MRI scan, was not related to the spasticity measures. Therefore, in a homogeneous stroke sample, a component of cerebral spasticity i.e., faculty Ia presynaptic inhibition, has been measured during a simulated functional movement in the lower extremity and was shown to differentiate this group from a matched, healthy, control sample. Joint stiffness did not contaminate the measures.
 ...
PMID:A reflex technique to measure presynaptic inhibition in cerebral stroke. 764 61

CVA is a very common problem that can lead to lower extremity complications. Impairment in gait pattern occurs often due to spasticity and less frequently due to prolonged flaccidity. This problem is manifested by equinus, varus, equinovarus, and toe flexion deformities. Therefore, prevention or elimination of spasticity must be achieved. Various modalities have been used, both conservative and surgical. Nonsurgical interventions include range of motion and strengthening exercises, pharmacologic agents, local anesthetic and phenol motor point blocks, and the use of orthoses. Surgical intervention should be considered after conservative treatment has failed. The goal of treatment is to reduce the deforming force as a result of spasticity and to allow for almost normal function to be achieved. This includes tendon transfers, tendon lengthenings, tenotomies, and arthrodeses of small toe joints. Preoperatively, the extent and progression of spasticity must be determined because this may affect the rate of recurrence of the deformity following surgical correction. The combination of arthrodeses of the interphalangeal joints and flexor tendon release is the best option in the presence of a spastic deformity. Arthrodesis provides for stability at the joint, whereas a flexor release eliminates the deforming force. Failure to address the plantar-flexor force of the long flexors can lead to instability at the fusion site. This may in turn lead to nonunion and recurrence of flexion contracture as shown in the case report in this article.
 ...
PMID:Stroke and its manifestations in the foot. A case report. 781 9

The spinal stretch reflex (SSR), or tendon jerk, is the simplest behavior of the vertebrate nervous system. It is mediated primarily by a wholly spinal, two-neuron pathway. Recent studies from several laboratories have shown that primates, human and nonhuman, can gradually increase or decrease the size of the SSR when reward depends on such change. Evidence of this training remains in the spinal cord after all supraspinal influence is removed. Thus, the learning of this simple motor skill changes the spinal cord itself. Comparable spinal plasticity probably plays a role in the acquisition of many complex motor skills. Intracellular physiological and anatomical studies are seeking the location and nature of this spinal cord plasticity. Attention focuses on the most probable sites of change, the group Ia afferent synapse on the alpha motoneuron and the motoneuron itself. Results to date indicate that modifications are present at several places in the spinal cord. Current clinical studies are investigating the use of spinal cord adaptive plasticity as a basis for a new therapeutic approach to spasticity and other forms of abnormal spinal reflex function that result from spinal cord injury, stroke, or other neurological disorders. In the future, understanding of spinal reflex plasticity may lead to development of improved training methods for a variety of motor skills.
 ...
PMID:Acquisition and maintenance of the simplest motor skill: investigation of CNS mechanisms. 786 82

An acute animal model (dorsal hemisection of the spinal cord in the decerebrate cat preparation) has been developed that closely mimics the spasticity in humans that occurs subsequent to partial spinal cord injury and hemiparetic stroke. In this animal model, there are severe disruptions in the pattern of recruitment and rate modulation of motoneurons. The cellular mechanisms of these deficits are being studied with a combined experimental/computer simulation approach. The initial studies indicate that changes in the intrinsic properties of motoneurons are not important, which means the mechanism for changes in recruitment and rate patterns must reside in an alteration in the organization of the synaptic input to motoneurons. Computer simulation studies of the effects of different synaptic inputs on motoneuron outputs show that inhibitory inputs can, under certain conditions, generate substantial disruptions in recruitment and rate modulation. Recent data indicate that the monoamines noradrenalin and serotonin, which are released by fiber tracts originating in the brainstem, may play an important role in maintaining normal levels of inhibition in spinal circuits. Pharmacological interventions based on the monoamines may provide effective means of reducing the deficits in recruitment and rate modulation.
 ...
PMID:Alterations in synaptic input to motoneurons during partial spinal cord injury. 786 83

This investigation estimated the mechanisms of tizanidine action on spasticity using a battery of neurophysiological methods. Thirty patients with old post-stroke spastic hemiparesis took part in the investigation. They were treated with tizanidine-mean daily dose 15.8 +/- 5.6 mg for a mean of 23.3 +/- 4.8 days. A questionnaire for assessment of subjective improvement after treatment used a 5-point scale. For standardization of the neurological examination 5-point scales were used to assess muscle tone, muscle force and tendon reflexes. A battery of neurophysiological methods was used to analyze different mechanisms of spasticity: for alpha motoneuron excitability--the F wave parameters; for presynaptic inhibition--the ratio of H reflex amplitudes before and after vibration of the achilles tendon (Hvibr/Hmax); for common interneuron activity--the flexor reflex parameters. Our results revealed that tizanidine reduces spastically increased muscle tone, but has no influence on muscle force, tendon reflexes, Babinski sign and ankle clonus. Tizanidine is supposed to act by increasing the presynaptic inhibition and decreasing of alpha motoneuron excitability. When spasticity has decreased presynaptic inhibition and increased motoneuron excitability, it is better to treat with tizanidine.
 ...
PMID:Mechanisms of tizanidine action on spasticity. 804 46

The relative importance of hyperreflexia and paresis in disturbances of voluntary arm movement was studied in a group of patients (n = 25) with spasticity arising from a unilateral ischemic cerebral lesion. Patient performance was evaluated against data obtained from normal subjects (n = 15). Spastic patients achieved lower maximum movement velocities during flexion or extension than did normal subjects. The more marked the paresis of the elbow flexor and extensor muscles of the patients, relative to the strength of the normal subjects, the greater was this reduction in maximum velocity. For a given velocity, however, the time taken to complete a movement and the time to reach the peak velocity were normal. No relationship was found between the degree of impairment of voluntary movement and the level of passive muscle hypertonia in the antagonist. Although overactivity of the antagonist muscle may play some role in disturbance of movements made at low velocities without an opposing load, antagonist activity during movements made against a load (i.e., under more natural conditions) was at or below normal levels, even in those patients with the most marked passive muscle hypertonia. It is concluded that agonist muscle paresis, rather than antagonist muscle hypertonia, plays the dominant role in the disturbance of voluntary elbow movement following stroke.
 ...
PMID:Voluntary movement at the elbow in spastic hemiparesis. 808 Feb 47

Secondary prevention is of importance when the patient is already suffering from a serious disease, e.g., from arterial obstruction causing a stroke or an amputation, from a hip fracture or other diseases that might threaten his independence. Secondary prevention covers a wide field of topics. First of all, the patient must recover from his acute disease. It is important to avoid complications which are not specific for the disease, but are typical for a bedridden old person (decubital ulcer, dehydration and others). Prevention also means to avoid recurrence of the same disease as well as complications that frequently occur during the clinical course and may influence the outcome (spasticity in stroke patients, muscular calcification following hip replacement). Frequently, old persons do not completely recover following serious disease, they are limited in their daily activities and their capability to leave home. Secondary prevention tries to fight isolation; the patient should live a meaningful life.
 ...
PMID:[Secondary prevention from the viewpoint of the geriatric specialist]. 814 79

The purpose of this investigation was to ascertain a complex of electromyographic methods suitable for evaluation of the basic segmental pathophysiological mechanisms of spasticity. Clinical and electromyographic examinations were performed on 120 patients with spastic hemiparesis after stroke. Patients muscle tone, muscle force and tendon reflexes were assessed by the well known clinical five point scales. A battery of electromyographic methods was used to analyze different segmental mechanisms of spasticity: for alpha motoneurone activity--the F-wave parameters; for gamma motoneurone activity--the TA/H amplitude ratio; for common interneurone activity--the flexor reflex parameters; for presynaptic inhibition--the Hvibrated/Hmaximal amplitude ratio. Our results revealed that nearly all of the patients have increased alpha motoneurone activity on the spastic side. In most of the patients at least two of the segmental mechanisms are altered. Different mechanisms participate with different frequency in development of spasticity. We suppose that alpha-motoneurone hyperactivity usually develops secondary after alteration of some other segmental mechanism. In conclusion the applied complex of electromyographic methods gives the possibility for evaluation of the individual pathophysiological profile of patients with spasticity. This is a background for appropriate treatment.
 ...
PMID:Examination of the segmental pathophysiological mechanisms of spasticity. 818 81

The frequency of prolonged muscular flaccidity (PMF) was examined in a series of stroke patients in chronic phase suffering from hemiplegia with minimal spontaneous recovery (MSR). The results indicated that in such a population with poor motor recovery, PMF was significantly more frequent than spasticity. PMF was found to be associated with left-sided hemiplegia and unilateral spatial neglect. The minimal spontaneous recovery of the series of stroke patients we studied could be dependent on the interaction of three negative prognostic factors: left sided hemiplegia, unilateral spatial neglect and prolonged muscular flaccidity.
 ...
PMID:Prolonged muscular flaccidity: frequency and association with unilateral spatial neglect after stroke. 829 27

The biomechanics of push-off and propulsion are described as part of normal gait. Deviations from a normal gait pattern, as well as secondary complications, are discussed in reference to common limps, such as gastrocnemius and soleus weakness and the hemiparetic stroke gait. In addition to the lack of propulsion, major abnormalities include the instability of the knee and the lack of motion at the ankle, associated with muscle imbalance and spasticity. The correction of the abnormalities by ankle-foot orthoses is described in quantitative terms. Proper adjustment of the orthosis is essential for optimal guided correction.
 ...
PMID:Push-off and propulsion of the body in normal and abnormal gait. Correction by ankle-foot orthoses. 838 38


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>