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more active than others At rest, with the muscles shortened to midposition, they are accid to palpation and electromyographically silent If the arm is extended or the leg exed very slowly, there may be little or no change in muscle tone By contrast, if the muscles are briskly stretched, the limb moves freely for a very short distance (free interval), beyond which there is an abrupt catch and then a rapidly increasing muscular resistance up to a point; then, as passive extension of the arm or exion of the leg continues, the resistance melts away This sequence constitutes the classic claspknife phenomenon With the limb in the extended or exed position, a new passive movement may not encounter the same sequence; this entire pattern of response constitutes the lengthening and shortening reaction Thus the essential feature of spasticity is a velocity-dependent increase in the resistance of muscles to a passive stretch stimulus Although a clasp-knife relaxation following peak resistance is highly characteristic of cerebral hemiplegia, it is by no means found consistently In some cases, the arm exors and leg extensors are spastic, while the antagonist muscles show an even resistance throughout the range of passive movement ie, rigidity (discussed in Chap 4); or rigidity may be more prominent than spasticity in all muscles This plastic or rigid resistance, in DennyBrown s view, is the mild form or precursor of an altered posture that he called dystonic (the term is used differently now) and considered to be a characteristic feature of hemiplegic spasticity Nor is there a constant relationship between spasticity and weakness In some cases, severe weakness may be associated with only the mildest signs of spasticity, detectable as a catch in the pronators on passive supination of the forearm and in the exors of the hand on extension of the wrist Contrariwise, the most extreme degrees of spasticity, observed in certain patients with cervical spinal cord disease, may so vastly exceed paresis of voluntary movement as to indicate that these two states depend on separate mechanisms Indeed, the selective blocking of small gamma neurons is said to abolish spasticity as well as hyperactive segmental tendon re exes but to leave motor performance unchanged Until recently, it was taught that the heightened myotatic or stretch re exes ( tendon jerks ) of the spastic state are release phenomena the result of interruption of descending inhibitory pathways This appears to be only a partial explanation Animal experiments have demonstrated that this aspect of the spastic state is also mediated through spindle afferents (increased tonic activity of gamma motor neurons) and, centrally, through reticulospinal and vestibulospinal pathways that act on alpha motor neurons The clasp-knife phenomenon appears to derive at least partly from a lesion (or presumably a change in central control) of a speci c portion of the reticulospinal system P Brown, in a discussion of the pathophysiology of spasticity, has emphasized the importance of two systems of bers: (1) the dorsal reticulospinal tract, which has inhibitory effects on stretch re exes, and (2) the medial reticulospinal and vestibulospinal tracts, which together facilitate extensor tone He postulates that in cerebral and capsular lesions, cortical inhibition is weakened, resulting in spastic hemiplegia In spinal cord lesions that involve the corticospinal tract, the dorsal reticulospinal tract is usually involved as well If the latter tract is spared, only paresis, loss of support re exes, and possibly release of exor re exes (Babinski phenomenon) occur Pantano and colleagues have suggested that primary involvement of the lentiform nucleus and thalamus is the feature that determines the persistence of accidity after stroke, but the anatomic and physiologic evidence for this view is insecure.

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