The anterior cerebral artery (ACA) arises as the medial branch of the bifurcation of the internal carotid artery (ICA) at the level of the anterior clinoid process. The ACA supplies the whole of the medial surfaces of the frontal and parietal lobes, the anterior four-fifths of the corpus callosum, the frontobasal cerebral cortex, the anterior diencephalon, and other deep structures. Ischemic stroke in the ACA territory is most often the result of emboli from the heart or the ICA. Transient loss of consciousness has been described in patients with ACA territory infarctions, but it is uncommon; sustained unresponsiveness most often indicates abulia or akinetic mutism. Anterograde amnesia has been known to follow rupture and related surgery for an anterior communicating artery (ACoA) aneurysm. Distinct syndromes of callosal disconnection resulting from ACA territory infarctions include ideomotor apraxia, agraphia, and tactile anomia restricted to the left hand in right-handed patients.

The arterial system supplying the midbrain is terminal for the midbrain itself, arising from the basilar artery and from the bifurcation of the basilar artery. According to magnetic resonance imaging (MRI)-based stroke registries, the midbrain was involved in 0.9% of strokes and 3% to 8% of posterior circulation infarcts. Oculomotor palsies are frequent in midbrain strokes and dominate the neurological picture. Combined upward- and downward-gaze palsy has been related to bilateral or unilateral midbrain infarcts. A lacunar infarct of the lateral midbrain affecting the pyramidal tract in the cerebral peduncle can cause pure motor stroke. Midbrain hematomas or infarcts that involve the sensory lemniscus have been reported as causes of pure sensory strokes. Bilateral, isolated small infarcts in the lateral midbrain involving the corticospinal tracts have been responsible for tetraplegia and mutism, leaving conscious patients with only gaze movements as a means to communicate.