Evaluation of Spasticity in Adults

Evaluation of Spasticity in Adults Philippe Decq, MD,* Paul Filipetti, MD,† and Jean-Pascal Lefaucheur, MD‡ Spasticity is one component of the upper motor neuron syndrome, which also includes motor deficits and loss of fine movement. Of these three components of the upper motor neuron syndrome, only spasticity is amenable to treatment, hence, the interest in this symptom. Evaluation of spasticity must therefore consider the patient as a whole. The patient presents a disorder of somatic motility that must be described precisely. Clinical examination must identify signs suggestive of spasticity such as alteration of passive mobilization of the limb segment, and abnormal deep tendon reflexes. Electrophysiology may help to define and quantify the altered reflexes. The most important step then consists of demonstrating that the spasticity, its consequences, or both, interfere with the patient’s natural movement (or with the patient’s remaining functional possibilities when voluntary movement is totally abolished), an essential prerequisite to determining a treatment program. Reversible tests (motor blocks, intrathecal baclofen test injections) provide a major contribution to the determination of functional impairment caused by spasticity and allow the objectives of treatment to be clearly defined. Oper Tech Neurosurg 7:100-108 © 2005 Elsevier Inc. All rights reserved. KEYWORDS spasticity, muscle retractions, motor blocks, intrathecal Baclofen, H reflex

T

he generally accepted definition of spasticity, adopted in all textbooks concerning this symptom, was proposed by Lance in 1980 at the end of a symposium on this subject:1 “Spasticity is a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (“muscle tone”) with exaggerated tendon jerk, resulting from hyperexcitability of the stretch reflex, as one of the components of the upper motor neuron syndrome.” This definition comprises three distinct parts, each of which is important. First, spasticity is primarily a clinical symptom described as a disorder of somatic motility related to exaggeration of the tonic component of the stretch reflex. It results from a known spinal reflex (stretch reflex or myotatic reflex) that has become hyperexcitable. Finally, it represents only one symptom among other components of the upper motor neuron syndrome. This definition adds three other concepts that remain a subject of discussion. First, exaggeration of the tonic stretch reflex is associated with exaggerated tendon jerks, which are considered to reflect the phasic component of the stretch reflex. Is spasticity therefore related to exaggeration of the entire stretch reflex and not just its tonic component? Sec-

*Service de Neurochirurgie, Hôpital Henri, Mondor, F-94010, Creteil, France. †Service de Médecine Physique et de Réadaptation, Centre de L’arche, F-72000 Le Mans, France. ‡Service d’Explorations Fonctionnelles, Hôpital Henri, Mondor, F-94010, Creteil, France. Address reprint requests to Philippe Decq, MD, Service de Neurochirurgie, Hôpital Henri Mondor, Boulevard du Maréchal de Lattre de Tassigny, F-94010 Creteil, France; [email protected].

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ond, the tonic stretch reflex is the basis for muscle tone, which remains a subject of controversy. Finally, exaggeration of the reflex depends on the velocity of stretching. Clinical experience has long shown that the intensity of the reflex is proportional to velocity, to a point. In the presence of intense reflex muscle contraction, however, continued stretching suddenly overcomes this contraction. This response is called the clasp-knife phenomenon and is easily demonstrated in the quadriceps muscle. In practice, clinicians do not always use this definition and tend to assess spasticity schematically in two different ways, thereby creating a certain degree of confusion.2 They either use Lance’s definition, reserving the term spasticity exclusively for exaggeration of the tonic stretch reflex, or they define spasticity by all of the positive signs of the upper motor neuron syndrome (Table 1). Therefore, spasticity is only one (or several depending on the point of view adopted) of the symptoms of the upper motor neuron syndrome whose main characteristic is various degrees of loss of control of movement. Movement is life; it is even the only sign by which man recognizes, in all living beings other than himself, the presence of sensitivity, as emphasized by Georges Canguilhem.2 The essential feature of life as an animal is therefore movement. It is so fundamental that research designed to restore movement remains and will always remain the lost cause of patients no matter what we tell them or try to explain to them. However, there are various qualities of movement. The essence of human dignity is willpower, in other words the ability to control one’s environment, starting with oneself. What is more essential than control of one’s own movements? In the

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Table 1 Upper Motor Neuron Syndrome Negative Symptoms

Positive Symptoms

Decreased muscle strength Loss of dexterity Fatiguability Loss of abdominal skin reflexes

Brisk and diffuse deep tendon reflexes Clonus Babinski’s sign Exaggerated tonic stretch reflex Flexion or extension reflexes Co-contractions and synkinesias

field of physiology, this accounts for the meticulous attention devoted to distinguishing involuntary, animal movements from voluntary movements, driven by reason. Patients confront a serious dilemma: They have trouble believing in the permanent loss of voluntary control of movement, which deprive them of part of their life. However, they are forced to live with this rudimentary reflex contraction, which does not belong to them and that they often consider to be the basis of their ills. How many patients deny the evidence of their paralysis and consult with the secret hope that treatment of their spasticity will restore their lost movement? Derived from the early stages of human evolution, exaggerated reflexes that constitute spasticity are nevertheless often preferable to flaccid paralysis. From this perspective, spasticity must not be considered a disease that must be treated at all costs. It is only a symptom, the intensity of which sometimes needs to be reduced when it interferes with the patient’s remaining or restored functional capacities. Evaluation of spasticity must therefore start by considering patients as a whole. Patients present a disorder of somatic motility that must be described precisely. The clinical examination is then used to identify signs suggestive of spasticity such as alteration of passive mobilization of the limb segment and abnormal deep tendon reflexes. The most important steps consist of demonstrating that the spasticity, its consequences, or both, interfere with patients’ natural movement (or with patients’ remaining functional possibilities when voluntary movement is totally abolished) and that treatment of spasticity will improve this movement.

First Step: Clinical Interview When patients consult about spasticity, the clinician must try to understand what patients mean by this term to determine their and their family’s expectations. Patients do not present an illness for which they can expect a cure. They present a limitation of their ability to move which can be accentuated by inappropriate reflex muscle contractions. The intensity of spasticity varies over time. The time since the neurological accident must be specified, and it may be useful to repeat the examination after an interval of several days or weeks. Variations in spasticity can sometimes be circadian. In the case of a recent and sudden modification of spasticity, the clinical examination must exclude the presence of an irritating factor (eg, urinary tract infection, bladder stones, pressure ulcer, ingrown toenail, altered bowel habit), which must be treated before considering the treatment of spasticity is considered.

Second Step: Description of the Patient’s Natural Movement In the Lower Limb The Patient Walks Gait is studied under conditions that are natural for patients (ie, with bare feet, and then with shoes) using the usual walking aids (eg, orthopedic shoes, antifoot drop or antirecurvatum splint, cane). Patients desire to walk as normally as possible (ie, walking easily with bare feet and in normal shoes). Therefore, the goal of treatment is to make this desire possible or to tend to satisfy this desire, for example, by allowing patients to walk with bare feet, by improving stability, or even by eliminating the need for a splint with shoes. Gait can be described precisely because it is an alternating automatic motor activity with a 180 degree phase difference between the two legs, during which the stance phase is longer than the swing phase or transfer phase. The result is a doublestance phase whose duration can vary (it is longer in elderly subjects with a slower walking speed, and it disappears with running).3 The clinical examination therefore measures global spatiotemporal parameters. Reduction of walking speed is measured by the time required for the patient to walk 10 meters. The duration of the swing phase (increased duration of the double stance phase) and its amplitude (does the swinging limb extend beyond the plane of the contralateral limb?) are also measured. Modifications of the angular variations of the main joints are described in the sagittal plane: At the hip, permanent flexion deformity, absence of extension at the end of the stance phase, and insufficient flexion at the beginning of the swing phase; at the knee, insufficient flexion during the swing phase and recurvatum during the stance phase; at the ankle, stepping gait because of insufficient dorsiflexion during heel strike or the swing phase and foot drop because of insufficient dorsiflexion during the stance phase and especially during the second rocker; and at the toes, presence of claw toes during the stance phase and insufficient dorsiflexion during the third rocker. Modifications are also described in the frontal plane: at the hip, pelvic tilting and excessive adduction responsible for “scissor” gait; at the ankle, varus of the hindfoot, forefoot, or both, during the various rockers of the stance phase or during the swing phase responsible for poor prepositioning of the foot at heel strike. A quantified gait analysis is the only complementary investigation providing a complete, objective,4 and reproducible5,6 analysis of the body during movement. Kinematic parameters (analysis of joint displacement by an opto-electronic system), kinetic parameters (analysis of the forces developed by ground force platforms), and electromyographic parameters [surface or intramuscular electromyography (EMG)] are measured during movement. This examination provides an objective description of gait and improves understanding of these abnormalities by means of kinetic and electromyographic data. The Patient Does Not Walk The behavior of the lower limbs is specified in all activities of daily life: sitting in a wheelchair, at rest and during movements, particularly on rough ground; during transfers; during personal hygiene; during dressing, especially of the lower limbs (pants) and feet (socks and shoes); during catheterizations and sexual intercourse; and at night.

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In the Upper Limb The activities of daily life require rapidity and precision. For an equal level of performance, the movement performed for the lowest effort should always be preferred. Most of the activities of daily life can be performed with one hand and rarely require two hands. Quadriplegics represent a special case, in whom it is essential to determine the dominant upper limb. The motor capacities of the upper limb are evaluated: The only automatic activities of the upper limb are related to gait and maintenance of posture. The upper limb is therefore examined during gait (from loss of swing to triple flexion, or even in dystonic rotation adduction) and in unstable situations (loss of balancing reactions). The range of movement and spatial exploration of the upper limb (depending on abduction, antepulsion and retropulsion of the shoulder and on flexion-extension of the elbow) are evaluated with the patient sitting and then upright. The possibilities of opening the hand and fingers are evaluated (opening of the hand possible with flexion of the wrist, presence of a crawling thumb in the palm, reduction of pronation-supination). At the end of this global evaluation of the motor possibilities of the upper limb, the clinical interview defines the activities that can be performed by the deficient limb: paperweight hand; temporary use (to relieve the contralateral limb) of a humero-thoracic grip, permanent flexion of the elbow, hand grasp; and investigation of possibly bimanual situations or situations requiring the deficient limb, during dressing (eg, to button a shirt or pants, to put on socks, to tie laces, to fasten a bra) or in other activities of daily life (eg, peel vegetables, open a jar of yogurt, put toothpaste on a toothbrush, wash the contralateral limb).

Third Step: Establish the Diagnosis of Spasticity Clinical Diagnosis Spasticity is a sign demonstrated by clinical examination during passive mobilization of limb segments. Exaggerated Stretch Reflex The stretch reflex was demonstrated by Liddel and Sherrington7 in the decerebrate cat. Muscle stretching induces reflex contraction of this muscle, which tends to oppose this stretching. Exaggeration of the tonic stretch reflex is detected clinically by resistance to passive mobilization of the joint. The intensity of this resistance is proportional to the rate of stretching. It disappears when stretching is stopped, as the limb segment tends to return to its initial position. This resistance is “elastic” and contrasts to the “plastic” resistance (the limb remains in the position at which mobilization was stopped) of extrapyramidal hypertonia observed in Parkinson’s disease. In the quadriceps, the stretch reflex can be evaluated by the pendulum test. The patient is placed in the supine position, with the trunk and thigh resting on a hard surface. The leg, in full extension, is held by the examiner. The leg is suddenly dropped and the angle of flexion at which the rate of flexion stops or declines, and the amplitude, frequency and number of oscillations are recorded with a goniometer. Spastic limbs have a smaller number and a smaller amplitude of oscillation, which can be described mathematically.8 Stretching a limb segment can also trigger a triple flexion or extension reflex. These reflexes can occur spontaneously or in

response to stimulation of cutaneous or articular nociceptive or nonnociceptive afferents. They are related to “disinhibition” of polysynaptic reflexes. They present clinically by triple flexion or extension postures. They are particularly frequent after spinal cord injuries. Finally, stretching can trigger clonus, which also corresponds to an exaggerated stretch reflex. It is always associated with exaggerated deep tendon reflexes, but the opposite is not always true. Clonus can be either exhaustible or inexhaustible. In the lower limb, it is often observed at the ankle and sometimes in the quadriceps, and can interfere with standing or gait. In the upper limb, clonus can interfere with the stability of standing and the residual function of the affected limb. It is always poorly tolerated in the upper limb, as it is perceived as an abnormal movement in addition to the handicap. Exaggeration of the stretch reflex is evaluated by the Ashworth score9 developed to assess the efficacy of antispastic treatment in patients with multiple sclerosis and presenting triple flexion paraplegia of the lower limbs (Table 2). It was modified by Bohannon in 198710 to evaluate elbow flexion “spasticity” in hemiplegic patients (Table 3). Despite many imperfections and criticisms, this simple score is widely used for the evaluation of spasticity, regardless of its site and its etiology. The intraobserver variability is satisfactory, but the interobserver variability is not.10 The Tardieu scale, used to describe spasticity associated with cerebral palsy, integrates the concept of velocity-related variations and the concept of clonus. The interobserver variability is better than that of Ashworth’s scale11 (Table 4). Tendon Hyperreflexia Tendon hyperreflexia is caused by hyperexcitability of the stretch reflex arc. Tendon reflexes are very brisk, diffuse, or even polykinetic. They can be absent in paraplegic patients with triple flexion. Tendon hyperreflexia can be evaluated by an intensity score (Table 5).

Electrophysiological Diagnosis The diagnosis of spasticity is clinical. However, it sometimes can be useful to complete the clinical evaluation by electrophysiological recordings, especially to quantify the effect of treatments. In humans stretch reflex in various muscles can be studied by several electrophysiological methods.12 H Reflex The H reflex, first described by Hoffman in 191813 in the soleus component of triceps surae (Fig. 1), can also be recorded at rest in the quadriceps muscle on the anterior surface of the thigh and in the flexor carpi radialis on the anterior surface of the forearm. However, an H reflex can be recorded

Table 2 Ashworth Scale Rating

Description

0 1

no increase in tone slight increase in tone giving a “catch” when the limb is moved during flexion or extension more marked increase in tone but limb easily flexed considerable increase in tone—passive movement difficult limb rigid during flexion or extension

2 3 4

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Table 3 Ashworth Scale Modified by Bohannon Rating 0 1

1ⴙ

2

3 4

Table 5 Deep Tendon Reflexes

Description

Rating

Description

no increase in muscle tone slight increase in muscle tone, manifested by a “catch” and release or by minimal resistance at end of range of motion when affected part(s) is moved during flexion or extension slight increase in muscle tone, manifested by a “catch,” followed by minimal resistance throughout the remainder (less than half) of range of motion more marked increase in muscle tone through most of range of motion, but affected part(s) easily moved considerable increase in muscle tone, passive movement difficult affected part(s) rigid during flexion or extension

0 1 2 3

absent present but weak normal brisk

on any muscle, provided a voluntary contraction performed at the same time is able to pre-excite spinal motoneurons so that they can respond to the reflex afferent pathway. Therefore, it is surprising that the H reflex can only be recorded at rest, without facilitation, in muscles clearly involved in the spastic process, such as the flexor carpi radialis and soleus muscles.

stimulus interval of 6 ms. In conditioned H reflex protocols, Ib inhibition lasts less than 10 ms.15

Presynaptic Inhibition The Ia afferent pathway involved in the stretch reflex also involves inhibitory interneurons able to negatively regulate this Ia stimulus, thereby adjusting the gain of the stretch reflex. This presynaptic Ia inhibition can be homonymous but also can be mediated heteronymously, for example, between the tibialis anterior and soleus or quadriceps. The Ia afferent pathway activates inhibitory interneurons that induce marked GABA-mediated axo-axonal depression of this specific Ia activity for a fairly prolonged period (several hundred ms before synaptic transmission to the motoneuron target.17 Presynaptic inhibition can therefore markedly modify the H reflex. Various electrophysiological methods can be used to study and quantify this presynaptic inhibitory influence.18

T Reflex The stretch reflex can be studied by recording the muscle response to tendon percussion, the T reflex. The amplitude of the T reflex response depends on the gain of the primary neuromuscular spindle nerve endings. In contrast, the H reflex is obtained by direct stimulation of proprioceptive fibers. This difference between these two types of reflex can be used to study control of the spindle system (ie, gamma motoneuron activity).14 Ib Inhibition Ib inhibition can be studied by various protocols of doubleshock conditioning of the H reflex. For example, the H reflex of the soleus can be conditioned by stimulation applied to the nerve to the medial head of the gastrocnemius with an interTable 4 Tardieu Score The affected part(s) is moved at different speeds: V1: as slowly as possible V2: intermediate speed (movement under gravity) V3: as rapidly as possible Two parameters are measured: X: type of muscle reaction Y: angle of the muscular event at the three different speeds Type of muscle reaction (X): 0 ⴝ no increase in muscle tone throughout the range of motion 1 ⴝ slight increase in muscle tone without any “catch” at a particular angle 2 ⴝ “catch” interrupting the movement at a defined angle, followed by muscular release 3 ⴝ exhaustible clonus (less than 10 seconds, for a permanent stretch), appearing at a defined angle 4 ⴝ inexhaustible clonus (more than 10 seconds, for a permanent stretch), appearing at a defined angle

Figure 1 Method of H-reflex recording, exploring the monosynaptic Ia-apha pathways. (A) Stimulation of the tibial nerve at the popliteal fossa (S) and recording of the motor response of the soleus muscle (R). B-H: increasing stimulation intensities resulting in the occurrence of H-reflex, which disappears by collision in parallel with the recruitment of motor fibers and the increasing amplitude of the direct motor response (M). R ⫽ recording electrodes, S ⫽ stimulating electrodes, G ⫽ ground electrode.

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Figure 2 Organization of presynaptic and reciprocal inhibiting pathways. On the right: inhibition curve of the soleus (SOL) H-reflex studied by conditioning stimulation of tibialis anterior (TA) Ia nerve fibers, defining a short-duration early period of reciprocal inhibition and a long-duration late period of presynaptic inhibition.13,16

Reciprocal Inhibition Reciprocal inhibition can be studied in the soleus muscle during contraction by a conditioning stimulation of the peroneal nerve or conversely in the tibialis anterior during contraction by conditioning stimulation of the tibial nerve.19 Rather than studying the repercussions on the various stretch reflexes and their electrophysiological manifestations, the methods of investigation focus on characterization of the electromyographic latency periods, especially their duration. After brief latency disynaptic inhibition, two longer periods of inhibition with an intermediate latency and a long latency are observed20,21 (Fig. 2).

Facilitation of Ia Afferents Facilitation of the H reflex by activating heteronymous Ia afferents can be demonstrated in the soleus muscle, especially by conditioning stimulation of the femoral nerve.22 This reflex facilitation is counterbalanced physiologically by inhibitory phenomena, especially presynaptic inhibition. Heteronymous projections also exist between the quadriceps and tibialis anterior.23 These projections indirectly allow the study of the regulation of presynaptic inhibition of the Ia afferent pathway projecting onto motoneurons controlling tibialis anterior.

Facilitation of Group II Afferents Facilitation phenomena of spinal reflexes related to activation of group II afferent fibers have been described. A large proportion of the mechanical response of a muscle to stretching appears to be related to a reflex meditated by group II afferent fibers arising from secondary muscle spindle nerve endings. For a given muscle, heteronymous motoneuron excitation by group II fibers could be more powerful than homonymous motoneuron excitation by group Ia fibers. Group II fibers, like Ia fibers, are activated according to the intensity of muscle stretching. Unlike Ia fibers, they are not sensitive to the velocity of stretching. The influence of these afferent fibers has been analyzed in recent studies by single motor unit post

stimulus time histogram (PSTH). Facilitation of the activity of the semitendinosus muscle by stimulation of the nerve to the medial head of gastrocnemius was observed in all subjects24 (Fig. 3). Role in Spasticity Hyperexcitability of the stretch reflex in spastic patients is characterized by an increase of the H max/M max ratio, because of exaggerated facilitation of the H reflex to voluntary contraction and to the absence of inhibition associated with relaxation.25,26 Disynaptic Ib inhibition appears to be depressed in patients with spasticity related to a brain lesion,27 but not in patients with spinal cord lesions.28 Discordant results according to the origin of spasticity have also been reported for recurrent inhibition. The H’ response recruitment curves, as defined above (recurrent inhibition), have been studied in particular detail in various groups of spastic patients.29 About 40% of spastic patients present an H’ response recruitment curve identical to that of healthy subjects (“bell-shaped” curve). In contrast with the hyperexcitability of the standard H reflex, absence of the H’ response is the most frequent abnormality observed in spastic patients, after stroke or spinal cord injury. This abnormality reflects an exaggeration of the recurrent inhibition phenomenon in these patients. In a minority of spastic patients, the amplitude of the H’ reflex remains maximal (“plateau-shaped” curve) or increases linearly despite an increasing intensity of stimulation. These two situations reflect a reduction of recurrent inhibition and are only observed in paraplegic patients with a progressive course. However, even when the segmental recurrent inhibition phenomenon is effective, descending control of this reflex pathway can be altered. This modifiability is reflected by the absence of modulation of recurrent inhibition during voluntary contractions in some spastic patients, in contrast with normal subjects. The role of a dysregulation of presynaptic inhibition is still controversial, as is the case for disynaptic Ib or recurrent inhibition. A reduction of presynaptic inhibition has been demonstrated by electrical double-shock protocols in the

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Figure 3 Organization of Ia facilitating pathways. On the right: facilitation curve of the soleus (SOL) H-reflex studied by conditioning stimulation of the femoral nerve.30

context of homonymous inhibition and heteronymous inhibition, at least in spinal injury patients.28,31,32 However, this finding may not apply to all spastic patients. Alterations of reciprocal inhibition in spastic patients appear to depend on the clinical severity and prognosis of spasticity.33-37 Finally, an exaggeration of facilitation phenomena by group II afferents has also been demonstrated.38 Electrophysiological studies of spinal cord reflex circuits have been conducted to determine the mechanisms of action of certain drug treatments for spasticity. Such studies have shown the presynaptic effect of alpha-2 agonists (clonidine)39-41 and the central and postsynaptic effect of GABA-B agonists (baclofen).42,43 Neurosurgical treatments for spasticity have also been evaluated by electrophysiological studies, such as spinal cord stimulation,44 selective dorsal rhizotomy45,46 or tibial neurotomy.47

Fourth Step: Distinguish Spasticity from Dystonia The term “dystonia” has been used since Denny Brown48 to describe prolonged abnormal postures observed in braindamaged patients. Dystonia causes a sustained involuntary movement. Some limb segments or a part of the body is placed in an extremely contorted positions. The movement occurs slowly, according to a tonic mode, or both. Dystonia and spasticity are two symptoms with a completely different pathophysiology. Furthermore, the topography of the lesions responsible for these two symptoms also differs: lesion of the basal ganglia for dystonia and lesion of corticospinal tracts for spasticity. Given the anatomical proximity of these two structures, both can be injured by the same pathological process. A subcortical hemorrhagic lesion affects both the internal capsule and the basal ganglia and can therefore induce both spasticity and dystonia. These two symptoms can sometimes be easily distinguished. The appearance of a retropulsion movement of the

arm, flexion of the forearm, extension of the hand, and flexion of the fingers in a hemiplegic patient can be attributed to dystonia, even in the presence of brisk deep tendon reflexes of the upper limb. Similarly, frequent extension of the large toe while walking is a dystonic phenomenon. Tonic flexion adduction of the forearm of hemiplegic patients can sometimes be diagnosed indifferently as either dystonic or spastic. The term “spastic dystonia” has been used but should be avoided because it is a source of confusion. In these cases, it is preferable to refer to the coexistence of these two symptoms. The physician must then decide which of the two symptoms causes the greatest disability for the patient and needs to be treated, or whether a treatment active on these two symptoms can be prescribed. It is sometimes possible to distinguish abnormal dystonic posture from spasticity. For example, claw toes, appearing on standing and during gait as soon as the flexor digitorum longus is stretched, and accompanied by a Rossolimo sign, can be described as spastic claw toes. Inversely, an analogous claw toe deformity, that appears gradually during gait, during the second or third step and more readily during a backward gait and without a Rossolimo sign can be described as dystonic claw toes. Unlike spastic claw toes, dystonic claw toes occur during the swing phase.

Fifth Step: Diagnose the Consequences of Spasticity Spastic reflex contraction, associated with a deficit of antagonist muscles, predisposes to muscle retraction phenomena because of the decreased number of sarcomeres.16,49,50 Limitation in the passive range of muscle movement result. Sherrington showed that the force opposing muscle stretching was always equal to the sum of the force exerted by the reflex contraction and the force related to the intrinsic viscoelastic properties of the muscles and tendons. It is not always simple for clinicians to attribute the resistance that they detect on stretching a muscle to one of these components. However,

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106 this distinction is fundamental, because treating the “spasticity” component does not modify muscle retraction. When retraction predominates over spasticity, a reduction of spasticity will not improve the patient’s functional disability. Muscle retractions are evaluated by measuring the passive range of movement of each joint (ie, the physiological limit of passive movement). The respective roles of spasticity and intrinsic muscle stiffness in the resistance to stretching up to the maximum limit are more difficult to evaluate. In the lower limbs and in the upper limbs after a spinal or supraspinal lesion,51-53 the increased resistance of the muscle to stretching could be exclusively related to a modification of the mechanical properties of the muscle itself, without any intervention of hyperexcitability of the stretch reflex.49,54 This mechanism can be demonstrated easily: increased resistance of the muscle to stretching is observed without any parallel recording of EMG activity from this muscle. It can be concluded that the increased tension observed is exclusively because of the mechanical properties of the muscle. Shortening induces a shift of the tension-length curve of the spastic muscle. It can then passively develop a strong force for low stretching. Some adult spastic hemiplegic patients can therefore remain upright. For example, with the ankle maintained at 90 degrees, the triceps surae develops a strong force (purely passive, ie, without EMG activity of the triceps).54 O’Dwyer51 studied spasticity-retraction relationships in 13 spastic hemiplegic patients. Increased resistance of the muscle to stretching in eight of these patients was not accompanied by a significant increase in EMG activity. The increased response to stretching could therefore be attributed to changes in the muscle itself. Longitudinal analysis of these patients revealed two important points. In patients who have never had an EMG response to stretching, muscle changes can occur two months after the lesion. In contrast with a widely held belief, retraction is not necessarily the consequence of untreated spasticity. Hyperactivity of the stretch reflex can also be because of retraction: spasticity can appear in some patients after retraction. This phenomenon can be explained by reducing the length of neuromuscular spindles in parallel with reduction of the length of the muscle itself. The same types of retractions are observed during prolonged experimental immobilization or in the case of an imbalance between antagonist muscles. According to the same authors, patients with central neurological lesions are immobilized and therefore offer every reason to develop retractions, even in the absence of spasticity.

Sixth Step: Attribute the Patient’s Functional Disability to Spasticity After the diagnosis of spasticity has been established, the most important step consists of demonstrating that this symptom interferes with the patient’s motor capacities and that reduction of this symptom by treatment can offer a real improvement. The Owestry scale (Table 6) can be used. This scale is based on the fact that spasticity interferes with the quality of movement.55 It attempts to evaluate the repercussions of muscle tone on movement and considers the influence of

Table 6 The Oswestry Scale Rating

Description

0

Solely spastic No willed movement. Tonic reflexes or spinal reflexes present. Very severe spasticity Movement very poor, total spastic synergy in one pattern only (ie, only total extension if limb is passively flexed or only total flexion from an extended position). Severe spasticity Movement poor, marked total spastic synergy but during both flexion and extension patterns (ie, patient can flex extended limb and extend flexed limb, with or without some isolated proximal control). Moderate spasticity Movement fair, spastic synergy, but some isolated control in a small range of movement at a distal joint (ankle or wrist). Mild spasticity Movement good with isolated distal control possible in a good range; spastic synergy still apparent on reinforcement by resistance to the movement or by effort exerted in another part of body. No spasticity Movement normal. No spastic synergy.

1

2

3

4

5

posture. This scale has not been the subject of validation studies and its reproducibility has not been studied. Clinicians can use two tests to significantly reduce or even temporarily eliminate the spasticity symptom to more effectively study its influence on movement: motor blocks (or test anesthetic block) and intrathecal Baclofen injection.

Motor Blocks The use of anesthetic blocks in the assessment of spasticity was first proposed by Liljestrand and Magnus in 1919.56 These authors reported a reduction of rigidity of the triceps surae after intramuscular injection of procaine in a decerebrate cat. At the same time, Walsche57 developed the first peripheral nerve infiltrations in humans. New anesthetic agents with more effective pharmacological properties and less toxicity were only developed after several decades. Lidocaine was developed in 1944, followed by bupivacaine in 1963.58-60 The later gradually replaced procaine, which was initially synthesized in 1905. In 1964 Tardieu and Harriga61 proposed a test injection of local anesthetic before injecting alcohol at motor points to treat cerebral palsy. In 1969,62 Zancolli, in his reference text devoted to the hand, described the surgical strategies used in spastic patients, based on the potentials revealed by anesthetic motor blocks. Since then, many specialized teams30,58,63-69 have used anesthetic blocks as a complementary modality for the evaluation of motor disorders related to spasticity.

Evaluation of spasticity Mechanism of Action Local anesthetics block nerve conduction when they are applied locally and at a sufficient concentration in nervous tissue. Their effect is reversible, creating no tissue injury. Histological Data At the cellular and molecular level, local anesthetics mainly act by blocking the kinetics of the rapid sodium channel. They can use two pathways to reach the receptor: a hydrophilic pathway, that used by highly ionized LA (lidocaine and derivatives) with binding to the cytoplasmic surface, and the hydrophobic pathway, preferentially used by neutral agents (Procaine) that penetrate the membrane and act on the sodium channel at this level. Physiological Data Installation and Regression of a Motor Block. The time to onset of the block, its intensity and its duration of action depend on the quantity of local anesthetics available to nerve fibers. This quantity depends on the dosage adopted and the availability of the product at the injection site. However, the physicochemical properties of the molecule play the most important role. The time to onset of action mainly depends on the pKa of the local anesthetic (ie, the pH at which half of the molecules in solution are dissociated and ionized). Local anesthetics with a relatively low pKa (pKa Lidocaine: 7.9, pKa Etidocaine: 7.7) diffuse easily across the membrane and have a shorter onset of action (3 minutes) than those with a high pKa (pKa Bupivacaine: 8.1, onset of action: 15 minutes). The intensity of the block depends on fat-solubility, which facilitates diffusion, and on the molecular weight. Highly fatsoluble local anesthetics (Procaine) must be administered at higher concentrations to obtain the same efficacy as very fatsoluble products with a high molecular weight (Bupivacaine, Etidocaine). The duration of action is determined by the intensity of binding to the receptor and by the absorption by lipids and muscles. These variables differ from one individual to another. The patient’s age must also be considered. Age is responsible for a reduction in the number of muscle fibers and for progressive thinning of the myelin sheath. As these changes occur, onset and intensity of a block increase with the same quantity of local anesthetic. Finally, the use of vasoconstrictors increases the duration of the block obtained with local anesthetics with a short duration of action. The indication for these nerve blocks is functionally bothersome focal spasticity of a muscle group (eg, thigh adductors, finger or wrist flexors, varus foot drop, elbow flexors). The effect of the block is predictive of a targeted surgical procedure or long-term treatment with a nerve-blocking agent (eg, botulinum toxin, phenol, alcohol). Concrete visualization of the efficacy of the motor block and resolution of the movement disorder gives the patient a better idea of the expected effects of treatment. Motor blocks are therefore useful to define the objectives of treatment.70

Intrathecal Baclofen Test Injection Baclofen, a GABA agonist, acts on presynaptic GABA-B receptors of nerve endings of type Ia fibers.71,72 It significantly reduces spasticity and polysynaptic flexion and extension reflexes.73,74 These test injections are performed by lumbar puncture or via a site communicating with the subarachnoid space. The initial dose is usually 50 g. Doses are then increased by increments of

107 25 g based on safety and the clinical response. These injections are used to verify the efficacy of baclofen on spinal reflexes (Ashworth, spasticity scale), to assess the efficacy of baclofen on the functional disability reported by the patient, and to demonstrate orthopedic limitations related to muscle retractions because it is sometimes difficult to distinguish between spasticity and retraction in cases of severe spasticity.

Conclusion The clinical evaluation of spasticity remains a complex problem.75 Observation of clonus or tendon hyperreflexia is easy, but it is not always easy to distinguish between resistance to stretching related to tonic spasticity and resistance related to increased intrinsic stiffness of the muscle. This difficulty could explain the absence of efficacy of antispastic treatments in some clinical situations. The other difficulty concerns attributing part of the impairment of the patient’s natural movements to spasticity. Establishing the therapeutic efficacy on the basis of a reduction of the Ashworth score may have no functional significance in these patients.

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