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Long-term effect of shock wave therapy on upper limb hypertonia in patients affected by stroke.

BACKGROUND AND PURPOSE: Spasticity is a disabling complication of stroke and different noninvasive treatments are used to reduce muscle hypertonia. Shock waves are defined as a sequence of single sonic pulses largely used in the treatment of diseases involving bone and tendon as well as muscular contractures. The effect and duration of extracorporeal shock wave therapy (ESWT) was investigated on muscle hypertonia of the hand and wrist. METHODS: A total of 20 patients affected by stroke associated with severe hypertonia in upper limbs were evaluated. Placebo stimulation was performed 1 week before active stimulation in each patient. Evaluation was performed using the National Institutes of Health and Ashworth scales and video monitoring with a digital goniometer before and immediately after placebo or active stimulation. Motor nerve conduction velocity from abductor digiti minimi were recorded. Patients were monitored at 1, 4, and 12 weeks after active treatment. RESULTS: After active ESWT, patients showed greater improvement in flexor tone of wrist and fingers compared with placebo stimulation. At the 1- and 4-week follow-up visits, a significant decrease of passive muscle tonicity was noted on muscles in all patients receiving active treatment. At 12 weeks after therapy, 10 of the 20 patients showed persistent reduction in muscle tone. There were no adverse events associated with ESWT. CONCLUSIONS: ESWT reduces hypertonia of the wrist and finger muscles for > or =12 weeks after treatment. The possible mechanisms of action of ESWT are discussed.

Adult↗

Reflex activity and muscle tone during elbow movements in patients with spastic paresis.

Reflex behavior and tension development in upper limb muscles were analyzed and comparisons made between the unaffected and spastic sides of patients with spastic hemiparesis. During sinusoidal (0.3-Hz) isometric or isotonic elbow tracking, with a control either of joint position or of torque, randomly timed displacements were induced (at one of three velocities) stretching either the activated flexor or the extensor muscles. On the spastic side, exaggerated short-latency reflexes were apparent, but in contrast, the amplitude of long-latency electromyography (EMG) responses was reduced. The latter responses were differentially modulated on the unaffected side, predominantly by the acceleration signal during control of position and more by the velocity signal during control of torque, while the mode of muscle contraction (isometric or isotonic) had little influence on this behavior. This difference in reflex modulation was lost on the spastic side. The functional consequence of this reduced EMG modulation could be difficulty in performing finely controlled arm movements. The ratio of torque to EMG activity during displacements was higher for both background and reflex-induced EMG on the spastic limb than on the unaffected side. This effect was more pronounced for the flexor than for the extensor muscles. Consequently, the development of spastic muscle hypertonia cannot be attributed to an increase in EMG activity. It is suggested that secondary to a supraspinal lesion, mechanical muscle properties change in such a way that the activated spastic muscle develops more tension when it is stretched.

Adolescent↗

Role of peripheral afferents and spinal reflexes in normal and impaired human locomotion.

For many years, electrophysiological investigations of locomotion were restricted to animals, largely the cat. They concentrated on and emphasized the role of spinal interneuronal networks responsible for the generation of the locomotor pattern. Following the introduction of perturbation impulses and electrical nerve stimulation during stance and gait, information became increasingly available concerning the role of the reflex systems involved in the regulation of gait, their afferent pathways and their control by supraspinal motor centres. During gait monosynaptic stretch reflexes are inhibited. From a knowledge of the behaviour of the cerebral potentials evoked during stance and gait, it can be deduced that during gait the signals of group I afferents are blocked at both segmental and supraspinal levels. Polysynaptic reflex responses are mainly responsible for the compensation of perturbations introduced during gait. They are most probably mediated by group II afferents via a spinal pathway closely connected with the spinal locomotor centres. The functioning of these responses depends on an intact supraspinal control. They are suggested to be incorporated in a more complex e.m.g. pattern mainly determined by central mechanisms. In contrast to the gait condition, segmental stretch reflex activity does contribute to activation of extensor muscles of the leg during fast movements, such as running and hopping. In children at an early stage in the development of gait (around 1 to 2 years of age), as well as in patients with spastic paresis, the polysynaptic reflex responses are reduced or absent, and isolated monosynaptic reflex potentials are present. This suggests a reciprocal modulation of mono- and polysynaptic reflex mechanisms, both being dependant on supraspinal control. When this control is either not yet matured (small children) or impaired (spastic paresis), inhibition of monosynaptic stretch reflexes is absent and associated with a reduced facilitation of polysynaptic spinal reflexes. In spastic muscle hypertonia, the tension developed at the Achilles tendon during gait cannot be explained by gastrocnemius activation alone. In patients with spastic hemiparesis gastrocnemius e.m.g. activity is reduced in the spastic leg as compared to the unaffected one. It can be concluded that the paretic muscle undergoes changes in its mechanical properties, secondary to the supraspinal lesion, which results in the development of spastic muscle hypertonia.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

Quantifying the effectiveness of the sustained muscle stretching treatments in stroke patients with ankle hypertonia.

Sustained muscle stretch (SMS) is commonly used to reduce hypertonia. The present study evaluates the effectiveness of three different SMS protocols, namely constant-angle, cyclic, and constant-torque stretching, in the immediate reducing of ankle hypertonia. Forty-seven hemiplegic subjects, 53.7+/-10.3 years old and 22.4+/-16.0 months after stroke, with hypertonic ankle joints were recruited to undergo three SMS applied to protocols treatment their hypertonic ankle joints using an integrated treatment/assessment system. The immediate post-treatment effectiveness of each stretching protocol was assessed by reference to the pre-treatment Modified Ashworth Scale (MAS), passive range of motion (ROM), and reactive torque measurement, from which the viscous-elastic components of the ankle joint were derived. All three SMS protocols successfully reduced MAS grade. Additionally, each stretching method yielded an increase in ankle ROM, from 9.7 degrees to 16 degrees , 9.6 degrees to 14.8 degrees , and 9.2 degrees to 18.3 degrees for the constant-angle, cyclic-stretching, constant-torque protocols, respectively, and reduction of the elastic and viscous properties of the ankle joint dorsiflexion (p<0.05). The changes in the ROM, elasticity, and viscosity were most pronounced in the case of the constant-torque stretching protocol. In addition to clinical scales, current biomechanical assessments indicate that three SMS protocols are all effective in reducing the immediate viscoelastic components of hypertonic ankle joints. Our quantitative analysis further shows that of the three treatment protocols, the constant-torque treatment is the most effective.

Adult↗

[Effects of tizanidine for refractory sleep disturbance in disabled children with spastic quadriplegia].

Tizanidine is a centrally acting alpha-2 adrenoreceptor agonist widely used in the treatment of spasticity in patients with cerebral or spinal injury, and it is causing drawsiness in some of them. Based on these drug actions, we administered tizanidine to 21 spastic quadriplegic children with severe sleep disturbance not improved by conventional therapies. All these patients were showing abnormalities of both the induction and maintenance of sleep. The dosage of tizanidine was 0.1 to 0.2 mg/kg/day, divided into two or three doses. If daytime drowsiness was severe, tizanidine admistration was restricted to just prior to bedtime. In 13 patients (61.9%), we found improvement in sleep induction and/or maintenance. Moreover, patients' families were satisfied with the treatment. There were no detectable side effects except facial pallor in two patients (9.5%) whose treatment was discontinued. Severe muscle hypertonia causes severe pain, which generates strong sympathetic nerve activity and subsequent sleep disturbance. We consider that tizanidine has direct effects on the induction of sleep, and promotes muscular relaxation bringing about good sleep. We conclude that tizanidine is useful for the treatment of refractory sleep disturbance in spastic quadriplegic patients.

Adolescent↗

[Malignant hyperthermia. Review of literature and case reports].

Malignant hyperthermia may appear during surgery. It has at least three features: 1) an anesthesiological trigger, usually the association of halothane and succinylcholine; 2) rapid increase in body temperature; 3) widespread muscle hypertonia. The literature is reviewed in an assessment of the physiopathological mechanism underlying the syndrome, with particular reference to the part played by calcium. Experimental data are cited and their similarity with the clinical, laboratory, anatomical, and histopathological picture in man is discussed. A detailed account is also given of two personal cases. Lastly, questions associated with the prevention and treatment of malignant hyperthermia are examined.

Acid-Base Equilibrium↗

Electrophysiological studies of gait in spasticity and rigidity. Evidence that altered mechanical properties of muscle contribute to hypertonia.

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.

Adolescent↗

Pathophysiology of gait in children with cerebral palsy.

The surface electromyogram (EMG) of leg muscles was recorded together with the changes of the angle at the ankle joint during slow gait in 10 normal children and 10 with cerebral palsy. The characteristic pattern of muscle activity recorded from the spastic legs mainly consisted of a co-activation of antagonistic leg muscles during the stance phase of a gait cycle and a general reduction in amplitude of EMG activity. The tension of the Achilles tendon, measured in 2 hemiparetic children during gait, increased much more steeply in the spastic leg than in the normal one at the beginning of the stance phase, when the electrically almost silent triceps surae was stretched. It is suggested that muscle hypertonia during gait in spastic children is mainly due to changed muscle fibre mechanical properties, as recently discussed also for spastic adults. While in the latter the reciprocal EMG activity of antagonistic leg muscles was preserved it is proposed that muscle co-activation recorded in spastic children is due to an impaired maturation of the locomotor pattern with an early neuronal adaptation to altered muscle fibre mechanical characteristics.

Adolescent↗

Tizanidine and electrophysiologic analysis of spinal control mechanisms in humans with spasticity.

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.

Clonidine↗

Comparison of the impact of a single session of isokinetic or isotonic muscle stretch on gait in patients with spastic hemiparesis.

OBJECTIVE: To establish if isokinetic and isotonic muscle stretch (with or without weight-bearing) of the ankle plantar flexors improves gait in hemiplegic patients. A further aim was to compare the effectiveness of these treatment methods. DESIGN: A randomized, parallel group prospective study. SETTING: A stroke rehabilitation unit. SUBJECTS: Ambulatory hemiparetic stroke patients with mild to moderately severe muscle hypertonia of the lower limb and a group of healthy control subjects. INTERVENTION: Subjects were randomized to receive a single 20-min session of isokinetic muscle stretch or isotonic muscle stretch with or without weight-bearing. OUTCOME MEASURES: Selected kinematic, kinetic and spatio-temporal gait parameters were measured at baseline, immediately after the muscle stretch and 24 h later. RESULTS: Sixty-six patients and 21 healthy control subjects were recruited and completed the study. There were statistically significant differences between the patient groups and the healthy subjects on most of the gait parameters studied. However, the differences between the patient groups or between the three measurements over time for each type of muscle stretch did not reach statistical significance. CONCLUSIONS: A single session of isokinetic or isotonic muscle stretch (with or without weight-bearing) of the ankle plantar flexors has no clinically observable effect on the gait of hemiplegic stroke patients.

Aged↗

Mesh-glove. 2. Modulation of residual upper limb motor control after stroke with whole-hand electric stimulation.

The effects of whole-hand electrical stimulation via a wired mesh-glove upon the residual motor control of the upper extremity are described. Clinical observations were made in 2 patients with nonfunctional upper limbs, 4 and 2 years after stroke, who had been enrolled in the home mesh-glove program for 6 and 4 months, respectively. The stimulation paradigm is novel and the target of stimulation is the hand. Preliminary results indicate beneficial effects such as reduction in muscle hypertonia and facilitation of isolated hand movements.

Aged↗

[New therapeutic methods for spasticity and dystonia in children with cerebral palsy require multidisciplinary team work. Comprehensive approach yields good results].

New effective methods to reduce spasticity and dystonia are now included in the treatment of children with cerebral palsy (CP): selective dorsal rhizotomy (SDR), continuous intrathecal infusion of baclofen by an implanted pump or intramuscular injections of botulinumtoxin A. SDR is the only method that can reduce the spasticity permanently. Strong evidence exists for a positive impact of SDR on the function of the children. A multidisciplinary approach is required as it is essential to choose the best treatment for each child in each developmental period. In Lund physicians and physiotherapeuts from different disciplines such as paediatric orthopaedic surgery, neurosurgery and neurology form a central spasticity team which co-operates with the local child habilitation services. We have found that a common structured and standardized follow-up programme with early intervention against muscle hypertonia and imbalance can prevent hip luxation and contractures in children with CP.

Cerebral Palsy↗

Botulinum toxin: dosing and dilution.

In the United States, the popularity of botulinum toxins as agents to treat muscle hypertonia has grown significantly over the last decade, despite lack of approval from the Food and Drug Administration for the indication of spasticity. Botox (botulinum toxin type A) and Myobloc (botulinum toxin type B) are Food and Drug Administration-approved for other indications, such as cervical dystonia. Another commercial preparation of type A, Dysport, has yet to reach the United States market as of this writing. Although botulinum toxin's efficacy in influencing spastic hypertonia is well accepted, the impact of certain clinical issues, such as dosing and dilution, on treatment outcome is not well established by published studies. This article will review important articles and selected abstracts on the use of botulinum toxin, specifically for spastic hypertonia in adults, with emphasis on current clinical practices as they relate to dosing and dilution.

Botulinum Toxins↗

Botulinum toxin in post-stroke patients: stiffness modifications and clinical implications.

OBJECTIVE: To objectively quantify stiffness and clinical changes in the upper limb of poststroke patients following botulinum toxin (BT) injection. METHODS: Eighteen consecutive chronic post-stroke spastic patients were injected Botulinum toxin A in the forearm flexor spastic muscles. Spasticity was clinically evaluated with the Ashworth scale. Stiffness was measured with indices (passive stiffness index (ISI) and total stiffness index (TSI) obtained by mechanical wrist displacements induced by a torque motor,which could also provide the stretch reflex threshold speed (SRTS) from flexor muscles. Functional status was measured with the Barthel index and a specific hand ability scale, pain with a visual analogue scale (VAS). The ranges of voluntary wrist extension (EROM) and flexion (FROM) and wrist isometric extension and flexion (IE-IF) strength were also calculated. RESULTS: IE and EROM significantly increased, being respectively p < 0.01 and p < 0.05; also SRTS was augmented (p < 0.001),while TSI showed lower values (p < 0.001); the Ashworth score decreased at least one point. Hand function for selected tasks improved in 50% of patients, the Barthel index only in 4 (22 %), forearm pain was completely relieved in 3 patients (17 %). CONCLUSIONS: BT can be considered a valid therapeutic tool in all spastic patients, because of immediate advantages: reduction of muscle hypertonia, pain relief, improvement in selected motor performances.

Adult↗

The relation between Ashworth scale scores and the excitability of the alpha motor neurones in patients with post-stroke muscle spasticity.

BACKGROUND: The modified Ashworth scale (MAS) is the most widely used method for assessing muscle spasticity in clinical practice and research. However, the validity of this scale has been challenged. OBJECTIVES: To compare the MAS with objective neurophysiological tests of spasticity. METHODS: The MAS was recorded in patients with post-stroke lower limb muscle spasticity and correlated with the excitability of the alpha motor neurones. The latter was evaluated by measuring the latency of the Hoffmann reflex (H reflex) and the ratio of the amplitude of the maximum H reflex (H(max)) to that of the compound action motor potential of the soleus muscle (M(max)). RESULTS: Data on 24 randomly recruited patients were analysed. Patients were divided into two groups according to their MAS score: 14 had a MAS score of 1 (group A) and 10 scored 2 (group B). The two groups were comparable with respect to age and sex, but in group A there was a longer period since the stroke. The H reflex latency was reduced and the H(max):M(max) ratio was increased in both groups. The H(max):M(max) ratio values were higher for group B but the differences were not statistically significant. CONCLUSIONS: There is a relation between the MAS scores and alpha motor neurone excitability, although it is not linear. This suggests that the MAS measures muscle hypertonia rather than spasticity.

Action Potentials↗