Central midbrain and subthalamic syndromes are a result of occlusion of the interpeduncular branches (Percheron vessel) of the posterior cerebral artery. The clinical syndromes include palsies of vertical gaze, stupor, or coma. Syndromes of the paramedian arteries, including the proximal posterior cerebral artery, have as their main feature a third-nerve palsy on the side of the lesion combined with contralateral hemiplegia (Weber syndrome), contralateral ataxic tremor (Claude syndrome), or contralateral ataxia and hemiplegia (Benedikt syndrome), as summarized in Table 33-5.
Anteromedial-inferior thalamic syndromes follow occlusion of the thalamoperforant branches. Here the most common effect is an extrapyramidal movement disorder (hemiballismus or hemichoreoathetosis or less often, asterixis). Deep sensory loss, hemiataxia, or tremor may be added in various combinations. Hemiballismus is usually a result of occlusion of a small branch to the subthalamic nucleus (of Luys) or its connections with the pallidum. Occlusion of the paramedian thalamic branches to the mediodorsal nucleus is a recognized cause of an amnesic (Korsakoff) syndrome; this simulates but is less common than infarction of the hippocampi from occlusion of the medial temporal branch of the posterior cerebral artery as noted below.
Cortical Syndromes of the Posterior Cerebral Artery
Occlusion of branches to the temporal and occipital lobes gives rise to a homonymous hemianopia as a result of involvement of the primary visual receptive areas (calcarine or striate cortex) or of the converging geniculocalcarine fibers. The hemianopia may be incomplete and involve the upper quadrants of the visual fields more than the lower ones (see Chap. 12). Macular, or central, vision is often spared (macular sparing) because of collateral blood supply of the occipital pole from distal branches of the middle (or rarely anterior) cerebral arteries. Other features seen in a few instances are visual hallucinations in the blind parts of the visual fields (Cogan) or metamorphopsia and palinopsia (Brust and Behrens). Occipital infarcts of the dominant hemisphere may cause alexia without agraphia, anomia (amnesic aphasia), a variety of visual agnosias, and rarely some degree of impaired memory. The anomias, when they occur, are most severe for colors, but the naming of other visually presented material such as pictures, mathematical symbols, and manipulable objects may also be impaired. The patient may treat objects as familiar—that is, describe their functions and use them correctly—but be unable to name them. Color anomia (a form of “central achromatopsia”) and amnesic aphasia are more often present in this syndrome than is alexia. The defect in retentive memory is of varying severity and may or may not improve with the passage of time. These syndromes are described in Chaps. 21 and 22.
A complete proximal arterial occlusion leads to a syndrome that combines cortical and anterior-proximal syndromes in part or totally. As mentioned, the vascular lesion may be either an embolus or an atherosclerotic thrombus, but more often the former.
These occur as a result of successive infarctions or from a single embolic or thrombotic occlusion of the upper basilar artery, especially if the posterior communicating arteries are unusually small or absent, or from global failure of circulation.