Clinical Policy Bulletin: Functional Electrical Stimulation and Neuromuscular Electrical Stimulation
Aetna considers functional electrical stimulation (FES) (e.g., Parastep I System) medically necessary durable medical equipment (DME) to enable members with spinal cord injury (SCI) to ambulate when all of the following criteria are met:
Member has intact lower motor units (L1 and below); and
Member can bear weight on upper and lower extremities to maintain an upright posture independently; and
Member demonstrated brisk muscle contraction to neuromuscular electrical stimulation and has sensory perception of electrical stimulation sufficient for muscle contraction; and
Member is highly motivated and has the cognitive ability to use such devices for walking; and
Member can transfer independently and stand for at least 3 minutes; and
Member possesses hand and finger function to manipulate the controls; and
Member is at least 6 months post recovery of spinal cord injury and restorative surgery; and
Member does not have hip and knee degenerative disease and has no history of long bone fracture secondary to osteoporosis; and
The member has successfully completed a training program, which consists of at least 32 physical therapy sessions with the device over a 3-month period.
Note: These criteria are adapted from the Food and Drug Administration (FDA) labeling for Parastep I System as well as information provided in published studies.
Functional electrical stimulation for walking (Parastep I System) has no proven value for members with SCI with any of the following:
Members with cardiac pacemakers; or
Members with severe scoliosis or severe osteoporosis; or
Members with skin disease or cancer at area of stimulation; or
Members with irreversible contracture; or
Members with autonomic dysreflexia.
Aetna considers neuromuscular electrical stimulators (NMES) medically necessary DME for disuse atrophy where the nerve supply to the muscle is intact and the member has any of the following non-neurological reasons for disuse atrophy:
Contractures due to burn scarring, or
Major knee surgery (when there is failure to respond to physical therapy), or
Previous casting or splinting of a limb, or
Recent hip replacement surgery (NMES is covered until physical therapy begins).
Note: More than 2 hours of NMES per day is considered not medically necessary; protocols reported in the literature recommend no more than 2 hours of NMES treatment within a 24-hour period.
Aetna considers FES of the upper extremities (e.g., NESS H200) experimental and investigational for all indications, including improvement of muscle strength, reduction of spasticity and atrophy, and facilitation of functional motor movement due to any of the following conditions because its effectiveness for these indications has not been established:
Spinal cord injury; or
Stroke (cerebrovascular accident/CVA); or
Traumatic brain injury; or
Other upper motor neuron disorders (e.g., Parkinson's disease).
Aetna considers FES and NMES experimental and investigational for all other indications, including any of the following because its effectiveness for indications other than the ones listed above as medically necessary has not been established:
Bell's palsy; or
Cerebral palsy; or
For cardiac conditioning; or
For general muscle strengthening in healthy individuals; or
For improving ambulatory function and muscle strength for progressive diseases (e.g., cancer, chronic heart failure, chronic obstructive pulmonary disease, multiple sclerosis) in persons without spinal cord injury; or
For the treatment of denervated muscles
For the treatment of knee osteoarthritis.
Note: Aetna considers the FES devices such as the FES Power Trainer, ERGYS, REGYS, NeuroEDUCATOR, STimMaster Galaxy, RT300 motorized FES ergometer, and SpectraSTIM to be exercise equipment. Most Aetna plans exclude coverage of exercise equipment; please check benefit plan descriptions for details.
Aetna considers a form-fitting conductive garment medically necessary DME only when it has been approved for marketing by the FDA, has been prescribed by a physician for use in delivering NMES that is considered medically necessary, and any of the following criteria is met:
The member can not manage without the conductive garment due to the large area or the large number of sites to be stimulated, and the stimulation would have to be delivered so frequently that it is not feasible to use conventional electrodes, adhesive tapes, and lead wires; or
The member has a skin problem or other medical conditions that precludes the application of conventional electrodes, adhesive tapes, and lead wires; or
The member requires electrical stimulation beneath a cast to treat disuse atrophy, where the nerve supply to the muscle is intact; or
The member has a medical need for rehabilitation strengthening following an injury where the nerve supply to the muscle is intact.
Aetna considers form-fitting conductive garments experimental and investigational for all other indications because its effectiveness for indications other than the ones listed above has not been established.
Aetna considers diaphragmatic/phrenic pacing (e.g., the Mark IV™ Breathing Pacemaker System, and the NeuRx DPS RA/4 Respiratory Stimulation System) medically necessary for the following indications:
For improvement of ventilatory function in stable, non-acute members with SCI when all of the following criteria are met:
Member has high quadriplegia at or above C-3; and
There are viable phrenic nerves; and
Member's diaphragm and lung function are adequate.
For the treatment of central alveolar hypoventilation.
For individuals with amyotrophic lateral sclerosis who have stimulatable diaphragms and are experiencing chronic hypoventilation.
Aetna considers diaphragmatic/phrenic pacing experimental and investigational for all other indications because its effectiveness for indications other than the ones listed above has not been established.
Aetna considers electrical stimulation of the sacral anterior roots (by means of an implanted stimulator, the Vocare Bladder System) in conjunction with a posterior rhizotomy medically necessary for members who have clinically complete spinal cord lesions (American Spinal Injury Association Classification) with intact parasympathetic innervation of the bladder and who are skeletally mature and neurologically stable, to provide urination on demand and to reduce post-void residual volumes of urine. The following selection criteria must be met:
3 months (female members) after or 9 months (male members) after complete supra-sacral spinal cord injury; and
A phasic detrusor pressure rise of 35 mm H2O (female members) or 50 cm H2O (male members) on cystometry; and
Presence of 3 of the 4 non-vesical sacral segment reflexes (i.e., ankle jerks, bulbo-cavernous reflex, anal skin reflex, and reflex erection).
Aetna considers electrical stimulation of the sacral anterior roots in conjunction with posterior rhizotomy (Vocare Blader System) experimental and investigational for all other indications because its effectiveness for indications other than the ones listed above has not been established.
Note: The Vocare Bladder System, also known as the implantable Finetech-Brindley stimulator, is different from the InterStim device (sacral nerve neuromodulation, see CPB 0223 - Urinary Incontinence Treatments). The Vocare Bladder System is patient-activated and is designed to elicit functional contraction of the innervated muscles. Implantation of the Vocare device is frequently performed in conjunction with a dorsal rhizotomy. The rhizotomy results in an areflexive bladder, limiting incontinence and autonomic hyperreflexia.
Aetna considers transurethral electrical stimulation experimental and investigational for the management of neurogenic bladder dysfunction and all other indications because its effectiveness for these indications has not been established.
Aetna considers peroneal nerve stimulators (e.g., the ODFS Dropped Foot Stimulator (Odstock), the WalkAide device, and the NESS L300 Foot Drop System) experimental and investigational for persons with foot drop and for all other indications because of insufficient evidence to support their use.
Aetna considers threshold (or therapeutic) electrical stimulation experimental and investigational for the management of cerebral palsy and other motor disorders because its effectiveness for these indications has not been established.
Note: The American Spinal Injury Association (ASIA) Impairment Scale is described in the background section below.
Spinal cord injury can (SCI) cause various degrees of neurological impairment depending on the location and severity of the injury. One method of categorizing the degree of injury is by a neurological examination that explores the segments of the cord which are still functional. The most caudal segment of the cord with normal sensory and motor functions is denoted as the neurological level of injury. The American Spinal Injury Association (ASIA) Impairment Scale is a classification system used to describe the extent of SCI.
The ASIA Impairment Scale
Complete: No motor or sensory function is preserved in the sacral segments S4 - S5
Incomplete: Sensory but not motor function is preserved below the neurological level and includes the sacral segments S4 - S5
Incomplete: Motor function is preserved below the neurological level, and more than half of key muscles below the neurological level have a muscle grade less than 3
Incomplete: Motor function is preserved below the neurological level, and at least half of key muscles below the neurological level have a muscle grade of 3 or more
Normal: Motor and sensory function are normal
Another factor that influences the severity of impairment is the neurological extent of injury, namely the degree of tissue trauma to the spinal cord at the level of injury. If the spinal cord is seriously damaged at the injury site, there is complete loss of sensation and voluntary muscle control below the level of lesion. On the other hand, if the damage is not complete, some sensory and/or motor functions may still be preserved. Thus, a complete injury to the cervical spine will result in quadriplegia, while an incomplete injury to the cervical spine will result in quadriparesis. Similarly, a complete lesion in the thoracic or lumbar spine will produce paraplegia, whereas an incomplete lesion at these levels will produce paraparesis. Spinal cord injury can result in damage to upper motor neurons (UMN), lower motor neurons (LMN), or a combination of both. The cell bodies of UMN originate from the primary motor area of the cerebral cortex and the brain stem, with their axons descending downward and terminating at each segmental level throughout the entire length of the spinal column to synapse with LMN that arise in the spinal cord and connect to a muscle or organ. The brain, through the UMN, exerts an inhibitory influence on the LMN so that they do not become hyperactive to local stimuli. The cell bodies of LMN are located in the central gray matter throughout the entire length of the spinal column, and their axons extend out via the spinal nerve roots and peripheral nerve branches to innervate skeletal muscles throughout the body.
Neuromuscular electrical stimulation (NMES) can be grouped into 2 categories: (i) stimulation of muscles to treat muscle atrophy, and (ii) enhancement of functional activity in neurologically impaired individuals. These devices use electrical impulses to activate paralyzed or weak muscles in precise sequence and have been utilized to provide SCI patients with the ability to walk (e.g., The Parastep I System). Neuromuscular electrical stimulation used in this manner is commonly known as functional electrical stimulation (FES).
Spinal Cord Injury:
The Parastep I System, a transcutaneous non-invasive and micro-computerized electrical stimulation system built into a battery-powered unit, is controlled by finger-touch buttons located on a walker's hand-bars for manual selection of stimulation menus. The microcomputer shapes, controls, and distributes trains of stimulation signals that trigger action potentials in selected peripheral nerves. Walker support is used for balance. The patient can don the system in less than 10 minutes. At least 32 training sessions are required.
Klose et al (1997) described performance parameters and effects on anthropometric measures in SCI patients (13 men and 3 women) training with the Parastep I system. Subjects with thoracic (T4 to T11) motor-complete SCI, mean age of 28.8 years, and mean duration post-injury of 3.8 years underwent 32 functional neuromuscular stimulation ambulation training sessions using the Parastep I System. The authors concluded that the Parastep I System enabled persons with thoracic-level SCI to stand and ambulate short distances but with a high-degree of performance variability across individuals. Furthermore, Graupe and Kohn (1998) reported that about 400 patients have used the Parastep I System and essentially all achieved standing and at least 30 feet of ambulation, with a few reaching as much as 1 mile at a time.
Bonaroti et al (1999) compared FES to long leg braces (LLB) as a means of upright mobility for children with motor-complete thoracic level SCI (n = 5). The authors found that FES system generally provided equal or greater independence in seven mobility activities as compared with LLB, provided faster sit-to-stand times, and was preferred over LLB in a majority of cases.
In addition to enhancement of walking abilities in SCI patients, other clinical applications of FES include diaphragmatic/phrenic pacing, and spasticity control. Functional electrical stimulation has had some success in improving ventilatory function in adult patients with SCI (Glenn et al, 1984; Carter et al, 1987; Glenn et al, 1988). Hunt et al (1988) reported that diaphragmatic pacing is also helpful for infants and children who need ventilatory support. Furthermore, in a 1992 review on the rehabilitation of children with SCI, Flett (1992) stated that diaphragmatic/phrenic pacing is indicated for children with quadriplegia at C3 or higher if they have viable phrenic nerves and adequate diaphragm and lung function. Candidates for diaphragmatic pacing should be stable and out of the acute phase of injury. The author stated that this approach of assisting ventilation in these patients resulted in psychological benefits to both the children and their families. Currently, bilateral stimulation at low frequency is more frequently used instead of stimulation of only one hemidiaphragm at a time, and adequate ventilation can be attained with 5 to 9 stimuli per minute.
Diaphragmatic pacing has also been used to treat patients with central alveolar hypoventilation syndrome. Yasuma and associates (1998) noted that the respiratory assistance by the diaphragm pacemaker or the use of a mechanical ventilator as a backup was highly useful for the home care of a patient with central alveolar hypoventilation. Garrido-Garcia and colleagues (1998) presented a series of patients with chronic ventilatory failure treated with electrophrenic respiration: 13 males and 9 females with a mean age of 12 +/- 11.5 years. The etiology was: 13 tetraplegia, 5 sequelae of surgical treatment of intracranial lesions, and 4 central alveolar hypoventilation. The mean duration of the conditioning period was 3 to 4 months. Eighteen patients (81.8 %) achieved permanent, diaphragmatically-paced breathing with bilateral stimulation and in 4 (18.2 %) patients, pacing was only during sleep. Five patients died (22.7 %): 2 during the hospital stay and 3 at home; 2 deaths had unknown cause and 3 were due respectively to, lack of at-home care, recurrence of an epidermoid tumor, and sequelae of accidental disconnection of the mechanical ventilation before beginning the conditioning period. Two cases were considered failures: 1 patient had transitory neurapraxia lasting 80 days, and the other had an ischemic spinal cord syndrome with progressive deterioration of the left-side response to stimulation. One patient had right phrenic nerve entrapment by scar tissue and 4 suffered infections. These results demonstrated that complete stable ventilation can be achieved using diaphragmatic pacing and that it improves the prognosis and life quality of patients with severe chronic respiratory failure.
Girsch et al (1996) noted that ventilatory insufficiency due to central hypoventilation syndrome and SCI can be treated even in children with diaphragm pacing, provided the indication for implantation, containing medical and social aspects, was made correctly. Additionally, Flageole et al (1995) stated that pediatric surgeons should be aware of congenital central hypoventilation syndrome (CCHS) because it may be treated with surgically implanted electrodes that allow for pacing of the diaphragm. The technique has an acceptable complication rate, and it can greatly decrease the impact of the disease on the lifestyle and activity of the patient. Shaul et al (2002) stated that diaphragmatic pacing can provide chronic ventilatory support for children who suffer from CCHS or cervical SCI.
Chen and Keens (2004) reported that all patients with CCHS require lifelong ventilatory support during sleep but some will be able to maintain adequate ventilation without assistance while awake once past infancy. However, some CCHS patients require ventilatory support for 24 hours/day. Modalities of home mechanical-assisted ventilation include positive pressure ventilation via tracheostomy, non-invasive positive pressure ventilation (bi-level ventilation), negative pressure ventilation and diaphragmatic pacers. Furthermore, Creasey et al (1996) reported that electrical stimulation has been used for over 25 years to restore breathing to patients with high quadriplegia causing respiratory paralysis and patients with central alveolar hypoventilation. Three groups have developed electrical pacing systems for long-term support of respiration in humans. These systems consist of electrodes implanted on the phrenic nerves, connected by leads to a stimulator implanted under the skin, and powered and controlled from a battery-powered transmitter outside the body. The systems differ principally in the electrode design and stimulation waveform. Approximately 1,000 people worldwide have received one of the three phrenic pacing devices, most with strongly positive results: reduced risk of tracheal problems and chronic infection, the ability to speak and smell more normally, reduced risk of accidental interruption of respiration, greater independence, and reduced costs and time for ventilatory care. For patients with partial lesions of the phrenic nerves, intercostal muscle stimulation may supplement respiration.
Neuromuscular respiratory failure is the cause of death in the majority of patients with amyotrophic lateral sclerosis (ALS). Respiratory muscle dysfunction impacts on quality of life and survival. Yun and associates (2007) noted that closed loop systems may facilitate the implementation of diaphragmatic pacing for the treatment of many indications. They may allow for wider adoption of ventilatory support in central sleep apnea and improve quality of life in diseases of chronic hypoventilation, such as ALS.
Onders and colleagues (2009a) summarized the complete worldwide multi-center experience with diaphragm pacing stimulation (DPS) to maintain and provide diaphragm function in ventilator-dependent SCI patients and respiratory-compromised patients with ALS. It high-lighted the surgical experiences and the differences in diaphragm function in these 2 groups of patients. In prospective Food and Drug Administration (FDA) trials, patients underwent laparoscopic diaphragm motor point mapping with intra-muscular electrode implantation. Stimulation of the electrodes ensued to condition and strengthen the diaphragm. From March of 2000 to September of 2007, a total of 88 patients (50 SCI and 38 ALS) were implanted with DPS at 5 sites. Age of patients at implantation ranged from 18 to 74 years. Time from SCI to implantation ranged from 3 months to 27 years. In 87 patients the diaphragm motor point was mapped with successful implantation of electrodes with the only failure the second SCI patient who had a false-positive phrenic nerve study. Patients with ALS had much weaker diaphragms identified surgically, requiring trains of stimulation during mapping to identify the motor point at times. There was no peri-operative mortality even in ALS patients with forced vital capacity (FVC) below 50 % predicted. There was no cardiac involvement from diaphragm pacing even when analyzed in 10 patients who had pre-existing cardiac pacemakers. No infections occurred even with simultaneous gastrostomy tube placements for ALS patients. In the SCI patients, 96 % were able to use DPS to provide ventilation replacing their mechanical ventilators; and in the ALS studies, patients have been able to delay the need for mechanical ventilation up to 24 months. The authors concluded that this multi-center experience has shown that laparoscopic diaphragm motor point mapping, electrode implantation, and pacing can be safely performed both in SCI and in ALS. In SCI patients it allows freedom from ventilator and in ALS patients it delays the need for ventilators, increasing survival.
Onders and co-workers (2009b) summarized the largest series of surgical cases in ALS during multi-center prospective trials of the laparoscopic DPS to delay respiratory failure. The overall strategy outlined includes the use of rapidly reversible short-acting analgesic and amnestic agents with no neuromuscular relaxants. A total of 51 patients were implanted from March 2005 to March 2008 at 2 sites. Age of patients ranged from 42 to 73 years and the percent predicted FVC ranged from 20 % to 87 %. On pre-operative blood gases, Pco(2) was as high as 60. Using this protocol, there were no failures to extubate or 30-day mortalities. The DPS system increase the respiratory system compliance by decreasing posterior lobe atelectasis and can stimulate respirations at the end of each case. The authors concluded that laparoscopic surgery with general anesthesia can be safely performed in patients with ALS undergoing DPS.
It has not been consistently shown that spasticity decreases with long-term FES. Yarkony et al (1992) claimed that no definitive statement can be made regarding the type, the magnitude, or even the direction of the effect of electrical stimulation on the spasticity of patients with SCI. Current management strategy for this condition ranges from rehabilitative physical therapy, re-education therapeutic exercise, oral medications such as Dantrium, Valium, and Lioresal (baclofen), intra-thecal infusion of baclofen, motor point blocks or nerve blocks, to destructive neurosurgical procedures (Merritt 1981).
Functional electrical stimulation exercise training has been claimed to strengthen and increase endurance of muscles paralyzed following UMN injuries, thereby improving physical fitness and health of individuals with SCI. However, fatigue of electrically stimulated muscles is a principal limiting factor in the applications of FES. Glaser (1986) stated that more research is needed to ascertain the mechanisms of fatigue of this type of peripherally induced exercise, and to substantiate the potential fitness and health benefits of FES exercise training. Sipski et al (1989) examined patient perceptions of FES bicycle ergometry. These researchers suggested that future studies should include a placebo control group. They also found that 6 of 9 patients with a history of neurogenic pain reported an increase in this pain which caused them to drop out of the training program. The cause of this intensification of pain was unclear. Leeds et al (1990) reported that bone mineral density did not increase in quadriplegic men who had undergone 6 months of FES cycle ergometry training. Sipski et al (1993) stated that more research is needed to document the benefits, if any, of the use of bicycle ergometry to justify the use of this equipment. Pentland (1993) claimed that much more research in FES techniques and treatment protocols is needed before this approach can be used widely as a means to provide cardiorespiratory fitness for quadriplegics.
The principal goal of stroke rehabilitation is to improve the functional abilities of these patients, thus affording them greater independence in activities of daily living and improving their quality of life. Conventional modalities of stroke rehabilitation comprise various combination of range of motion (ROM) and muscle strengthening exercises, mobilization activities, and compensatory techniques. Other therapies include neurophysiological and/or developmental based methods in which the therapeutic program incorporates neuromuscular re-education techniques. In this regard, FES has been employed in the rehabilitation of stroke patients. It has been utilized to manage contracture of joints, maintain ROM, facilitate voluntary motor control, and reduce spasticity. However, there is insufficient evidence that FES is effective as a rehabilitative tool for patients who suffered strokes. In particular, there are little data supporting the long-term effectiveness of this modality for stroke rehabilitation.
In a review on the clinical applications of FES, Kumar et al (1995) stated that advances in electrode technology and control and command sources activation systems as well as development of close-loop systems are needed if wide patient acceptance of this modality (FES) is to be ensured. The Agency for Health Care Policy and Research's clinical guideline on “Post-stroke Rehabilitation” maintains that neither research evidence nor expert consensus adequately supports recommendation concerning the use of FES in the rehabilitation of stroke patients (Gresham, 1995). Furthermore, Hummelsheim et al (1997) reported that repetitive electrical muscle stimulation did not improve biomechanical or functional motor parameters of the centrally paretic hand and arm of stroke patients.
In a randomized controlled study, Yan and colleagues (2005) evaluated whether FES was more effective in promoting motor recovery of the lower extremity and walking ability than standard rehabilitation alone. A total of 46 patients were assigned randomly to one of three groups receiving standard rehabilitation with FES or placebo stimulation or alone (control). They received treatment for 3 weeks, starting shortly after having the stroke. Outcome measurements included composite spasticity score, maximum isometric voluntary contraction of ankle dorsi-flexors and planter-flexors, and walking ability. After 3 weeks of treatment, those receiving FES plus standard rehabilitation did better on several measures of lower limb functioning compared to the other 2 groups. All patients in the FES group were able to walk after treatment, and 84.6 % of them returned home, in comparison with the placebo (53.3 %) and control (46.2 %) groups. However, these authors stated that generalization of the results from this study should be performed with caution because of subject selection criteria, which did not cover all stroke categories or subjects aged younger than 45 or older than 85 years. Further studies are now needed to see whether FES can work with a wide range of stroke patients.
Although a number of studies suggested that electrical stimulation may be effective for reducing shoulder pain and subluxation or improving the function of wrist and finger extensors following stroke (Chantraine et al, 1999; Wang et al, 2002; and Yozbatrian et al, 2006), more research is needed to validate these findings. Chantraine et al (1999) reported that FES program was significantly effective in reducing the severity of subluxation and pain and possibly may have facilitated recovery of the shoulder function in hemiplegic patients. However, they noted that more research addressing the mechanism of the actions of FES on pain and subluxation of the hemiplegic shoulder is needed.
Chae and Yu (2000) critically evaluated the clinical effectiveness of NMES in treating motor dysfunction in hemiplegia. Three distinct applications were reviewed in the areas of motor relearning, shoulder dysfunction, and neuroprostheses. Assessment of clinical effectiveness and recommendations on clinical implementation were based on the weight of published scientific evidence. With respect to motor relearning, evidence supports the use of NMES to facilitate recovery of muscle strength and coordination in hemiplegia. However, effects on physical disability are uncertain. With respect to shoulder dysfunction, NMES decreases shoulder subluxation, at least in the short term. However, effects on shoulder pain and disability are also uncertain. With respect to neuroprosthesis systems, clinically deployable upper extremity systems must await the development of more sophisticated control methods and greater fundamental understanding of motor dysfunction in hemiplegia. The evidence for clinical feasibility of lower extremity neuroprostheses is stronger, and investigations on clinical effectiveness should be pursued. The authors concluded that the application of NMES for motor relearning and shoulder dysfunction are ready for more rigorous scientific and clinical assessment via large, multi-center, randomized clinical trials.
In a Cochrane review, Price and Pandyan (2000) ascertained the effectiveness of any form of surface ES in the prevention and/or treatment of pain around the shoulder at any time after stroke. These investigators concluded that the evidence from randomized controlled studies so far does not confirm or refute that ES around the shoulder after stroke influences reports of pain, but there do appear to be benefits for passive humeral lateral rotation. A possible mechanism is through the reduction of glenohumeral subluxation. The authors stated that further studies are needed.
Turner-Stokes and Jackson (2002) noted that although a wide variety of physical changes are associated with hemiplegic shoulder pain (HSP), these can be categorized into 2 presentations; (i) "flaccid", and (ii) "spastic". Management should vary accordingly; each presentation requiring different approaches to handling, support and intervention. In the "flaccid" stage, the shoulder is prone to inferior subluxation and vulnerable to soft-tissue damage. The arm should be supported at all times and FES may reduce subluxation and enhance return of muscle activity. In the "spastic" stage, movement is often severely limited. Relieving spasticity and maintaining range requires expert handling; over-head exercise pulleys should never be used. Local steroid injections should be avoided unless there is clear evidence of an inflammatory lesion. The authors concluded that HSP requires coordinated multi-disciplinary management to minimize interference with rehabilitation and optimize outcome. They stated that more research is needed to determine effective prophylaxis and document the therapeutic effect of different modalities in the various presentations.
The New Zealand Guidelines Group's guideline for management of stroke (2003) stated that the use of FES and transcutaneous electrical nerve stimulation for post-stroke patients is not recommended. Furthermore, Van Peppen et al (2004) determined the evidence for physical therapy interventions aimed at improving functional outcome after stroke. These researchers reported that while strong evidence was found regarding NMES for glenohumeral subluxation, no or insufficient evidence in terms of functional outcome was found for FES and NMES aimed at improving dexterity or gait performance; orthotics and assistive devices; and physical therapy interventions for reducing hemiplegic shoulder pain and hand edema. Furthermore, in a review on therapeutic orthosis and ES for upper extremity hemiplegia after stroke, Aoyagi and Tsubahara (2004) stated the longer term effectiveness after discontinuation as well as the motor recovery mechanism of ES or robotic devices remains unclear. More research is needed to determine the evidence-based effectiveness of ES or other devices for stroke survivors.
In a Cochrane review on ES for promoting recovery of movement or functional ability after stroke, Pomeroy et al (2006) concluded that "[a]t present, there are insufficient robust data to inform clinical use of electrostimulation for neuromuscular re-training. Research is needed to address specific questions about the type of electrostimulation that might be most effective, in what dose and at what time after stroke".
Functional Electrical Stimulation of the Upper Extremities:
Functional electrical stimulation is being investigated as a means to improve hand and arm function after stroke-related paralysis or spinal cord injury. The NESS H200 hand rehabilitation system (Bioness, Valencia, CA), formerly the Handmaster, is a neuroprosthesis that uses mild ES in an attempt to activate muscle groups in the forearm to produce functional movement patterns in the hand. It is designed to be used as part of a self-administered home-based rehabilitation program for the treatment of upper limb paralysis from hemiplegic stroke, traumatic brain injury or C5 to C6 spinal cord injury. The system contains a custom-fitted orthosis and a control unit. The control unit allows the user to adjust the stimulation intensity and training mode. Exercise sessions can be gradually increased to avoid muscle over-fatigue.
Initial case studies have indicated that the use of FES as an adjunct to physical therapy can improve patient outcomes (Weingarden et al, 1998; Alon et al, 2002; Alon et al, 2003; Berner et al, 2004). However, the studies lacked a control group, involved small study populations with limited periods of follow-up. Thus, it is difficult to ascertain the significance of the treatment effects and their durability.
De Kroon et al (2002) systematically reviewed the evidence for ES to improve motor control and functional abilities of the upper extremity after stroke. The authors reported that "[t]he results suggest that electrical stimulation has a positive effect on motor control, although it is not known if this improvement is clinically relevant." The review stated that "[n]o conclusions can be drawn concerning the effect of electrical stimulation on functional abilities."
Ring and Rosenthal (2005) evaluated the effects of daily neuroprosthetic (NESS Handmaster) FES in sub-acute stroke. Patients were clinically stratified to 2 groups: (i) no active finger movement, and (ii) partial active finger movements, and then were randomized to control and neuroprosthesis groups. Observer blinded evaluations were performed at baseline and completion of the 6-week study. A total of 22 patients with moderate-to-severe upper limb paresis 3 to 6 months after stroke were enrolled in this study. They were in day hospital rehabilitation, receiving physical and occupational therapy 3 times weekly. The neuroprosthesis group used the device at home. The neuroprosthesis group had significantly greater improvements in spasticity, active ROM and scores on the functional hand tests (those with partial active motion). Of the few patients with pain and edema, there was improvement only among those in the neuroprosthesis group. There were no adverse reactions. These investigators concluded that supplementing standard outpatient rehabilitation with daily home neuroprosthetic activation improves upper limb outcomes.
In a systematic review, Meilink et al (2008) evaluated if electromyography-triggered NMES (EMG-NMES) applied to the extensor muscles of the forearm improves hand function after stroke. A total of 8 studies, selected out of 192 hits and presenting 157 patients, were included in quantitative and qualitative analyses. The methodological quality ranged from 2 to 6 points. The meta-analysis revealed non-significant effect sizes in favor of EMG-NMES for reaction time, sustained contraction, dexterity measured with the Box and Block manipulation test, synergism measured with the Fugl-Meyer Motor Assessment Scale and manual dexterity measured with the Action Research Arm test. The authors concluded that no statistically significant differences in effects were found between EMG-NMES and usual care. Most studies had poor methodological quality, low statistical power and insufficient treatment contrast between experimental and control groups. In addition, all studies except 2 investigated the effects of EMG-NMES in the chronic phase after stroke, whereas the literature suggests that an early start, within the time window in which functional outcome of the upper limb is not fully defined, is more appropriate.
In a retrospective cohort study, Meijer et al (2009) evaluated the short-term and long-term use of a hybrid orthosis for NMES of the upper extremity in patients (n = 110) after chronic stroke. The Modified Ashworth Scale (0 to 5) for wrist (primary outcome) and elbow flexor hypertonia, visual analog scale (0 to 10) for pain, edema score (0 to 3), and passive range of wrist flexion and extension (pROM, degrees) were assessed prior to Handmaster orthosis prescription (T0), after 6 weeks try-out (T1) and a subsequent 4 weeks withhold period (T2). Long-term use was evaluated using a questionnaire. Non-parametric analyses and predictive values were used for statistical analyses. Of the 110 patients, 78.2 % were long-term Handmaster orthosis users. Long-term users showed significant short-term (T0 to T1) improvements on all impairment scores and a significant relapse of wrist and elbow Modified Ashworth Scale (T1 to T2). Non-users showed significant short-term effects on elbow Modified Ashworth Scale and visual analog scale only. Positive predictive values of short-term effects for long-term use varied between 75 % and 100 %, with 85 % (95 % confidence interval (CI): 0.72 to 0.93) for wrist Modified Ashworth Scale. Negative predictive values were low (11 to 27 %). The authors concluded that short-term Handmaster orthosis effects were generally beneficial for hypertonia, pain, edema, and pROM, especially in long-term users and that short-term beneficial effects were highly predictive for long-term use, but not for non-use.
The results of these studies are promising, however, these findings need to be validated by further investigation with more patients and follow-up data.
Rehabilitation Following Ligament/Knee Surgery:
On the other hand, NMES has been shown to be an effective rehabilitative regimen for patients following ligament/knee surgery. It prevents muscle atrophy associated with knee immobilization, enables patients to ambulate sooner, and reduces the use of pain medication as well as length of hospital stay (Arvidsson, 1986; Lake, 1992; Gotlin et al, 1994; Snyder-Mackler et al, 1995).
Bax et al (2005) systematically reviewed the available evidence for the use of NMES in increasing strength of the quadriceps femoris. The authors concluded that limited evidence suggests that NMES can improve strength in comparison with no exercise, but volitional exercises appear more effective in most situations. The authors' cautious conclusions reflect the general poor quality of the included studies.
Neurogenic Bladder Dysfunction:
Neurogenic bladder dysfunction is due to lesions of the innervation either within the central nervous system or in the peripheral nerves of the bladder and urethra. The Lapides Classification is the scheme most frequently used by urologists to classify patients with neuropathic voiding dysfunction. This classification system is divided into 5 categories: (i) sensory neurogenic bladder, (ii) motor paralytic bladder, (iii) uninhibited neurogenic bladder, (iv) reflex neurogenic bladder, and (v) autonomous neurogenic bladder.
A sensory neurogenic bladder is caused by diseases that selectively disrupt the sensory fibers between the bladder and spinal cord or the afferent pathways to the brain. This is commonly observed in patients with peripheral neuropathies such as diabetes mellitus, tabes dorsalis, folic acid avitaminosis, and pernicious anemia. A motor paralytic bladder is the consequence of diseases/processes that interrupt the parasympathetic motor innervation of the bladder. It can be produced by extensive pelvic surgery or trauma or herpes zoster. An uninhibited neurogenic bladder is due to the absence of cerebral inhibition of the micturition reflex as a result of injury or disease in the cortico-regulatory tract. Cerebral lesions such as stroke, tumors, arteriosclerosis, and traumatic lesions are the most common causes of this type of voiding disorder. A reflex neurogenic bladder is often observed in the post-spinal shock condition existing following the complete transection of the sensory and motor tracts between the sacral spinal cord and the brain stem. This is often the result of traumatic SCI and transverse myelitis, but may also occur with severe demyelinating disease or tumor. An autonomous neurogenic bladder is caused by complete motor and sensory separation of the bladder from the sacral spinal cord. Diseases that destroy the sacral spinal cord or cause extensive damage to the sacral roots or pelvic nerves can produce this type of disorder. It should be noted that many patients do not exactly fit into one or another of these categories because of gradations of sensory, motor, and mixed lesions. Thus, the patterns produced after different types of peripheral denervation may vary greatly from those that are classically described (Barrett and Wein, 1991).
Neurogenic bladder dysfunction can also be associated with other neurological diseases including cerebellar ataxia, multiple sclerosis, Parkinson's disease, and Shy-Drager syndrome. In children, the common causes of neurogenic bladder dysfunction are sacral agenesis, tethered cord syndrome, and myelomeningocele. The main results of neurogenic bladder dysfunction are renal damage and urinary incontinence (UI). The former is due to either high intravesical pressure or the association of vesicoureteral reflux and infection. The mechanisms for UI are multiple including (i) overflow incontinence caused by detrusor atonia with a non-relaxing sphincter, (ii) lack of storage capacity caused by hyperreflexia or poor compliance, and (iii) low urethral resistance caused by denervation of the sphincters. Oftentimes, the causes of UI are mixed (Wein 1992; Fernandes et al, 1994).
The management of patients with neurogenic bladder dysfunction entails clean intermittent catheterization, pharmacotherapy (e.g., oxybutynin, phenoxybenzamine, and anti-cholinergic medications such as tolterodine), and surgical interventions (e.g., urinary diversion or bladder augmentation). Moreover, stimulation of sacral anterior nerve roots in association with posterior rhizotomy has been used in the treatment of patients with suprasacral SCI. The FDA approved the Vocare Bladder System as a humanitarian use device based on a study of 23 patients who received device in association with posterior rhizotomy and were followed for a minimum of 3 months. Comparisons were made with the implanted stimulator turned either on or off; thus patients served as their own controls. The primary outcome measures were improvement in bladder emptying as evidenced by the ability to void more than 200 ml on demand with post-void residual urine volumes of less than 50 ml. Secondary endpoints included reduction in the use of urinary catheters, number and severity of episodes of UI, reduction in incidence of urinary tract infections, and results of a user satisfaction survey.
After 3 months, 90 % of the patients were able to urinate more than 200 ml on demand and 81 % had post-void residual urine volumes of less than 50 ml. A total of 73 % of patients reported fewer urinary tract infections and at 6 months, about 50 % of the patients were using the device exclusively for micturition, and no external devices (e.g., catheters) were needed. The results reported in this study were in agreement with those reported by Van Kerrebroeck et al (1996) as well as Egon et al (1998). The former group of investigators reported on the outcomes of 47 patients who were followed for a minimum of 6 months. Complete continence was observed in 43 of the 47 patients, and 41 of the 47 patients used only the stimulator for bladder emptying. The residual urine volume also decreased to less than 50 ml in 41 patients. The incidence of urinary tract infections also decreased. The latter group of researchers reported on a case series of 93 patients. A total of 83 of the 93 patients used their implants for micturition with residual volumes of less than 50 ml.
Jamil (2001) stated that the Finetech-Brindley stimulator can be recommended to female patients after 3 months and to male patients after 9 months of complete supra-sacral SCI. The presence of 3 of the 4 non-vesical sacral segment reflexes (ankle jerks, bulbo-cavernous reflex, anal skin reflex, and reflex erection) and a phasic detrusor pressure rise of 35 mm H2O in the female and 50 cm H2O in the male on cystometry indicates intact efferent nerve supply to the bladder and consequently the possibility of success of the implanted stimulator.
A less widely used method for the treatment of neurogenic bladder is transurethral electrical bladder stimulation (TEBS). This modality was first introduced in Europe by Katona and Berenyi (1975) to treat patients with myelomeningocele. It was introduced in the United States by Kaplan and Richards (1986). This procedure has been utilized with the theory that bladder stimulation promotes new sensory awareness of bladder filling and a restoration of detrusor contractility (i.e., disappearance of uninhibited bladder contractions and replacement with normal contractions). Briefly, this procedure involves the filling of the bladder to approximately half capacity with normal saline via an electrocatheter under sterile conditions. The catheter is then connected to a pressure recorder for continuous monitoring of bladder pressure. A rectal balloon catheter is employed to subtract abdominal pressure and a ground electrode is placed on the leg. Stimulation parameters are as follow: (i) voltage -- 0.5 to 10 mA, (ii) frequency -- 40 to 100 Hz, (iii) duration -- 2 to 8 msec, and (iv) interval -- 1 to 10 sec. Patients undergo one or more series of bladder stimulation. The first series of stimulation begins with an evaluation session, which is followed by 10 to 30 90-min daily sessions. Each of these sessions comprises a 15-min period of monitoring of bladder activity followed by 60 mins of bladder stimulation and then another 15 mins of observation of bladder activity. Between series there is a rest period of 3 to 6 months during which no stimulation is given. Following the rest interval, a subsequent series consisting of 5 to 15 daily sessions will commence (Boone et al, 1992; Kaplan and Richards, 1988; Kaplan et al, 1989).
Although earlier reports (Katona and Berenyi, 1975; Kaplan and Richards, 1986; Kaplan and Richards, 1988; Kaplan et al, 1989) claimed that TEBS is effective in treating patients with neurogenic bladder dysfunction, recent studies (Boone et al, 19921; Decter et al, 1992; Lyne and Bellinger, 1993; Decter et al, 1994) have not been able to replicate such findings. The 2 most relevant outcome measures in assessing the effectiveness of TEBS are restoration of normal detrusor contractility and urinary continence. Lyne and Bellinger (1993) treated 17 patients with neurovesical dysfunction with TEBS. Overall, only 5 (41.7 %) of the 12 patients with fully standardized serial cystometry experienced a durable increase in bladder capacity, and no patient achieved volitional voiding. Decter et al (1992) treated 21 patients with neurogenic bladder dysfunction using TEBS. They found that 20 % of the patients showed an increase in bladder capacity and 30 % experienced a decrease in end filling pressures. However, these effects did not significantly change patients' daily voiding regimens. In a follow-up study, Decter et al (1994) stated that TEBS is a time consuming and labor intensive procedure. Additionally, the limited urodynamic benefits attained by patients have not changed their daily routine of bladder management. Because of the afore-mentioned factors, these investigators are not accepting any new patients in their TEBS program. In an earlier study, Nicholas and Eckstein (1975) reported their findings of TEBS in the treatment of 20 patients with neurogenic bladder dysfunction due to spina bifida. No patient attained bladder sensation and the essential pattern of detrusor activity in these patients was unchanged by TEBS.
Boone et al (1992) performed the only prospective, randomized, sham controlled and blinded clinical trial on the use of TEBS in 36 children with myelomeningocele. Patients were allocated to either a 3-week period of TEBS or sham treatment, which was followed by a 3-month rest period, and then all patients were treated with TEBS for an additional 3 weeks. Bladder capacity, sensation, and compliance as well as continence were evaluated. Transurethral electrical bladder stimulation did not produce any beneficial effects even in patients who had undergone a total of 6 weeks of active stimulation.
Van Balken et al (2004) reviewed the literature on the application of various devices and techniques for the ES treatment of lower urinary tract (e.g., bladder) dysfunction with respect to mechanism of action and clinical outcome. These investigators concluded that randomized clinical trials to compare different techniques and evaluate placebo effects are urgently needed, as are further studies to elucidate modes of action to improve stimulation application and therapy results. The introduction of new stimulation methods may provide treatment alternatives as well as help answer more basic questions on ES and neuromodulation.
Cerebral palsy (CP) refers to a wide variety of non-progressive brain disorders resulting from insults to the central nervous system during the perinatal period. Infants born prematurely and full-term infants with low birth-weight have the highest risk of developing CP. Infants whose birth weights are less than 2,500 g account for approximately 1/3 of all babies who later demonstrate signs of CP. Moreover, the rate of CP is about 30 times higher in babies who weigh less than 1,500 g at birth than in full-term babies with normal weight (Kuban and Leviton, 1994). Traditionally, the adverse effects of spasticity are managed by means of pharmacotherapy, physical therapy, bracing, casting, splinting, orthopedic surgeries, and more recently selective posterior rhizotomy. Various forms of ES have also been employed for the management of patients with CP including NMES, which has been used to increase ROM, decrease spasticity, and enhance muscle rehabilitation.
The exact mechanisms by which NMES might improve motor function in children with CP remain unclear. It may be related to its ability to increase ROM, temporarily decrease spasticity, and enhance muscle rehabilitation. Moreover, Pape et al (1993) suggested that NMES applied during sleep might encourage the differential growth of atrophic non-spastic antagonistic muscles. As a result, the decreased imbalance at the end-organ level might improve motor function.
Pape et al (1993) reported their findings regarding the use of NMES for improving motor deficits in children with CP. Six patients with mild ambulatory spastic hemiplegia or diplegia underwent a study of over-night low intensity sub-threshold transcutaneous ES. Only 5 of the 6 patients completed the study. After 6 months of ES, significant improvement was observed on the Peabody Developmental Motor Scales scores in gross motor, locomotor, and receipt/propulsion skills. However, balance and non-locomotor scores showed no significant changes. On the other hand, when ES was withdrawn for 6 months, there was uniform partial regression in scores. Moreover, re-institution of treatment by ES resulted in additional improvement in total gross motor, balance, locomotor, and receipt/propulsion skills, but not for non-locomotor skills. The authors concluded that in selective cases, especially children with mild CP, over-night ES may be a useful adjunct to conventional rehabilitation services. Although the findings by Pape et al appear to be encouraging, this was an uncontrolled study with 5 children who were 3 to 5 years old, a time when rapid changes are expected in these children. More importantly, no attempt was made to standardize physical therapy throughout the study. All but 1 subject continued to receive rehabilitative procedures which may have a confounding effect on the outcome of the study. It is unclear whether these improvements were translated into improvements in activities of daily living. Additionally, there were no data regarding the long-term effects of this treatment modality.
Hazlewood et al (1994) evaluated the effectiveness of ES in treating children with hemiplegic CP. Ten patients were given ES of the anterior tibial muscles by their parents daily for 1 hour for 35 consecutive days in conjunction with their physical therapy (PT) regimen. Ten patients who were matched for age, severity of gait pattern, and for limitation of range of passive dorsiflexion of the ankle served as controls and continued with their current PT program. Active and passive ranges of movement of the ankle, as well as knee and ankle motion during ambulation were recorded by means of electrogoniometers before and after ES. For passive joint-range measurements, there were no significant changes in the range of ankle plantar-flexion, or dorsiflexion with the knee flexed for patients who received tibial muscles ES. However, there was a significant increase in dorsiflexion of the ankle with the knee extended. The mean ranges of the stimulated group of patients for dorsiflexion with the knee extended increased from 40 to 60 % of the range of the non-affected side. For active joint-range measurements, there was a significant difference in the range of voluntary dorsiflexion when the patient was sitting, comparing the experimental and control groups post-test, but no significant differences comparing the pre-and post-changes of the 2 groups. Furthermore, gait analysis and ankle motion showed little change. The authors concluded that because of the complex and diverse pathology associated with CP, the application of ES for the treatment of children with this disorder requires further investigations to determine which types of CP patients are likely to benefit from ES as well as the desired parameters of stimulation before this modality should be used widely in the clinical setting.
Steinbok et al (1997) concluded that therapeutic ES may be beneficial in children with spastic CP who have undergone a selective posterior rhizotomy more than 1 year ago. However, the authors concluded that more research is needed to confirm these results. More importantly, it must be emphasized that these findings can not be extrapolated to the larger population of children with spastic CP who have not undergone selective posterior rhizotomy.
In a systematic review of the literature on ES for CP, Kerr et al (2004) concluded that "[t]here is more evidence to support the use of NMES than TES [threshold electrical stimulation]. However, the findings should be interpreted with caution as the studies had insufficient power to provide conclusive evidence for or against the use of these modalities." An earlier systematic evidence review by Boyd et al (2001) reached similar conclusions about the paucity of evidence for the use of ES for CP.
Acute idiopathic facial paresis is often known as Bell's palsy. Treatment of idiopathic Bell's palsy is still not well-defined. Conservative approaches entail physiotherapies such as facial exercises, massage, and muscle relaxation, which may support rehabilitation and possibly reduce the production of pathological synkinesia. Medical treatments include botulinum toxin type A (Botox) as well as a combined regimen of cortisone, virostatic agents, hemorrheologic substances, and possibly antibiotics. Moreover, available evidence from randomized controlled trials does not show significant benefit from treating Bell's palsy with corticosteroids (Salinas et al, 2002). Surgical decompression of the facial nerve remains controversial.
Adour (1991) stated that decompression of the facial nerve and electrotherapy are not advised for the management of patients with idiopathic (Bell's) palsy. This is in agreement with Wolf who stated that ES should not be used in the treatment of Bell's palsy. Buttress and Herren (2002) reviewed the medical literature to ascertain whether ES had any advantages over facial exercises in promoting recovery after Bell's palsy. Of the 270 papers reviewed by the authors, only 1 presented the best evidence to answer the clinical question. The authors stated that there is no evidence to suggest that either facial exercises or ES is beneficial to patients with acute Bell's palsy. However, evidence does exist to suggest the use of ES in patients with chronic Bell's palsy, although the study design was not rigorous.
Individuals with stroke, CP, multiple sclerosis, and SCI/traumatic brain injury may exhibit foot drop, a condition caused by weakness or paralysis of the muscles involved in lifting the front part of the foot. The WalkAide is a product of Myo-Orthotics Technology, a term coined by the manufacturer, Innovative Neurotronics (Austin, TX). According to the manufacturer, it represents the convergence of orthotic technology (which braces a limb) and ES (which restores specific muscle function). The WalkAide device is intended to counteract foot drop by producing dorsiflexion of the ankle during the swing phase of the gait. The device attaches to the leg, just below the knee, near the head of the fibula. During a gait cycle, the WalkAide stimulates the common peroneal nerve, which innervates the tibialis anterior and other muscles that produce dorsiflexion of the ankle. The WalkAide is designed to offer persons with foot drop increased mobility, functionality and independence. It was cleared by the FDA through the 510(k) process. However, there is currently insufficient evidence to support its use for foot drop and other indications. Prospective clinical studies of the WalkAide device are necessary to evaluate whether it improves function and reduces disability compared to standard bracing in persons with foot drop.
Sheffler and associates (2007) reported the findings of peroneal nerve stimulation in patients with hemiplegia. Two chronic stroke survivors who utilized an ankle foot orthosis (AFO) prior to study entry were evaluated at baseline and after 4 weeks of daily use of a surface peroneal nerve stimulator. Participants were assessed without their dorsiflexor assistive device, using the modified Emory Functional Ambulation Profile (mEFAP). The participants demonstrated improvement in all 5 components of the mEFAP relative to baseline. These case reports indicated that enhanced functional ambulation may be an important therapeutic effect of peroneal nerve stimulation. The authors stated that controlled trials are needed to demonstrate a cause-and-effect relationship.
In a randomized controlled study, Kottink and colleagues (2008) examined the effect of an implantable peroneal nerve stimulator for 6 months versus an AFO in patients with chronic stroke and foot drop (n = 29). The mean time from stroke was 7.3 years (SD = 7.3), and all subjects were community ambulators. The FES group received the implantable stimulation system for correction of their foot drop. The control group continued using their conventional walking device (i.e., AFO, orthopedic shoes, or no walking device). All subjects were measured at baseline and at 4, 8, 12, and 26 weeks in the gait laboratory. The therapeutic effect of FES on the maximum value of the root mean square (RMSmax) of the tibialis anterior (TA) muscle with both flexed and extended knees and walking speed were selected as the primary outcome measures. The RMSmax of the peroneus longus (PL), gastrocnemius (GS), and soleus (SL) muscles with both flexed and extended knees and muscle activity of the TA muscle of the affected leg during the swing phase of gait were selected as secondary outcome measures. A significantly higher RMSmax of the TA muscle with extended knee was found after using FES. No change in walking speed was found when the stimulator was not switched on. A significantly increased RMSmax of the GS muscle with both flexed and extended knees was found after using FES. The authors concluded that functionally, no therapeutic effect of implantable peroneal nerve stimulation was found. However, the significantly increased voluntary muscle output of the TA and GS muscles after the use of FES suggested that there was a certain extent of plasticity in the subjects in this study.
The American Association of Neuromuscular and Electrodiagnostic Medicine, the American Academy of Neurology, and the American Academy of Physical Medicine & Rehabilitation (Bril et al, 2011) developed a scientifically sound and clinically relevant evidence-based guideline for the treatment of painful diabetic neuropathy (PDN). The basic question that was asked was: "What is the efficacy of a given treatment (pharmacological: anticonvulsants, antidepressants, opioids, others; non-pharmacological: electrical stimulation, magnetic field treatment, low-intensity laser treatment, Reiki massage, others) to reduce pain and improve physical function and quality of life (QOL) in patients with PDN"? A systematic review of literature from 1960 to August 2008 was performed, and studies were classified according to the American Academy of Neurology classification of evidence scheme for a therapeutic article. Recommendations were linked to the strength of the evidence. The results indicated that pregabalin is established as effective and should be offered for relief of PDN (Level A). Venlafaxine, duloxetine, amitriptyline, gabapentin, valproate, opioids (morphine sulfate, tramadol, and oxycodone controlled-release), and capsaicin are probably effective and should be considered for treatment of PDN (Level B). Other treatments have less robust evidence, or the evidence is negative. Effective treatments for PDN are available, but many have side effects that limit their usefulness. Few studies have sufficient information on their effects on function and QOL.
Neuromuscular Electrical Stimulation for Ambulatory Function in Patients with Multiple Sclerosis:
In a case-series study, Wahls et al (2010) examined if NMES would improve gait disability in patients with secondary progressive multiple sclerosis (SPMS) or primary progressive multiple sclerosis (PPMS). Participants were treated using NMES coupled with a home-exercise program (HEP) to treat MS-related gait disability. Between June 2007 and June 2009, a licensed physical therapist used NMES coupled with a HEP to work with patients who had SPMS/PPMS and MS-related gait disability. All of the cases in which an NMES test session of NMES was conducted were included in the case series. Data regarding MS symptoms, treatment, gait, and function were abstracted from the PT clinic notes. Results of assessment with the expanded Kurtzke Disability Status Scale (EDSS) at presentation and at most recent visit were abstracted from the clinical record by the treating physical therapist. A total of 9 patients (7 with SPMS and 2 with PPMS) met inclusion criteria for review. Mean of years of diagnosis was 10.4 (range of 4 to 15), and mean EDSS score at presentation was 5.9 (range of 4.5 to 6.5). Mean of days of NMES was 140 (range of 22 to 495). Mean EDSS scores improved by 0.78 (range of 0 to 2.0). The authors concluded that NMES was associated with measurable gains in ambulatory function in patients with gait disability associated with SPMS and PPMS. Moreover, they stated that additional studies are needed.
Neuromuscular Electrical Stimulation for Knee Osteoarthritis:
Giggins et al (2012) evaluated the effectiveness of surface NMES in the treatment of knee osteoarthritis. A systematic review and meta-analysis of randomized controlled trials (RCTs) and controlled clinical trials was performed. Studies were identified from databases (MEDLINE, EMBASE, CINAHL, Sports Discus, PEDro and the Cochrane Library) searched to January 2011 using a battery of keywords. Two reviewers selected studies meeting inclusion criteria. The methodological quality of the included studies was assessed using the Thomas Test and the strength of the evidence was then graded using the Agency for Health Care Policy and Research guidelines. Data were pooled and meta-analyses were performed. A total of 9 RCTs and 1 controlled clinical trial, studying a total of 409 participants (n = 395 for RCTs, and n = 14 for controlled trial) with a diagnosis of osteoarthritis were included. Inconsistent evidence (level D) was found that NMES has a significant impact on measures of pain, function and quadriceps femoris muscle strength in knee osteoarthritis. The authors concluded that the role of NMES in the treatment of knee osteoarthritis is ambiguous. Thus, future work is needed in this field to clearly establish the role of NMES in this population.
Threshold Electrical Stimulation:
Threshold electrical stimulation (also known as therapeutic electrical stimulation) entails the use of of low-intensity ES, usually at night. For patients with CP, threshold electrical stimulation (TES) aims to (i) strengthen muscles weakened by non-use and (ii) to increase joint mobility, thus, resulting in improved voluntary motor function.
In a randomized, controlled, cross-over trial, Sommerfelt et al (2001) evaluated the effect of TES applied to antagonists of spastic leg muscles on gross motor function in children with spastic diplegic CP. A total of 12 children between 5 and 12 years of age completed a 24-month cross-over study in which 6 were randomly assigned to receive TES for the first 12 months and the remaining 6 for the last 12 months. Physiotherapy and a home training program were not altered. All were evaluated blindly in terms of tests of motor function and video recordings at the start and at 12 and 24 months. At the end of the study parents/carers gave a subjective assessment of the effect of TES. No significant effect of TES on motor or ambulatory function was found on the blinded evaluation, but parents of 11 of the 12 children stated that TES had a significant effect. The authors concluded that it is unlikely that TES has a significant effect on motor and ambulatory function in chilren with spastic diplegia CP.
In a randomized, double-blind, placebo-controlled clinical trial, Dali et al (2002) studied whether a group of stable children with CP (36 boys, 21 girls; mean age of 10 years 11 months with a range of 5 to 18 years) would improve their motor skills after 12 months of TES; 2/3 received active and 1/3 received inactive stimulators. The primary outcome was change in summary indices of the performance measurements in a set of motor function tests. Tests were videotaped and assessed blindly to record qualitative changes that might not be reflected in performance measurements. Fifty-seven of 82 subjects who were able to walk at least with a walker, completed all 12 months of treatment (hemiplegia n = 25; diplegia n = 32). There was no significant difference between active and placebo treatment in any of the tested groups, nor combined. Visual and subjective assessments favored TES (non-significant), whereas objective indices showed the opposite trend. The authors concluded that TES in these patients did not have any significant clinical effect during the test period.
In a randomized placebo-controlled study, Kerr et al (2006) examined the effectiveness of NMES and TES in strengthening the quadriceps muscles of both legs in children with CP. A total of 60 children (38 males, 22 females; mean age of 11 years [SD 3 years 6 months]; age range of 5 to 16 years) were randomized to one of the following groups: NMES (n = 18), TES ( n= 20), or placebo (n = 22). Clinical presentations were diplegia (n = 55), quadriplegia (n = 1), dystonia (n = 1), ataxia (n = 1), and non-classifiable CP (n = 2). Thirty-four children walked unaided, 17 used posterior walkers, 6 used crutches, and the remaining 3 used sticks for mobility. Peak torque of the left and right quadriceps muscles, gross motor function, and impact of disability were assessed at baseline and end of treatment (16 weeks), and at a 6-week follow-up visit. No statistically significant difference was demonstrated between NMES or TES versus placebo for strength or function. Statistically significant differences were observed between NMES and TES versus placebo for impact of disability at the end of treatment, but only between TES and placebo at the 6-week follow-up. The authors concluded that further evidence is needed to show whether NMES and/or TES may be useful as an adjunct to therapy in ambulatory children with diplegia who find resistive strengthening programs difficult.
In a systematic review with meta-analysis of randomized trials, Scianni et al (2009) examined if strengthening interventions increase strength without increasing spasticity and improve activity, and if there is there any carry-over after cessation in children and adolescents with CP? Children with spastic CP between school age and 20 years were included in this analysis. Strengthening interventions involved repetitive, strong, or effortful muscle contractions and progressed as ability changed; and they included biofeedback, ES, and progressive resistance exercise. Strength was measured as continuous measures of maximum voluntary force or torque production. Spasticity was measured as velocity-dependent resistance to passive stretch. Activity was measured as continuous measures, e.g., 10-m Walk Test, or using scales e.g., the Gross Motor Function Measure. A total of 6 studies were identified and 5 had data that could be included in a meta-analysis. Strengthening interventions had no effect on strength (SMD 0.20, 95 % CI: -0.17 to 0.56), no effect on walking speed (MD 0.02 m/s, 95 % CI: -0.13 to 0.16), and had a small statistically-significant but not clinically-worthwhile effect on Gross Motor Function Measure (MD 2 %, 95 % CI: 0 to 4). Only 1 study measured spasticity but did not report the between-group analysis. The authors concluded that in children and adolescents with CP who are walking, the current evidence suggests that strengthening interventions are neither effective nor worthwhile.
Cauraugh et al (2010) performed a systematic review and meta-analysis using the International Classification of Functioning to determine the summary effect of ES on impairment and activity limitations relevant to gait problems of children with CP. These researchers identified 40 CP and ES studies, and 17 gait studies qualified for inclusion. Applying enablement classification methods to walking abnormalities created 2 subgroups: impairment (n = 14) and activity limitations (n = 15). Overall, 238 subjects experienced ES treatments and 224 served as a no stimulation control group. Calculations followed conventional data extraction and meta-analysis techniques: (a) individual standardized mean differences, (b) summary effect size, (c) I² heterogeneity test, (d) fail-safe N analysis and (e) moderator variable analyses. The authors cited reservation about recommending ES as an effective intervention for individuals with CP. Outside of the laboratory-testing experiments, "no quantitative, functional immediate or longitudinal effects beyond the testing situations were reported in the studies. Thus, long-term effects of various types of electrical stimulation on gait challenges in children with cerebral palsy would advance our understanding."
Improvement of Ambulatory Function/Muscle Weakness in Individuals with Progressive Diseases:
Pereira et al (2012) conducted a systematic review on the effectiveness of FES in improving lower extremity function in chronic stroke. Multiple databases (PubMed, CINAHL, EMBASE, and Scopus) were searched for relevant articles. Studies were included for review if (i) greater than or equal to 50 % of the study population has sustained a stroke, (ii) the study design was a RCT, (iii) the mean time since stroke was greater than or equal to 6 months, (iv) FES or NMES was compared to other interventions or a control group, and (v) functional lower extremity outcomes were assessed. Methodological quality was assessed using the PEDro tool. A standardized mean difference (SMD ± SE and 95 % CI) was calculated for the 6-min walk test (6MWT). Pooled analysis was conducted for treatment effect of FES on the 6MWT distance using a fixed effects model. A total of 7 RCTs (PEDro scores 5 to 7) including a pooled sample size of 231 participants met inclusion criteria. Pooled analysis revealed a small but significant treatment effect of FES (0.379 ± 0.152; 95 % CI: 0.081 to 0.677; p = 0.013) on 6MWT distance. The authors concluded that FES may be an effective intervention in the chronic phase post-stroke. However, its therapeutic value in improving lower extremity function and superiority over other gait training approaches remains unclear.
In a Cochrane review, Maddocks et al (2013) evaluated the effectiveness of NMES for improving muscle strength in adults with advanced disease. The secondary objective of this study was to examine the acceptability and safety of NMES, and changes in muscle function (strength or endurance), muscle mass, exercise capacity, breathlessness and health-related quality of life. Studies were identified from searches of The Cochrane Library, MEDLINE, EMBASE, CINAHL and PsycINFO databases to July 2012, citation searches, conference proceedings and previous systematic reviews. These investigators included RCTs in adults with advanced chronic obstructive pulmonary disease (COPD), chronic heart failure, cancer or human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) comparing a program of NMES as a sole or adjunct intervention to no treatment, placebo NMES or an active control. They imposed no language restriction. Two review authors independently extracted data on study design, participants, interventions and outcomes. They assessed risk of bias using the Cochrane Collaboration's tool; and calculated mean differences (MD) or standardized mean differences (SMD) between intervention and control groups for outcomes with sufficient data; for other outcomes these researchers described findings from individual studies. A total of 11 studies involving 218 participants met the inclusion criteria across COPD, chronic heart failure and thoracic cancer. Neuromuscular ES significantly improved quadriceps strength by a SMD of 0.9 (95 % CI: 0.33 to 1.46), equating to approximately 25 Newton meters (Nm) (95 % CI: 9 to 41). Mean differences across various walking tests, favoring NMES, were 40 m (95 % CI: -4 to 84) for the 6MWT, 69 m (95 % CI: 19 to 119) for the incremental shuttle walk test and 160 m (95 % CI: 34 to 287) for the endurance shuttle walk test. Limited evidence was available for the assessment of other secondary outcomes. The authors concluded that NMES appears an effective means of improving muscle weakness in adults with progressive diseases such as COPD, chronic heart failure and cancer. Moreover, they stated that further research is needed to clarify its place in clinical practice, by determining the optimal parameters for a NMES program, the patients most likely to benefit, and its impact on morbidity and service use.
CPT Codes / HCPCS Codes / ICD-9 Codes
Functional Electrical Stimulation (FES) for spinal cord injury (e.g., Parastep I System):
CPT codes covered if selection criteria are met:
HCPCS codes covered if selection criteria are met:
Electrodes (e.g., apnea monitor), per pair
Lead wires (e.g., apnea monitor), per pair
Conductive gel or paste, for use with electrical device (e.g., TENS, NMES), per oz.
Electrical stimulator supplies, 2 lead, per month, (e.g. TENS, NMES)
Form-fitting conductive garment for delivery of TENS or NMES (with conductive fibers separated from the patient's skin by layers of fabric)
Neuromuscular stimulator, electronic shock unit
Transcutaneous electrical joint stimulation device system, includes all accessories
Functional neuromuscular stimulator, transcutaneous stimulation of muscles of ambulation with computer control, used for walking by spinal cord injured, entire system, after completion of training program
Functional electrical stimulator, transcutaneous stimulation of nerve and / or muscle groups, any type, complete system, not otherwise specified
Implantable neurostimulator electrode, each
Patient programmer (external) for use with implantable programmable neurostimulator pulse generator
Radiofrequency transmitter (external) for use with implantable sacral root neurostimulator receiver for bowel and bladder management, replacement
Implantable neurostimulator pulse generator, single array, rechargeable, includes extension
Implantable neurostimulator pulse generator, single array, non-rechargeable, includes extension
Implantable neurostimulator pulse generator, dual array, rechargeable, includes extension
Implantable neurostimulator pulse generator, dual array, non-rechargeable, includes extension
External recharging system for battery (internal) for use with implantable neurostimulator
ICD-9 codes covered if selection criteria are met:
Neurogenic bladder dysfunction
Other ICD-9 codes related to the CPB:
788.20 - 788.29
Retention of urine
788.30 - 788.39
Incontinence of urine
Peroneal Nerve Stimulators:
There is no specific code for peroneal nerve stimulators:
ICD-9 codes not covered for indications listed in the CPB (not all-inclusive):
Other acquired deformities of ankle and foot
The above policy is based on the following references:
Functional Electrical Stimulation for Walking:
Granat M, Keating JF, Smith AC, et al. The use of functional electrical stimulation to assist gait in patients with incomplete spinal cord injury. Disabil Rehabil. 1992;14(2):93-97.
Stein R, Belanger M, Wheeler G, et al. Electrical systems for improving locomotion after incomplete spinal cord injury: An assessment. Archiv Physical Med Rehabil. 1993;74(9):954-959.
Winchester P, Carollo JJ, Habasevich R. Physiologic costs of reciprocal gait in FES assisted walking. Paraplegia. 1994;32(10):680-686.
U.S. Food and Drug Administration (FDA). Parastep I electrical stimulation for quadriplegics. Sigmedics, Inc. PMA No. P900038. Rockville, MD: FDA; April 20, 1994.
Gallien P, Brissot R, Eyssette M, et al. Restoration of gait by functional electrical stimulation for spinal cord injured patients. Paraplegia. 1995;33(11):660-664.
Thoumie P, Perrouin-Verbe B, Le Claire G, et al. Restoration of functional gait in paraplegic patients with the RGO-II Hybrid Orthosis. A multicentre controlled study. I. Clinical evaluation. Paraplegia. 1995;33(11):647-653.
Chaplin E. Functional neuromuscular stimulation for mobility in people with spinal cord injuries. The Parastep I System. J Spinal Cord Med. 1996;19(2):99-105.
Heller BW, Granat MH, Andrews BJ. Swing-through gait with free-knees produced by surface functional electrical stimulation. Paraplegia. 1996;34(1):8-15.
Moynahan M, Mullin C, Cohn J, et al. Home use of a functional electrical stimulation system for standing and mobility in adolescents with spinal cord injury. Archiv Physical Med Rehabil. 1996;77(10):1005-1013.
Sykes L, Ross ER, Powell ES, Edwards J. Objective measurement of the use of the Reciprocating Gait Orthosis (RGO) and the Electrically Augmented RGO in adult patients with spinal cord lesions. Prosthetics Orthotics Int. 1996;20(3):182-190.
Klose KJ, Jacobs PL, Broton JG, et al. Evaluation of a training program for persons with SCI paraplegia using the Parastep I Ambulation System: Part 1, Ambulation Performance and Anthropometric Measures. Archiv Physical Med Rehabil. 1997;78(8):808-814.
Jacobs PL, Nash MS, Klose KJ, et al. Evaluation of a training program for persons with SCI paraplegia using the Parastep 1 ambulation system. Part 2. Effects on physiological responses to peak arm ergometry. Arch Phys Med Rehabil. 1997;78(8):794-798.
Needham-Shropshire B, Broton JG, Klose KJ, et al. Evaluation of a training program for persons with SCI paraplegia using the Parastep 1 Ambulation System: Part 3. Lack of effect on bone mineral density. Archiv Physical Med Rehabil. 1997;78(8):799-803.
Guest RS, Klose KJ, Needham-Shropshire BM, Jacobs PL. Evaluation of a training program for persons with SCI paraplegia using the Parastep 1 ambulation system. Part 4. Effect on physical self-concept and depression. Arch Phys Med Rehabil. 1997;78(8):804-807.
Nash M, Jacobs PL, Montalvo BM, et al. Evaluation of a training program for persons with SCI paraplegia using the Parastep 1 Ambulation System: Part 5. Lower extremity blood flow and hyperemic responses to occlusion are augmented by ambulation training. Archiv Physical Med Rehabil. 1997;78(8):808-814.
Solomonow M, Reisin E, Aguilar E, et al. Reciprocating gait orthosis powered with electrical stimulation (RGO II). Part II: Medical evaluation of 70 paraplegic patients. Orthopedics. 1997;20(5):411-418.
Graupe D, Kohn K. Ambulation by traumatic T4-T12 paraplegics using functional neuromuscular stimulation. Crit Rev Neurosurg. 1998;8(4):221-231.
Wieler M, Stein RB, Ladouceur M, et al. Multicenter evaluation of electrical stimulation systems for walking. Archiv Physical Med Rehabil. 1999;80(5):495-500.
Bonaroti D, Akers JM, Smith BT, et al. Comparison of functional electrical stimulation to long leg braces for upright mobility for children with complete thoracic level spinal injuries. Archiv Phys Med Rehabil. 1999;80(9):1047-1053.
Center for Medicare and Medicaid Services (CMS). Neuromuscular electrical stimulation (NMES) for spinal cord injury. Decision Memorandum #CAG -00153R. Baltimore, MD: CMS; July 22, 2002.
Center for Medicare and Medicaid Services (CMS). Neuromuscular electrical stimulation (NMES) for spinal cord injury. National Coverage Analysis (NCA). Baltimore, MD: CMS; effective April 1, 2003. Available at: http://www.cms.hhs.gov/mcd/search.asp. Accessed November 16, 2004.
Robbins SM, Houghton PE, Woodbury MG, Brown JL. The therapeutic effect of functional and transcutaneous electric stimulation on improving gait speed in stroke patients: A meta-analysis. Archiv Phys Med Rehab. 2006;87(6):853-859.
Weingarden HP, Kizony R, Nathan R, et al. Upper limb functional electrical stimulation for walker ambulation in hemiplegia: A case report. Am J Phys Med Rehabil. 1997;76(1):63-67.
Hausdorff JM, Ring H. Effects of a new radio frequency-controlled neuroprosthesis on gait symmetry and rhythmicity in patients with chronic hemiparesis. Am J Phys Med Rehabil. 2008;87(1):4-13.
Functional Electrical Stimulation of the Upper Extremities:
Weingarden HP, Zeilig G, Heruti R, et al. Hybrid functional electrical stimulation orthosis system for the upper limb: Effects on spasticity in chronic stable hemiplegia Am J Phys Med Rehabil. 1998;77(4):276-281.
Alon G, McBride K, Ring H. Improving selected hand functions using a noninvasive neuroprosthesis in persons with chronic stroke. Stroke Cerebrovasc Dis. 2002;11(2):99-106.
Alon G, Ring H. Gait and hand function enhancement following training with a multi-segment hybrid-orthosis stimulation system in stroke patients. J Stroke Cerebrovasc Dis. 2003;12(5):209-216.
Alon G, Sunnerhagen KS, Geurts AC, Ohry A. A home-based, self-administered stimulation program to improve selected hand functions of chronic stroke. NeuroRehabilitation. 2003;18(3):215-25.
Berner YN, Lif Kimchi O, Spokoiny V, Finkeltov B. The effect of electric stimulation treatment on the functional rehabilitation of acute geriatric patients with stroke--a preliminary study. Arch Gerontol Geriatr. 2004;39(2):125-132.
Ring H, Rosenthal N. Controlled study of neuroprosthetic functional electrical stimulation in sub-acute post-stroke rehabilitation. J Rehabil Med. 2005;37(1):32-36.
Meijer JW, Voerman GE, Santegoets KM, Geurts AC. Short-term effects and long-term use of a hybrid orthosis for neuromuscular electrical stimulation of the upper extremity in patients after chronic stroke. J Rehabil Med. 2009;41(3):157-161.
Snoek GJ, IJzerman MJ, in 't Groen FA, et al. Use of the NESS handmaster to restore handfunction in tetraplegia: Clinical experiences in ten patients. Spinal Cord. 2000;38(4):244-249.
Hendricks HT, IJzerman MJ, de Kroon JR, et al. Functional electrical stimulation by means of the 'Ness Handmaster Orthosis' in chronic stroke patients: An exploratory study. Clin Rehabil. 2001;15(2):217-220.
Urbano E, Cappello A, Davalli A. A PC-based system for evaluating the efficacy of the NESS Handmaster orthosis. IEEE Trans Neural Syst Rehabil Eng. 2003;11(4):438-442.
Alon G, Levitt AF, McCarthy PA. Functional electrical stimulation enhancement of upper extremity functional recovery during stroke rehabilitation: A pilot study. Neurorehabil Neural Repair. 2007;21(3):207-215.
Ring H, Weingarden H. Neuromodulation by functional electrical stimulation (FES) of limb paralysis after stroke. Acta Neurochir Suppl. 2007;97(Pt 1):375-380.
Alon G, Levitt AF, McCarthy PA. Functional electrical stimulation (FES) may modify the poor prognosis of stroke survivors with severe motor loss of the upper extremity: A preliminary study. Am J Phys Med Rehabil. 2008;87(8):627-636.
Neuromuscular Electrical Stimulation for Disuse Atrophy:
Gould N, Donnermeyer D, Gammon GG, et al. Transcutaneous muscle stimulation to retard disuse atrophy after open meniscectomy. Clin Orthop. 1983;178:190-197.
Morrissey MC, Brewster CE, Shields CL Jr, Brown M. The effects of electrical stimulation on the quadriceps during postoperative knee immobilization. Am J Sports Med. 1985;13(1):40-45.
Arvidsson I, Arvidsson H, Eriksson E, Jansson E. Prevention of quadriceps wasting after immobilization: An evaluation of the effect of electrical stimulation. Orthopedics. 1986;9(11):1519-1528.
Snyder-Mackler L, Ladin Z, Schepsis AA, Young JC. Electrical stimulation of the thigh muscles after reconstruction of the anterior cruciate ligament. J Bone Joint Surg. 1991;73(7):1025-1036.
Lake DA. Neuromuscular electrical stimulation: An overview and its application in the treatment of sports injuries. Sports Med. 1992;13(5):320-336.
Gotlin RS, Hershkowitz S, Juris PM, et al. Electrical stimulation effect on extensor lag and length of hospital stay after total knee arthroplasty. Arch Phys Med Rehabil. 1994;75(9):957-959.
Snyder-Mackler L, Delitto A, Bailey SL, Stralka SW. Strength of the quadriceps femoris muscle and functional recovery after reconstruction of the anterior cruciate ligament. A prospective, randomized clinical trial of electrical stimulation. J Bone Joint Surg Am. 1995;77(8):1166-1173.
Lieber RL, Silva PD, Daniel DM. Equal effectiveness of electrical and volitional strength training for quadriceps femoris muscles after anterior cruciate ligament surgery. J Orthop Res. 1996;14(1):131-138.
Bax L, Staes F, Verhagen A. Does neuromuscular electrical stimulation strengthen the quadriceps femoris: A systematic review of randomised controlled trials. Sports Med. 2005;35(3):191-212.
Monaghan B, Caulfield B, O'Mathúna DP. Surface neuromuscular electrical stimulation for quadriceps strengthening pre and post total knee replacement. Cochrane Database Syst Rev, 2010;(1):CD007177.
Neuromuscular Electrical Stimulation for Stroke:
Gresham SE, Duncan PW, Stason WB, et al. Post-stroke rehabilitation. Clinical Practice Guideline No. 16. AHCPR Publication No. 95-0662. Rockville, MD: Agency for Health Care Policy and Research (AHCPR); May 1995.
Kumar VP, Lau HK, Liu J, et al. Clinical applications of functional electrical stimulation. Ann Acad Med Singapore. 1995;24(3):428-435.
Daly JJ, Marsolais EB, Mendell LM, et al. Therapeutic neural effects of electrical stimulation. IEEE Trans Rehabil Eng. 1996;4(4):218-230.
Pandyan AD, Granat MH, Stott DJ. Effects of electrical stimulation on flexion contractures in the hemiplegic wrist. Clin Rehabil. 1997;11(2):123-130.
Hummelsheim H, Maier-Loth ML, Eickhof C. The functional value of electrical muscle stimulation for the rehabilitation of the hand in stroke patients. Scand J Rehabil Med. 1997;29(1):3-10.
Francisco G, Chae J, Chawla H, et al. Electromyogram-triggered neuromuscular stimulation for improving the arm function of acute stroke survivors: A randomized pilot study. Arch Phys Med Rehabil. 1998;79(5):570-575.
Kagaya H, Sharma M, Kobetic R, Marsolais EB. Ankle, knee, and hip moments during standing with and without joint contractures: Simulation study for functional electrical stimulation. Am J Phys Med Rehabil. 1998;77(1):49-54.
Chae J, Bethoux F, Bohine T, et al. Neuromuscular stimulation for upper extremity motor and functional recovery in acute hemiplegia. Stroke. 1998;29(5):975-979.
Dent THS. Functional electrical stimulation for limb motor dysfunction following stroke. STEER: Succinct and Timely Evaluated Evidence Reviews. Bazian, Ltd., eds. London, UK: Wessex Institute for Health Research and Development, University of Southampton; 2001;1(16):1-9.
Yan T, Hui-Chan CW, Li LS. Functional electrical stimulation improves motor recovery of the lower extremity and walking ability of subjects with first acute stroke: A randomized placebo-controlled trial. Stroke. 2005 Jan;36(1):80-85.
de Kroon JR, van der Lee J , Ijzerman MJ, et al. Therapeutic electrical stimulation to improve motor control and functional abilities of the upper extremity after stroke: A systematic review. Clin Rehab. 2002;16(4):350-360.
Chantraine A, Baribeault A, Uebelhart D, Gremion G. Shoulder pain and dysfunction in hemiplegia: Effects of functional electrical stimulation. Arch Phys Med Rehabil. 1999;80(3):328-331.
Chae J, Yu D. A critical review of neuromuscular electrical stimulation for treatment of motor dysfunction in hemiplegia. Assist Technol. 2000;12(1):33-49.
Price CI, Pandyan AD. Electrical stimulation for preventing and treating post-stroke shoulder pain. Cochrane Database Syst Rev. 2000;(4):CD001698.
Wang RY, Yang YR, Tsai MW, et al. Effects of functional electric stimulation on upper limb motor function and shoulder range of motion in hemiplegic patients. Am J Phys Med Rehabil. 2002;81(4):283-290.
Turner-Stokes L, Jackson D. Shoulder pain after stroke: A review of the evidence base to inform the development of an integrated care pathway. Clin Rehabil. 2002;16(3):276-298.
New Zealand Guidelines Group (NZGG). Life after stroke. New Zealand guideline for management of stroke. Wellington, New Zealand: NZGG; November 2003.
Van Peppen RP, Kwakkel G, Wood-Dauphinee S, et al. The impact of physical therapy on functional outcomes after stroke: What's the evidence? Clin Rehabil. 2004;18(8):833-862.
Aoyagi Y, Tsubahara A. Therapeutic orthosis and electrical stimulation for upper extremity hemiplegia after stroke: A review of effectiveness based on evidence. Top Stroke Rehabil. 2004;11(3):9-15.
Yozbatiran N, Donmez B, Kayak N, Bozan O. Electrical stimulation of wrist and fingers for sensory and functional recovery in acute hemiplegia. Clin Rehabil. 2006;20(1):4-11.
Pomeroy VM, King L, Pollock A, et al. Electrostimulation for promoting recovery of movement or functional ability after stroke. Cochrane Database Syst Rev. 2006;(2):CD003241.
Meilink A, Hemmen B, Seelen HA, Kwakkel G. Impact of EMG-triggered neuromuscular stimulation of the wrist and finger extensors of the paretic hand after stroke: A systematic review of the literature. Clin Rehabil. 2008;22(4):291-305.
van Swigchem R, Vloothuis J, den Boer J, et al. Is transcutaneous peroneal stimulation beneficial to patients with chronic stroke using an ankle-foot orthosis? A within-subjects study of patients' satisfaction, walking speed and physical activity level. J Rehabil Med. 2010;42(2):117-121.
Neuromuscular Electrical Stimulation for Spinal Cord Injury:
Merritt JL. Management of spasticity in spinal cord injury. Mayo Clin Proc. 1981;56(10):614-622.
Glaser RM. Physiologic aspects of spinal cord injury and functional neuromuscular stimulation. Cent Nerv Syst Trauma. 1986;3(1):49-62.
Sipski ML, Delisa JA, Schweer S. Functional electrical stimulation bicycle ergometry: Patient perceptions. Am J Phys Med Rehabil. 1989;68(3):147-149.
Leeds EM, Klose KJ, Ganz W, et al. Bone mineral density after bicycle ergometry training. Arch Phys Med Rehabil. 1990;71(3):207-209.
Yarkony GM, Roth EJ, Cybulski GR, Jaeger RJ. Neuromuscular stimulation in spinal cord injury II: Prevention of secondary complications. Arch Phys Med Rehabil. 1992;73(2):195-200.
National Spinal Cord Injury Association (NSCIA). Functional electrical stimulation, clinical applications in spinal cord injury. Fact sheet no. 9. Silver Spring, MD: NSCIA; March 1992.
Pentland B. Rehabilitation. Quadriplegia and cardiorespiratory fitness. Lancet. 1993;341(8842):413-414.
Sipski ML, Alexander CJ, Harris M. Long-term use of computerized bicycle ergometry for spinal cord injured subjects. Arch Phys Med Rehabil. 1993;74(3):238-241.
Krauss JC, Robergs RA, Depaepe JL, et al. Effects of electrical stimulation and upper body training after spinal cord injury. Med Sci Sports Exerc. 1993;25(9):1054-1061.
American Spinal Injury Association (ASIA). ASIA Impairment Scale Clinical Syndromes. Chicago, IL: ASIA; revised 2000. Available at: www.asia-spinalinjury.org/publications/index.html. Accessed November 16, 2004.
Mehrholz J, Kugler J, Pohl M. Locomotor training for walking after spinal cord injury. Cochrane Database Syst Rev. 2008;(2):CD006676.
Alon G, McBride K. Persons with C5 or C6 tetraplegia achieve selected functional gains using a neuroprosthesis. Arch Phys Med Rehabil. 2003;84(1):119-124.
Glenn WW, Haak B, Sasaki C, Kirchner J. Characteristics and surgical management of respiratory complications accompanying lesions of the brainstem. Ann Surg. 1980;191(6):655-663.
Glenn WW, Hogan JF, Loke JS, et al. Ventilatory support by pacing of the conditioned diaphragm in quadriplegia. N Engl J Med. 1984;310(18):1150-1155.
Stover SL, Fine PR, eds. Spinal Cord Injury: The Facts and Figures. Birmingham, AL: University of Alabama at Birmingham; 1986: 25 - 27.
Carter RE, Donovan WH, Halstead L, Wilkerson MA. Comparative study of electrophrenic nerve stimulation and mechanical ventilatory support in traumatic spinal cord injury. Paraplegia. 1987;25(2):86-91.
Glenn WW, Brouillette RT, Dentz B, et al. Fundamental considerations in pacing of the diaphragm for chronic ventilatory insufficiency: A multi-center study. Pacing Clin Electrophysiol. 1988;11(2):2121-2127.
Hunt CE, Brouillette RT, Weese-Mayer DE, et al. Diaphragm pacing in infants and children. Pacing Clin Electrophysiol. 1988;11(2):2135-2141.
Flett PJ. The rehabilitation of children with spinal cord injury. J Paediatr Child Health. 1992;28(2):141-146.
Esclarin A, Bravo P, Arroyo O, et al. Tracheostomy ventilation versus diaphragmatic pacemaker ventilation in high spinal cord injury. Paraplegia. 1994;32(10):687-693.
Chervin RD, Guilleminault C. Diaphragm pacing for respiratory insufficiency. J Clin Neurophysiol. 1997;14(5):369-377.
Krieger LM, Krieger AJ. The intercostal to phrenic nerve transfer: An effective means of reanimating the diaphragm in patients with high cervical spine injury. Plast Reconstr Surg. 2000;105(4):1255-1261.
Elefteriades JA, Quin JA, Hogan JF, et al. Long-term follow-up of pacing of the conditioned diaphragm in quadriplegia. Pacing Clin Electrophysiol. 2002;25(6):897-906.
Flageole H, Adolph VR, Davis GM, et al. Diaphragmatic pacing in children with congenital central alveolar hypoventilation syndrome. Surgery. 1995;118(1):25-28.
Comite d'Evaluation et de Diffusion des Innovations Technologiques (CEDIT). Implantable phrenic stimulation. Ref. 96.07.1. Paris, France: CEDIT; 1996.
Girsch W, Koller R, Holle J, et al. Vienna phrenic pacemaker--experience with diaphragm pacing in children. Eur J Pediatr Surg. 1996;6(3):140-143.
Creasey G, Elefteriades J, DiMarco A, et al. Electrical stimulation to restore respiration. J Rehabil Res Dev. 1996;33(2):123-132.
Yasuma F, Sakamoto M, Okada T, Abe K. Eight-year follow-up study of a patient with central alveolar hypoventilation treated with diaphragm pacing. Respiration. 1998;65(4):313-316.
Garrido-Garcia H, Mazaira Alvarez J, Martin Escribano P, et al. Treatment of chronic ventilatory failure using a diaphragmatic pacemaker. Spinal Cord. 1998;36(5):310-314.
Shaul DB, Danielson PD, McComb JG, Keens TG. Thoracoscopic placement of phrenic nerve electrodes for diaphragmatic pacing in children. J Pediatr Surg. 2002;37(7):974-978.
Chen ML, Keens TG. Congenital central hypoventilation syndrome: Not just another rare disorder. Paediatr Respir Rev. 2004;5(3):182-189.
Yun AJ, Lee PY, Doux JD. Negative pressure ventilation via diaphragmatic pacing: A potential gateway for treating systemic dysfunctions. Expert Rev Med Devices. 2007;4(3):315-319.
Onders RP, Elmo M, Khansarinia S, et al. Complete worldwide operative experience in laparoscopic diaphragm pacing: Results and differences in spinal cord injured patients and amyotrophic lateral sclerosis patients. Surg Endosc. 2009a;23(7):1433-1440.
Onders RP, Carlin AM, Elmo M, et al. Amyotrophic lateral sclerosis: The Midwestern surgical experience with the diaphragm pacing stimulation system shows that general anesthesia can be safely performed. Am J Surg. 2009b;197(3):386-390.
National Institute for Health and Clinical Excellence (NICE). Intramuscular diaphragm stimulation for ventilator-dependent chronic respiratory failure due to neurological disease. Interventional Procedure Guidance 307. London, UK: NICE; July 2009.
Dibidino R, Morrison, A. Laparoscopic diaphragm pacing for tetraplegia [Issues in emerging health technologies issue 115]. Ottawa: Canadian Agency for Drugs and Technologies in Health; 2009.
Hirschfeld S, Exner G, Luukkaala T, Baer GA. Mechanical ventilation or phrenic nerve stimulation for treatment of spinal cord injury-induced respiratory insufficiency. Spinal Cord. 2008;46(11):738-742.
Sacral Nerve Stimulation With Dorsal Rhizotomy (Vocare Bladder System):
Creasey GH. Electrical stimulation of sacral roots for micturition after spinal cord injury. Urol Clin North Am. 1993;20(3):505-515.
Brindley GS. The first 500 patients with sacral anterior root stimulator implants: General description. Paraplegia. 1994;32(12):795-805.
Van Kerrebroeck PE, Koldewijn EL, Rosier PF, et al. Results of the treatment of neurogenic bladder dysfunction in spinal cord injury by sacral posterior root rhizotomy and anterior sacral root stimulation. J Urol. 1996;155(4):1378-1381.
Wielink G, Essink-Bot M L, van Kerrebroeck PEV, Rutten FFH. Sacral rhizotomies and electrical bladder stimulation in spinal cord injury 2: Cost-effectiveness and quality of life analysis. Eur Urol. 1997;31(4):441-446.
Egon G, Barat M, Columbel P, et al. Implantation of anterior sacral root stimulators combined with posterior sacral rhizotomy in spinal injury patients. World J Urol. 1998;16(5):342-349.
Wyndaele JJ, Madersbacher H, Kovindha A. Conservative treatment of the neuropathic bladder in spinal cord injured patients. Spinal Cord. 2001;39(6):294-300.
Jamil F. Towards a catheter free status in neurogenic bladder dysfunction: A review of bladder management options in spinal cord injury (SCI). Spinal Cord. 2001;39(7):355-361.
Jezernik S, Craggs M, Grill WM, et al. Electrical stimulation for the treatment of bladder dysfunction: Current status and future possibilities. Neurol Res. 2002;24(5):413-430.
U.S. Food and Drug Administration (FDA). Vocare Bladder System. Humanitarian Use Devices. H980005. Rockville, MD: FDA; December 28, 1998. Available at: http://www.fda.gov/cdrh/ode/hdeinfo.html. Accessed November 16, 2004.
American Spinal Injury Association (ASIA). ASIA Impairment Scale Clinical Syndromes. Chicago, IL: ASIA; revised 2000. Available at: www.asia-spinalinjury.org/publications/index.html. Accessed November 16, 2004.
Herbison P, Arnold E. Neuromodulation with implanted electrodes for urinary storage and voiding dysfunction in adults (Protocol for Cochrane Review). Cochrane Database Syst Rev. 2003;(2):CD004202.
Transurethral Electrical Bladder Stimulation:
Katona F, Berenyi M. Intravesical transurethral electrotherapy in meningomyelocele patients. Acta Paed Acad Sci Hung. 1975;16(3-4):363-374.
Nicholas JL, Eckstein HB. Endovesical electrotherapy in treatment of urinary incontinence in spina-bifida patients. Lancet. 1975;2(7948):1276-1277.
Barrett DM, Wein AJ. Voiding dysfunction: Diagnosis, classification, and management. In: Adult and Pediatric Urology. Vol. 1. 2nd Ed. JY Gillenwater, et al., eds. St. Louis, MO: Mosby Year Book; 1991; Ch. 28B, pp. 1001-1099.
Wein AJ. Neuromuscular dysfunction of the lower urinary tract. In: Campbell's Urology. Vol. 1. 6th Ed. PC Walsh, et al., eds. Philadelphia, PA: W.B. Saunders Company; 1992; Ch. 13, pp. 573-642.
Kaplan WE, Richards I. Intravesical transurethral electrotherapy for the neurogenic bladder. J Urol. 1986;136(1 pt 2):243-246.
Kaplan WE, Richards I. Intravesical bladder stimulation in myelodysplasia. J Urol. 1988;140(5 Pt 2):1282-1284.
Fernandes ET, Reinberg Y, Vernier R, Gonzalez R. Neurogenic bladder dysfunction in children: Review of pathophysiology and current management. J Pediatr. 1994;124(1):1-7.
Boone TB, Roehrborn CG, Hurt G. Transurethral intravesical electrotherapy for neurogenic bladder dysfunction in children with myelodysplasia: A prospective, randomized clinical trial. J Urol. 1992;148(2 Pt 2):550-554.
Lyne CJ, Bellinger MF. Early experience with transurethral electrical bladder stimulation. J Urol. 1993;150(2 Pt 2):697-699.
Decter RM, Snyder P, Laudermilch C. Transurethral electrical bladder stimulation: A follow-up report. J Urol. 1994;152(2 Pt 2):812-814.
Van Kerrebroeck EV, van der Aa HE, Bosch JL, et al. Sacral rhizotomies and electrical bladder stimulation in spinal cord injury. Part I: Clinical and urodynamic analysis. Dutch Study Group on Sacral Anterior Root Stimulation. Eur Urol. 1997;31(3):263-271.
Wielink G, Essink-Bot ML, van Kerrebroeck PE, Rutten FF. Sacral rhizotomies and electrical bladder stimulation in spinal cord injury. 2: Cost-effectiveness and quality of life analysis. Eur Urol. 1997;31(4):441-446.
Aslan AR, Kogan BA. Conservative management in neurogenic bladder dysfunction. Curr Opin Urol. 2002;12(6):473-477.
van Balken MR, Vergunst H, Bemelmans BL. The use of electrical devices for the treatment of bladder dysfunction: A review of methods. J Urol. 2004;172(3):846-851.
Electrical Stimulation for Cerebral Palsy:
Dubowitz L, Finnie N, Hyde SA, et al. Improvement of muscle performance by chronic electrical stimulation in children with cerebral palsy. Lancet. 1988;1(8585):587-588.
Atwater SW, et al. Electromyography-triggered electrical muscle stimulation for children with cerebral palsy: A pilot study. Pediatr Phys Ther. 1991;3:190-199.
Lake DA. Neuromuscular electrical stimulation: An overview and its application in the treatment of sports injuries. Sports Medicine. 1992;13(5):320-336.
Pape KE, Kirsch SE, Galil A, et al. Neuromuscular approach to the motor deficits of cerebral palsy: A pilot study. J Pediatr Orthop. 1993;13(5):628-633.
Carmick J. Clinical use of neuromuscular electrical stimulation for children with cerebral, Part 1: Lower extremity. Phys Ther. 1993;73(8):505-513, discussion 523-527.
Carmick J. Clinical use of neuromuscular electrical stimulation for children with cerebral, Part 2: Upper extremity. Phys Ther. 1993;73(8):514-522, discussion 523-527.
Hazlewood ME, Brown JK, Rowe PJ, Salter PM. The use of therapeutic electrical stimulation in the treatment of hemiplegic cerebral palsy. Dev Med Child Neurol. 1994;36(8):661-673.
Kuban KC, Leviton A. Cerebral Palsy. N Engl J Med. 1994;330(3):188-195.
Steinbok P, Reiner A, Kestle JR. Therapeutic electrical stimulation following selective posterior rhizotomy in children with spastic diplegic cerebral palsy: A randomized clinical trial. Dev Med Child Neurol. 1997;39(8):515-520.
Detrembleur C, Lejeune TM, Renders A, Van Den Bergh PY. Botulinum toxin and short-term electrical stimulation in the treatment of equinus in cerebral palsy. Mov Disord. 2002;17(1):162-169.
Boyd RN, Morris ME, Graham HK. Management of upper limb dysfunction in children with cerebral palsy: A systematic review. Eur J Neurol. 2001;8(Suppl 5):150-166.
Kerr C, McDowell B, McDonough S. Electrical stimulation in cerebral palsy: A review of effects on strength and motor function. Dev Med Child Neurol. 2004;46(3):205-213.
Electrical Stimulation for Bell's Palsy:
Huizing EH, Mechelse K, Staal A. Treatment of Bell's Palsy. An analysis of the available studies. Acta Otolaryngol. 1981;92(1-2):115-121.
Adour KK. Medical management of idiopathic (Bell's) palsy. Otolaryngol Clin North Am. 1991;24(3):663-673.
Fitzgerald DC. Role of electrical stimulation therapy for Bell's palsy. Am J Otol. 1993;14(4):413-414.
Wolf SR. Idiopathic facial paralysis. HNO. 1998;46(9):786-798.
Buttress S, Herren K. Towards evidence based emergency medicine: Best BETs from the Manchester Royal Infirmary. Electrical stimulation and Bell's palsy. Emerg Med J. 2002;19(5):428.
Quinn R, Cramp F. The efficacy of electrotherapy for Bell's palsy: A systematic review. Phys Ther Rev. 2003;8(3):151-164.
Foot Drop (Walkaide device):
Weber DJ, Stein RB, Chan KM, et al. BIONic WalkAide for correcting foot drop. Conf Proc IEEE Eng Med Biol Soc. 2004;6:4189-4192.
Weber DJ, Stein RB, Chan KM, et al. BIONic WalkAide for correcting foot drop. IEEE Trans Neural Syst Rehabil Eng. 2005;13(2):242-246.
Weber DJ, Stein RB, Chan KM, et al. Functional electrical stimulation using microstimulators to correct foot drop: A case study. Can J Physiol Pharmacol. 2004;82(8-9):784-792.
Kido Thompson A, Stein RB. Short-term effects of functional electrical stimulation on motor-evoked potentials in ankle flexor and extensor muscles. Exp Brain Res. 2004;159(4):491-500.
Sheffler LR, Hennessey MT, Naples GG, Chae J. Improvement in functional ambulation as a therapeutic effect of peroneal nerve stimulation in hemiplegia: Two case reports. Neurorehabil Neural Repair. 2007;21(4):366-369.
Kottink AI, Hermens HJ, Nene AV, et al. Therapeutic effect of an implantable peroneal nerve stimulator in subjects with chronic stroke and footdrop: A randomized controlled trial. Phys Ther. 2008;88(4):437-448.
Laufer Y, Ring H, Sprecher E, Hausdorff JM. Gait in individuals with chronic hemipareisis: One-year follow-up of the effects of a neuroprosthesis that ameliorates foot drop. J Neurol Phys Ther. 2009;33(2):104-110.
Laufer Y, Hausdorff JM, Ring H. Effects of a foot drop neuroprosthesis on functional abilities, social participation, and gait velocity. Am J Phys Med Rehabil. 2009;88(1):14-20.
Ring H, Treger I, Gruendlinger L, Hausdorff JM. Neuroprosthesis for footdrop compared with an ankle-foot orthosis: Effects on postural control during walking. J Stroke Cerebrovasc Dis. 2009;18(1):41-47.
Neuromuscular Electrical Stimulation for Ambulatory Function in Patients with Multiple Sclerosis:
Wahls TL, Reese D, Kaplan D, Darling WG. Rehabilitation with neuromuscular electrical stimulation leads to functional gains in ambulation in patients with secondary progressive and primary progressive multiple sclerosis: A case series report. J Altern Complement Med. 2010;16(12):1343-1349.
Neuromuscular Electrical Stimulation for Knee Osteoarthritis:
Giggins OM, Fullen BM, Coughlan GF, et al. Neuromuscular electrical stimulation in the treatment of knee osteoarthritis: A systematic review and meta-analysis. Clin Rehabil. 2012 Feb 9. [Epub ahead of print]
Threshold Electrical Stimulation:
Sommerfelt K, Markestad T, Berg K, Saetesdal I. Therapeutic electrical stimulation in cerebral palsy: A randomized, controlled, crossover trial. Dev Med Child Neurol. 2001;43(9):609-613.
Dali C, Hansen FJ, Pedersen SA, et al. Threshold electrical stimulation (TES) in ambulant children with CP: A randomized double-blind placebo-controlled clinical trial. Dev Med Child Neurol. 2002; 44(6):364-369.
Kerr C, McDowell B, Cosgrove A, et al. Electrical stimulation in cerebral palsy: A randomized controlled trial. Dev Med Child Neurol. 2006;48(11):870-8766.
Scianni A, Butler JM, Ada L, Teixeira-Salmela LF. Muscle strengthening is not effective in children and adolescents with cerebral palsy: A systematic review. Aust J Physiother. 2009;55(2):81-87.
Cauraugh JH, Naik SK, Hsu WH, et al. Children with cerebral palsy: A systematic review and meta-analysis on gait and electrical stimulation. Clin Rehabil. 2010;24(11):963-978.
Improvement of Ambulatory Function/Muscle Weakness in Individuals with Progressive Diseases:
Pereira S, Mehta S, McIntyre A, et al. Functional electrical stimulation for improving gait in persons with chronic stroke. Top Stroke Rehabil. 2012;19(6):491-498.
Maddocks M, Gao W, Higginson IJ, Wilcock A. Neuromuscular electrical stimulation for muscle weakness in adults with advanced disease. Cochrane Database Syst Rev. 2013;1:CD009419.
Copyright Aetna Inc. All rights reserved. Clinical Policy Bulletins are developed by Aetna to assist in administering plan benefits and constitute neither offers of coverage nor medical advice. This Clinical Policy Bulletin contains only a partial, general description of plan or program benefits and does not constitute a contract. Aetna does not provide health care services and, therefore, cannot guarantee any results or outcomes. Participating providers are independent contractors in private practice and are neither employees nor agents of Aetna or its affiliates. Treating providers are solely responsible for medical advice and treatment of members. This Clinical Policy Bulletin may be updated and therefore is subject to change.