Clinical and electrophysiologic observations indicate that the extension movement of the great toe is a component of a larger synergistic flexion or shortening reflex of the leg—that is, toe extension when viewed from a physiologic perspective is a protective (nocifensive, or defensive) response. The most characteristic of these is the “triple flexion response,” in which the hip, thigh, and ankle flex (dorsiflex) slowly, following an appropriate stimulus. These spinal flexion reflexes, of which the Babinski sign is the most characteristic, are common accompaniments to—but not essential components of—spasticity. They are present because of disinhibition or release of motor programs of spinal origin. Important characteristics of these responses are their capacity to be induced by weak superficial stimuli (such as a series of pinpricks) and their tendency to persist for a few moments after the stimulation ceases. With incomplete suprasegmental lesions, the response may be fractionated; for example, the hip and knee may flex but the foot may not dorsiflex, or vice versa.
The hyperreflexic state that characterizes spasticity may take the form of clonus, a series of rhythmic involuntary muscular contractions occurring at a frequency of 5 to 7 Hz in response to an abruptly applied and sustained stretch stimulus. It is usually designated in terms of the part of the limb to which the stimulus is applied (e.g., patella, ankle). The frequency is constant within 1 Hz and is not appreciably modified by altering peripheral or central nervous system activities. Clonus requires an appropriate degree of muscle relaxation, integrity of the spinal stretch reflex mechanisms, sustained hyperexcitability of alpha and gamma motor neurons (suprasegmental effects), and synchronization of the contraction–relaxation cycle of muscle spindles.
The cutaneomuscular abdominal and cremasteric reflexes (“cutaneous, or superficial reflexes”) are elicited by rapid, gentle stroking of the skin overlying these muscles, and are usually abolished when the upper motor neuron is damaged acutely. They are difficult to interpret because they are absent in some normal individuals and may disappear after acute spinal injury, only to reappear at a later time.
Spread, or radiation of reflexes, is regularly associated with spasticity, although it may be observed to a slight degree in normal persons with brisk tendon reflexes. Tapping of the radial periosteum, for example, may elicit a reflex contraction not only of the brachioradialis but also of the biceps, triceps, or finger flexors. This spread of reflex activity is probably not the result of radiation of impulses in the spinal cord, but a result of the propagation of a vibration wave from bone to muscle, stimulating the excitable muscle spindles in its path (Lance). Other manifestations of the hyperreflexic state are the Hoffmann sign and the crossed adductor reflex of the thigh muscles. Also, reflexes may be “inverted,” as in the case of a lesion of the fifth or sixth cervical segment. Here the biceps and brachioradialis reflexes are abolished and in response to a tap over the distal radius or the biceps tendon, only the remaining triceps and finger flexor reflex arcs are engaged.
With bilateral cerebral lesions, exaggerated stretch reflexes may be elicited in cranial as well as limb and trunk muscles because of interruption of the corticobulbar pathways. These are seen as easily triggered masseter contractions in response to a brisk downward tap on the chin (“jaw jerk”) and brisk contractions of the orbicularis oris muscles in response to tapping the philtrum or corners of the mouth. In advanced cases, weakness or paralysis or slowness of voluntary movements of the face, tongue, larynx, and pharynx are added (bulbar spasticity or “pseudobulbar” palsy; see also Chap. 24).