DISSERTATION SYNOPSIS

SUBMITTED TO

RAJIVGANDHI UNIVERSITY OF HEALTH SCIENCES, KARNATAKA

BANGALORE

TOWARD PARTIAL FULFILMENT OF

MASTER OF PHYSIOTHERAPY DEGREE COURSE

By

ANISH A K

UNDER THE GUIDANCE OF

B A BOOMADEVI

VIKAS COLLEGE OF PHYSIOTHERAPY

MARYHILL, KONCHADY, MANGALORE-575006

2009-11

RAJIVGANDHI UNIVERSITY OF HEALTH SCIENCES, KARNATAKA

BANGALORE

REGISTRATION OF SUBJECTS FOR DISSERTATION

1. / Name of the Candidate
and Address / ANISH A K
VIKAS COLLEGE OF PHYSIOTHERAPY
AIRPORT ROAD
MARYHILL, KONCHADY
MANGALORE – 575008
2. / Name of the Institution / VIKAS COLLEGE OF PHYSIOTHERAPY
Mangalore.
3. / Course of study and subject / Master of Physiotherapy (MPT)
Physiotherapy in Neurological and Psychosomatic Disorders
4. / Date of admission to Course / 01-06-2009
5. / Title of the Topic
A COMPARATIVE STUDY BETWEEN THE EFFECTS OF NEUROMUSCULAR ELECTRICAL STIMULATION AND EMG BIOFEEDBACK IN REDUCING SPASTICITY AND IMPROVING HAND FUNCTION IN CHRONIC HEMIPLEGIC STROKE PATIENTS
6 / BRIEF RESUME OF THE INTENDED WORK
6.1) Need for the study
Among the neurological diseases that lead to death and disability in the adult population, stroke is the most common.1 After stroke, voluntary control of movement is typically impaired. Poststroke recovery of motor skills depends on neurological recovery and adaptation as well as on the learning of new strategies and motor programs.2 Rehabilitation after hemiplegia has typically involved training patients in the use of compensatory strategies. It has been shown that motor control can improve progressively with task-specific training that incorporates increased use of proximal and distal movements during intensive practice of real-life activities.3
Spasticity is a common symptom seen in stroke.4 Spasticity is abnormal muscle tone recognised clinically as resistance to passive muscle stretch which increases with velocity of stretch.5 It is more formally defined as: 'a motor disorder characterised by velocity dependent increase in tonic stretch reflexes with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex'.6
Central to the generation of spasticity is overactivity of the alpha motor neuron (α-MN) pool. Lesions restricted to corticospinal tracts cause muscle weakness, loss of dexterity and a Babinski response, but not spasticity.5 Loss of descending input from cerebral cortex and basal ganglia, through medial and dorsal reticulospinal and vestibulospinal fibres, is thought to be important in causing impaired modulation of monosynaptic input from primary afferent (la) fibres (segmental myotatic reflex), and polysynaptic afferent input from cutaneous receptors and Golgi tendon organs contributing to α -MN hyperexcitability.6 Spinal interneurons play a crucial part in this modulation, in particular through presynaptic and reciprocal la inhibition. Inappropriate muscle co-contraction may arise through reduced reciprocal la inhibition impeding voluntary limb movement.7 In addition, nocioceptive and motor pathways have considerable influence on each other, emphasising the clinical importance of pain management in treating spasticity.5
Stroke affecting the motor cortex or internal capsule commonly produces initial hypotonia and absent tendon jerks, followed several days or weeks later by spastic hypertonia in the antigravity muscles. The upper limb adopts an adducted posture at the shoulder and a flexed posture at the elbow and wrist, with the fingers flexed into the palm. In the lower limb there is hip and knee extension, with plantarflexion at the ankle.5 In patients with no functionally useful voluntary limb movement, spasticity can maintain an abnormal resting limb posture leading to contracture formation. In the arm, severe flexion deformity of the fingers and elbow may interfere with hand hygiene and dressing, as well as affecting self image.5
In patients with functionally useful voluntary limb movement, inappropriate co-activation of agonist and antagonist muscles can impede normal limb movement. In the arm, co-activation of the biceps and triceps may affect the placement function. Co-contraction of the forearm flexor and extensor muscles may prevent voluntary extension of the fingers and thus impede relaxation of grip.5
As spasticity may disturb walking and functional abilities of patients,8 there is a general agreement that its treatment is important.9 Effective management of spasticity requires a multidisciplinary approach both for assessment and treatment and should not be viewed in isolation from the patient's other problems.5 Treatment should be directed at preventing abnormal limb or trunk posture and facilitate normal movement in the context of functional activities.5 The management of spasticity can be broadly divided into5: identifying exacerbating factors and their treatment; positioning the patient during sitting and lying to discourage the development of abnormal posture10; and having access to treatments directed at established spasticity.
Various treatments have been recommended to reduce spasticity, including surgical, medical and physiotherapy techniques.11,12,13 Methods such as drug therapy, chemical nerve block or neurosurgical treatments may reduce spasticity but may cause muscle weakness or paralysis.14 The aims of physiotherapy techniques used for the treatment of spasticity are to favour sensorimotor recovery, which leads to optimal independence in daily life activities.15 For stroke and head injury patients there are several techniques, sometimes based on opposing principles.16 Physiotherapy techniques for the management of spasticity includes positioning, cryotherapy, splinting and casting, biofeedback, electrical stimulation, and education on causative factors, most of which have little evidence to support their application.17
Physiotherapy techniques aim to improve motor performance partly through manipulation of muscle tone.5 Several approaches are used during rehabilitation, although there is lack of evidence to show which is most effective.18 A wide range of treatment techniques for hemiplegic patients have been studied in recent decades. The mechanical approach, however, has gradually been abandoned and has been replaced by forms of treatment that emphasise the reorganisation of motor activities.19
Many authors have employed functional electrical stimulation (FES) and have achieved success in terms of improved upper extremity function.20-30 Electrical stimulation has been shown to have positive effects on motor performance, sensation, and the configuration of somatosensorial evoked potential of the paretic limb in chronic stroke patients.31
Evidence for direct antispasticity effects of electrical stimulation is limited.5 Transcutaneous nerve stimulation applied over the dermatome corresponding to the nerve supply of the spastic muscle can produce short-lived reduction in spasticity.5 Possible mechanisms underlying the improvements could be attributable to an enhancement of presynaptic inhibition of the hyperactive stretch reflexes in spastic muscles, decrease in the cocontraction of spastic antagonists, and disinhibition of descending voluntary commands to the motoneurons of paretic muscles are suggested.32 However, electrical stimulation directed at improving strength of paretic muscles33 may augment the functional effects of BTA treatment in the antagonist muscles.
Neuromuscular electrical stimulation over the agonist or antagonist muscles of spastic muscle is shown to reduce spasticity.8,34 There is some evidence that electrical stimulation of the antagonist muscles can reduce spasticity immediately following treatment.14,34,35 It has also been claimed that spasticity reduction by this method is achieved without any muscle weakness or paralysis.14 Bogataj et al. found that neuromuscular electrical stimulation may increase sensory inputs into the central nervous system and so accelerate nervous plasticity and lead to faster motor learning.12 It has been claimed that electrical stimulation may reduce muscle tonicity via the reduction of the stretching reflex, causing lower spasticity and allowing a larger range of motion,36,37 and preventing soft tissue stiffness and contracture.38,39 However, there are controversial reports about the spasticity reduction effect of electrical stimulation.40,41
Some authors have demonstrated that surface electromyographic biofeedback (EMG-BFB) results in progressive increases in voluntary control of movement and meaningful improvement in patient functional capacity.42,43,44
Electromyographic biofeedback is defined as the use of instrumentation applied to the patient's muscle(s) with external electrodes to capture motor unit electrical potentials.45 The patient is asked to activate or lessen the activity of the muscle(s). The instrumentation converts the potentials into visual or audio information for the patient and the therapist. It is usually used to augment desired muscle action or to decrease unwanted muscle activity.45 Wolf, posited that visual and auditory feedback activate unused or underused synapses in executing motor commands.46 As such, continued training could establish new sensory engrams and help patients perform tasks without feedback.46 Overall, biofeedback may enhance neural plasticity by engaging auxiliary sensory inputs, thus making it a plausible tool for neurorehabilitation. Traditional EMG biofeedback studies showed that patients can improve voluntary control of the activity of the trained muscle and/or increase the range of motion of a joint that the trained muscle controls.47,48,49 The overall effect of this type of biofeedback training on motor recovery is inconsistent, however. Meta-analyses of studies on stroke patients exemplify this.44,45,50,51
Due to these conflicting results and the dearth of studies that compare directly the efficacy of electrical stimulation and EMG biofeedback in reducing spasticity and improving hand function in stroke patients, further studies are necessary.
6.2) Review of Literature
Bakhtiary and Fatemy conducted a RCT to investigate the therapeutic effect of electrical stimulation and a combination of ES and Bobath technique on plantarflexor spasticity in 46 stroke patients. Passive ankle dorsiflexion ROM, dorsiflexion strength, plantarflexor muscle tone by Modified Ashworth Scale (MAS) and soleus muscle H-reflex were measured as outcome results. Results showed that passive ankle joint dorsiflexion and dorsiflexor muscle strength in the combination therapy group was significantly higher, while MAS was significantly lower compared with the Bobath group. However, no significant change in the amplitude of H-reflex was found between groups. They concluded that therapy combining Bobath inhibitory technique and electrical stimulation may help to reduce spasticity effectively in stroke patients.52
Armutlu at al conducted a study to examine the effects of transcutaneous electrical nerve stimulation on spasticity in patients with multiple sclerosis. Patients were assessed by electromyography, Modified Ashworth Scale, and Ambulation Index. After 4 weeks of treatment, there were statistically significant reductions in spasticity of both extremities as assessed by myoelectric activity and the Modified Ashworth Scale. Ambulation Index level was not improved significantly.53
Miller et al conducted a study to evaluate the effectiveness of two weeks of 60 minutes and 8 hours daily of TENS applications on spasticity in 32 MS subjects. Outcomes were examined using the Global Spasticity Score (GSS), the Penn Spasm Score (PSS), and a visual analogue scale (VAS) for pain. The results of the study demonstrated that there were no statistically significant differences in the GSS following either 60 minutes or 8 hours daily of TENS. The 8-hour application time led to a significant reduction in muscle spasm and pain. They concluded that TENS does not appear to be effective in reducing spasticity, but longer applications may be useful in treating MS patients with pain and muscle spasm.40
Vodovnik et al applied cyclical electrical stimulation of 30 minutes to the hamstrings followed by another 30 minutes to the hamstrings and quadriceps of 10 hemiparetic patients with clinical signs of knee joint spasticity. The reduction in spasticity ranged from none to substantial with some other beneficial side-effects. No conclusions could be drawn as to whether hamstring stimulation is preferred to combined stimulation or to quadriceps stimulation alone. It is suggested that small portable stimulators be introduced for chronic use in spastic patients after an optimum stimulation regimen is individually established for each patient.54
Walker in a double blind, controlled study has shown that contralateral electrical subcutaneous nerve stimulation of radial, median, and saphenous nerves produced prolonged analgesia and also suppressed ankle clonus for 3 hours after stimulation ceased in subjects with spasticity. He proposed that because stimulation of the nerve in the wrist suppressed ankle clonus, the mechanism mediating the effect must be centrifugal inhibition. He concluded that subcutaneous nerve stimulation may also be a tool in the management of spasticity.55
Hesse et al tested the spasmolytic effect of Botulinum toxin A in two groups of hemiparetic patients with lower limb spasticity, with one group receiving injection alone, while the second received additional repetitive alternating electrical stimulation for 30 min six times per day during the 3 days following the injection. Muscle tone, rated by the Ashworth spasticity score, and gait analysis including recording of vertical ground reaction forces, were assessed before and 4 weeks after injection. The results showed that the combined treatment proved to be more effective.56
Given et al studied the effects of electrical stimulation of the skin for a period of ten minutes at a 20 Hz frequency, pulse duration 0.1 ms, with an intensity level between sensory and motor thresholds on upper extremity spasticity in 9 hemiparetic stroke subjects. In a subset of subjects, the protocol was repeated using frequencies of 1 and 100 Hz. The effects were quantified by comparing reflex torque responses during ramp and hold angular perturbations of the elbow. Results showed peak torque responses were reduced for at least 30 minutes and significantly increased in threshold onset angle of the reflex torque without changes in reflex stiffness. They concluded that the long-term changes may reflect synaptic plasticity of spinal circuitry outside the stretch reflex loop and comparable reductions in spasticity were observed when repeating the same protocol with different stimulation frequencies.57
Lourenção et al conducted a study to determine the effect that electromyographic biofeedback (EMG-BFB), used in conjunction with occupational therapy (OT) and functional electrical stimulation (FES), on spasticity, range of motion, and upper extremity function in 59 hemiplegic patients. 31 received twice-weekly sessions of OT+FES, together with weekly sessions of EMG-BFB, and 28 received only the twice-weekly sessions of OT+FES. The patients were evaluated at baseline, at 6 months, and at 12 months, using the hand function test, the Minnesota manual dexterity test, the joint range of motion scale, and the modified Ashworth scale. At 6 months, the patients receiving EMG-BFB presented significantly greater improvement in upper extremity function than those receiving only OT+FES. They concluded that incorporating EMG-BFB into the treatment regimen had a positive effect on the range of motion and on the recovery of upper extremity function in hemiplegic patients and it might represent an important therapeutic tool for the rehabilitation of stroke patients.58
Chae et al conducted a randomized placebo study to assess the efficacy of neuromuscular stimulation in enhancing the upper extremity motor and functional recovery of forty-six acute stroke survivors. The treatment group received surface neuromuscular stimulation 1 hour per day, for a total of 15 sessions to produce wrist and finger extension exercises while the control group received placebo stimulation over the paretic forearm. Outcomes were assessed in a blinded manner with the upper extremity component of the Fugl-Meyer Motor Assessment and the self-care component of the Functional Independence Measure at pretreatment, after treatment, and at 4 and 12 weeks after treatment. Results revealed significantly greater gains in Fugl-Meyer scores for the treatment group after treatment, at 4 weeks after treatment, and at 12 weeks after treatment. Functional Independence Measure scores were not different between groups at any of the time periods. They concluded that neuromuscular stimulation enhances the upper extremity motor recovery of acute stroke survivors.28