Background: Posterior cerebral arteries (PCAs) supply the ventrolateral thalamic sensory nuclei and white matter sensory tracts to the somatosensory parietal cortex. Patients with PCA territory strokes often have visual, memory, cognitive, and sensory signs. Clinicoanatomic correlation of visual, cognitive, and memory functions are well defined but, to our knowledge, no systematic study has analyzed the anatomy of sensory abnormalities.Objective: To assess the frequency and anatomic correlation of sensory symptoms and signs in patients with PCA territory infarction.Patients and Methods: Sixty patients with hemispheral and hemispheral and deep PCA territory infarcts apparent on computed tomographic and magnetic resonance imaging scans were studied for the presence of sensory findings and location of infarcts.Results: Sensory symptoms or signs were present in 15 (25%) of 60 patients. Among patients with sensory findings, 11 of 15 had infarcts in the ventrolateral thalamus in the territory of the thalamogeniculate or lateral posterior choroidal arteries. The other 4 patients had no ventrolateral thalamic or white matter infarction but had severe proximal vascular occlusive lesions that could have caused temporary thalamic ischemia. One of these 4 patients had a medial thalamic infarct and transient hemisensory symptoms. Twelve patients had thalamic infarcts and no recorded sensory findings. Seven patients with thalamic infarcts (6 medial and 1 ventrolateral) had no sensory findings, and sensory findings could not be accurately assessed in 4 patients with ventrolateral and 1 patient with medial thalamic infarcts.Conclusions: All patients with PCA territory infarcts and sensory findings either had thalamic infarcts in thalamogeniculate or lateral posterior choroidal artery territory or had thalamic ischemia. Sensory findings in PCA territory infarction indicate ventrolateral thalamic ischemia.

PURPOSE To review our experience with intracranial angioplasty, including the complications we encountered. METHODS During a 3-year period, from 1993 to 1996, 10 patients had intracranial percutaneous transluminal angioplasty (PTA). The stenosed vessels included three internal carotid arteries, one middle cerebral artery, one basilar artery, and five vertebral arteries. Stenosis in all patients was 75%, or greater. PTA was technically successful in eight patients; in two patients it could not be performed owing to inability to traverse the stenosed area. RESULTS Two patients had successful and uneventful PTA. Five patients had vasospasm, which resolved with local vasodilators in two and with repeat PTA in one. Vasospasm led to stroke in two patients. Compromise of perforating vessels and arterial dissection were associated with stroke in two patients. CONCLUSION Intracranial PTA is technically feasible but associated with risks related to vasospasm, arterial trauma, and compromise of perforating vessels.

Basilar artery (BA) occlusion is generally believed to have a high mortality. A favorable outcome is rarely reported, A consecutive series of 20 survivors with angiographically proven symptomatic BA occlusion not treated with thrombolysis or selected for outcome were analyzed for clinical presentation and neuroradiologic features to find outcome predictors. Long-term functional outcome (Rankin scale) was good in 12 (60%), moderate in 4 (20%), and poor in 4 (20%) patients who had complete mid-segmental BA occlusions and bilateral large pontine infarcts. Prominent retrograde collateral supply from the carotids and/or anterograde from the cerebellar arteries was present in all patients with adequate angiographic studies (n = 18). BA occlusion was proximal in 12, mid-segmental in 7, and distal in 1 patient. Stroke etiology was considered atherothrombotic in 14 (70%), embolic in 2 (10%), and related to migraine in 4 (20%). Clinical outcome following BA occlusion is more heterogenous than usually presumed and influenced by the temporal course, length of BA occlusion, availability of collateral circulation, and extent of brainstem infarction. The etiology of benign BA occlusion is mostly local thrombosis.

Cirsoid aneurysms of the scalp are notoriously difficult lesions to manage. The authors report a patient in whom a large traumatic cirsoid aneurysm of the scalp was eliminated using a combined neurosurgical and interventional neuroradiological approach. Transarterial embolization was utilized to reduce arterial blood supply to the fistula. Thrombogenic Gianturco spring coils were then introduced via direct percutaneous puncture of the aneurysm. The aneurysm thrombosed and the multiple tortuous scalp vessels disappeared. One month after embolization, a small area of skin necrosis over the aneurysm necessitated surgical excision of the lesion. The thrombosed aneurysm was easily resected with minimal blood loss. Percutaneous embolization with thrombogenic coils in this case was a safe and effective ablative technique.

We reviewed CTs from 47 patients with 48 spontaneous, supratentorial brain hemorrhages to determine the effect of ventricular blood on outcome. We correlated volumetric analysis of the parenchymal (P) and ventricular (V) blood, as well as other clinical and CT features, with clinical outcome in a statistical analysis. Hemorrhages were located in putamen 20/48 (42%), thalamus 13/48 (27%), lobar 9/48 (19%), caudate 3/48 (6%), and miscellaneous locations 3/48 (6%). Outcome in putaminal hemorrhages was highly correlated with the total (P+V) and P blood volumes, whereas the V blood was less important. For thalamic hemorrhages, outcome correlated more highly with the V and P+V volumes than with the P portion. Outcome for ail hemorrhages was significantly correlated, in descending order of importance, with the severity of the initial neurologic deficit, P+V blood, hydrocephalus, the number of ventricles containing blood, P, V, and blood in the 4th ventricle. In general patients with more than 20 cc of V blood did poorly. Although hydrocephalus was associated with poor outcome, ventricular drainage did not benefit 8 of 9 patients.

One aneurysm of the basilar artery and three large, paraclinoid aneurysms of the internal carotid artery (ICA) were treated with the aid of intraoperative temporary balloon occlusion of the vessel. Optimal clip placement was confirmed using intraoperative angiography. This technique provided excellent proximal vascular control and for the large aneurysms of the paraclinoid ICA obviated the need for surgical exposure of the ICA in the neck. We think this is a useful adjunct in the surgical management of aneurysms of both the basilar artery and proximal ICA.

Extracranial internal carotid artery occlusive disease usually produces stroke in the middle cerebral artery territory or the border zone between the middle and anterior cerebral arteries. It is unusual for occipital infarction in the posterior cerebral artery territory to be caused by internal carotid artery disease despite the fact that the posterior cerebral artery may arise directly from the internal carotid artery as an anatomic variation. We describe a patient with a fetal posterior cerebral artery originating from the internal carotid artery, and the initial manifestation of his extracranial internal carotid artery occlusive disease was hemianopsia from occipital infarction.

We studied seven patients with brainstem infarction and large fusiform vertebrobasilar (VB) aneurysms to clarify the clinical, radiologic, and pathologic features. All presented with pontine infarcts; one also had a cerebellar infarct. VB TIAs preceded brainstem infarction in four patients. Angiography and CT documented VB fusiform aneurysmal dilatation. Four had intraluminal thrombi and one had severe basilar artery stenosis. Two distinct clinical pictures emerged: unilateral pontine infarcts with favorable outcome, presumably related to obstruction of a pontine penetrating artery at its origin from the posterior wall of the aneurysmal basilar artery, and major fatal bilateral pontine infarcts from basilar artery occlusion. Two patients came to autopsy. One had thrombus in the dilated basilar artery and a posterior cerebral artery branch embolus with hemorrhagic occipital infarction; the other had basilar artery thrombus with aneurysmal rupture and subarachnoid hemorrhage. Fusiform VB aneurysms caused brainstem stroke by intraluminal thrombus, local embolism, atherostenosis, and obstruction of paramedian penetrating arteries. Subarachnoid hemorrhage is an uncommon complication.

Basilar artery territory stroke may result from embolism arising from the site of vertebral artery occlusion. This stroke mechanism (local embolism) has been well documented in the middle cerebral artery territory from extracranial internal carotid artery disease but not fully appreciated in the vertebral basilar circulation. We report two patients whose clinical presentation indicated major basilar artery territory infarction documented by angiography to be the result of vertebral artery occlusion and artery-to-artery embolism. Vertebral artery occlusion has often been associated with a benign course, but under certain circumstances embolism to the basilar artery may complicate the outcome.

We describe four patients and review prior reports to clarify the clinical, radiographic, and pathologic findings of intracranial vertebral artery (VA) dissection. A 43-year-old man and a 33-year-old woman had chronic bilateral VA dissecting aneurysms. The man had multiple episodes of subarachnoid hemorrhage (SAH) and necropsy showed multiple dissections and defects in the internal elastica. The woman had many brainstem TIAs and strokes during 3 years. Two other patients had SAH and unilateral dissections. Intracranial VA dissection causes four overlapping syndromes: (1) brainstem infarcts are usually due to subintimal dissection extending into the basilar artery, affect younger patients, and often are single fatal events; (2) SAH is due to subadventitial or transmural dissection; (3) aneurysms cause mass effect on the brainstem and lower cranial nerves; and (4) chronic dissections due to connective tissue defects cause extensive bilateral aneurysms and repeated TIAs, small strokes, and SAH.

A new catheter system was used in ten patients (16 infusions) for infusion of chemotherapeutic agents to the sites of malignant gliomas. Thirteen infusions to the supraophthalmic region were successful, as were three infusions to the posterior cerebral region. There were no complications after the infusions. A neurologic complication occurred in one patient in whom two successful supraophthalmic infusions were previously carried out. In this patient the guide wire separated during catheter placement into the posterior cerebral artery.

We analyzed the clinical features of symptomatic posterior cerebral artery (PCA) stenosis in 6 patients selected from 15 patients with angiographically documented PCA atherostenosis occurring during a 7‐year period. Transient ischemic attacks (TIAs) were the major presentation in 5 patients. A homonymous visual field defect was present in 2 patients. TIA symptoms were predominantly visual or sensory, or both. The most common visual symptom was difficulty seeing to one side. One patient saw flashing lights. Sensory spells were always paresthetic, usually involving the arm and hand and occasionally the face and leg. Three patients had visual and sensory spells together. Two patients with a visual field defect had calcarine infarcts found by computed tomography. All patients were treated with warfarin. During followup (4 months to 4 years), no patient had a new stroke in the PCA territory, and only one continued to have TIAs. PCA atherostenosis is rarer than PCA embolic occlusion. In contrast to those with PCA embolism, our patients with PCA atherostenosis had more TIAs and fewer infarcts. The clinical features of PCA stenosis—preponderance of visual and sensory TIAs‐distinguish this vascular lesion from stenosis of the middle cerebral artery.

We report the clinical features and prognosis in nine patients with angiographically documented basilar artery stenosis of the middle and distal segments. Six patients had transient ischemic attacks (TIAs), and in two this was their only clinical manifestation. The TIAs in four patients included two or more of the following symptoms: dizziness, diplopia, perioral numbness, dysphagia, weakness, or loss of consciousness. Two other patients had isolated symptoms of transient dizziness and unilateral weakness. Seven patients had posterior circulation strokes, preceded by TIAs in four. Basilar artery occlusive disease can affect any segment of the artery. The short-term prognosis of middle and distal basilar artery stenosis was good especially when patients were treated with warfarin or platelet antiaggregants.

To clarify the clinical features and mechanism of infarction in the posterior cerebral artery territory, we investigated 35 consecutive patients who presented with homonymous visual field defects and occipital infarction documented by computed tomography. Cerebral angiographic findings in 23 patients, and the clinical features of rare transient ischemic attacks and maximal deficit occurring at stroke onset, were consistent with embolism of the posterior cerebral artery. Visual field defects were the only neurological abnormality in 17 patients; the remainder had additional findings. Three patients had a major brainstem stroke. Stroke in the posterior cerebral artery territory was found in a heterogeneous group of patients, although embolism was the most common stroke mechanism. Several distinct patient groups were identified: cardiac source embolism (10 patients), vertebrobasilar atheroma with local embolism (6), migraine (5), systemic illness with presumed coagulopathy (3), and "unknown source embolism" after negative cardiac investigation (11 patients). During follow-up, 26 patients had no further neurological events (the majority on anticoagulation or antiplatelet treatment), 3 suffered new strokes, and 6 died.