Electrical Stimulation in the Management of Spasticity:
A Review
Joyce M. Campbell, Member,
IFESS
Abstract
Despite
successful reports of spasticity management by electrical stimulation [ES] over
the past 246 years, this potentially effective and economical tool is often
overlooked in clinical practice in favor of oral medications with serious
side-effects, intrathecal drug administration, or surgical procedures including
tendon lengthening and long-term muscle denervation. The body of literature on
ES and spasticity provides a rationale for critical review of the relative
merits of all strategies employed to manage spasticity as well as for the
development of criteria to use these available tools in concert for optimal
patient outcomes.
Index terms: Spasticity; Electrical Stimulation; Stroke; Brain
Injury; Spinal Cord Injury; Cerebral Palsy; Multiple Sclerosis; Amyotrophic
Lateral Sclerosis.
Historical
Perspective
Electrical
stimulation has been used therapeutically for over 2,000 years. It has been
employed to manage spasticity for 246 years, or more. In 1752, Benjamin
Franklin wrote a case report describing his use of electricity to manage
involuntary muscle contractions in a young patient. In 1871, Duchenne used
electrical stimulation [ES] to inhibit spastic antagonist muscles that
interfered with function. [1-2]
Following
the interest in the neurophysiological mechanisms underlying spasticity in the
early 1900's, practical electrical stimulation devices became available in the
1960's. Success with cutaneous, or skin, electrodes was replicated when
implanted electrodes were employed.
Cerebellar
and spinal cord stimulation studies in the early 1970's appeared to reduce
spasticity and improve the lives of the patients implanted, but the statistical
outcomes were not universally rewarding. [3-4]
Despite
the proliferation of studies in the past 20 years, this body of knowledge has
been ignored by many clinicians. In many
centers, medications are the first treatment of choice and intrathecal drug
administration is commonly employed. Surgical intervention, including phenol
nerve block and tendon lengthening is recommended without prior trials of
electrical stimulation. It is time to consider the development of criteria for
the use of electrical stimulation in concert with, or as an alternative to
medications and surgery.
Consensus of Results
in Peripheral Nerve Stimulation
Study
protocols, using objective measures of spasticity, ranging from single
assessment to two year follow-up have demonstrated statistically significant
reduction in spasticity as a result of peripheral nerve stimulation. [5-16]
Cutaneous electrodes, implanted electrodes and implanted neural prosthetic
systems have led to reduced interference from spastic muscles, improvements in
volitional control and positive changes in the energy demand of walking.
[11-12] Carry-over effects ranged from 30 minutes to 24 hours, or more.
Functional outcomes were realized when ES was combined with goal directed
physical therapy. [7-8,17-18]
Results of
Cerebellar and Spinal Cord Stimulation
Cerebellar
ES in cerebral palsy and multiple sclerosis resulted in reduced spasticity in
the majority of subjects along with improvement in bladder function,
respiratory function, volitional control,
active and passive movement and mood state. [3] Spinal cord ES outcomes were
similar with carry-over effects lasting up to 24 hours.[4] Functional test
scores in many of the studies did not reflect the other improvements observed.
[3-4]
Problems in Study
Design
Among
the problems in some study designs have been small subject samples with
extremely varied diagnoses and severity of disability. Objective measures of
spasticity have not been uniformly employed. Gross functional scales have been
used as the primary measurement tool and the statistical significance criteria
imposed would have required relatively miraculous changes in function in order
to be considered efficacious. In addition, many final publications have
disregarded reports of improvement from patients, families and physicians.
[2-4]
Critical Concepts
Confusion
exists in terminology, selection of assessment tools, methods of patient
evaluation and the importance of specificity in goal setting, treatment and
outcome evaluations. Terms such as "muscle tone" and "muscle
spasm" are not objectively measurable and should be replaced by
"spasticity" which can be measured. Spasticity
must be assessed in the upright or most functional position if interference is
to be accurately defined. It must be recognized that interfering muscle
activity [ie in walking or transfers] may be the result of a spastic response
to voluntary use of antagonist muscles or it may be that the inappropriate
muscle is being recruited in the wrong phase of movement. In the latter case,
spasticity is not the culprit and we have no evidence that therapy will alter
the cortical recruitment pattern. Surgical relocation of the muscle's action to
its functioning phase would then be appropriate. [19-20]
The only
way to determine if inappropriate muscle activity is responsible [spastic or
out of phase, or both] is to do intramuscular electromyography [EMG] recordings
during movement such as walking or grasp and release. Cutaneous EMG recordings
are contaminated by volume conduction from all muscles in the limb and are
useless for diagnostic purposes of this nature. [21-22] It must be recognized
that each patient has his or her own "neurological fingerprint" of
neurological dysfunction and treatment must be tailored to each individual.
It must
be recognized that ES alone is usually not an encompassing treatment for
spasticity. ES can "unmask" residual control and result in early
recovery of selected functional movement. In most instances when the patient is
in the phase of "neural recovery" after insult to the CNS, reduction
of spasticity with ES is only the first step. ES can then be employed to
improve muscle recruitment and performance [force, work, power, and fatigue
resistance] as well as enhance timing of recruitment for function. When
recovery is incomplete, ES may be used as a neural prosthetic for maintained
daily function.
Goals
must be individualized and small achievements that result in even minimal
improvements in function and quality of life must be delineated. Whether the goal
is improved sitting position and tolerance resulting in less frequent
repositioning by an attendant or the ability to bring the body weight forward
over the base of support in order to allow a reasonable contralateral step
length, improved safety in walking, increased free pace velocity and reduced
energy demand, objective documentation of goal achievement is invaluable. It is
not necessary to change from bedridden to walking independently to show
efficacy of ES in the modulation of spasticity.
Common
Misconceptions
There
are a variety of misconceptions in the treatment of spasticity. One serious
pitfall relates to the amount of ES required per day to reduce spasticity and
the need for immediate ES treatment when spastic episodes occur. There is agreement
among researchers that 1-2 hours of ES per day will suppress spasticity on a 24
hour/day basis. In addition, the ES may be administered at any time, including
nighttime. Even cutaneous, or sub-motor, intensities of ES result in 24
hour/day suppression of interfering spasticity. [15-16]
One of
the biggest impediments to the use of spasticity is the misconception that ES
for spasticity modulation is expensive or esoteric. There are a variety of ES
devices available through wholesale vendors for less than the cost of a single
physician or therapy clinical visit [ie less than $45-100.00,
ES
can be used anywhere in the world to modulate spasticity for a minimum cost
[$45.00 to $100.00 and the cost of 1-3 physical therapy visits]. The lack of recognition
of this opportunity by clinicians and publishers of consumer education
materials is revealing of the lack of understanding of the clinical needs of
patients and the ES research and clinical outcome reports available in the
literature.
Considerations of
Risk
ES for
spasticity modulation is relatively risk free. Although it is possible that
spasticity may be temporarily exacerbated, especially if abrupt muscle
contraction is generated, any adverse effect is significantly reduced or absent
within 30-60 minutes. If the patient uses spasticity to allow standing,
transfers or limited stepping, the reduction of spasticity by ES may reduce
function until ES control of muscle or ES facilitation of muscle recruitment
can be instituted. When ES is applied as one component of an integrated
rehabilitation protocol, this is not a problem.
In
comparison to the muscle weakness, depression of CNS and respiration associated
with drugs and the risk of infection with implanted medication dispensing
devices, ES is extremely safe. [24] In comparison with the muscle weakness,
severe post-operative pain, subluxation of the hip, spinal deformity, increased
incidence of spondylolisthesis and potential for recurrence of spasticity
associated with rhizotomy, ES is very safe. [25] In comparison with the muscle
weakness or even complete denervation associated with botulinum toxin and
phenol nerve block, ES is a preferred initial treatment. [19-20,26-27]
Summary of Clinical
Suggestions
Individual
patient care can be improved through clarity of terminology [ie omission of
terms like tone and spasm and replacement with spasticity when applicable] and
the use of objective measurements [ie measurable resistance to passive joint
movement, available joint range of motion, sitting tolerance, specific hand
function assessment, manual muscle test or instrumented assessment of force,
work, power and fatigue, and mechanical as well as metabolic characteristics of
gait]. Attention to specific
changes in function is critical. It is not necessary to improve from bedridden
to independent ambulation, for example, to realize the benefits of reduced
spasticity. Careful documentation of ES protocols is important. For example,
the use of a comfortable, balanced pulse duration [ie 300 usec] and a long ramp
in intensity [2 seconds or more] along with a minimal intensity will minimize
the potential for aggravation of spasticity in the early days of an ES
protocol.
When
prospective data collection is planned,
categorization of patients by diagnosis, severity and specific goals will
improve outcome evaluation and statistical analyses.
Suggestions For
Future Spasticity Studies
There
are many options for successful use of ES to modulate spasticity and accomplish
reasonable, efficacious goals for the patient. When ES alone is not adequate to
resolve the penalties of severe spasticity, it may offer a first line of
evaluation as well as an adjunct to the overall rehabilitation outcomes.
[28-29]
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Author's Address:
Joyce M. Campbell, Ph.D., P.T., Professor
562 985-5455
JCampb8116@AOL.com