An essential skill in the care of patients with CNS disorders and injuries
16th September, 2002
By Catharine M. Farnan, MS, RN, CRRN, & Michael Saulino, MD, PhD
Spasticity is a complex phenomenon that affects many persons living with central nervous system diseases. Key points of this challenging topic include advantages and disadvantages of spasticity, various management strategies with special emphasis on the intrathecal baclofen therapy and nursing interventions for patients living with spasticity.
The word "spasticity" originates from the Greek word for "to tug or to draw." The appearance of spasticity has been described as more difficult to quantify and to characterize than to recognize. Spasticity is one of the hallmarks of upper motor neuron disorders (i.e. involving the brain and/or spinal cord). It can be an important impairment for the nurse caring for patients with these diseases. Simply stated, spasticity is stiffness of muscles and occurs when injury to the spinal cord or brain prevents nerve signals from reaching areas of the spinal cord that release the neurotransmitter gamma aminobutyric acid (GABA).
This substance is believed to assist in allowing muscles to relax. After an injury, this neural system is disrupted and the muscles remain uncontrollably tight. Disorders such as stroke, cerebral palsy, multiple sclerosis, spinal cord and brain injuries can be associated with spasticity.
A review of the literature puts forth the definition of spasticity as a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex. It is fundamental to understand that muscle tone is a sensation of resistance as one moves a joint through range of motion, with the patient attempting to relax. Muscle tone involves three key points: physical inertia of the limb, elastic-mechanical characteristics of muscular and connective tissue, and reflex muscle contraction (tonic stretch reflexes). Changes in spastic muscles can lead to stiffness, contracture, fibrosis or muscular atrophy.
Before any intervention is undertaken to modulate hypertonicity, it is important to attempt to assess spasticity severity. Three grading scales are commonly used to quantify this syndrome. These grading systems address the degree of muscle tone, the frequency of spontaneous spasms and the extent of hyperreflexia. These scales are described in Table 1.
Advantages and Disadvantages
Spasticity can have both desirable and undesirable effects. It can be used to assist with mobility, especially by those patients with some voluntary motor control. It can be useful in maintaining posture. It can improve circulation and may be useful for decreasing the risk of deep vein thrombosis. It may decrease the risk of osteoporosis in affected limbs. Spasticity can assist in maintaining muscle mass and bulk. It can aid in reflexive bowel and bladder function. Conversely, spasticity can also interfere with positioning, mobility, and hygiene. In patients with voluntary muscle movement, spasticity can interfere with dexterity.
It can limit the range of motion about a joint and result in pain. Excessive hypertonia has been linked to increased metabolic demands. Spontaneous spasms can interfere with sleep or duration of wheelchair use. These spasms can lead to skin breakdown because of a shearing effect or due to poor healing of surgical wounds due to tension along suture lines. A decision to intervene must consider both the positive and negative aspects of a patient's spasticity. Additionally, the practitioner may not desire complete elimination of spasticity, rather titration the hypertonia to maximize the risk / benefit ratio. Thus, any antispasticity regimen must be customized to the individual patient.
Spasticity can be modulated by a number of factors. Stretching of the involved muscles has been demonstrated to be efficacious in spasticity reduction. Continuous or static stretching is preferred over short duration or ballistic stretching. Long duration stretch techniques can be applied manually or can utilize adaptive equipment, such as casts or splints. Other therapeutic modalities such as cold application and transcutaneous electrical nerve stimulation units can decrease hypertonicity in some patients. Co-morbidities of neurological disease can serve as "triggers" for increased spasticity. Any patient with a sudden change in their spasticity pattern should be queried for these noxious stimuli. Examples would include urinary tract infections, bladder distention, urolithiasis, bowel impaction, decubitus ulcers, osteomyelitis, etc. These interventions should be undertaken prior to initiation of medical treatment.
Nursing interventions for positioning patients with spasticity can be significant for many patients. Key points in positioning patients with spasticity in bed are aimed at maintaining range of motion and improving respiratory and gastrointestinal (an effect of trunk extension) as well as the advantages described above.
Specific actions include:
If pharmacological treatment of spasticity is warranted, health care providers have a number of available agents at their disposal. Table 2 summarizes the major oral medications that are used for spasticity reduction. Individualized treatment regimens are common with some patients requiring multiple medications for effective management. Some drugs require laboratory monitoring (specifically, treatment with tizadine and dantrolene mandates monitoring of liver function tests). Monitoring of medication levels is unnecessary since the efficacy of these medications is determined by clinical means. It is important to recognize that many patients require medication amounts that are above the FDA-advised limits. It is reasonable to consider treatment above these limits if the patient is achieving inadequate hypertonicity reduction and is not experiencing serious side effects.
Occasionally non-oral agents are utilized for spasticity management. This would include neurolytic blockage with phenol or Botulinium toxin as well as intrathecal baclofen. The underlying principle of neurolytic blockade is the use of a chemical agent to induce a contained amount of neural destruction that results in a decrement in neuromuscular hyperactivity. Phenol can be injected into either muscles or nerves. This substance denatures the protein structures within these tissues. Botulinium toxins are injected into the involved muscles and migrate to the neuromuscular junction. These toxins inhibit the release of acetylcholine into the synaptic cleft. This blockade results in a controlled degree of paralysis within the injected muscle. Currently, there are two Botulinium toxins commercially available in the United States: type A (Botox®) and type B (Myobloc®).
Intrathecal baclofen therapy is an advanced spasticity management technique that delivers baclofen directly to the central nervous system. This delivery system is indicated when patients are poorly controlled with their current regimen or poorly tolerant of other treatments. It is also useful when patients require the precise control that the intrathecal delivery system affords. Patients must be clinically stable (i.e. greater than one year post- central nervous system injury, not in an exacerbation, etc.) understand the risks and benefits of therapy and have resources available to return to clinic for refills.
This therapy delivers medication from a small pump directly to the cerebrospinal fluid (i.e. the intrathecal space). The pump is about the size of a hockey puck (3.5 x 3.5 inches) and is implanted surgically in the abdominal subcutaneous tissue. A catheter is attached to the pump and then tunneled along the patient's flank to the vertebral column. The catheter then pierces the dura and is left unattached within the intrathecal space. The implantation of this pump and catheter system is accomplished via 2 or 3 incisions (abdominal and lumbar and possibly flank). Patients are usually hospitalized for a few days for this procedure. One of the more common complications of pump implantation that may require nursing intervention is spinal headache. Classically, spinal headache has an orthostatic component that is present when the patient is upright and relieved when the patient is supine. Treatment of spinal headache can include bedrest, overhydration, caffeine, abdominal binder placement and in recalcitrant cases epidural blood patch.
Immediately following implant, baclofen leaves the pump's reservoir, travels within the catheter and enters the cerebrospinal fluid. Intrathecal baclofen dosing is adjusted by utilizing a radiotelemetry portable computer. In the immediate post-implant phase, the patient is maintained on his/her baseline amount of oral antispasticity medication. This protocol is used to prevent any withdrawal syndrome. Over the intervening weeks, the oral medications are slowly weaned off as the intrathecal baclofen dosage is titrated.
Patients with intrathecal baclofen pumps require chronic maintenance care. The pump's reservoir is refilled with additional medication every 1-3 months, depending on the individual patient's dosage. Reservoir refills are a sterile, office-based procedure. The patient is continually assessed for any potential pump malfunction. Any dramatic change in the patient's spasticity pattern should prompt an evaluation. Potential problems of this therapy include catheter disruption, failure to refill the pump reservoir and failure of the pump's power source. In order to avoid this last complication, patients should be electively scheduled for battery replacement every 4-5 years. Abrupt disruption of intrathecal baclofen can be a serious scenario with continuous spasms, tremors, temperature elevation, seizure and death having been reported.
Critical to the success of intrathecal baclofen therapy is the nurse's in-depth knowledge of spasticity, astute assessment as oral baclofen is weaned and intrathecal baclofen is titrated upwards, and mechanics of the pump and its potential complications. Post pump implantation, nurses need to closely monitor the patient's respiratory status for depression and educate both family and patient to the side effects of the baclofen. In collaboration with the physician and other members of the team, these interventions are beneficial.
A fundamental knowledge of spasticity is essential in the quality nursing
care of many patients who are living with a variety of central nervous
system disorders and injuries. At times spasticity can be functional for
the patients who need it for transfers, but often it may be painful and
interfere with basics of hygiene and activities of daily living. The management
of spasticity can be as intricate as the phenomenon itself. Nurses can
improve painful spasticity by understanding how positioning affect tone.
Intrathecal baclofen therapy is one advanced method of management in the
gamut of interventions for people who live with spasticity everyday.
|Table 1 — Spasticity assessment systems|
|Ashworth scale||Degree of muscle tone|
|No increase in tone
Slight increase in tone
More marked increase in muscle tone but affected limb easily moved
Considerable increase in muscle tone, passive movement difficult
Affected part is rigid and in flexion
|Spasm scale||Intensity of spasms|
|No spontaneous or elicited spasms
No spontaneous spasms, spasms elicited with vigorous stimulation
Occasional spontaneous and easily inducible spasms
More than 1, but fewer than 10 spontaneous spasms per hour
More than 10 spontaneous spasms per
|Reflex scale||Degree of hyperreflexia|
3-4 beats clonus
Greater than 4 beats of clonus
(Clonus is a repetitive cyclical contraction between agonist and antagonist
muscle groups when a rapid stretch is applied)
|Table 2: Oral Pharmacological agents for the treatment of spasticity|
|Drug||Neuro-transmitter affected||Daily Dosage Range||Common side effects||Comments|
|Baclofen (Lioresal®)||GABAB||5-200 mg in 3-6 divided doses||Sedation
|Intrathecal delivery available|
|Diazepam (Valium®)||GABAA||2-40 mg in 1-4 divided doses||Sedation
|Intravenous delivery available|
|a-2 adrenergic||0.1-2.4 mg in 2-4 divided doses||Hypotension
|Transdermal delivery available|
|a-2 adrenergic||2-36 mg in 1-3 divided doses||Hypotension
|Need to check liver function tests every few months|
|Intracellular calcium||25-400 mg in 1-4 divided doses||Hepatotoxicity
|Need to check liver function tests every few months|
|Exact mechanism unknown||300-3600 mg in 1-4 divided doses||Leukopenia
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Catharine M. Farnan is a clinical nurse specialist in the department
of nursing at Thomas Jefferson University Hospital and Dr. Michael Saulino
is an assistant professor in the department of rehabilitation medicine
at Thomas Jefferson University, Philadelphia.
© Copyright 2002, Merion Publications, Inc