The arterial patterns associated with internal carotid disease and cerebral infarcts

In 20 necropsies with 15 stenosed and 17 thrombotic occluded internal carotid arteries there were 46 cerebral infarcts larger than 1 cm diameter. Using portmortem arteriographic and pathological techniques the patterns of the neck and brain artery systems were correlated with the situation and extent of the brain infarcts. Massive infarcts involving two major cerebral artery territories were associated with distal internal carotid artery occlusion and grossly ineffective cervical and circle of Willis anastomoses. Isolated middle cerebral artery territory infarcts were associated with internal carotid occlusion or stenosis and impairment of the circle of Willis anastomoses, perhaps with middle cerebral artery stenosis. The pattern of adequate size arteries determined if these infarcts were total, deep central, anterior, medium or posterior partial territory infarcts. Boundary zone infarcts were associated with internal carotid artery disease and limitation of anterior or posterior circle of Willis anastomoses. These limitations determined which boundary zones were affected. Isolated anterior cerebral artery territory infarcts were associated with bilateral internal carotid disease and an anterior cerebral artery stenosis or small caliber anterior communicating artery. Isolated posterior cerebral artery territory infarcts were associated with internal carotid disease and a direct impairment of the ipsilateral posterior cerebral artery capability.     

单侧颈动脉闭塞脑梗死和侧支代偿情况分析

目的 通过计算机断层扫描（computer tomography,CT）和磁共振成像（magnetic resonance imaging,MRI）研究闭塞颈动脉同侧半球的梗死情况,分析不同侧支的代偿能力,增进我们对梗死机制的理解。方法 颈部血管彩色超声证实的43例单侧颈动脉闭塞患者,将颈动脉闭塞同侧的大脑半球分为大脑中动脉皮层区域、前皮层分水岭区域、后皮层分水岭区域、内分水岭区域、穿支动脉供血区域,比较各个解剖区域发生梗死情况,并分析侧支代偿种类和不同解剖部位梗死的关系。结果 颈动脉闭塞时,内分水岭区发生梗死最多见19例（44.2%）,8例前皮层分水岭梗死有6例伴有内分水岭区梗死。后交通动脉（posterior communicating artery,PCoA）出现是减少内分水岭区梗死的保护性因素[比值比（odd ratio,OR）为0.226,95%可信区间（confidence interval,CI）在0.058～0.833间,P =0.027]。结论 颈动脉闭塞时,内分水岭区发生梗死最多见,提示内分水岭区是对血流下降最敏感的区域。PCoA开放能够减少内分水岭区梗死。     

Neurovascular territory involved in different etiological subtypes of ischemic stroke in the Perugia Stroke Registry

We studied the correlation between the potential causes of stroke (TOAST etiological groups) and the involvement of different vascular territories seen on computed tomography (CT) scans in patients with ischemic stroke. Information from consecutive patients with a first-ever stroke have been prospectively coded and entered into a computerized data bank (Perugia Stroke Registry). A population of 1,719 patients were evaluated: 1,284 patients (74.7%) had ischemic stroke. Large artery disease was the main cause of entire middle cerebral artery (MCA) territory infarcts (40.9%), superficial MCA territory infarcts (35.7%), and watershed infarcts (68.2%). The highest presence of emboligenic heart disease was found in the entire MCA territory infarcts (28.8%) or superficial (29.4%) supratentorial infarcts and in cerebellar infarcts (36.8%). Small artery disease was the most common presumed cause of deep MCA infarcts (75.0%) and posterior cerebral artery (PCA) territory infarcts (52.1%). In conclusion: stroke location could depend on its etiology. Lacunar infarcts are the most prevalent (36.7%), being mostly localized in the deep MCA territory; large artery disease includes more than two-thirds of watershed infarcts; the most prevalent territories involved in cardioembolic stroke are the entire MCA and posterior fossa.     

Site and pathogenesis of infarcts associated with carotid endarterectomy

We analyzed perioperative strokes in 658 carotid endarterectomies with the purpose of explaining the pathogenesis from the morphologic aspect of the infarct on cerebral computed tomograms. All endarterectomies were performed with continuous electroencephalographic monitoring. Of the 42 ischemic strokes (6.4% of all endarterectomies), 34 could be studied. Seven infarcts were hemodynamically induced (five watershed infarcts, two patients with bilateral ischemia); all seven occurred during surgery. Twenty-three of the remaining 27 infarcts were within the territory of the middle cerebral artery (20) or anterior cerebral artery (three) and were probably of thromboembolic origin; 13 of these 23 occurred during surgery (57%). If intraoperative stroke was heralded by permanent electroencephalographic changes, these were not related to the moment of cross-clamping. In four patients the computed tomogram was normal. We believe these facts favor the hypothesis that thromboembolism is the most important factor in the pathogenesis of perioperative stroke associated with carotid endarterectomy under conditions of optimal cerebral monitoring.     

Centrum ovale infarcts: subcortical infarction in the superficial territory of the middle cerebral artery.

The centrum ovale, which contains the core of the hemispheric white matter, receives its blood supply from the superficial (pial) middle cerebral artery (MCA) system through perforating medullary branches (MBs), which course toward the lateral ventricles. Though vascular changes in the centrum ovale have been emphasized in dementia, stroke from acute infarction in the centrum ovale is less well documented. We studied 36 patients with infarct limited to MB territory, without involvement of the lenticulostriate territory. Ten patients had a large infarct, associated with severe disease of the ipsilateral carotid artery and with neurologic-neuropsychological impairment not different from that of large MCA infarcts. In 26 patients, the infarct was small and round or ovoid, and was associated with hypertension or diabetes and with "lacunar syndromes," usually of progressive onset. These findings show that two forms of centrum ovale infarcts can be delineated according to infarct size and shape, clinical picture, risk factors, and associated vascular disease. We propose to classify subcortical infarcts in the carotid system into four main territory groups: (1) deep perforator territory (from the MCA trunk, carotid siphon, anterior choroidal artery, anterior cerebral artery trunk, Heubner's artery, and posterior communicating artery); (2) perforating MB territory (from the superficial MCA branches); (3) junctional (territory between 1 and 2); and (4) combined territories.     

Mechanisms of single and multiple borderzone infarct: transcranial Doppler ultrasound/magnetic resonance imaging correlates

BACKGROUND AND PURPOSE: Hemodynamic patterns after borderzone (BZ) infarction are variable and dynamic. However, stroke mechanisms in different types of BZ infarctions have not been systematically studied by magnetic resonance angiography (MRA) and transcranial Doppler ultrasonography (TCD). METHODS: Forty-nine patients who experienced a stroke limited to the territory of either the superficial or internal borderzone proved on MRI included in our registry, corresponding to 4% of 1,200 patients with ischemic stroke, were studied. All these patients underwent MRA, extracranial Doppler ultrasonography, TCD and other investigations from the standard protocol of our registry. Twenty of them (41%) had a posterior BZ infarct, 14 (29%) an anterior BZ infarct, 10 (20%) a subcortical BZ infarct and 5 (10%) bilateral BZ infarcts. RESULTS: Unilateral internal carotid artery (ICA) tight stenosis or occlusion ipsilateral to the lesion was present in 14 patients (70%) with a posterior BZ infarct, in 72% of those with an anterior BZ infarct, in 80% of those with a subcortical BZ infarct and in 80% of those with bilateral BZ infarcts. TCD showed cross-filling of the middle cerebral artery via the anterior communicating artery in 5 patients (25%) with a posterior BZ infarct and 10% had an increased mean flow velocity (MFV) in the ipsilateral P1 posterior cerebral artery (PCA). In patients with an anterior BZ infarct, 3 (23%) had an MFV increase in the contralateral A1 anterior cerebral artery (ACA), and 2 (15%) had a higher MFV in the ipsilateral PCA. An elevated velocity at midline depths with reversed A1 ACA flow direction was seen in 2 patients (20%) with a subcortical infarct, and 1 patient (10%) had an MFV increase in the ipsilateral P1 PCA. Left ventricular systolic dysfunction (ejection fraction <40%) was present in 50% of patients with a posterior BZ infarct, in 36% of those with an anterior BZ infarct, in 20% of those with a subcortical BZ infarct and bilateral BZ infarcts each. CONCLUSION: The association of severe ICA stenosis or occlusion with cardiopathies and left ventricular dysfunction may play a critical role in those with BZ infarcts having inadequate collateral supply, while a cardioembolism or acute ICA dissection may also cause BZ infarction due to the rapidity of the occlusive process and the inability of the cerebral vasculature to recruit collateral pathways quickly enough.     

Clinical manifestations of cerebrovascular hypoplasias in childhood

The aim of the study was to analyze cerebrovascular hypoplasia in childhood and its clinical manifestations in a clinical population of 205 children aged 3 to 14 years. Cerebrovascular hypoplasias were diagnosed using angiography (n=63), magnetic resonance angiography, and transcranial Doppler ultrasonography. Hypoplasias were localized in the internal carotid artery in 41.9% of patients, in the middle cerebral artery in 54.1%, the anterior cerebral artery in 1.0%, and in the vertebro-basilar system in 3.0%. Clinical manifestations included transient ischemic attacks (21% of patients), cerebral infarcts (17%), progressive unilateral cerebral hemisphere atrophy (1.0%), focal and secondary generalized epileptic seizures (56.1%), and migraine-like headache (4.9%). Hypoplasias of the internal carotid artery and middle cerebral artery manifested as focal and secondary generalized epileptic seizures, transient ischemic attacks, cerebral infarcts, migraine-like headache, and progressive unilateral cerebral hemisphere atrophy, in descending order of frequency. Hypoplasias in the anterior cerebral artery or the basilar artery caused cerebral infarcts, and hypoplasias in the vertebral arteries caused transient ischemic attacks. This article discusses the pathophysiology of ischemia in the territory of the hypoplastic cerebral artery in childhood, as well as possibilities for noninvasive neuroimaging for diagnosis of cerebrovascular hypoplasias.     

Clinical and radiologic features of lacunar versus nonlacunar minor stroke

We determined the angiographic presence of extracerebral and intracerebral arterial disease in 122 patients with minor stroke within the carotid territory; we excluded patients with a recognized cardiac source of emboli. Based on clinical features and computed tomographic findings, patients were classified as having lacunar infarcts (n = 61), nonlacunar infarcts (n = 53), and infarcts of indeterminate type (n = 8). Severe carotid bifurcation disease (greater than or equal to 50% stenosis or occlusion) was significantly more common in nonlacunar than in lacunar infarcts, on both the ipsilateral (p less than 0.001) and the contralateral (p less than 0.01) sides; 79% of the patients with nonlacunar infarcts had severe carotid bifurcation and/or middle cerebral artery disease on the ipsilateral side compared with 3.3% of the patients with lacunar infarcts. Our data underscore the need for classification of patients by the underlying mechanisms in future studies of treatment of ischemic stroke.     

Double infarction in one cerebral hemisphere

Thirty-two patients whose first stroke was due to double infarct in one cerebral hemisphere were identified among 1,911 consecutive patients from the Lausanne Stroke Registry. The double infarct involved territories of the superficial middle cerebral artery, superficial posterior cerebral artery, lenticulostriate, anterior choroidal artery, or borderzone. The most common combination involved territories of the anterior middle cerebral artery plus the posterior middle cerebral artery. In the patients with the double infarct, the prevalence of potential cardiac sources of embolism (19%) was similar to that found in the registry in general, but the double infarct was closely associated with tight (greater than or equal to 90% of the lumen diameter) stenosis or occlusion (75%) of the internal carotid artery. The most common neurological picture mimicked large infarction in the middle cerebral artery territory, but nearly half of the patients with double infarct in one cerebral hemisphere had a specific clinical syndrome, which was not found in the 1,879 remaining patients from the registry, including hemianopia-hemiplegia (in 6), acute conduction aphasia-hemiparesis (in 2), and acute transcortical mixed aphasia (in 6), in relation to characteristic combinations of infarcts. These unique clinical and etiological correlates warrant the recognition of double infarct in one cerebral hemisphere from other acute ischemic strokes.     

Risk of stroke during coronary artery bypass graft surgery in patients with internal carotid artery disease documented by angiography

We retrospectively identified 144 patients who underwent coronary artery bypass graft (CABG) surgery in the presence of angiographically documented greater than or equal to 50% internal carotid stenosis or occlusion. Of these, 115 patients had bilateral carotid lesions and received combined operations involving carotid endarterectomy on only one side. The remaining 29 patients, including 11 with bilateral carotid lesions, underwent coronary bypass alone. Nine cerebral infarcts occurred (6%), but only three strokes (2%) were appropriate to the cerebral hemisphere ipsilateral to unoperated carotid stenosis. There was one stroke (3%) among the 29 patients who did not undergo combined procedures. In the group of 115 patients with bilateral carotid disease who received unilateral combined carotid endarterectomy there were 8 perioperative strokes (7%), of which 6 were ipsilateral to the endarterectomy. Asymptomatic unilateral less than 90% ICA stenosis or ICA occlusion does not increase stroke risk during CABG surgery.     

Transesophageal echocardiographic findings in patients with anterior and posterior circulation infarcts

Objectives - The aim of this study was to assess the role of transesophageal echocardiography in detecting the source of cerebral embolism in ischemic stroke patients and to evaluate the difference in occurrence of heart abnormalities in anterior and posterior circulation infarcts. Material and Methods - The study group included 104 patients, 51 males and 53 females with ischemic stroke without significant atherosclerosis in the carotid arteries. Age of the patients ranged from 14 to 82 years (mean 55). The clinical picture of stroke suggested the embolic etiology, 34 of them had atrial fibrillation. Transthoracic and transesophageal echocardiography were performed in all patients. All patients were separated as anterior or posterior circulation infarcts. The control group consisted of 100 patients aged from 14 to 73 years (mean 53) without stroke history. Results - Transesophageal echocardiography (TEE) examination revealed left atrial thrombus in 12%, left atrial spontaneous contrast in 16%, interatrial communication in 31%, mitral valve prolapse in 20%, atrial septal aneurysm in 14%, ventricular thrombus in 6% and aortic atheromas of 5 mm or more in size in 7% of stroke patients. In the control group left atrial spontaneous contrast was found in 10%, interatrial communication in 17%, mitral valve prolapse in 4%, atrial septal aneurysm in 8%, neither atrial nor ventricular thrombi were found. At least one abnormal TEE finding was present in 70 (67%) of stroke patients. Abnormal TEE findings were more often seen in patients with anterior circulation infarct than in those with posterior circulation infarcts, although the difference was not statistically significant. Left atrial thrombus and mitral valve prolapse occurred statistically significantly more often in stroke patients than in the control group. Conclusions - Echocardiographic examination is often abnormal in patients with ischemic stroke. The study did not reveal the statistically significant difference in the prevalence of abnormal transesophageal echocardiography findings between patients with anterior and posterior circulation infarcts.     

Multiple acute infarcts in the posterior circulation.

OBJECTIVE--to evaluate clinical, radiological, and prognostic features of patients with multiple acute infarcts in remote arterial territories of the posterior circulation. DESIGN--Data analysis from a prospective acute stroke registry in a community based primary care centre using a standard protocol including MRI and MRA. RESULTS--In three and a half years, 27 of the 236 patients (11%) with posterior circulation stroke had multiple acute infarcts in the posterior circulation as shown by gadolinium enhancement on MRI. Eighteen patients had multiple infratentorial and supratentorial infarcts including the cerebellum and posterior cerebral artery territory, with coexisting brainstem involvement in seven patients. Fourteen patients had a rostral basilar artery syndrome and cerebellar signs; four patients had a visual field defect with cerebellar signs. Causes were vertebral (six) or basilar (four) artery atheromatosis, and cardioembolism (four). Seven patients had multiple acute infarcts in the posterior circulation of the cerebellum and lower brainstem. Brainstem and cerebellar signs were found in most patients (five); aetiologies were small vessel disease (four), cardioembolism (one), and vertebral artery dissection (one). Two patients with large artery atheromatosis had multiple acute infarcts in the posterior circulation in the brainstem and posterior cerebral artery territory. One month after stroke more than 25% of the patients were dependent or had died. There was no difference in the outcome between the three groups, and recovery was linked to the size of infarcts rather than to a high number of infarcts. CONCLUSIONS--multiple acute infarcts in the posterior circulation usually involve the cerebellum. Simultaneous brainstem and posterior cerebral artery territory infarcts sparing the cerebellum are uncommon. They can be suspected clinically before neuroimaging, mainly when supratentorial and infratentorial infarcts coexist. This may be important, because different patterns of infarction are associated with different causes of stroke.     

Mechanisms of acute cerebral infarctions in patients with middle cerebral artery stenosis: a diffusion-weighted imaging and microemboli monitoring study

Although most therapeutic efforts and experimental stroke models focus on the concept of complete occlusion of the middle cerebral artery as a result of embolism from the carotid artery or cardiac chamber, relatively little is known about the stroke mechanism of intrinsic middle cerebral artery stenosis. Differences in stroke pathophysiology may require different strategies for prevention and treatment. We prospectively studied 30 consecutive acute ischemic stroke patients with middle cerebral artery stenosis detected by transcranial Doppler and magnetic resonance angiography. Patients underwent microembolic signal monitoring by transcranial Doppler and diffusion-weighted magnetic resonance imaging. Characteristics of acute infarct on diffusion-weighted magnetic resonance imaging were categorized according to the number (single or multiple infarcts) and the pattern of cerebral infarcts (cortical, border zone, or perforating artery territory infarcts). The data of microembolic signals and diffusion-weighted magnetic resonance imaging were assessed blindly and independently by separate observers. Diffusion-weighted magnetic resonance imaging showed that 15 patients (50%) had single acute cerebral infarcts and 15 patients had multiple acute cerebral infarcts. Among patients with multiple acute infarcts, unilateral, deep, chainlike border zone infarcts were the most common pattern (11 patients, 73%), and for single infarcts, penetrating artery infarcts were the most common (10 patients, 67%). Microembolic signals were detected in 10 patients (33%). The median number of microembolic signals per 30 minutes was 15 (range, 3-102). Microembolic signals were found in 9 patients with multiple infarcts and in 1 patient with a single infarct (p = 0.002, chi(2)). The number of microembolic signals predicted the number of acute infarcts on diffusion-weighted magnetic resonance imaging (linear regression, adjusted R(2) =0.475, p < 0.001). Common stroke mechanisms in patients with middle cerebral artery stenosis are the occlusion of a single penetrating artery to produce a small subcortical lacuna-like infarct and an artery-to-artery embolism with impaired clearance of emboli that produces multiple small cerebral infarcts, especially along the border zone region.     

Should computed tomography appearance of lacunar stroke influence patient management?

Patients with a lacunar stroke syndrome may have cortical infarcts on brain imaging rather than lacunar infarcts, and patients with the clinical features of a small cortical stroke (partial anterior circulation syndrome, PACS) may have lacunar infarcts on imaging. The aim was to compare risk factors and outcome in lacunar syndrome (LACS) with cortical infarct, LACS with lacunar infarct, PACS with cortical infarct, and PACS with lacunar infarct to determine whether the clinical syndrome should be modified according to brain imaging. As part of a hospital stroke registry, patients with first ever stroke from 1990 to 1998 were assessed by a stroke physician who assigned a clinical classification using clinical features only. A neuroradiologist classified recent clinically relevant infarcts on brain imaging as cortical, posterior cerebral artery territory or lacunar. Of 1772 first ever strokes, there were 637 patients with PACS and 377 patients with LACS who had CT or MRI. Recent infarcts were seen in 395 PACS and 180 LACS. Atrial fibrillation was more common in PACS with cortical than lacunar infarcts (OR 2.3, 95% confidence interval (95% CI) 0.9-5.5), and in LACS with cortical than lacunar infarcts (OR 3.9, 1.2-12). Severe ipsilateral carotid stenosis or occlusion was more common in PACS with cortical than lacunar infarcts (OR 3.5, 1.3-9.5); and in LACS with cortical than lacunar infarcts (OR 3.7, 1.1-12). In conclusion, patients with cortical infarcts are more likely to have severe ipsilateral carotid stenosis or atrial fibrillation than those with lacunar infarcts irrespective of the presenting clinical syndrome. Brain imaging should modify the clinical classification and influence patient investigation.     

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.     

Capsular hypesthetic ataxic hemiparesis

Twenty-three patients with hypesthetic ataxic hemiparesis underwent computed tomography or magnetic resonance imaging. Twenty-two patients had infarcts of lacunar or slightly larger size in the contralateral posterior limb of the internal capsule. In 15 patients the infarct extended superiorly into the adjacent paraventricular region, and in seven it extended into the lateral thalmus. In eight patients the infarct was limited to the posterior limb of the internal capsule, and in only two patients was an ipsilateral to capsular pontine lacune found. Despite a location similar to that of pure motor and pure sensory lacunar stroke, hypesthetic ataxic hemiparesis correlates with larger infarcts, most often located in the posterior medial superior territory of the anterior choroidal artery. Some infarcts appeared to be localized immediately posterolateral to this region, in the posterior cerebral artery territory. The presence and extent of infarction is better detected by the addition of magnetic resonance imaging to computed tomography.     

Significance of acute multiple brain infarction on diffusion-weighted imaging

BACKGROUND AND PURPOSE: Diffusion-weighted imaging (DWI) is superior to conventional MRI in identification of small new ischemic lesions and discrimination of recent infarcts from old ones. Thus, this technique is useful in the detection of acute multiple brain infarcts (AMBI). We sought to determine the frequency and the topographical and etiologic patterns of AMBI detected on DWI. METHODS: We studied 329 consecutive ischemic stroke patients who underwent DWI and MRI/MR angiography within 4 days of stroke onset. AMBI was defined as noncontiguous high signal intensities on DWI in >1 vascular territory. Stroke mechanism was determined according to the criteria of the Trial of Org 10172 in Acute Stroke Treatment (TOAST). RESULTS: We detected AMBI in 95 patients (28.9%). AMBI in anterior circulation was found in 62 cases: in 1 hemisphere in 42 (group A) and in bilateral hemispheres in 20 (group B). Twenty-two patients had AMBI in the posterior circulation (group C) and 11 in both anterior and posterior circulations (group D). The most frequent cause of stroke was large-artery atherosclerosis in groups A (33/42), B (9/20), and C (15/22) (P=0.02) and cardioembolism in group D (6/11) (P=0.02). Elevated fibrinogen or hematocrit was significantly associated with group B (P=0.01). In 9 patients in groups B and D, anatomic variations of anterior or posterior cerebral arteries or patent posterior communicating artery contributed to AMBI. CONCLUSIONS: Different topographical patterns of AMBI are associated with different vascular pathologies and stroke mechanisms. Hemorheologic abnormality or vascular anatomic variations may be contributing factors in the pathogenesis of AMBI in bilateral cerebral hemispheres or in both anterior and posterior circulations.     

Stroke with internal carotid artery stenosis

BACKGROUND: Stroke patterns in patients with different degrees of carotid stenosis have not been systematically studied. OBJECTIVE: To determine first-ever stroke subtypes in nonselected patients with extracranial internal carotid artery (ICA) stenosis, based on a primary care hospital stroke registry. METHODS: One hundred seventy-three patients who experienced their first-ever stroke and who had 50% or greater (North American Symptomatic Carotid Endarterectomy Trial method) ipsilateral extracranial ICA stenosis, corresponding to 6.5% of 2649 patients with anterior circulation stroke included in the Lausanne Stroke Registry, were studied. All these patients underwent Doppler ultrasonography, carotid angiography (conventional or magnetic resonance angiography), neuroimaging (computed tomography or magnetic resonance imaging), and other investigations from the standard protocol of the Lausanne Stroke Registry. RESULTS: We found the following types of infarct in the middle cerebral artery territory: anterior pial in 54 (31%) of the patients; subcortical, 34 (20%); posterior pial, 32 (19%); large hemispheral, 20 (12%); and border zone, 17 (10%). There were multiple pial in 14 (8%) and multiple deep infarcts in 2 (1%) of the patients. Moderate (50%-69%) ICA stenosis was significantly associated with large hemispheral infarcts and a normal contralateral ICA (P =.04 and P =.02, respectively). Seventy percent to 89% of ICA stenosis was associated with prior transient ischemic attacks (P =.02). After adjusting for cardioembolism, border zone infarcts showed a strong trend to appear mostly in patients with 90% to 99% ICA stenosis (P =.06). CONCLUSIONS: The association of a large hemispheral infarct with moderate ICA stenosis suggests a large embolism and/or an inadequate collateral supply. While an embolism may also contribute, the association of border zone infarcts with 90% to 99% ICA stenosis emphasizes the significance of hemodynamic disturbance in the pathogenesis of these types of infarct.     

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.     

Thalamic infarcts in young adults: relationship between clinical-topographic features and pathogenesis.

BACKGROUND: Most reports on thalamic infarcts have focused on clinicoanatomical correlations while the mechanisms of stroke have rarely been investigated. Moreover, most series have included mainly elderly stroke patients, whereas scarce information is available about the etiology of thalamic infarcts in the young. OBJECTIVE: To investigate the mechanisms of thalamic infarcts according to vascular territory in a series of young adults. METHODS: A sample of 24 consecutive patients with thalamic infarcts were found in an unselected series of 129 patients with cerebral infarction aged 18-45 years. Diagnostic investigation included computed tomography and magnetic resonance imaging scans, ultrasonic scanning of the extracranial and intracranial arteries, conventional angiography and magnetic resonance angiography, transthoracic and transesophageal echocardiography and extensive thrombophilic studies. The affected vascular territory within the thalamus was determined using standard templates. RESULTS: Thalamic infarcts constituted almost one fifth of the ischemic strokes in our series. Ten patients (42%) had infarct in the territory of the thalamogeniculate pedicle (group 1), 10 (42%) in the territory of the paramedian thalamosubthalamic artery (group 2) and 3 (12%) in the territory of the tuberothalamic artery (group 3). In 1 patient (4%), the lesion involved more than one vascular thalamic territory. A significant association between cardioembolism and paramedian infarcts was found when comparing the mechanisms of stroke of group 2 with those of the group including infarcts in other thalamic territories (p = 0.002) and with those of group 1 (p = 0.02). CONCLUSIONS: Our findings provide information about the epidemiology of thalamic infarcts in young adults and point to a differential association between the distribution of infarcts in specific vascular territories and the mechanism of stroke.