Spasticity
Spasticity
Definition
Spasticity is often defined as a velocity-
dependent increase in muscle tone.
This means that the faster the passive
movement of the limb through its range,
the greater the increase in muscle tone.
The definition usually also includes clonus
and flexor and extensor muscle spasms.
Spasticity occurs in the context of an
upper motor neuron (UMN) lesion (brain or
spinal cord pathology) and in association
with exaggerated deep tendon reflexes.
Symptoms
Spasticity reduces an individual's
ability
to move affected limbs actively or
passively.
Spasms may be a feature, and pain is
present in some cases.
Physical Examination
Spasticity occurs in the presence of other signs and
symptoms of UMN damage, including hyperreflexia,
Babinski responses, reduced motor control, and other
evidence of brain and/or spinal cord damage.
Increased muscle tone in the absence of these findings
should lead to consideration of alternative causes of
increased muscle tone, such as dystonia, Parkinson's
disease, paratonia associated with Alzheimer's disease, or
pain-associated muscle spasm.
Contracture and spasticity commonly co-exist, though in
some cases it may be difficult to determine how much
contracture is present in an individual with severe
spasticity.
The "clasp-knife" phenomenon, seen more commonly
in spasticity of spinal origin, is characterized by a
relaxation of the involved muscle after spasticity has
been overcome.
The presence and severity of ankle clonus, withdrawal
reflexes, and extensor spasms should be noted.
The skin should be inspected because abnormal
positioning due to spasticity may directly cause skin
injury (e.g., maceration of the palm due to a clenched
fist) or contribute to decubitus ulcer formation.
Functional Limitations
Functional limitations include difficulty with ambulation or
brace usage, positioning in a wheelchair, urinary
catheterization and/or hygiene, and interrupted sleep.
Impaired sexual function may result from adductor muscle
or other muscle spasms.
In some cases spasticity may interfere with volitional
function; yet in others, it may serve as a partial substitute
for voluntary muscle contraction.
In the rehabilitation setting, patients who use their
increased tone to help them ambulate are often noted to be
"walking on their spasticity."
A common example of substitution for voluntary
muscle function is the hip and knee extensor
spasticity seen after stroke, which may allow
successful weight bearing through the weak leg
and contribute to restored walking ability.
Therefore, one must always be cognizant of this
phenomenon, because overly aggressive
treatment of spasticity may actually worsen an
individual's ability to function.
Diagnostic Studies
Spasticity is a clinical diagnosis without any
specific laboratory confirmation. Clinical
measurement scales to quantify the severity
of spasticity may be useful to monitor the
efficacy of treatment.
The most commonly used scales are the
Ashworth scale, which measures resistance
of the muscle to passive stretch, and the
Spasm Frequency scale, which characterizes
the frequency of muscle spasms.
Treatment
Pharmacotherapy with oral medications is most effective in
spasticity of spinal origin, as occurs in spinal cord injury or many
cases of multiple sclerosis.
Oral medications are often less effective in spasticity resulting
from stroke or traumatic brain injury.
Medications commonly used include baclofen, benzodiazepines,
tizanidine, and dantrolene.
With the exception of dantrolene, these medications work centrally
at the GABA-A receptors (benzodiazepines), GABA-B receptors
(baclofen), and the alpha-adrenoreceptors (tizanidine).
Dantrolene exerts its effects directly at the muscle, preventing
calcium influx at the sarcoplasmic reticulum level and thereby
reducing muscle force.
Rehabilitation
Stretching and passive range of
motion are key elements of spasticity
management, regardless of etiology.
These activities serve to prevent
contracture and to temporarily
reduce increased muscle tone.
Splinting a spastic limb is another critical aspect of a comprehensive
rehabilitation program for spasticity and can include pre-fabricated splints,
low temperature thermoplastic custom splints, and plaster or fiberglass casts.
Physical therapists can instruct the patient and caregivers regarding
appropriate stretching techniques.
Physical therapists with experience in casting can fabricate plaster or
fiberglass casts or assist in selecting a prefabricated leg splint from a
commercial vendor.
If a sturdier device is needed (e.g., one that permits weight bearing through
the device), an orthotist may be called upon to fabricate a custom brace.
Occupational therapists can similarly provide instruction in stretching and
splinting of the upper extremity.
Most occupational therapists are trained in fabrication of custom hand splints.
Procedures
Injections for spasticity are an effective means of
obtaining substantial reduction in spasticity in specific
muscles with little risk of systemic side effects.
Local anesthetic injections may be useful to assess the
efficacy and benefits of more permanent injections.
Intramuscular botulinum toxin type A injection
provides local relief of spasticity for 3 to 4 months.
Botulinum toxin type B is likely to prove effective as
well, although efficacy and dosing are not yet
established.
Perineural phenol injection may provide more long-term
relief and may in some cases cause permanent reduction of
spasticity.
Botulinum toxin injections may use anatomic guidance for
large, easily identified muscles (e.g., biceps brachii), but
EMG or nerve stimulator guidance is necessary for smaller,
harder to identify muscles (e.g., forearm muscles).
Botulinum toxin type A doses for spasticity generally vary
from 30–200 units per muscle, with larger muscles requiring
higher doses.
Dosage for spasticity management has not been
established for type B.
Type A is generally diluted to 100 units/cc with
nonpreserved sterile saline, although more dilute
concentrations are useful for small doses.
After dilution, the toxin is drawn into a small syringe (1–3
cc), and a Teflon-coated injection needle is connected via a
wire to either an EMG machine or a nerve stimulator.
Given the limited motor control and muscle synergies seen
in spasticity, nerve stimulator guidance often proves more
useful than EMG guidance in distinguishing different
muscles.
With nerve stimulator guidance, the muscle is stimulated
and the clinical response observed (e.g., finger flexion when
the flexor digitorum profundus is stimulated).
Toxin is then injected in small aliquots distributed in the
muscle.
Early post-injection symptoms are unusual, and related
more to the effects of an intramuscular injection than to the
botulinum toxin itself.
There are no specific activity restrictions necessary post-
injection. Clinical effects are generally evident 24–72 hours
after the injection.
Surgery
Neurosurgical intervention includes the placement
of an intrathecal baclofen pump—a highly effective
treatment for individuals with intractable bilateral
lower extremity spasticity.
Alternative neurosurgical procedures useful in
carefully selected patients include rhizotomy and
myelotomy.
Orthopedic surgery, including tendon lengthening,
tenotomy, or joint fusion, can be used after failure
of more conservative measures (e.g., stretching,
casting, and blocks) to provide adequate control of
spasticity and contracture.
Potential Disease
Complications
Permanent loss of range of motion can
result from inadequately controlled
spasticity or insufficient stretching and
splinting.
Contractures can hinder seating; contribute
to skin breakdown; and interfere with
hygiene, ambulation, and transfers.
Potential Treatment
Complications
As noted earlier, some individuals function better with a
degree of spasticity because it can substitute for lost motor
function.
Therefore, overly aggressive treatment of spasticity may
result in a decline in functional ability.
All centrally acting medications can cause significant
sedation, which often determines the upper limit of the
dose that can be tolerated.
In individuals with pre-existing cognitive impairments (e.g.,
stroke, TBI), this maximally tolerated dose may be
insufficient to control the symptoms of spasticity and may
indicate the need to consider alternative therapies.
Abrupt discontinuation of oral antispasticity medications is
inadvisable, since seizures have been described after
abrupt discontinuation of baclofen, and rebound spasticity
is a concern with all of these medications.
Phenol poses some risk of painful dysesthesia if peripheral
nerves with cutaneous sensory representation are injected.
Botulinum toxin is generally very well tolerated in
therapeutic doses but can cause transient (3 to 4 months)
weakness of muscles adjacent to those targeted by
treatment due to diffusion of toxin.
Dysphagia has been described after injection of the
sternocleidomastoid and other cervical muscles.
Injection of excessive doses of botulinum toxin could lead to
symptoms of systemic botulism, though this can be prevented by
restricting injection to 6 units/kg of botulinum toxin type A or less
within any 1-month period.
Antibodies to botulinum toxin can develop after repeated injection—
this causes lack of efficacy; however, allergic or anaphylactic
reactions have not been reported.
Intrathecal baclofen pump treatment can result in iatrogenic
meningitis or infection of the external surface of the pump.
Catheter failures can result in need for surgical intervention.
Both overdosage due to programming errors and severe withdrawal
symptoms due to pump failure have been described.