Damage to the corticospinal and corticobulbar tracts in the upper portion of the brainstem also causes paralysis of the face, arm, and leg of the opposite side (see Fig. 3-2). The lesion in the brainstem may be localized by the presence of a cranial nerve palsy or other segmental abnormality on the same side as the lesion (opposite the hemiplegia). These “crossed paralyses” are characteristic of brainstem lesions. With midbrain lesions there is a third nerve palsy (Weber syndrome); in low pontine lesions, an ipsilateral abducens or facial palsy is combined with a contralateral weakness or paralysis of the arm and leg (Millard-Gubler syndrome). Lesions in the medulla affect the tongue and sometimes the pharynx and larynx on one side and the arm and leg on the other. Even lower in the medulla, a unilateral infarct in the pyramid causes a flaccid paralysis of the contralateral arm and leg, with sparing of the face and tongue. The crossed brainstem syndromes are further described in Chaps. 33 and 44.
In some cases, an ipsilateral hemiplegia may be caused by a lesion in the corticospinal tract of the cervical spinal cord. In the spinal cord, however, the pathologic process is more often large and induces bilateral signs. A hemiparesis that spares the face, if combined with a loss of vibratory and position sense on the same side and a contralateral loss of pain and temperature, signifies disease of the spinal cord on the side of the hemiparesis (Brown-Séquard syndrome, as discussed in Chap. 42).
As indicated above, in general there is little or no muscle atrophy following upper motor neuron lesions, as there is in diseases of the lower motor neuron. The atrophy in the former case is mainly a consequence of disuse.
When the motor cortex and adjacent parts of the parietal lobe are damaged in infancy or childhood, normal development of the muscles, as well as the skeletal system in the affected limbs, may be impaired. The limbs and even the trunk are smaller on one side than on the other. This does not happen if the paralysis occurs after puberty, by which time the greater part of skeletal growth has been attained. In hemiplegia caused by spinal cord lesions, muscles at the level of the lesion may atrophy as a result of damage to anterior horn cells or ventral roots.
In the causation of hemiplegia, ischemic and hemorrhagic vascular diseases of the cerebrum and brainstem exceed all others in frequency. Trauma (brain contusion, epidural and subdural hemorrhage) ranks second. Other important causes, less acute in onset, are, in order of frequency, brain tumor, demyelinating disease, brain abscess, and the vascular complications of meningitis and encephalitis. Most of these diseases can be recognized by their mode of evolution and characteristic imaging, which are presented in the chapters on specific neurologic diseases. Alternating transitory hemiparesis may be the result of a special type of migraine (see discussion in Chap. 9). Hysteria (conversion disorder) is another common cause of hemiplegia, as discussed further on.