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.