Distinguishing capsular from pontine hemiplegia It is often not possible to distinguish a hemiplegia of pontine origin from one of deep cerebral origin unless there is an associated cranial nerve palsy to triangulate the lesion to a specific part of the brainstem. In both, the face, arm, hand, leg, and foot are affected because of the location of the descending motor fibers into a small segmental region in both structures. With brainstem lesions, as with cerebral ones, a flaccid paralysis gives way to spasticity after a few days or weeks, and there is no satisfactory explanation for the occurrence in some cases of spasticity from the onset of the stroke. There is also may be a combined hemiparesis and ataxia of the limbs on the same side. With a hemiplegia of pontine origin, however, the eyes may deviate to the side of the paralysis, that is, the opposite of what occurs with supratentorial lesions. The pattern of sensory disturbance may also be helpful. A dissociated sensory deficit over the ipsilateral face and contralateral half of the body usually indicates a lesion in the lower brainstem, while a hemisensory loss including the face and involving all modalities indicates a lesion in the upper brainstem, in the thalamus, or deep in the white matter of the parietal lobe. When position sense, two-point discrimination, and tactile localization are affected relatively more than pain or thermal and tactile sense, a cerebral lesion is suggested; the converse indicates a brainstem localization. Bilateral motor and sensory signs are almost certain evidence that the lesion lies in the brainstem. When hemiplegia or hemiparesis and sensory loss are coextensive, the lesion usually is situated supratentorially. Additional manifestations that strongly favor a brainstem site are vertigo, diplopia, cerebellar ataxia, a Horner syndrome, and deafness. The numerous brainstem syndromes illustrate the important point that the cerebellar pathways, spinothalamic tract, trigeminal nucleus, and sympathetic fibers can be involved at different rostral-caudal levels so that “neighboring” phenomena are required to identify the exact site of the infarction.
A myriad of proper names have been applied to the brainstem syndromes, as noted in Tables 33-5 and 44-1. Many of them were originally described in relation to tumors, trauma, and other nonvascular diseases. The diagnosis of vascular disorders in this region of the brain is not greatly facilitated by knowledge of these eponymic syndromes; it is much more profitable to be closely familiar with the anatomy of the brainstem.
To recapitulate, the principal syndromes to be recognized are the full basilar, vertebral–PICA, posteroinferior cerebellar, anteroinferior cerebellar, superior cerebellar, pontomedullary, and medial medullary. Figures 33-12 through 33-16, supplied originally by C.M. Fisher and used in previous editions of this book. Other syndromes can usually be identified as fragments or combinations of the major ones.