Spasticity is a commonly encountered condition that can have a devastating impact on affected patients. Lance described it as “a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon reflexes, resulting from excitability of the stretch reflex.” It can also be defined as the constant and unwanted contractions of one or more muscle groups as a result of an injury or insult to the brain or spinal cord. The condition can be mild, with patients experiencing only minor discomfort or inconvenience, or major, with the spasticity leading to immobility and the development of contractures and pressure sores. However, clinicians must use caution when applying such descriptors of severity to muscle overactivity so as not to misrepresent their clinical impact to the patient. For example, relatively slight resistance to passive motion, evaluated as “mild” by a physician, may have a quite significant functional impact for a patient, who might describe the same phenomenon as “severe.” Even mild degrees of spasticity can impair the ability to perform basic activities of daily living, including hygiene, dressing, and toileting. In addition, spasms associated with spasticity can cause pain, interrupt sleep, negatively influence mood, and impair mobility.

Although appropriate and timely treatment is needed to obtain optimal results, there is some evidence that spasticity is undertreated. Delayed or inadequate treatment can lead to maladaptive remodeling of the affected body part, leading to shortening of muscles and contracture of tendons or soft muscle and, ultimately, to a permanent physical deformity.

Symptoms & Signs

Pathologic changes in the central nervous system often create a constellation of symptoms or signs that encompass both positive and negative components. Weakness and loss of dexterity, the most commonly encountered negative phenomena, are relatively easy to define. Other negative signs include atrophy, fatigability, and loss of selective motor control. The positive components are more complex, with diverse pathophysiologic mechanisms. Observable phenomena include increased resistance to passive stretch, muscle–tendon hyperreflexia, clonus, co-contraction of synergistic muscle groups, and spontaneous flexor–extensor spasms. Spasticity is only one of these features, namely, a velocity-dependent increase in resistance to passive range of motion (ROM). Collectively, all of the positive signs can be called “muscle overactivity,” with the qualification that abnormal pathology extends beyond the muscle itself. Frequently, and perhaps unfortunately, the term spasticity is often applied to the entire collection of signs. Given this common practice, spasticity and muscle overactivity are used somewhat interchangeably for remainder of this chapter.

The causes of spasticity are heterogeneous. This syndrome is usually seen in conditions that involve damage to the portion of the brain or spinal cord that controls voluntary movement. Spasticity can be associated with spinal cord injuries, multiple sclerosis, cerebral palsy, stroke, and traumatic or anoxic brain injury, as well as metabolic or degenerative diseases such as adrenoleukodystrophy, amyotrophic lateral sclerosis, hereditary spastic paraparesis, stiff-person syndrome, and phenylketonuria. Although spasticity is a common condition, its incidence and prevalence are difficult to determine because of its association with a wide variety of disease processes. By combining several sources, it is reasonable to estimate that upward of 2 million people in the United States experience spasticity. The estimated prevalence of spasticity for the most common etiologies is shown in Table 6–1.

Patterns of Spasticity

The clinical presentation of spasticity is quite diverse owing to the range of central nervous system disease that may produce muscle overactivity. One approach used to differentiate spasticity focuses on the number of muscle groups involved. Diffuse patterns of spasticity can involve all four limbs (quadriplegic), both lower extremities (paraplegic or diplegic), or the upper and lower extremities on the same side of the body (hemiplegic). Combination of these patterns can also be seen (eg, paraplegic and hemiplegic) in the same patient. The axial musculature of the cervical, thoracic, and lumbar spine can similarly be involved. Alternatively, a more localized appearance that involves only a few muscles or muscle groups can be detected. Mixtures of focal and diffuse patterns can also be recorded in the same patient.

Flexion (the movement of a limb to decrease the angle of a joint), extension (the opposite movement) or combined flexion–extension synergies can be observed. Motor synergies are stereotyped movements of the entire limb that reflect loss of independent joint control and that limit a person’s ability to coordinate his or her joints in flexible and adaptable patterns, thereby precluding performance of many functional motor tasks. In the upper extremity, the flexion synergy is often characterized by simultaneous shoulder abduction and elbow flexion. Conversely, upper extremity extension synergy is characterized by simultaneous shoulder adduction and elbow extension. In the lower limb, flexion synergy consists of hip flexion, abduction, and external rotation, along with knee flexion, ankle dorsiflexion, and inversion. Lower limb extension synergy consists of hip extension, adduction, internal rotation, knee extension, ankle plantar flexion, inversion, and toe plantar flexion. These synergistic patterns can appear as both a static positioning of an affected limb and a nonspecific movement pattern. Consider the following example: A man is asked to feed himself; in doing so, he abducts his shoulder and flexes his elbow but does not pick up his spoon. When the same man is asked to open a door, he also abducts his shoulder and flexes his elbow.

Measurement of Spasticity

Spasticity can be graded according to severity (mild, moderate, or severe) using both objective and subjective measures. However, as previously noted, clinicians must be careful when applying severity descriptors to muscle overactivity so as not to misrepresent their clinical impact to the patient. From a technical standpoint, spasticity levels can be affected by many factors, including temperature, emotional status, time of day, level of pain, body position, and the amount of prior stretching. Given this potential variability, interpretation of serial measurements can be problematic.

A. Clinical Rating Scales

Hypertonia can be evaluated clinically using a number of well-established rating scales. The most commonly used are the Ashworth, Modified Ashworth, and Tardieu scales (Table 6–2), which are generally considered to have fair to good interrater and intrarater reliability. One criticism of the Ashworth and Modified Ashworth scales is their inability to distinguish between the rheologic properties of the soft tissues and the neural contributions to hypertonia. The Tardieu scale attempts to address this difficulty by measuring two angles: R1, the angle at which resistance is first encountered during a quick muscle stretch, and R2, the final angle, which reflects the maximum range of movement during a slow muscle stretch. The difference between the two is claimed to represent the true amount of spasticity, or spasticity angle.

B. Neurophysiologic and Other Tests

More sophisticated measures of hypertonia include neurophysiologic tests that attempt to quantify the muscle response to stretch (surface electromyographic activity, H-reflex response, the H-reflex standardized to the M-wave max, or the F-wave response) or instrumented measurements of stiffness and torque with accelerometers. The pendulum test is a biochemical method of assessing spasticity in a limb by extending the limb and then letting it swing freely against gravity. The oscillating pattern observed is mathematically assessed to obtain data such as time delay and muscle stretch reflex threshold, which can identify subtle changes in spasticity. One drawback to the use of the pendulum test is great variability when testing the same individual multiple times. This makes it less reliable when measuring treatment outcomes. Another issue is that force velocity and force length do not have a linear relationship. Therefore, positioning of the limb, muscle length, relaxation, and multiple other factors affect test reliability. The Wartenberg pendulum score is calculated during the gravity-induced pendulum-like movement of the lower limb as the ratio of joint angles measured by goniometry or computerized video motion analysis.

C. Subjective Measures

Subjective measures include patient assessment of spasm intensity and logs of spasm frequency. There is an inconsistent correlation between subjective report and objective measures of spasticity.

Spasticity can have beneficial or deleterious effects, and both may be noted in the same patient. Advantageous effects potentially include assistance with mobility, maintenance of posture, improvement of vascular circulation, preservation of muscle mass and bone mineral density, prevention of venous thrombosis, and assistance in reflexive bowel and bladder function. Conversely, spasticity can interfere with positioning, mobility, comfort, and hygiene. Spasticity has also been linked to increased metabolic demands, which can be problematic in the nutritionally compromised patient. Spontaneous spasms can interfere with sleep or duration of wheelchair use. Spasms can also lead to skin breakdown because of the shearing effect or impaired healing of surgical wounds due to tension along suture lines.

The relationship of spasticity to pain is complex. Spasticity can limit the range of motion about a joint, causing musculoskeletal pain. In this scenario, reduction of spasticity may decrease the pain associated with biomechanical limitations. However, central nervous system disease can also produce neuropathic pain, for which modulation of spasticity may not be effective in reducing symptoms. Clinicians must therefore consider all aspects of a patient’s spasticity before embarking on a treatment plan. Rather than complete elimination of spasticity, a more realistic goal may be titration to maximize the risk–benefit ratio.

Rehabilitation Techniques

Therapeutic interventions are essential to the management of spasticity, both in isolation and in combination with other treatment modalities described in this chapter. A multitude of different techniques have been reported to modulate muscle overactivity, including range of motion exercises, stretching, therapeutic exercise, constraint-induced therapies, neurodevelopmental techniques, positioning, splinting, neuroprosthetics, serial casting, and functional electrical stimulation. Ideally, therapy will attempt to maximize the beneficial aspects of muscle overactivity and mitigate the detrimental aspects.

A. Stretching

Stretching is one of the primary strategies used by physical and occupational therapists for spasticity management. Static or low-velocity stretching has been the hallmark of this technique as applied manually by the treating therapist. Traditionally, a minimum of 30 seconds is recommended to achieve therapeutic benefit, with some data suggesting that longer duration stretches are more beneficial. Mechanical stretching devices such as dynamometers (Cybex, Kin-Com, Biodex, etc) are increasingly utilized. These devices allow for longer therapy sessions with programmed adjustability based on intelligent design biofeedback. Cost can be a limiting factor in the use of these devices, but this must be balanced against the operational benefit of freeing up clinician time. Several studies have shown positive effects of stretching, such as decreased motor activity on electromyography (EMG), greater range of motion, and decreased stiffness, but there is limited evidence of the long-term benefits of this intervention.

B. Casting

Serial casting involves the sequential application of casting material, either plaster or fiberglass, in a circumferential manner around the spastic joint. The area to be casted (eg, foot and ankle) is covered with a stocking, bony prominences are carefully padded, and the cast is applied at a comfortable end range of motion. Casts are changed weekly at an enhanced joint angle. Serial casting is discontinued when no incremental increase in range of motion is seen on two sequential castings. Patients are then transitioned to a bivalved cast as a long-term maintenance strategy. The purported mechanism of spasticity reduction for this intervention is that casts minimize changes in muscle length and tension, thus reducing the excitatory input from muscle spindles. This diminished input, in turn, decreases the activity of the spinal reflex arc. Alternatively, casting might reduce sensory input with similarly diminished reflex activity. Potential complications of serial casting include skin breakdown, venous thrombosis, compartment syndrome, and regional decreases in bone mineral density.

C. Splinting

Splinting is a useful, noninvasive method for preventing contractures associated with spastic conditions and maintaining range of motion. A variety of prefabricated and constructed splints are available. Examples include resting hand splints, wrist cock-up splints, elbow extension splints, and posterior foot splints. Dynamic splints have a self-adjusting elastic component such as spring wire or rubber band and can serve both as passive assistance for movement of weaker muscles and as a resistant component for muscles with increased tone. Proprietary dynamic splinting devices (eg, Saeboflex, Dynasplints) are commonly used. Saeboflex was designed to allow training of grasp-and-release activities when a hemiplegic patient has upper extremity flexor hypertonicity with limited extensor activity. Dynasplints consist of padded cuffs and struts that are hinged at the joint axis. They allow tension and force to be adjusted across a given joint.

D. Strength Training

Perhaps the most commonly utilized rehabilitation modality is strength training. This technique is particularly important in the spastic patient given the potential for coexistence of muscle overactivity and weakness. Additionally, several approaches described later in this chapter have the potential to increase weakness.

Findings from several studies support the idea that the capacity for strength can be increased in individuals with central nervous system disease without exacerbation of spasticity. The parameters of strength training protocols are almost limitless, with no particular approach being preferential in the spastic patient. Although there is minimal evidence to suggest that strength training reduces spasticity, the potential for comorbid weakness in this patient population mandates consideration of these techniques following other interventions.

E. Nerve Stimulation

Both functional electrical stimulation (FES) and transcutaneous electrical nerve stimulation (TENS) can be used to reduce pain and spasticity, improve muscle tone, and facilitate function in patients with upper motor neuron injury. In FES, an electrical current is applied to intact nerves of the body in order to generate a muscle contraction. Several studies have reported benefits after use of FES (improved range of motion, decreased spasticity, and improved foot drop) and TENS (improved motor function and spasticity) in post-stroke patients.

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