spinal reflex pathways, results in "positive" symptoms including spasticity, hyperactive muscle stretch reflexes, abnormal cutaneous and autonomic reflexes, and co-contraction of agonist and antagonist muscles (dystonia).
Immediately after an acute brain or spinal cord injury muscles generally become weak and hypotonic (O'Brien et al., 1996). This is referred to as "spinal shock" and is accompanied by loss of muscle stretch reflexes and impaired F-wave responses on nerve conduction testing (Hiersemenzel et al., 2000). Spasticity then often develops days to weeks after the acute injury; this is thought to be due to upregu-lation of spinal cord receptors and synaptic reorganization (McGuire and Harvey, 1999). Patients with cerebral lesions tend to recover reflexes and tone within a few days of injury, while patients with spinal cord injuries may have a period of spinal shock last for weeks (Calancie et al., 2002). Generally, the longer it takes for tone to return the worse the prognosis is for meaningful motor recovery (Young, 2002).
The pattern of spasticity often differs depending on the location of the upper motor neuron lesion. For example, spasticity tends to preferentially involve upper extremity flexors and lower extremity extensor groups following cerebral injuries, and flexor groups in both the upper and lower extremities following spinal cord injuries. Although not seen following cerebral injury, patients with spinal lesions often have grossly exaggerated cutaneous reflexes, such as a "triple flexion" lower extremity withdrawal reflex following cutaneous stimulation (Young, 2002).
Spasticity is not always detrimental and relief of spasticity does not ensure improvement in clinical disability. In patients with severe muscle weakness an increase in muscle tone, especially in the antigravity muscles of the trunk and lower extremities, may actually facilitate transfers, standing, and ambulation. The spastic posture of the upper extremity, with the adducted arm held close to the body, may help with balance. A spastic urinary sphincter may help maintain continence. As well, spasticity may help prevent muscle atrophy, decrease peripheral edema, and reduce the risk of deep venous thrombosis (Gelber and Jozefczyk, 1999).
However, in many patients with brain and spinal cord disorders, spasticity can interfere with functional mobility and activities of daily living. For example, in stroke patients, spasticity of the lower extremity extensor muscles can result in a stiff-legged gait with toe dragging (Riley and Kerrigan, 1999). Excessive ankle plantarflexion spasticity can affect the ability to comfortably wear an ankle foot orthosis. Spasticity of the upper extremity musculature can lead to difficulties with self-feeding, grooming, and hygiene. Other spasticity-related factors, which often contribute to overall disability, include impairment of posture (e.g., affecting wheelchair seating), and painful spasms. The presence of spas-ticity also increases skin friction, especially over extensor surfaces of limbs; if severe this can lead to the development of decubitus skin ulcers (Peerless et al., 1999).
Spasticity can be evaluated at bedside during the physical examination. Manual muscle stretch should be assessed at different rates of movement. When spasticity is mild it often takes high velocities of movement to elicit resistance. With moderate spas-ticity, resistance to passive movement may be noted with slower rates of stretch. With severe spasticity, the resistance to passive stretch may be so marked as to stop movement entirely, the so-called clasp-knife phenomenon (Dimitrijevic, 1995).
Table 17.2. Modified Ashworth and Spasm Scales (Ashworth, 1964; Bohannon and Smith, 1987).
Score Degree of muscle tone
0 No increase in muscle tone
1 Slight increase in tone, elicit a "catch when affected part is moved in flexion or extension"
2 Moderate increase in tone, passive movement difficult
3 Considerate increase in tone, passive movement difficult
Spasticity can be more formally assessed using quantitative scales and laboratory measures. This can be of particular benefit in assessing response to spasticity treatment. The most commonly used semiquantitative clinical scale to assess spasticity is the Modified Ashworth Scale (Ashworth, 1964) (Table 17.2). The examiner rates the resistance on a scale of 0-4 when muscles are passively lengthened. This scale has been found to be a reliable and reproducible method of measuring spasticity with good interrater reliability (Bohannon and Smith, 1987; Brashear et al., 2002).
For research trials spasticity can also be measured in the laboratory by biomechanical methods. The Pendulum Drop Test quantitates spasticity in knee muscles by recording a ratio of two angles of knee angular displacement. The patient sits with their hanging over the edge of a table. The leg is held at full extension and then dropped, allowing free swinging of the extremity. The flexion angle of the first swing of the leg is defined as the acute angle. The final resting angle is then determined and the ratio of these angles is calculated (Jamshidi and Smith, 1996). Measurements can be made by videotape, electrogoniometry, or with an isokinetic dynamometer (Bohannon, 1986). Other laboratory measurements of spasticity include assessment of the H-reflex and the tonic vibratory reflex (Allison and Abraham, 1995). Variable correlation has been demonstrated between these measures and the Modified Ashworth Scale (Leslie et al., 1992; Bohannon, 1999; Prandyan et al., 2003).
Treatment for spasticity is generally initiated when the increase in muscle tone interferes with functional activities, such as positioning in bed or wheelchair, mobility (walking or transfers), activities of daily living, or hygiene (e.g., if excessive hip adductor tone impairs the ability to catheterize). Furthermore, treatment should be considered when spasticity causes discomfort or painful spasms, or if excessive tone leads to complications such as decubitus ulcers or early contractures.
Again, it is important to recognize that in some patients spasticity may actually be of benefit, especially in those with marginal strength; in these individuals the increase in tone may actually allow them to stand or walk. Reducing tone in these patients may be functionally detrimental and should either be avoided or done cautiously.
When planning treatment the patient's underlying neurologic and medical conditions should always be considered. For example, spinal cord injured patients with autonomic dysreflexia, patients on antihypertensive medications, or elderly patients often do not tolerate antispasticity medications with hypotensive side effects. Patients with traumatic brain injury, stroke, or multiple sclerosis who have significant cognitive impairments may not tolerate drugs that are sedating. Furthermore, patients with marginal strength may lose functional abilities if treated with medications that cause muscle weakness. Therefore, the pros and cons of the various treatments must always be considered for each individual patient. An algorithm for the management of spasticity is presented in Fig. 17.1. This is by no means exhaustive.
It is important that the specific goals of treatment always be discussed in detail with the patient, family, and caregivers so all understand fully what the targeted outcomes of management are. As an example, spasticity treatment goals for a spinal cord injured patient with paraplegia might include a reduction in painful spasms and more comfortable positioning in a wheelchair, but not be expected to improve strength in the lower extremities or facilitate the ability to walk.
Realistic expectations must be carefully reviewed for all those involved in the patient's care.
In all patients with spasticity, medical conditions or extrinsic factors that can worsen spasticity should always be sought. For example, fever can worsen spasticity. Certain medications, such as the interferons, commonly used in multiple sclerosis management, can result in an increase in spasticity (Walther and Hohfield, 1999). The most common precipitants of a sudden worsening in spasticity and spasms are painful stimuli, especially those involving the lower extremities. This is thought to be mediated by nociceptive sensory afferents (that release substance P), which increase segmental spinal reflex activity. Initial evaluation of a spastic patient, or one in whom spasticity or flexor spasms suddenly worsens should always include a search for potential noxious stimuli, including urinary tract infections, bladder distension, bowel impaction, ingrown toenails, decubitus ulcers, and deep venous thrombosis (Merritt, 1981). Treatment of these underlying conditions will often improve tone and spasms.
There are alterations that occur in muscles and connective tissue associated with chronic spasticity. Spastic muscles have been shown to have shorter resting sarcomere length with evidence of changes in connective tissue constituents, such as collagen and titin (Friden and Lieber, 2003). Biomechanical interventions, including range of motion exercises and splinting, may help minimize these changes.
Passive range of motion of spastic muscles, performed at least 2-3 times a day, should be an integral part of any treatment regimen for spasticity. Although the improvement in tone is only temporary (several hours), routine range of motion exercises may help prevent the development of contractures (Nuyens et al., 2002).
There are certain physical therapy philosophies that stress the inhibition of spasticity in their treatment approach. For example, the neurodevelopmen-tal technique is based on the attempt to inhibit tonic reflexes by passively bringing patients into reflex inhibitory postures (Kabat and Knott, 1954). The techniques of proprioceptive neuromuscular facilitation (PNF) emphasizes the instruction of normal patterns of movement to spastic patients (Pierson, 2002). Although studies have not demonstrated better functional outcomes in patients treated with this particular technique compared to others, patients with marked spasticity might be ones to benefit from these therapy approaches (Gelber et al., 1995).
Anecdotal reports suggest that other therapy modalities might help reduce muscle tone. Vibration, especially of antagonist muscles, may help reduce tone in a spastic limb (Lee et al., 2002). Topical cold and anesthetics may reduce tone by decreasing the sensitivity of cutaneous receptors and slowing nerve conduction (Miglietta, 1973; Sabbahi et al., 1981). There are also case reports of improved spasticity following magnetic stimulation of the spinal cord and acupuncture (Nielsten 1995; Moon et al., 2003).
Orthotic devices may also be considered in the management of spasticity, to reduce tone, improve range of motion, prevent contractures, and reduce pain. Orthoses also control joint instability and may alter the loading of a limb to prevent stretch reflex activity in antagonist muscles. The theory behind tone inhibiting orthoses suggests that prolonged stretch may actually change the mechanical properties of spastic muscles, perhaps by reducing muscle spindles' reaction to stretch (Kogler, 2002). Although clinical observations suggest tone to be reduced with splints, experimental evidence is scarce and studies have not determined the most effective splint design (Langlois, et al., 1989). However, most commonly splints are fabricated to position affected joints opposite to the tonal response (Kogler, 2002).
Ankle-foot orthoses (AFO's) are commonly prescribed in patients with spastic lower extremity paresis to inhibit tone, and if possible, improve ambulation (Lehmann et al., 1987, Sankey et al., 1989). Rarely, knee-ankle-foot orthoses (KAFO's) are used in the management of young patients with cerebral palsy (Kogler, 2002).
The goals of upper extremity splinting are to reduce tone, improve range of motion, and prevent palm maceration. Some of the commonly used wrist-hand-finger orthoses include the Snook splint (Snook, 1979), cone splint, Bobath splint, and finger-abductor splint. Static or dynamic orthoses can also be considered for management of elbow flexion spasticity (Kogler, 2002).
Serial casting is an effective means for managing early soft tissue contractures resulting from spasticity, and is often combined with the use of botulinum toxin or medications (Mortenson and Eng, 2003). This process involves positioning an extremity at the end of passive range of motion and casting in that position. The cast is left in place for several days and is then removed (Pohl et al., 2002). The patient undergoes range of motion therapy between castings and is then recasted at the new (reduced) angle; this is repeated 4-5 times until as close as possible to a normal range of motion can be reestablished. It is suggested that serial casting is most effective when initiated within 6 months of acute neurologic injury, while neurologic recovery is still possible. Once the cast is removed, if the overall spasticity has not been reduced the likelihood of maintaining the improvement in range of motion without further splinting or bracing is poor (Conine et al., 1990).
Electrical stimulation has also been used to reduce spasticity in patients with hemiplegia and spinal cord injury, often as adjunctive therapy with other physical therapy modalities (Armutulu et al., 2003; Scheker and Ozer, 2003). The most common technique is to stimulate antagonist muscles; this causes activation of polysynaptic spinal cord pathways resulting in inhibition of agonist muscle activity and tone (Alfieri, 1982). The decrease in spasticity generally lasts from 15 min to 3 h, allowing the therapists to do more aggressive range of motion and strengthening exercises during this time. However, the long-term benefit of electrical stimulation in reducing muscle tone is probably limited (Dali et al., 2002).
A number of medications are effective in the treatment of spasticity (Table 17.3). These drugs all decrease the excitability of spinal reflexes, but act through different mechanisms. Such mechanisms of action include a reduction in the release of excitatory neurotransmitters from presynaptic terminals of primary Ia afferent fibers, facilitation of the action of inhibitory interneurons involved in reflex pathways, interference with the contractile mechanism of skeletal muscle, and inhibition of supraspinal influences on the spinal reflex arc (Davidoff, 1985). The choice of drug should take into account the patient's underlying neurologic disease, concurrent medications, and medical conditions.
Baclofen is a GABA agonist, active primarily at GABAb fibers, that inhibits monosynaptic extensor and polysynaptic flexor reflexes (Davidoff, 1985).
Baclofen acts presynaptically to reduce the release of excitatory neurotransmitters from the descending corticospinal tracts and primary spinal cord Ia afferent fibers, and possibly of substance P from afferent nociceptive fibers (Young and Delwaide, 1981). At high concentrations, baclofen also acts postsynaptically to decrease the effects of the excitatory neurotransmitters, thus inhibiting activation of motor neurons in the ventral horn (Rossi, 1994).
Baclofen is most effective for the treatment of spasticity secondary to spinal cord injuries, but is also approved for the treatment of spasticity of cerebral origin (Albright et al., 1993). The advantages of baclofen are that it is less sedating than the benzodi-azepines, especially when started at a low dose and titrated slowly upward and works extremely well in treating painful flexor and extensor muscle spasms (Fromm, 1994). Its major drawback is that it can cause muscle weakness at moderate and high doses, although much less than dantrolene (Roussan et al., 1985). Less common side effects include ataxia, confusion, headache, hallucinations, dyskinesias, respiratory, and cardiovascular depression (Young and Delwaide, 1981). Baclofen can also lower seizure threshold and should be used cautiously in epileptic
Major adverse effects
Reduces release of excitatory neurotransmitters and substance P in the
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