[Effect of local hypothermia on the muscle tonus in spastic paresis].
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Spinal cord injury can lead to an exaggeration of transmission through spinal pathways, resulting in muscle spasticity, chronic pain, and abnormal control of blood pressure and bladder function. These conditions are mediated, in part, by N-methyl-D-aspartate (NMDA) receptors on spinal neurons, but the effects of cord injury on the expression or function of these receptors is unknown. Therefore, antibodies to the NMDA-R1 receptor subunit and binding of [3H]MK-801 were used to assess NMDA receptors in the spinal cord. Receptor density in rats with intact spinal cords was compared to that in rats 1 and 2 weeks after spinal cord transection (SCT) at the mid-thoracic level. At 1 and 2 weeks after SCT, [3H]MK-801 binding was reduced in most laminae in cord segments caudal to the injury, whereas no decrease in amount of R1 subunit immunoreactivity was observed. No significant changes in [3H]MK-801 binding and NMDA-R1 immunoreactivity could be seen rostral to the transection. Since [3H]MK-801 binding requires an open ion channel, the discrepancy between [3H]MK-801 binding and immunocytochemistry may indicate a loss of functional receptors without a consistent change in their total number. Therefore, the exaggerated reflexes that are well established in rats 2 weeks after cord injury must be mediated by a mechanism that withstands attenuation of NMDA receptor function.
Between April 1987 and March 1996, 32 deformed hands of 31 patients with cerebral palsy were treated with combined release of the flexor digitorum profundus, flexor digitorum superficialis, and intrinsic muscles. Of these 31 patients, 26 patients (27 hands) were followed up after treatment. Improvements were evaluated by the modified classification of Zancolli et al, the classification of House et al, the object handling score, and the activity of daily living score. Improvements of more than one level on an average were observed in the modified classification of Zancolli et al and the classification of House et al. The ability to grasp, pinch, and release increased with improvement of 2.5 points in the object handling score, and activities of daily living were enhanced with improvement of 2.4 points. The fine motor skills could be facilitated, and dexterity was restored in most patients.
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Neuromuscular biopsies were obtained in 10 patients with traumatic spinal cord lesions at various levels and in one patient with cerebral lesions due to a long lasting coma. In all cases, there was a rapid onset of both fibers types atrophy, with numerous transitional type III and intermediate fibers. Only the two patients with cervical lesions had an increased terminal innervation ratio suggesting denervation. Our observations do not support the hypothesis of a transneuronal degeneration. These changes cannot be related to disuse only as the atrophy does not preferentially involve type II fibers. The underlying neural mechanism of spasticity in muscle of patients with cortico-spinal lesions could explain the change of the histochemical pattern of the muscle fibers.
Dantrolene sodium or dantrolene1 is 1([5-(nitrophenyl)furfurylidend] amino) hydantoin sodium hydrate. It is indicated for use in chronic disorders characterised by skeletal muscle spasticity, such as spinal cord injury, stroke, cerebral palsy and multiple sclerosis. Dantrolene is believed to act directly on the contractile mechanism of skeletal muscle to decrease the force of contraction in the absence of any demonstrated effects on neural pathways, on the neuromuscular junction, or on the excitable properties of the muscle fibre membranes. Controlled trials have demonstrated that dantrolene is superior to placebo in adults or children with spasticity from various causes, as evidenced by clinical assessments of disability and daily activities, and by muscle and reflex responses to mechanical and electrical stimulation. It is somewhat less effective in patients with multiple sclerosis than in those with spasticity from other causes. There has been a general clinical impression in controlled trials that dantrolene caused less sedation than would have been expected from therapeutically comparable doses of diazepam. In 2 controlled trials, there was no significant difference between dantrolene and diazepam in terms of reductions in spasticity, clonus, and hyperreflexia, but side-effects such as drowsiness and inco-ordination occurred significantly more frequently on diazepam. Long-term studies have indicated continuing benefit for patients taking dantrolene, though the incidence of side-effects has often been high and there has been a suggestion of exacerbation of seizures in children with cerebral palsy. Dantrolene may be of value in the medical treatment of spasm of the external urethral sphincter due to neurological and non-neurological disease, and animal studies suggest a potential use in the management of malignant hyperpyrexia. Chemical evidence of liver dysfunction may occur in 0.7 to 1% of patients on long-term treatment with dantrolene, with symptomatic hepatitis in 0.35 to 0.5% and fatal hepatitis in 0.1 to 0.2%. The drug commonly causes transient drowsiness, dizziness, weakness, general malaise, fatigue and diarrhoea at the start of therapy. Muscle weakness may be the principal limiting side-effect in ambulant patients, particularly in those with multiple sclerosis, and therapy could be hazardous in patients with pre-existing bulbar or respiratory weakness. The dosage of dantrolene has been fixed in most controlled trials, though long-term studies have indicated the need for individualisation of dosage. The initial dose is usually 25mg once daily, increasing to 25mg two, three or four times daily, and then by increments of 25mg up to as high as 100mg two, three or four times daily. The lowest dose compatible with optimal response is recommended.
The relative contributions of variations in stretch reflex threshold and total joint stiffness to changes in stretch-evoked torque were assessed in the spastic elbow muscles of 14 hemiparetic spastic subjects. For a given subject, variations in torque, measured after a constant angular deflection, were mediated largely by changes in stretch reflex threshold, rather than by changes in reflex stiffness. Between-subject comparisons were sensitive to stiffness differences between limbs, but reflex thresholds were still broadly correlated with torque magnitude, suggesting that reductions in stretch reflex threshold are uniformly present in spastic muscles. These findings, coupled with the apparent similarity of reflex stiffness estimates in voluntarily activated spastic and normal muscles, suggest that the central disturbance in spasticity is a reduction in the threshold of the stretch reflex, without a significant enhancement of reflex gain.
Spasticity after a stroke interferes with the normal function of a limb. Electric stimulation has been used in a variety of ways to decrease spasticity. The purposes of this study were (1) to quantify the effectiveness of electric stimulation on decreasing ankle spasticity and (2) to develop a quantitative assessment of muscle tone, which could be replicated in the clinic. Ten patients with hemiparesis resulting from ischemic stroke participated in the study according to the selection criteria. Their mean age was 57 yr, with a mean stroke interval of 12.5 months. Patients received electric stimulation for 45 min through surface electrodes applied to the skin in the 12th thoracic and 1st lumbar areas. All patients received five electric stimulation treatment sessions. The electrical pulses were amplitude modulated frequency beat with a carry frequency of 2500 Hz and a stimulation frequency of 20 Hz. The stimulation intensity was adjusted to each patient to produce a sensory stimulation. The pre- and posttreatment evaluation included surface electromyography activity during passive ankle dorsiflexion, passive ankle dorsiflexion resistance at different angular velocities, as measured by an isokinetic machine and the modified Ashworth scale. Our results indicate that the surface spinal cord stimulation with middle frequency modulated to low frequency for sensory stimulation on the skin of 12th thoracic and first lumbar area is effective in reducing calf muscle spasticity of hemiplegic patients. The isokinetic torque measures for spasticity are a sensitive tool to document the effects of the treatment.
Lesions of the central nervous system often result in an upper motor neuron syndrome including spasticity, paresis with pyramidal signs, and painful spasms. Pharmacological treatment with oral antispasticity drugs is frequently associated with systemic side effects which limit their clinical use. Botulinum Toxin A (BtxA) injected in spastic muscles has been shown to be effective in reducing muscle tone, but only few studies have reported pain relief as additional benefit. Therefore, we investigated the effects of local BtxA injections in 60 patients with acute (< 12 months) and chronic spasticity and pain in a prospective multicenter study. Target muscles for BtxA were selected on the basis of clinical examination. Intramuscular BtxA injections were placed in muscles exhibiting increased muscle tone in combination with pain during passive joint movement. Patients received a mean total dose of 165.7 +/- 108.2 [30-400] units BOTOX((R)) per treatment session in a mean 3.4 +/- 1.5 muscles. Baseline and follow-up (mean 5.9 weeks) measures included a patient self-assessment of pain and function on a five-level scale, a physician's evaluation of function, and a global rating of response to BtxA. Fifty-four of sixty patients experienced improvement in pain without subjective functional improvement. The effects were comparable in acute (n = 17) and chronic (n = 43) spasticity. Physician's assessment of gain in function increased significantly (p < 0.05) only in patients with chronic spasticity. No serious adverse event was observed. Mild reversible side effects (local pain, hematoma, edema, mild weakness) were observed in four patients. In conclusion, we found that intramuscular BtxA injections are a potent, well-tolerated treatment modality to significantly reduce spasticity-related local pain. This problem may be a main indication, especially in patients with poor response or intolerable side effects to oral medication.
BACKGROUND AND PURPOSE: We sought to define an effective and safe dose of botulinum toxin type A (Dysport) for the treatment of upper limb muscle spasticity due to stroke. METHODS: This was a prospective, randomized, double-blind, placebo-controlled, dose-ranging study. Patients received either a placebo or 1 of 3 doses of Dysport (500, 1000, 1500 U) into 5 muscles of the affected arm. Efficacy was assessed periodically by the Modified Ashworth Scale and a battery of functional outcome measures. RESULTS: Eighty-three patients were recruited, and 82 completed the study. The 4 study groups were comparable at baseline with respect to their demographic characteristics and severity of spasticity. All doses of Dysport studied showed a significant reduction from baseline of muscle tone compared with placebo. However, the effect on functional disability was not statistically significant and was best at a dose of 1000 U. There were no statistically significant differences between the groups in the incidence of adverse events. CONCLUSIONS: The present study suggests that treatment with Dysport reduces muscle tone in patients with poststroke upper limb spasticity. Treatment was effective at doses of Dysport of 500, 1000, and 1500 U. The optimal dose for treatment of patients with residual voluntary movements in the upper limb appears to be 1000 U. Dysport is safe in the doses used in this study.
Isometric contractile properties of human elbow flexor muscles were examined in 27 normal subjects (7 females and 20 males). Contractions of elbow flexors were elicited by application of electrical pulses to the biceps motor points. The tension development was recorded at the wrist with the elbow angle fixed at 90 degrees--100 degrees. The data for the time to peak and time to half relaxation of the twitch, the twitch tension-to-tetanus tension ratio, and the posttetanic twitch potentiation are reported. The contractile properties of spastic elbow flexor muscles from 7 subjects who had been hemiparetic for periods ranging from 4 months to 60 months were found to be similar to those of muscles in normal subjects and unaffected muscles in hemiparetic subjects.
This research paper compares dental casts and lateral cephalometric radiographs of thirty children with spastic cerebral palsy with those of a control group to determine what effect spasticity and cerebral palsy have on dental occlusion and skeletal formation. Muscle spasticity can retard bone growth. Variations in the normal tonus of head and neck muscles can cause malocclusion and arch deformity.
This investigation quantified pre- and postsurgery (8 months) hamstring muscle spasticity and strength in children with cerebral palsy (CP) undergoing a selective dorsal rhizotomy. Nineteen children with CP (CP group) and six children with able bodies (AB group) underwent testing with a dynamometer. For the spasticity measure, the dynamometer measured the resistive torque of the hamstring muscles during passive knee extension at four different speeds. Torque angle data were processed to calculate the work done by the machine to extend the knee for each speed. Linear regression was used to calculate the slope of the line of best fit for the work velocity data. The slope simultaneously encompassed three key elements associated with spasticity (velocity, resistance, and stretch) and was considered the measure of spasticity. For the strength test, the dynamometer moved the leg from full knee extension to flexion while a maximum concentric contraction of the hamstring muscles was performed. Torque angle data were processed to calculate the work done on the machine by the child. Hamstring spasticity values for the CP group were significantly greater than similar values for AB group prior to surgery; however they were not significantly different after surgery. Hamstring strength values for the CP group remained significantly less than those for the AB group after surgery, but were significantly increased relative to their presurgery values. The results of spasticity testing in the present investigation agreed with previous studies indicating a reduction in spasticity for the CP group. The results of strength testing did not agree with those in the previous literature; a significant increase in strength was observed for the CP group.
Botulinum A toxin (BT) has been successfully used for the management of spasticity in cerebral palsy (CP). However, the long-term results of BT have not yet been determined. We have studied the evolution of a homogeneous group of patients with CP treated with BT. All these patients had an equinus gait resulting from calf muscle spasticity without other muscle group involvement. All of these patients were treated with the same total dose (4 microg/kg) at the same time interval (three months). The mean follow-up time was 33 months. Gait evaluation was made blind on videotape recordings by two independent physicians according to five point scale. All our patients exhibited a progressive improvement in their gait pattern. None of our patients developed fixed contractures nor did any of them need surgical correction. No significant side-effects were seen. The response observed in our study could be due to a progressive symptomatic effect of BT, but it might be also explained by a change in the natural history of the spasticity related to CP, at least in this selected group of patients.