If the upper motor neurons are interrupted above the level of the facial nucleus in the pons, hand and arm muscles are affected most severely and the leg muscles to a lesser extent; of the cranial musculature, only muscles of the tongue and lower part of the face are involved to any significant degree (Fig. 3-5). Because Broadbent was the first to call attention to this distribution of facial paralysis that relatively spares the forehead muscles, it has been referred to as “Broadbent’s law.” The precise course taken by fibers that innervate the facial nucleus is still somewhat uncertain; however, the majority crosses in the mid-pons to innervate the contralateral facial nerve nucleus. Some fibers may descend to the upper medulla and then ascend recurrently to the pons (Pick’s bundle), accounting for the rare, mild facial weakness that may be seen with lesions of the lower pons and upper medulla.
At lower levels, such as the cervical cord, complete, acute, and bilateral lesions of the upper motor neurons not only cause a paralysis of voluntary movement but also temporarily abolish the spinal reflexes of segments below the lesion. This is the condition referred to earlier as spinal shock, a state of acute flaccid paralysis that is replaced later by spasticity. A comparable state of areflexia and hypotonia may occur with acute cerebral lesions but is less sharply defined than is the spinal state. With some acute cerebral lesions, spasticity and paralysis develop together; in others, especially with parietal lesions, the limbs remain flaccid but reflexes are retained.
Spasticity, Hyperreflexia, and the Babinski Sign
The identifying characteristics of paralysis from an upper motor neuron lesion are a predilection for involvement of certain muscle groups, a specific pattern of response of muscles to passive stretch (where resistance increases linearly in relation to velocity of stretch), and a manifest exaggeration of tendon reflexes. The antigravity muscles—the flexors of the arms and the extensors of the legs—are predominantly affected. The arm tends to assume a flexed and pronated position and the leg an extended and adducted one, indicating that certain spinal neurons are reflexly more active than others.
At rest, with the muscles shortened to midposition, they are flaccid to palpation and electromyographically silent. If the arm is extended or the leg flexed 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 flexion of the leg continues, the resistance melts away. This velocity-dependent tone constitutes the “clasp-knife” phenomenon of spasticity. With the limb in the extended or flexed position, a new passive movement may not encounter the same sequence. 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. At times, a form of velocity-independent hypertonia is found that is termed rigidity and is more characteristic of basal ganglia lesions as discussed in Chap. 4.
Clinicians have known for some time that there is not a constant relationship between spasticity and weakness. Severe weakness may be associated with only the mildest signs of spasticity; in contrast, the most extreme degrees of spasticity, observed in certain patients with cervical spinal cord disease, may seem disproportionate to the extent of weakness, signifying that these two states depend on separate mechanisms. Indeed, the selective blocking of small gamma neurons abolishes spasticity as well as hyperactive segmental tendon reflexes but leaves power unchanged.