The heightened stretch reflexes (tendon jerks) of the spastic state may be a “release” phenomenon—the result of interruption of descending inhibitory pathways. Animal experiments have demonstrated that this aspect of the spastic state is mediated through disinhibition of spindle efferents (increased tonic activity of gamma motor neurons) and through loss of the influence of 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 specific portion of the reticulospinal system.
The pathophysiology of spasticity is further dependent on two more refined descending tracts: (1) the dorsal reticulospinal tract, which has inhibitory effects on stretch reflexes; and (2) the medial reticulospinal and vestibulospinal tracts, which together facilitate extensor tone. In cerebral and capsular lesions, cortical inhibition from these pathways is reduced, 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 reflexes, and possibly release of flexor reflexes (Babinski phenomenon) occur. In some instances, flaccidity persists after hemiplegic stroke, possibly as a result of primary involvement of the lenticular nucleus of the basal ganglia and the thalamus as suggested by Pantano and colleagues.
The most reliable indications of an upper motor neuron lesion are the signs described by Babinski in 1896 (the great toe sign) and 1903 (the toe abduction, or fan sign) (Fig. 3-6). In modern parlance, the toe and fan signs have generally been conflated and termed the Babinski sign. Numerous monographs and articles have been written about the sign: a comprehensive one, by van Gijn, and an elegant but more arcane one by Fulton and Keller. A worthwhile biography of Babinsk has been written by Phillipon and Poirer.
In its essential form, the sign consists of extension of the large toe and extension and fanning of the other toes during and immediately after stroking the lateral plantar surface of the foot. The stimulus is applied along the dorsum of the foot from the lateral heel and sweeping upward and across the ball of the foot. The stimulus must be firm but not necessarily painful. Several dozen surrogate responses (with numerous eponyms) have been described over the years, most utilizing alternative sites and types of stimulation, but all have the same significance as the Babinski response.
As Babinski himself indicated, a movement resembling the Babinski sign is present in normal infants (see Phiilipon and Poirer), but it disappears and its persistence or emergence in late infancy and childhood or later in life is an invariable indicator of a lesion at some level of the corticospinal tract. There has been considerable discussion regarding the form and meaning of the sign in infants, some surveys such as the one by Hogan and
Milligan indicating that the first movement of the great toe is flexor, others, that the four toes fan outward but do not extend and that the sign differs from the one in adults. To some extent, the nature of the stimulus is responsible for variation in the response.