Among 4200 consecutive patients admitted to three hospitals with acute ischemic stroke, we found only 11 patients in whom magnetic resonance imaging (MRI) had proved that they had medial medullary infarction (MMI). In our centers, patients with MMI were less than 1% of those with vertebrobasilar stroke. The infarcts documented by MRI were unilateral in 10 patients and bilateral in one. On clinico-topographical analysis there were four clinical patterns: (1) Classical Dejerine's syndrome was the most frequent, consisting of contralateral hemiparesis, lemniscal sensory loss and ipsilateral lingual palsy in 7 of the eleven patients. (2) Pure hemiparesis was present in 2 patients; (3) Sensorimotor stroke was present in 1 patient with contralateral hemiparesis, hypesthesia and mild decrease in pain sensation without lingual palsy; (4) Bilateral MMI syndrome in 1 patient, accompanied by tetraparesis, bilateral loss of deep sensation, dysphagia, dysphonia and anarthria. Presumed causes of MMI were intrinsic branch penetrator artery disease with concomitant vertebral artery stenosis in 6 of the 11 patients, vertebral artery occlusion in 2, dolichoectatic vertebrobasilar arteries in 2, a source of cardiac embolism in 1. Prognosis at 3 months was favorable in 8 patients, but the patient with bilateral MMI syndrome had persisting motor deficit causing limitation of daily activities, and 2 died from systemic causes. The classical triad of acute MMI facilitates the diagnosis, although the recognition of this syndrome in patients with incomplete manifestations can be difficult and occurs more frequently than commonly thought. Moreover, vertebral artery atherosclerosis and branch atheromatous disease of the penetrating arteries are the main causes of medullary infarction.

To evaluate and review the clinical spectrum of anterior cerebral artery (ACA) territory infarction, we studied 48 consecutive patients who admitted to our stroke unit over a 6-year period. We performed magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) in all patients, and diffusion magnetic resonance imaging (DWI) in 21. In our stroke registry, patients with ACA infarction represented 1.3% of 3705 patients with ischemic stroke. The main risk factors of ACA infarcts was hypertension in 58% of patients, diabetes mellitus in 29%, hypercholesterolemia in 25%, cigarette smoking in 19%, atrial fibrillation in 19%, and myocardial infarct in 6%. Presumed causes of ACA infarct were large-artery disease and cardioembolism in 13 patients each, small-artery disease (SAD) in the territory of Heubner's artery in two and atherosclerosis of large-arteries (<50% stenosis) in 16. On clinico-radiologic analysis there were three main clinical patterns depending on lesion side; left-side infarction (30 patients) consisting of mutism, transcortical motor aphasia, and hemiparesis with lower limb predominance; right side infarction (16 patients) accompanied by acute confusional state, motor hemineglect and hemiparesis; bilateral infarction (two patients) presented with akinetic mutism, severe sphincter dysfunction, and dependent functional outcome. Our findings suggest that clinical and etiologic spectrum of ACA infarction may present similar features as that of middle cerebral artery infarction, but frontal dysfunctions and callosal syndromes can help to make a clinical differential diagnosis. Moreover, at the early phase of stroke, DWI is useful imaging method to locate and delineate the boundary of lesion in the territory of ACA.

Posterior cerebral artery (PCA) territory infarction is not uncommon. Published series were concentrated either on isolated deep PCA territory infarcts or on incomplete calcarine artery territory infarcts. Although, correlations between clinical symptoms, causes of stroke and outcome at 6-months in patients with superficial PCA territory stroke are less well known. We sought prospectively stroke causes, infarct topography, and clinical findings of 137 patients with superficial PCA territory infarcts with or without mesencephalic/thalamic involvement, representing 11% of patients with posterior circulation ischemic stroke in our Stroke Registry. We analyzed patients by subdividing into three subgroups; (1). cortical infarct (CI) group; (2). cortical and deep infarcts (CDI) (thalamic and/or mesencephalic involvement) group; (3). bilateral infarcts (BI) group. We studied the outcomes of patients at 6-month regarding clinical findings, risk factors and vascular mechanisms by means of comprehensive vascular and cardiac studies. Seventy-one patients (52%) had cortical (CI) PCA infarct, 52 patients (38%) had CDI, and 14 patients (10%) had bilateral PCA infarct (BI). In the CDI group, unilateral thalamus was involved in 38 patients (73%) and unilateral mesencephalic involvement was present in 27% of patients. The presumed causes of infarction were intrinsic PCA disease in 33 patients (26%), proximal large-artery disease (PLAD) in 33 (24%), cardioembolism in 23 (17%), co-existence of PLAD and cardioembolism in 7 (5%), vertebral or basilar artery dissection in 8 (6%), and coagulopathy in 2. The death rate was 7% in our series and stroke recurrence was 16% during 6-month follow-up period. Features of the stroke that was associated with significant increased risk of poor outcome included, consciousness disturbances at stroke onset (RR, 66.6; 95% CI, 8.6-515.5), mesencephalic and/or thalamic involvement (RR, 3.79; 95% CI, 1.49-9.65), PLAD (RR, 2.71; 95% CI, 1.09-6.73), and basilar artery disease (RR, 5.94; 95% CI, 1.73-20.47). The infarct mechanisms in three different types of superficial PCA territory stroke were quite similar, but cardioembolism was found more frequent in those with cortical PCA territory infarction. Although, the cause of stroke could not reliably dictate the infarct topography and clinical features. Visual field defect was the main clinical symptom in all groups, but sensorial, motor and neuropsychological deficits occurred mostly in those with CDI. Outcome is good in general, although patients having PLAD and basilar artery disease had more risk of stroke recurrence and poor outcome rather than those with intrinsic PCA disease.

Background and Purpose-The purposes of this study were to evaluate and review the risk factors and clinical features of patients with posterior circulation stroke involving mesencephalon and neighboring structures and to describe the clinical syndromes according to the mesencephalic arterial territory involved. Methods-We studied all patients with acute posterior circulation stroke involving mesencephalon who were admitted consecutively to our stroke unit over a 6-year period. We selected these patients (3%) from 1296 patients with posterior circulation infarct. Neurological and radiological investigations, including MRI and angiography, were performed in all cases. We classified patients into 4 groups on the basis of MRI findings: (1) isolated mesencephalic infarcts (9 patients); (2) distal territory infarcts (19 patients), including mesencephalon, thalamus, medial temporal and occipital lobes, and cerebellum; (3) middle territory infarcts (12 patients), including the pons and anterior inferior cerebellar artery territory; and (4) proximal territory infarcts (1 patient), including the medulla and posterior inferior cerebellar artery territory. Results-Middle mesencephalon involvement was the most common in all groups, and the anteromedial territory was frequently affected, depending on the direct perforators of basilar artery. In patients with isolated mesencephalic infarct, the clinical picture was dominated by nuclear or fascicular third-nerve palsy and contralateral motor deficits. The distal territory involvement was the most common and associated with consciousness disturbances, gait ataxia, ocular motor disturbances, and visual field deficits. The neurological picture of middle territory infarcts was dominated by consciousness disturbances with dysarthria, horizontal ocular motor disorders, and hemiparesis. Proximal territory involvement was rare and associated with acute unsteadiness, vertigo, dysphagia, dysphonia, tetra-ataxia, and motor weakness. The most common cause of stroke was large-artery disease in 16 patients (39%), cardioembolism in 8 (20%), and small-artery disease with lacunar mesencephalic infarct in 10 (24%). Bilateral mesencephalic infarcts were not uncommon (27%), mainly in patients with multiple and extended infarcts in the posterior circulation, and were associated with poor outcome compared with unilateral infarct. Conclusions-Our study highlights the topographic and clinical heterogeneity of the acute posterior circulation infarcts involving mesencephalon. The variety of the underlying potential causes of stroke requires detailed investigations of the extra and intracranial arteries and the heart.

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