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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Torque curves were recorded during passive and active ankle joint movements at three preset angular velocities (30, 60 and 120 degrees/s) with the subject in the supine position and 45 degrees hip and knee angles. Recordings were performed in normal subjects (n = 11), patients with clinical spasticity (n = 10) and patients with Parkinson's disease (n = 7). The torque curves recorded during passive dorsiflexion followed by plantar flexion showed a counterclockwise hysteresis loop with minimal area in the normal subjects and a large area in patients, especially at the highest velocity. The torque increase during dorsiflexion was proportional to the angular velocity in the patients with spasticity but not in the patients with Parkinson's disease. In the patients with spasticity, a good correlation was found between clinical assessment of hypertonia and measurements of torque during passive movements but not torque values during maximal voluntary dorsiflexion. A model for data reduction and estimation of instant slope values on different parts of the torque-angle curve is suggested. The use of ankle torque recordings for evaluation of treatment effects is exemplified.
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PMID:Measurement of torque during passive and active ankle movements in patients with muscle hypertonia. A methodological study. 658 32

Electromyographic (EMG) recordings from multiple muscle groups with surface electrodes during systematic evaluation of phasic and tonic stretch reflexes, cutaneomuscular reflexes, long loop reflexes, postural reflexes, and volitional activation have been used to provide a neurophysiologic basis for selection of the appropriate treatment for spasticity, and to gain further insights into the general mechanisms of spasticity. Pharmacologic methods are useful as a temporary measure. Hypertonia of a single muscle can be effectively treated with 40% alcohol injections to the motor points and hypertonia of a muscle group with partial denervation through 6% phenol in water injected into the nerve trunk. Hypertonia of several muscle groups can be treated by chemical or surgical rhizotomy or myelotomy. Generalized hypertonia involving limb and trunk muscles can be modified through chronic epidural stimulation of the spinal cord. Modification of reciprocal antagonistic muscle activity may be achieved through electrical stimulation of the involved nerve trunks.
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PMID:Spasticity: medical and surgical treatment. 699 92

The surface electromyogram (EMG) of mm. tibialis anterior and triceps surae was recorded in 10 patients with spasticity, 10 patients with rigidity and 20 normal subjects and correlated with the changes in ankle joint angle during the different phases of the gait cycle. While the strength and timing of EMG activity recorded from triceps surae during the stance phase of gait did not differ from that of normal subjects, the EMG of tibialis anterior was significantly stronger during the swing phase in both groups of patients. Although the reciprocally organized innervation pattern of the leg muscles was preserved, spastic patients could hardly lift up the affected foot during the swing phase despite the enhanced activity of tibialis anterior. There was no coactivation of the calf muscles during the hyperactivity of tibialis anterior. Therefore, no electrophysiological explanation could be found for the increased muscle tone in either group of patients. The possibilities of reduced force development by the muscle fibres of tibialis anterior or of some mechanical obstruction in the ankle joint were largely excluded as alternative explanations underlying the impeded elevation of the foot. We suppose that in both diseases the muscle fibres undergo changes which are responsible for increased muscle tone in spasticity and rigidity. The pathophysiological mechanism of these changes remains unknown.
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PMID:Electrophysiological studies of gait in spasticity and rigidity. Evidence that altered mechanical properties of muscle contribute to hypertonia. 727 9

The effects of various cerebral cortical lesions on motor function and in particular on muscle tone have been studied quantitatively in the squirrel monkey (Saimiri sciureus) in an attempt to define the cause of muscular hypertonia and to develop a reliable model for human cerebral spasticity. Unilateral ablation of the primary motor area (MI), either alone or together with the supplementary motor area (MII), produced a contralateral hemiparesis especially marked for fine motor tasks, but did not cause hypertonia. Bilateral ablation of the supplementary motor area alone produced no impairment of motor function or change in muscle tone. Bilateral lesions of the primary motor area, either alone or together with the supplementary motor area, caused a disabling quandriparesis with striking hypertonia affecting chiefly the upper limb flexors and lower limb extensors. Quantitative electromyography revealed augmented stretch responses proportional to the rate of muscle lengthening. This velocity-dependent exaggerated stretch reflex, with a predominantly dynamic component reflecting hyperactivity of the Ia spindle afferents, is similar to that seen in human hemiplegic spasticity. Out results indicate that decorticate hypertonia depends upon the bilateral interruption of fiber tracts originating in motor cortex and distributed both ipsilaterally and contralaterally. Bilateral decortication in the primate seems to be a suitable laboratory model for the objective evaluation of measures proposed for the relief of spasticity in humans.
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PMID:Quantitative assessment of muscular hypertonia resulting from cortical lesions in primates. 727 72

Spasticity is one of the major problems affecting the outcome of rehabilitation in paraplegic patients. Orphenadrine citrate possesses an effective muscle relaxant action in many pathologies. Nevertheless, despite a recognized central site of action, no controlled data are available on its use in the treatment of spastic hypertonia in patients with spinal cord injuries. Therefore, the effect of intravenous administration of 60mg of orphenadrine citrate versus placebo on spastic hypertonia after spinal cord injury was studied in 11 patients. The threshold of the flexion reflex of the lower limb was studied as a neurophysiological correlate of spastic hypertonia. Clinical assessment was made using the Ashworth Spasticity Scale. The threshold, expressed in mAmp, was studied for 60 minutes after the treatment. A significant difference was found using the active drug compared with placebo (p < 0.0001). In 9 patients, the reduction of the abnormal flexion responses after orphenadrine appeared to begin only after 30 minutes. In one patient the onset of the therapeutic effect was early but weak. One patient with severe spastic hypertonia leading to triple flexion when the limb was manipulated did not gain any relief with orphenadrine. The clinical and neurophysiological results suggest an efficacy of orphenadrine citrate in the control of spastic hypertonia in paraplegics. This could be relevant in the rehabilitation strategy, although further studies are needed on the duration of its action.
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PMID:Reduction of spastic hypertonia in patients with spinal cord injury: a double-blind comparison of intravenous orphenadrine citrate and placebo. 760 86

Today it is accepted that chronic infusion of baclofen produces significant relaxation and drastic reduction of spasms, amelioration of cramping pain and improvement of sphincter functions in spasticity of spinal cord origin. Based on these results our group had the opportunity of treating 11 cases with refractory spasticity and dystonic symptoms due to central damage caused by head injury in 8 cases and to cerebral palsy in 3 using cervical intrathecal infusion of baclofen. During the trial period with percutaneous intrathecal infusion of a daily bolus of 12.5-75 micrograms of baclofen through a reservoir, improvement of mentation and speech conditions, marked improvement of dystonic and abnormal movements of the upper limbs and trunk and a notable reduction of hypertonia were observed in all cases, which led to a better performance of motor activities in skilled acts and transfer. With these preliminary results in mind, in all cases the previous cervical subarachnoid catheter was attached to a programmable pump that infused a daily total dose varying from 100 to 190 micrograms of baclofen in a continuous or multistep complex mode. After a mean follow-up of 21 months previous results were long-lasting. Neither overdose side effects nor malfunction of the system were observed.
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PMID:Management of intractable spasticity of supraspinal origin by chronic cervical intrathecal infusion of baclofen. 763 Oct 54

Herein we report the development of a canine model to examine transplacental and/or transmammary transmission of Neospora caninum. Six pregnant bitches were experimentally infected with N. caninum on day 21 of gestation. One bitch successfully delivered a litter of 3 live pups. These pups showed slight proprioception deficits, increased muscle tone, and spasticity in both pelvic limbs; however, N. caninum was neither demonstrated by bioassay in cell culture nor seen in histological sections of tissues from these pups. The remaining 5 bitches aborted. Neospora caninum was isolated from tissues of 4 of the experimentally infected bitches and pups from 2 of the miscarried litters. Experimental infections of 2 litters of 5-day-old nursing pups produced variable results. Neospora caninum was isolated from 2 of 2 inoculated pups in 1 litter and 3 of 6 inoculated pups in the second litter.
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PMID:Vertical transmission of Neospora caninum in dogs. 770 95

The use of phenol motor nerve blocks is advantageous in the early period of acquired spasticity (ie, that occurring following traumatic brain injury or incomplete spinal cord injury), when increased muscle tone is often the most severe. Because acquired spasticity is dynamic and usually improves slowly, a temporary treatment method used to ameliorate increased muscle tone is desirable. Phenol nerve infiltration provides a temporary motor nerve block that lasts for weeks or months. It allows passive limb mobilization in a comprehensive rehabilitation program that attempts to prevent fixed soft tissue contractures. Permanent or irreversible methods such as operative tendon lengthening, muscle release or recession, or neurectomy are usually best delayed until the spasticity has become static, when the need for surgical correction becomes more firmly indicated, and outcomes of operative intervention are more predictable. Although phenol nerve blocks were initially administered at the spinal cord level to control spasticity, the potential side effects have caused a loss of popularity of this method of administration. The safer and more common use of phenol infiltration at the peripheral nerve level is now more accepted for brain injury and spinal cord injury patients. This report reviews the indications, current concepts, and development of the different methods used to administer phenol nerve blocks. Comparisons to other methods to control spasticity are discussed.
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PMID:Treatment of acquired muscle spasticity using phenol peripheral nerve blocks. 774 50

Spasticity results from various pathophysiologic abnormalities in spinal cord neuronal circuits. Noninvasive electrophysiologic techniques can be used to study these circuits in humans. The best correlation between briskness of reflexes and results of electrophysiologic testing is found with reduction in vibratory inhibition, a test that reflects presynaptic inhibition. For increase in muscle tone, the best correlation is found with reduction of Ib nonreciprocal inhibition. These test results, which are stable under controlled conditions, are influenced by myorelaxant drugs and may be used to analyze the mode of action of new products because the tests study specific circuits involving known neurotransmitters. Tizanidine reinforces presynaptic inhibition and two types of postsynaptic inhibition: Ia reciprocal and Ib nonreciprocal. It also markedly reduces flexor reflexes. These effects are explained by an action exerted on spinal interneurons deprived of their normal monoaminergic descending innervation. The spectrum of activity for tizanidine is thus broad, making it likely that tizanidine corrects more than one pathophysiologic abnormality. Because tizanidine reinforces presynaptic as well as Ib nonreciprocal inhibition, it may reduce both brisk tendon jerks and muscle hypertonia.
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PMID:Tizanidine and electrophysiologic analysis of spinal control mechanisms in humans with spasticity. 797 7

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.
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PMID:Mechanisms of tizanidine action on spasticity. 804 46


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