Mechanisms, Measurement, and Management of Spastic Hypertonia after Head Injury

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MECHANISMS, MEASUREMENT, AND MANAGEMENT OF SPASTIC HYPERTONIA AFTER HEAD INJURY Richard T. Katz, MD

Spasticity is the hallmark of an upper motor neuron disorder and is one of the most important impairments of patients suffering from head injury. Any professional caring for the brain-injured hemiplegic who is not in decerebrate coma is familiar with the common synergic patterns of flexion in the upper extremity and extension in the lower. This article attempts to provide the physician caring for the head injury patient with a comprehensive discussion of the treatment of this disorder. Preceding the discussion of management is a brief overview of pathophysiologic mechanisms and techniques used in the quantification of spasticity. These subjects are dealt with in greater depth in a recent review.52 A widely accepted definition of spasticity is "a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome."66 Muscle tone may be characterized as "the sensation of resistance as one manipulates a joint through a range of motion, with the subject attempting to relax."67 Although this definition of tone is adequate for bedside evaluation, a more vigorous analysis indicates that muscle tone is likely to consist of several distinct components: (1)physical inertia of the extremity, (2) mechanical-elastic characteristics of muscular and connective tissues, and (3) reflex muscle contraction (tonic From the SSM Rehabilitation Institute, St. Louis, Missouri; and the University of Medicine and Dentistry of New Jersey, Newark, New Jersey

PHYSICAL MEDICINE AND REHABILITATION CLINICS OF NORTH AMERICA VOLUME 3 NUMBER 2 . MAY 1992

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stretch reflexes). As the inertia of the limb does not change after an upper motor neuron lesion, it is clear that the heightened resistance found during bedside examination represents changes in the musculotendinous unit (e.g., contracture) and/or changes within the segmental reflex arc (hyperactive stretch reflexes). The intrinsic stiffness of a muscle is one contributor to muscle tone. Like a spring, muscle has a biomechanical stiffness that may be estimated, at least in part, by studying the tension elicited when a joint is extended a given angle at varying angular velocities. Changes in muscle stiffness appear as increases in the resistance to limb extension without a commensurate increase in muscle excitation as measured by electromyography (EMG) (increased reflex activity appears as an increase in resistance with an increase in EMG activity). One group of authors has promoted changes in muscle stiffness as the primary mechanism of muscular hypertonia.27Their studies consisted of EMG and tension analysis of leg muscles in hemiplegic adults and children during ambulation. Their findings may be equally well explained, however, by degenerative or atrophic changes within the muscle structure. Moreover, this "intrinsic" muscle hypothesis does not account for the various changes in reflex activity commonly encountered in spastic patients. NEURAL MECHANISMS OF SPASTIC HYPERTONIA

Neural mechanisms of muscular hypertonia imply that the nervous system produces an enhanced reflex response to muscle stretch. These can be understood by examining the role of the segmental reflex arc (Fig. 1).This arc consists of muscle receptors, their central connections with spinal cord neurons, and the motoneuronal output to muscle. Within this arc, the alpha motor neuron may be likened to a final conduit for motoneuronal outflow. This outflow is the summation of a host of different synaptic and modulatory influences, including (1)excitatory postsynaptic potentials from Group Ia and I1 muscle spindle afferents, (2) inhibitory postsynaptic potentials from interneuronal connections from antagonistic muscles, and (3) presynaptic inhibition initiated by descending fiber input. There are two distinctly different ways in which the nervous system can produce an enhanced reflex response. First, there can be increased motoneuronal excitability, also known as alpha motor neuron hyperexcitability ("a-spasticity" in the older nomenclature). In this scenario less synaptic input is needed to cause the alpha motor neuron to fire (reach threshold at which depolarization occurs). Various mechanisms can promote alpha motor neuron hyperexcitability. There can be increased excitatory or decreased inhibitory influences upon the cell. Alternatively, there can be changes to the intrinsic membrane properties of the cell itself which alter its electrochemical characteristics. A second way in which an increased motoneuronal response to stretch can arise is secondary to augmented stretch-evoked excitatory

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Supraspinal Pathways

Muscle

Inhibitory

y -motor neuron

Skin Figure 1. Diagrammatic representation of the spinal cord circuitry basic to the understanding of spastic hypertonia.

synaptic input. This occurs (1)if muscle spindle afferents show enhanced responses to stretch because of increased dynamic fusimotor bias ("y-spasticity" in the old nomenclature), (2) if interposed excitatory neurons are more responsive to muscle afferent input, or (3) if the level of baseline presynaptic inhibition is reduced. Microneurographic recordings of spindle afferent discharge do not support the concept of enhanced dynamic fusimotor bias, and the concept of "y-spasticity" has fallen into disfavor. Hypertonia due to loss of presynaptic inhibition remains a possibility. SPASTIC HYPERTONIA AND THE UPPER MOTOR NEURON SYNDROME

The wide variety of motor dysfunctions that occur in the patient with spasticity is not simply a result of hypertonic changes. The upper motor neuron ( U M N )syndrome is a more general term used to describe abnormal motor function secondary to lesions of cortical, subcortical, or spinal cord structures. Careful study of patients with UMN syndrome reveals that their motor difficulties can be divided into a series of abnormal behaviors (positive symptoms) and performance deficits (negative symptoms). Examples of positive symptoms in the head-injured patient include the Babinski response or clonus. Negative symptoms are exhibited by the hemiparetic patient as motoric actions that are weak, easily fatigued, and

lacking in dexterity. The loss of motor control is due to the loss of orderly recruitment and rate modulation of motoneurons within the motoneuron pool, as well as to alteration in the activation of a muscle in relationship to its agonists and antagonists. It may be concluded in this brief sketch of abnormal mechanisms that relief of the hypertonic spastic components of the UMN syndrome does not necessarily imply enhanced performance. Disturbances in motor control are probably more disabling in many patients than the muscle hypertonia itself. QUANTIFICATION OF SPASTIC HYPERTONIA

The quantification of spasticity has been a difficult and challenging problem and has been based primarily on highly observer-dependent measurements. The lack of effective measurement techniques has been restrictive because quantification is necessary to evaluate various modes of treatment. No uniformly useful clinical measurements have emerged, but certain methods may be quite practical and useful in the hemiplegic patient .51 Clinical scales assess muscle tone on an ordinal scale-often zero to four-but suffer from clustering within the middle grades. The Pedersens9and Ashworth4 scales are examples that have been used. Although they offer only qualitative information, they have been widely used in the study of spasticity and are the present yardstick against which newer, more exact methods must be compared. The Fugl-Meyer scale is an accurate and objective method of assessing function (but not necessarily spastic hypertonia) in hemiplegic patients33based on the natural progression of function return.15 Motor control, light touch, position sense, and joint movement are assessed in the upper and lower hemiplegic extremity, and postural and balance evaluations complete the 100 point scale. Biomechanical evaluations consist of (1) torque-the amount of force elicited by moving a limb over a specified angle; (2) threshold-that particular angle at which torque or EMG starts to increase significantly; and (3) electromyography-rectified signal analysis from superficial muscle groups. By definition, spastic limbs demonstrate abnormal resistance to externally imposed joint movement. This resistance is augmented by increasing the angle of deflection and the rate at which the limb is moved. The pendulum test has proven to be a rather simple and highly reliable method of quantifying spastic hypertonia and correlates well . ~ ~patient is placed in a supine position with the clinical e ~ a m i n a t i o nThe with the hemiparetic lower extremity extended over the edge of a table but supported only as far as the distal thigh. The lower limb segment is allowed to fall freely from a fully extended position and oscillates about the vertical in the manner of a pendulum. The limb is damped by the viscoelastic properties of the limb, which are dramatically altered in spasticity.

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Finally, a wide variety of electrophysiologic reflex studies have been performed to assess spasticity and explore neuronal circuits within the spinal cord. Although they are easily recorded, analyzed, and quantified, they have yet to be proven clinically useful. A ratio of the maximal H-reflex and M-response (H to M ratio) is an example of such a study. Although the ratio is clearly abnormal in spastic patients, there is no correlation between the clinical severity of muscle hypertonia and the numerical ratio.51 Other electrophysiologic parameters that have been used include F waves, tonic vibration reflex inhibition of the H reflex, flexor withdrawal responses, and lumbosacral spinal evoked responses, among others. The reader is referred to other sources for a more complete discussion of these 52' 92 TREATMENT OF SPASTIC HYPERTONIA

Before treatment is initiated, the physician needs to address several important questions. Is there a functional impairment due to the spastic hypertonia? How is gait disturbed? Does the pain that can be associated with "spasms" disturb the patient's sleep? Is the lower extremity extensor tone useful to the patient in supporting him during his gait pattern? A stereotyped therapeutic approach has been proposed,79but, as in many aspects of neurologic rehabilitation, treatment is best individualized to a particular patient.48 A daily stretching program is an integral component of any management program for spastic hypertonia. A common bedside observation is that the resistance perceived as one continuously ranges a limb progressively diminishes as one repeats the motion. Regular ranging of a patient's limbs helps prevent contractures, and clinical experience suggests that it can reduce the severity of spastic tone for several hours. Recently it was documented that prolonged stretch in cerebral palsied children results in prolonged inhibition in ankle muscles which lasted up to 35 minutes.l12 The reasons for the "carry-over" of ranging for several hours are not completely clear but could be related to mechanical changes in the musculotendinous unit, as well as to plastic changes that occur within the CNS. These plastic events may correlate with short- and long-term modulation of synaptic efficacy associated with neurotransmitter changes on a cellular level. Habituation of reflex activity has been studied in the marine snail Aplysia califounica, which has a simple nervous system. The snail has a reflex for withdrawing its respiratory organ and siphon which is similar to the leg-flexion withdrawal reflex in humans. Repetitive activation results in a decrease in synaptic transmission, partly due to an inactivation of calcium channels in the presynaptic terminal. The decrease in calcium influx diminishes the release of neurotransmitter, probably owing to the calcium-dependent exocytosis of neurotransmitter vesicles.17, Related studies of the muscle stretch reflex in a primate model have demonstrated that the monosynaptic two-neuron pathways can be operantly conditioned. Memory traces responsible for this behav-

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ioral change reside in the spinal cord, probably at the terminal of the Ia afferent neuron on the motor neuron and/or the motoneuron itself.lZ7 Finally, muscle stretch can be a short-term strategy to help improve motor control (see below). Recently it was shown that manual stretch of extrinsic finger flexor muscles can improve motor control of finger extension in hemiparetic subjects.16 Short-term Strategies

Certain interventions may be valuable as temporizing strategies when a specific goal is in mind. Several schools of therapeutic exercise have suggested that reflex-inhibiting postures may temporarily decrease s astic hypertonia so that underlying movements may be unmasked.6, 69 Utilizing these strategies, therapists are able to help hemiplegic head injury patients produce voluntary movements. Topical cold has been reported to decrease tendon reflex excitability, reduce clonus, increase range of motion of the joint, and improve power in the antagonistic muscle group. These effects can be used to faciliTone tate improved motor function for short periods of time.42r713 76, may be decreased very shortly after the application of ice, probably owing to decreased sensitivity in cutaneous receptors and slowing of nerve conduction. Central factors, changes in CNS excitability, may take longer to occur. Thus a therapist might apply a cold pack for 20 minutes or more to obtain maximum effect.19Topical anesthesia may have similar effects.84,loo Casting and splinting techniques can improve the range of motion in a joint subject to hypertonic contracture, and positioning the limb in a tonic stretch has been observed to decrease reflex tone.13, 22,47, 60, 75, lo5,lo9In one study, long-term but not short-term casting resulted in a significant decrease in both dynamic and static reflex sensitivity. Elongation of the series elastic component of the musculotendinous unit and an increase in the number of sarcomeres within muscle fibers may each have contributed to the decrease in tone.88Biofeedback techniques have also been observed to modulate spastic hypertonia but have not demonstrated much widespread usef~lness.~, lZ5,lZ6

P

' I

Pharmacologic I n t e r v e n t i ~ n 503 ~12'~ ~

No medication has been uniformly useful in the treatment of spastic hypertonia (Table 1). Considering the variety of problems associated with spasticity after head injury, it is unlikely that one agent will be beneficial to all parties. More importantly, all drugs have potentially serious side effects, and these negative features should be carefully weighed when beginning a patient on any drug. Continued use of a drug should be contingent on a clearly beneficial effect. Baclofen (Lioresal) is an analog of gamma-aminobutyricacid (GABA),

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Table 1. PHARMACOLOGIC TREATMENT OF SPASTIC HYPERTONIA Agent

Daily Dosage

Half-life (hrs)

Mechanism of Action

Baclofen

10-80+ mg

3.5

Diazepam

4-60+ mg

27-37*

Presynaptic inhibitor by activation of GABA "B" receptor Facilitates postsynaptic effects of GABA, resulting in increased presynaptic inhibition Reduces calcium release, interfering with excitation-contraction coupling i n skeletal muscle

Dantrolene

25-400 m g

8.7

* Half-life of active primary metabolite is significantly longer

a neurotransmitter involved in presynaptic inhibition. Baclofen does not bind to the classic GABA " A receptor but rather to a recently discovered and less well-characterized " B receptor. Agonism at this site inhibits calcium influx into presynaptic terminals and suppresses release of excitatory neurotransmitter^.^^ Baclofen inhibits both mono- and polysynaptic reflexes and also reduces activity of the gamma efferent.l14Recent work has also demonstrated that part of its relaxant effect may be mediated through the substantia nigra.'ll Although therapeutic effects have been shown to occur when plasma levels exceed 400 ng/mL,74optimal responses have been obtained at very different plasma and CSF levels.63Baclofen is completely absorbed after oral administration and is eliminated predominantly by the renal route. Half-life is approximately 3.5 hours. Baclofen readily crosses the blood-brain barrier, in contrast to GABA.31r 62 Although baclofen is probably the drug of choice in spinal forms of asti tic it^,^^, lol the role of baclofen in the treatment of spasticity after head injury remains unsettled.44, 64, It may interfere with attention and memory in brain-injured patients.lo2Baclofen may improve bladder control by decreasing hyperreflexive contraction of the external urethral sphincter.59It has been shown to be safe and effective in long-term use.97 Dosage begins at approximately 5 mg orally two or three times a day and may be slowly titrated upwards toward a recommended maximum dose of 80 mglday. This "recommended maximum dose" may not necessarily be the most effective dose for the patient, however, and higher doses may be well tolerated by the patient as well as additionally therapeutic.61 There is a low incidence of side effects, which may include hallucinations, confusion, sedation, hypotonia, and ataxia.44,98 Sudden withdrawal of the drug may lead to seizures and hallucination^.^^^ Stereospecific L-baclofenhas been shown to be more effective than the currently used racemic form in treatment of pain.32tlo3L-Baclofen deserves evaluation for treatment of spastic hypertonia. Intrathecal baclofen has received a great deal of attention for the treatment of spinal forms of spasticity, but recent trials have begun to include patients with cerebral forms of spasticity due to cerebral palsy as well as head injury.', 68 The

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reader is referred to another recent review for a fuller discussion of intrathecal drug delivery.50 Diazepam (Valium)facilitates postsynaptic effects of GABA, resulting It has no direct GABA-mimetic in an increase in presynaptic inhibiti~n.'~ effect but exerts indirect mimetic effect only when GABA transmission is f ~ n c t i o n a 1 .In l ~ addition ~ to its known effects in the brain,51it has been shown to have effect in patients with demonstrated spinal cord diviits effect in complete spinal lesions was not confirmed ~ i o n . 'However, ~ in one report.'l6 Diazepam is generally unsuitable in patients with head injury owing Other side effects to deleterious effects on attention and mem01-y.~~ include intellectual impairment and reduced motor coordination. Evidence of abuse and addiction is rare, but true physiologic addiction may occur. Withdrawal symptoms may appear if diazepam is tapered too rapidly. There is some synergistic depression of the CNS when administered with alcohol. Although the potential for overdose exists, the benzodiazepines have an extremely large margin of safety.39Dosage begins at approximately 2 mg orally twice a day and may be slowly titrated up to 60 mglday or more in divided doses. Dantrolene sodium (Dantrium) reduces muscle action potentialinduced release of calcium into the sarcoplasmic reticulum, decreasing the force produced by excitation-contraction coupling.'l5 Thus, dantrolene is the only drug that intervenes in spastic hypertonia at a "muscular" rather than a segmental reflex level. It reduces the activity of phasic greater than tonic stretch reflexes.93Dantrolene affects fast muscle fibers more greatly than slow muscle fibers, and, for unknown reasons, seems to have little effect on smooth and cardiac muscle tissues. It is metabolized largely in the liver and eliminated in urine and bile. Half-life is 8.7 hours. 93 Dantrolene is the preferred agent for spastic hypertonia after brain injury.55 Patients who may benefit the most are those with emerging motor control that is limited by severe hypertonia. It is less likely than baclofen or diazepam to cause lethargy or cognitive disturbance^.^^ Although dantrolene theoretically "weakens" muscles, the effects on spastic hypertonia are generally without impairment of motor performance. Its most pronounced effects may be a reduction in clonus and muscle spasms resulting from innocuous stimuli.46 Dantrolene is mildly to moderately sedative and may cause malaise, nausea and vomiting, dizziness, and diarrhea. The most commonly considered side effect is hepatotoxicity, which may occur in approximately 1%of patients. Generally, liver function tests are monitored periodically, and the drug can be tapered or discontinued if enzyme elevations are noted. Fatal hepatitis has been reported in 0.1% to 0.2% of patients treated for longer than 60 days.'' One expert9 in the use of dantrolene believes that its hepatotoxic effects may have been overstated, however. Dosage begins at 25 mglday and may slowly increase up to 400 mg/day,93 but clinical results are not clearly related to dose and may plateau at a dosage of 100 mg/da~.~O

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Tizanidine, an imidazoline derivative, has an agonistic action at central alpha2-adrenergic receptor sites. It may facilitate the action of glycine, , ~ ~ prevents the release of excitatory an inhibitory n e ~ r o t r a n s m i t t e r and amino acids, i.e., L-glutamate and L-aspartate, from the presynaptic terminal of svinal inter neuron^.'^ It reduces tonic stretch reflexes and enhances presynaptic inhibition in animals. It enhances vibratory inhibiTizanidine has tion of H reflex and reduces abnormal co-contra~tion.'~~ the unusual effect of increasing the torque of spastic muscle by increasing the amplitude of the agonist EMG It has been shown to be equivalent to baclofen as an antispastic agent but may be better tolerated in divided doses up to 36 mg/day.45,78 It has been shown to be equally efficacious and better tolerated than diazevam in vatients with chronic hemiplegia.1° Common side effects incluhe mild hypotension, sleepiness, weakness, and dry mouth.lo7 Both tizanidine and baclofen are more effective in extensor than flexor m u s ~ u l a t u r eTizanidine .~~ is not currentlv available for use in the United States, and it is auestionable whethe; Sandoz will pursue FDA approval for treatment oi spastic hypertonia (Katz RT, personal communication with Sandoz Pharmaceuticals.' Aueust 21. 1989). " ~ h l o r ~ r o m a z i nhei s been applied to the treatment of hypertonia because of its alpha-adrenergic blocking affect. Clinical and electrophysiologic studies in humans before and after administration of alpha and beta blocking agents suggest that descending adrenergic and noradrenergic pathways may have important modulatory effects on spastic hypert ~ n i aThe . ~ ~depression of motor function by phenothiazines is thought to be due largely to its effects upon the brain stem reticular formation, however. A small double-blind study of chlorpromazine with phenytoin suggests that a combination of these drugs may be beneficial in the treatment of spastic hypertonia. Neither drug alone was as efficacious as the combination of the two, although chlorpromazine alone was nearly as effective. Phenytoin serum levels did not correlate with therapeutic effect as long as this concentration was above 7 pg/mL. The addition of phenytoin lowered the needed optimally therapeutic dose of chlorpromazine, decreasing its sedative effect." Progabide, a systemically active GABA agonist at both the " A and "B" receptors, and THIP (tetrahydroisoxazolopyridin), a second GABA agonist, have been proposed as possible antispasticity Electrophysiologic studies suggest that progabide's likely site of action is spinal inter neuron^.^^ A median dose of 24.3 mglkg (1800 mglday) resulted in satisfactory reduction in spastic hypertonia, tendon reflexes, and flexor spasms without a significant improvement in voluntary strength.86The beneficial effects of progabide in higher doses seem to be limited by serious side effects-fever, weakness, and elevated liver enzymes.99 Glucine. a neurotransmitter involved in recivrocal inhibition. has not been thoroughly investigated in the treatmen't of spastic hypertonia. Glycine passes the blood-brain barrier in amounts sufficient to affect reflex activity and has decreased spasticity in small groups of patient^.^ Glycine is rapidly depleted in the spinal cord ventral gray matter after

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spinal cord transection, and the depletion correlates with onset of spasticity in a canine model.40Similarly, threonine, a glycine precursor, has shown potential efficacy in a preliminary in~estigation.~ Electrical Stimulation

The concept of using electrical stimulation to improve patient function, or "functional electrical stimulation," has received wide medical and lay press. Cyclic use of electrical stimulation has been shown to decrease upper extremity contractures,' improve motor activity in agonistic muscles, and reduce tone in antagonistic muscle groups of the hemiplegic and quadriplegic patient.3, 38, 70, 117In a carefully performed study, stimulation of a flexor reflex afferent, the sural nerve, resulted in decreased extensor tonus and increased strength of ankle d o r s i f l e x i ~ n . ~ ~ The therapeutic effect may last for an hour or more after stimulation has been discontinued,l18,'19, lZ1perhaps owing to neurotransmitter modulation within the segmental reflex. Peroneal nerve stimulation may suppress ankle clonus in ambulatory hemiplegic patients via reciprocal inhib i t i ~ n . 'Electrical ~ stimulation has limited but defined applications as a dorsiflexor-assist during hemiplegic gait and as a hand-opening educational device in the plegic upper extremity.', lZ3 ' 1

Phenol Injections

Nerve and motor point blocks with injectable phenol offer the physician a somewhat effective method of reducing spastic tone on a local, albeit temporary basis. Two percent to 6% aqueous phenol solutions produce chemical neurolysis when applied to a nerve trunk or its terminal nerve fibers (motor point 34, 41, 56-58, 91 Concentrations of phenol greater than 5% cause protein coagulation and necrosis. Neurolyses of motor points are generally ineffective by themselves, perhaps owing to the multiplicity of motor points within a muscle.73Nerve blocks may be quite effective and may last 3 to 6 months or more.30,35' 41' 57 Musculocutaneous blocks can be helpful in the hemiplegic with severe elbow flexion c~ntracture.~' Elbow flexion is preserved through the action of the brachioradialis muscle, which, unlike other elbow flexors, is innervated by the radial nerve. Median nerve blocks help relax tightly contracted hemiplegic wrist and fingers. Tibia1 nerve block can reduce severe equinovarus ankle p~sturing.'~, 91 A preliminary diagnostic block with local anesthetic is often useful to predict the effect of a longer-acting phenol procedure. Implantable reservoirs can be used to repeatedly inject long-acting anesthetic agents onto the brachial plexus in hemiplegics with severely spastic upper e~tremities.'~ Nerve blocks may'be associated with dysesthesias and causalgia in approximately 10% of patients; the patient should be advised of this before the block is administered.lZ8Severe persistent dysesthesias may

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Open be treated with oral steroids or repetition of the phenol phenol nerve blocks may be more successful by selectively blocking fibers destined for muscle groups while leaving sensory fibers unharmed. Presumably, the incidence of dysesthesias should also be lower using this method.35 Venous thromboses may complicate phenol injection for chemical n e u r o l y ~ i s . ~ ~ Botulinum toxin injection to weaken muscle is a procedure that may complement or supplant the phenol nerve or motor point block. Botulinum toxin has been used investigationally for many years in the treatment of ocular muscle disorders-blepharospasm and strabismus. It has also been used in a variety of other dystonias such as torticollis and hemifacial spasm. Type A toxin produced by Clostridiumbotulinum causes an irreversible blockade of cholinergic junctions at the motor endplate by inhibiting release of acetylcholine, functionally denervating the muscle.14Recently botulinum toxin has been shown to produce a significant improvement in adductor spastic tone in nine patients who were either chair-bound or bed-bound with chronic stable multiple sclerosis.lo6 Orthopedic Procedures

Tenotomy, the release of a tendon to a severely hypertonic muscle, is a more advanced treatment that may provide benefit in selected patients. Selective quadriceps release may help patients who suffer from a stifflegged gait. Out-of-phase firing of the rectus femoris and vastus intermedius is the most common cause of such a gait deviation.lo4 Achilles tenotomies are a valuable asset in many patients with plantar flexion contractures that interfere with functional goals. Although various methods of lengthening the heelcord exist, it is generally conceded that an open procedure is desirable for precision. Toe flexor tenotomies may be beneficial in the hemiplegic patient when hypertonicity of the foot intrinsics results in claw foot deformities.''' Tendon transfer in various upper extremity muscle groups has been suggested for the augmentation of motor function in hemiplegic individu a l ~Transfer . ~ ~ of the flexor digitorum sublimis to the profundus, brachioradialis transfer to the long finger extensor^,^^ and fractional lengthening of long flexors have been advocated in head injury patients,120but these procedures are not universally acknowledged to improve the patient's functional activities. Overlengthening of the finger flexors can result in a loss of grip strength.54Adequate sensory function must be present before any type of upper extremity surgery is contemplated. V-Y lengthening of the triceps muscle has been advocated in the occasional hemiplegic in whom severe triceps tone limits function.95The marked complexity of upper extremity function limits the use of transfer surgery in that limb because patients tend to perform activities of daily living with the remaining functional extremity. Lower extremity tendon transfer is undoubtedly the most successful and useful type of rehabilitative surgery in the hemiplegic patient and is

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used for the remediation of equinovarus posturing. The SPLATT procedure-split anterior tibia1 transfer-is a procedure to help reduce excessive supination at the subtalar joint. The tibialis anterior tendon is split along its length, and the distal end of the lateral half is tunneled into the third cuneiform and cuboid bones. This creates an eversion force that is slightly greater than the varus pull of the remaining medial portion. It is generally performed in combination with an Achilles tendon lengthening.lZ4The SPLATT procedure is one of the most useful types of hemiplegic rehabilitative procedures and may substantially improve affected gait.lZ2

SUMMARY

Therapeutic intervention for the post-head injury hemiplegic with spastic hypertonia must be individualized to the patient's needs but generally includes frequent range of motion. Therapeutic exercise, cold, or topical anesthesia may decrease reflex activity for short periods of time in order to facilitate minimal motor function. Casting and splinting techniques are extremely valuable to extend joint range diminished by hypertonicity. Sodium dantrolene is the most efficacious pharmacologic agent available in the United States for the treatment of spastic hypertonia after head injury; it is the only drug that acts directly on muscle tissue. Peripheral electrical stimulation may have limited use in diminishing tone and facilitating paretic muscles. Phenol injections provide a valuable transition between short-term and long-term treatments and offer remediation of hypertonia in selected muscle groups. Tenotomies and tendon transfers offer significant benefit in carefully chosen head injury patients, and the SPLATT procedure is one of the most successful rehabilitative surgeries. Achilles tendon lengthening and release of long toe flexors may complement the SPLATT procedure in the management of the hemiplegic with spastic equinovarus. References 1. Albert A, Andre JM: State of the art of functional electrical stimulation in France. Int Rehabil Med 6:13-18, 1984 2. Albright AL, Cervi A, Singletary J: Intrathecal baclofen for spasticity in cerebral palsy. JAMA 165:1418-1422,1991 3. Alfieri V: Electrical treatment of spasticity: Reflex tonic activity in hemiplegic patients and selected specific electrostimulation. Scand J Rehabil Med 14:177-182, 1982 4. Ashworth B: Preliminary trial of carisoprodol in multiple sclerosis. Practitioner 192:540-542,1964 5. Baker LL, Yeh C, Wilson D, Waters RL: Electrical stimulation of wrist and fingers for hemiplegic patients. Phys Ther 59:1495-1499, 1979 6. Barbeau A: Preliminary study of glycine administration in patients with spasticity [abstract]. Neurology 24392, 1974 7. Barbeau A, Roy M, Chouza C: Pilot study of threonine supplementation in human spasticity. Can J Neurol Sci 9:141-145, 1982

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