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This is a long, narrow artery that springs from the internal carotid, just above the origin of the posterior communicating artery It supplies the internal segment of the globus pallidus and posterior limb of the internal capsule and various contiguous structures, including (in most patients) the optic tract (Fig 34-5); then it penetrates the temporal horn of the lateral ventricle, where it supplies the choroid plexus and anastomoses with the posterior choroidal artery Only a few complete clinicopathologic studies have been made of the syndrome caused by occlusion of this artery It was found by Foix and colleagues to consist of contralateral hemiplegia, hemihypesthesia, and homonymous hemianopia due to involvement of the posterior limb of the internal capsule and white matter posterolateral to it, through which the geniculocalcarine tract passes Cognitive and language functions are notably spared in most cases This combination of extensive motor, sensory, and visual impairment in an individual with well-preserved language and cognition distinguishes this stroke syndrome from the more common syndromes involving the major cerebral arteries Decroix and colleagues reported 16 cases (identi ed by CT) in which the lesion appeared to lie in the vascular territory of this artery In most of their cases the clinical syndrome fell short of what was expected on anatomic grounds With right-sided lesions, there may be a left spatial neglect and constructional apraxia; slight disorders of speech and language may accompany left-sided lesions Hupperts and colleagues have discussed the controversy regarding the effects of occlusion of the anterior choroidal artery and in particular the variability of its supply to the posterior paraventricular area of the corona radiata and adjacent regions They concluded, also from a survey of CT scans, that there was no uniform syndrome attributable to occlusion of this vessel and that in most cases its territory of supply was overlapped by small surrounding vessels Of course, in both these studies, the lesions may have extended beyond the territory of this artery, since postmortem con rmation was lacking It should be remembered that for a time, in order to abolish the tremor and rigidity of unilateral Parkinson disease, the anterior choroidal artery was being surgically ligated without these other effects having been produced.

Posterior Cerebral Artery In about 70 percent of persons, both posterior cerebral arteries are formed by the bifurcation of the basilar artery, and only thin posterior communicating arteries join this system to the internal carotid arteries In 20 to 25 percent, one posterior cerebral artery arises from the basilar in the usual way, but the other arises from the internal carotid, a so-called persistent fetal circulation; in the remainder, both arise from the corresponding carotids The con guration and branches of the proximal segment of the posterior cerebral artery (P1 segment) are illustrated in Figs 34-6, 34-8, and 34-9 The interpeduncular branches, which arise

Ant choroidal A Post communicating A Cerebral peduncle Red nucleus 3rd nerve nucleus Sup colliculus C Post cerebral A B Peduncular arteries Ant temporal A Thalamo-geniculate A Midbrain (thalamo) perforating A Long quadrigeminal A Post temporal A Visual cortex Calcarine A

9:

Figure 34-8 Inferior aspect of the brain showing the branches and distribution of the posterior cerebral artery and the principal anatomic structures supplied Listed below are the clinical manifestations produced by infarction in its territory and the corresponding regions of damage

Thalamic syndrome: sensory loss (all modalities), spontaneous pain and dysesthesias, choreoathetosis, intention tremor, spasms of hand, mild hemiparesis Thalamoperforate syndrome: (1) superior, crossed cerebellar ataxia; (2) inferior, crossed cerebellar ataxia with ipsilateral third nerve palsy (Claude syndrome) Weber syndrome third nerve palsy and contralateral hemiplegia Contralateral hemiplegia Paralysis or paresis of vertical eye movement, skew deviation, sluggish pupillary responses to light, slight miosis and ptosis (retraction nystagmus and tucked-in eyelids may be associated) Contralateral ataxic or postural tremor Decerebrate attacks

Ventral posterolateral nucleus of thalamus in territory of thalamogeniculate artery Involvement of the adjacent subthalamic nucleus or its pallidal connections results in hemiballismus and choreoathetosis Dentatothalamic tract and issuing third nerve

Issuing third nerve and cerebral peduncle Cerebral peduncle Supranuclear bers to third nerve, high midbrain tegmentum ventral to superior colliculus (nucleus of Cajal, nucleus of Darkschevich, rostral interstitial nucleus of the MLF, and posterior commissure) Dentatothalamic tract ( ) after decussation Precise site of lesion unknown Damage to motor tracts between red and vestibular nuclei

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Peripheral territory Homonymous hemianopia Calcarine cortex or optic radiation; hemiachromatopsia may be present Macular or central vision is preserved if posterior striate area is spared Bilateral occipital lobe, possibly with involvement of parieto-occipital region

Bilateral homonymous hemianopia, cortical blindness, unawareness or denial of blindness; achromatopsia, failure to see toand-fro movements, inability to perceive objects not centrally located, apraxia of ocular movements, inability to count or enumerate objects Dyslexia without agraphia, color anomia Memory defect Topographic disorientation and prosopagnosia Simultagnosia Unformed visual hallucinations, metamorphopsia, teleopsia, illusory visual spread, palinopsia, distortion of outlines, photophobia

Dominant calcarine lesion and posterior part of corpus callosum Lesion of inferomedial portions of temporal lobe bilaterally; occasionally of the dominant side only Nondominant calcarine and lingual gyri, usually bilateral Dominant visual cortex, sometimes bilateral Calcarine cortex

Note: Tremor in repose has been omitted because of the uncertainty of its occurrence in the posterior cerebral artery syndrome Peduncular hallucinosis may occur in thalamicsubthalamic ischemic lesions, but the exact location of the lesion is unknown