The thalamoperforate branches (also called paramedian thalamic arteries) arise slightly more distally from the stem, nearer the junction of the posterior cerebral and posterior communicating arteries (P2 segment of the artery) and supply the inferior, medial, and anterior parts of the thalamus. The thalamogeniculate branches arise still more distally, opposite the lateral geniculate body, and supply the geniculate body and the central and posterior parts of the thalamus. Medial branches emerging from the posterior cerebral artery as it encircles the midbrain, supply the lateral part of the cerebral peduncle, lateral tegmentum and corpora quadrigemina, and pineal gland. Posterior choroidal branches run to the posterosuperior thalamus, choroid plexus, posterior parts of the hippocampus, and psalterium (decussation of deep white matter fornices).
Most importantly, the terminal or cortical branches of the posterior cerebral artery supply the inferomedial part of the temporal lobe and the medial occipital lobe, including the lingula, cuneus, precuneus, and visual Brodmann areas 17, 18, and 19 (see Figs. 33-6, 33-10, and 33-11).
Occlusion of the posterior cerebral artery produces a profusion of clinical because both the upper brainstem, which is replete with important structures, and the inferomedial parts of the temporal and occipital lobes lie within its supply. The site of the occlusion and the arrangement of the circle of Willis will, in large measure, determine the location and extent of the resulting infarct. For example, occlusion proximal to the posterior communicating artery may be asymptomatic or have only transitory effects if the collateral flow is adequate from the Circle of Willis (see Figs. 33-2, 33-10, and 33-11).
In older series of posterior cerebral artery strokes, such as the one by studied by Milandre and coworkers, the causes were mainly atherosclerotic. Our experience has differed in that the proportion of presumed embolic occlusions has been far greater than that of other causes.
For convenience of exposition, it is helpful to divide the posterior cerebral artery syndromes into three groups: (1) proximal (involving interpeduncular, thalamic perforant, and thalamogeniculate branches), (2) cortical (inferior temporal and medial occipital), and (3) bilateral.
Proximal PCA Syndromes (See Figs. 33-10 and 33-11)
The thalamic syndrome of Dejerine and Roussy (see also Chap. 7) follows infarction of the sensory relay nuclei in the thalamus, the result of occlusion of thalamogeniculate branches. Occlusion of the small vessels supplying these territories from in situ atherothrombosis or embolic occlusion of the posterior cerebral artery is the most common cause. There is both a deep and cutaneous sensory loss, usually severe in degree, of the opposite side of the body, including the trunk and face, sometimes accompanied by a transitory hemiparesis. A homonymous hemianopia may be conjoined. In some instances, there is a dissociated sensory loss—pain and thermal sensation being more affected than touch, vibration, and position—or only one part of the body may be anesthetic. The characteristic feature is always sensory loss that includes the entire hemibody up to the midline. After an interval, sensation begins to return, and the patient may develop pain, paresthesia, and hyperpathia in the affected parts. The painful paresthetic syndrome may persist for years. There may also be distortion of taste, athetotic posturing of the hand, and alteration of mood. Mania and depression have occasionally been observed with infarction of the diencephalon and adjacent structures, but the data are usually incomplete.