Eddie S. Kwan

Chinese‐white differences in the distribution of occlusive cerebrovascular disease

The distribution of cerebrovascular lesions is affected by race. Blacks and Japanese have more intracranial occlusive cerebrovascular disease, while whites have more extracranial disease. Despite a high incidence of stroke in China, there are few formal studies of the distribution of vascular occlusive disease in Chinese populations. We compared clinical and angiographic features of 24 white and 24 Chinese patients with symptomatic occlusive cerebrovascular disease. In symptomatic vascular territories, whites had more severe (≥50% stenosis) extracranial lesions, while Chinese had more severe intracranial lesions. When we counted mild and severe lesions in a symptomatic territory, whites had more extracranial lesions while Chinese had more intracranial lesions. When we combined symptomatic and asymptomatic temtories, whites had more extracranial lesions, while Chinese had more intracranial lesions. White patients reported more transient ischemic attacks. The distribution of lesions, however, was not explained by differences in incidence of transient ischemia, hypertension, diabetes, hypercholesterol-emia, or ischemic heart disease between the groups. The preponderance of intracranial vascular lesions in Chinese patients is similar to that seen in blacks and Japanese. Racial differences in the occurrence of extracranial and intracranial lesions raise the possibility of a different underlying pathophysiology for the 2 locations.

Dissection of the intracranial vertebral artery

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.

Prognostic significance of ventricular blood in supratentorial hemorrhage A volumetric study

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.

Stroke in patients with fusiform vertebrobasilar aneurysms

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 stenosis Middle and distal segments

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.

Mechanisms and clinical features of posterior border-zone infarcts

Background: Previous studies link posterior border-zone cerebral infarcts between the middle cerebral artery (MCA) and the posterior cerebral artery (PCA) to hemodynamic causes, not embolism. Objective: To study the cause of these infarcts. Methods: We studied 21 patients (unilateral = 18, bilateral = 3) with acute, symptomatic posterior border-zone infarcts shown on CT or MRI to clarify stroke mechanisms. Patients were identified by review of CT and MRI logs and medical records during a 35-month period. An embolic mechanism was assigned when a source of embolism from either the heart, aorta, or parent large artery was present in the absence of intrinsic MCA or PCA disease. A hemodynamic mechanism was assigned when systemic hypotension was present. Results: Among patients with unilateral lesions, 10 were embolic (7 cardiac, 3 carotid), 7 were unknown, and one patient had vasospasm from a ruptured aneurysm. Visual field abnormalities predominated over motor, sensory, and language abnormalities. All patients with bilateral posterior border-zone lesions had perioperative hypotension. Prolonged lethargy, bilateral limb weakness, and cortical blindness were common. Conclusions: Embolism, either cardiac or from the parent carotid artery, is the predominant stroke mechanism in unilateral posterior border-zone infarcts, not distal field perfusion failure. Bilateral posterior border-zone infarcts have a distinctive clinical presentation and are caused by systemic hypotension. Variability of irrigation of the major arteries, passage of emboli to border-zone areas, and decreased clearance of emboli in these areas explain the findings in the patients with unilateral lesions.

Survival with Basilar Artery Occlusion

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 o

Thrombus in Vertebrobasilar Dolichoectatic Artery Treated with Intravenous Urokinase

Background: Vertebrobasilar dolichoectasia is often found in patients with posterior circulation ischemia. Brain ischemia is caused by abnormal flow in the dilated artery and obstruction of paramedian arteries or intraluminal thrombus with artery-to-artery embolism. We report a patient with vertebrobasilar dolichoectasia and luminal thrombus treated with intravenous urokinase who did well but died 2 months later of subarachnoid hemorrhage. Case Description: A 60-year-old man developed right-hand clumsiness, dysarthria and ataxia. Computed tomography showed vertebrobasilar dolichoectasia and thrombus in the basilar artery. Symptoms quickly resolved on heparin but recurred on warfarin and again resolved on heparin. Two weeks later, while on warfarin and aspirin 325 mg, he developed hand numbness, oscillopsia and ataxia. Symptoms again resolved on heparin. Angiography showed severe dolichoectasia of the distal right vertebral artery and basilar artery. A large mural thrombus was detected in the ventral part of the distal basilar artery narrowing the lumen by 50%. He was treated with intravenous urokinase 4,400 units/kg as a bolus followed by 4,400 units/kg/h for 12 h. Repeat angiography showed almost complete recanalization and improved filling of basilar artery branches. He was maintained on warfarin and aspirin 81 mg and had no further ischemic episodes. He died 2 months later of rupture of the basilar artery and subarachnoid hemorrhage. Conclusion: Some patients with thrombosis of vertebrobasilar dolichoectactic arteries continue to have ischemic symptoms despite adequate anticoagulation. Intravenous thrombolysis may be effective in reducing the risk of stroke, but the risk/benefit ratio needs to be assessed in each patient.

Local embolism from vertebral artery occlusion.

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.

Occipital infarction with hemianopsia from carotid occlusive disease.

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.