SUMMARY We studied 8 patients with cerebral infarction in the deep territory of the middle cerebral artery (MCA). All patients had a definite cardiac source of emboli and no known factors for thrombosis. Mixed sensory and motor deficit was found in all but one patient and CT scan showed larger lesions than usually reported in lacunar infarcts. Contrast enhancement was seen in all cases in which CT scan was performed in the second or third week. It is concluded that embolic infarcts in deep cerebral territory of MCA from a cardiac source are more frequent than previously reported. This diagnosis has to be consid ered when CT scan demonstrates a deep cerebral infarct.Stroke Patients and MethodsWe reviewed records of all patients with deep cere bral infarcts confirmed by CT seen during the period 1979-1981. Patients with hypertension (blood pres sure equal or more than 160/95 mm Hg in several determinations) diabetes, blood hematocrit greater than 45%, heavy cigarette smoking or vasculitis were excluded. This review yielded 8 patients without known risk factors for a thrombotic disease and with a definite heart disease with high probability of cerebral embolization. Six patients had rheumatic heart disease and mitral valve stenosis, five of them with atrial fi brillation. The disease was diagnosed by clinical histo ry and auscultation. In three cases it was confirmed at surgery. One patient had an aortic prosthetic valve (Starr-Edwards) and anticoagulation had been stopped one year before the stroke because of gastrointestinal bleeding. Another patient had a subacute bacterial en docarditis with blood cultures positive for Streptococ- cus salivarius and infected vegetations were confirmed at surgery. Results Clinical and CT findings are summarized in table 1.The clinical deficit had an abrupt onset, reaching its peak in a few minutes in half of the patients. In two patients, the deficit progressed during the next 3 hours; and in the remaining 2, a fluctuating course over sever al hours was seen before stabilization occurred. Neuro logical examination showed a complete (5 cases) or incomplete (3 cases) hemiplegia, accompanied by hypesthesia in 6 patients. A pure motor hemiplegia was only seen in one case. In three of them, a transitory anosognosia was clearly observed. In a further patient (case 8), the motor hemiplegia was accompanied by an expressive dysphasia. Her language disorder was char acterized by nonfluent conversational speech, naming and reading difficulties, dysgraphia and a normal audi tory comprehension. She was almost normal one year after the stroke. Recovery of the motor and sensory deficit was complete in two patients, moderate in four, and poor in two. EEG was performed on 7 patients. In all but one case, EEG showed a discrete focal slowing. The most common CT abnormality, seen in four cases, was a well-defined low density area placed in caudate, putamen and anterior limb of internal capsule ( fig. 1). In a further 3 cases, CT showed a posterior extension (fig. 2). The patient with aphasia had...

We describe a man aged 42 years with mitral valve regurgitation who suffered from subacute bacterial endocarditis caused by Streptococcus morbillorum. The clinical picture began with a toxic syndrome. Five months later, the patient had an embolic episode and a right rostral pontine stroke, which was followed a few days later by an adversive focal seizure on the right. Despite antibiotic treatment, he suffered complete third nerve palsy. Arteriography, magnetic resonance imaging, and computed tomography of the brain showed a giant aneurysm in the rostral end of the basilar artery; the aneurysm was clipped. We discuss the clinical features, radiology, and characteristics of this aneurysm as a unique case of a giant bacterial aneurysm in the vertebrobasilar system. ; brain stem localization is rare. Mycotic aneurysm is the next most frequent complication of endocarditis, appearing mainly in the distal branches of the middle cerebral artery. Case ReportOur patient was a 45-year-old man with a medical history of moderate mitral regurgitation. He was a heavy drinker and smoker (40 cigarettes/day) and had gout. Five months before admission, he began a toxic syndrome with joint pain, asthenia, anorexia, weight loss of 8-10 kg, and anemia. He came to our hospital with an acute picture consisting of dizziness, vomiting, instability, pulsatile left oculofrontal headache, left gaze diplopia, left hemiparesis, and left hemifacial paresthesias. He had a normal arterial blood pressure, a normal body temperature, and a systolic murmur at the cardiac apex and the left sternal border that radiated into the axilla and the base of the heart. The neurologic examination showed a dysarthric patient with a right horizontal gaze paresis and a right internuclear ophthalmoplegia that led to the one-and-a-half syndrome, 6 a vertical nystagmus appearing during upward gaze, a left hemiparesis (facial 3/5, arm 3-4/5, and leg 4/5) with the plantar reflexes in flexion, a left cerebellar deficit, and left arm and face sensory loss.An initial nonenhanced computed tomogram (CT scan) of the brain was normal (Figure 1). The results of urine and blood analyses were normal except for an erythrocyte sedimentation rate of 113 mm/hr; hematocrit was 31%, hemoglobin was 10.2 g/dl, leukocyte count was 11,290/mm 3 , platelet count was 431,000/mm 3 , and fibrinogen concentration was 405 mg/100 ml. A chest roentgenograph showed cardiomegaly due to enlargement of the left chambers. The electrocardiogram was normal with a QRS axis of -30°.On the sixth day of hospitalization, the patient began to have a severe occipital headache and later developed a focal seizure on turning his head and eyes to the right, followed by a secondary generalized tonic-clonic seizure.His leukocyte and platelet counts rose to 18,910/mm 3 and 591,000/mm 3 , respectively, and Streptococcus morbillorum grew in six blood cultures. An echocardiogram demonstrated the presence of vegetations in the mitral valve with severe mitral regurgitation, minimal tricuspid regurgitation, and enlargement...

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The relevance of abnormalities in the distribution of peripheral blood T lymphocyte subsets to the clinical manifestations of multiple sclerosis is not firmly established. A clinical and immunological follow‐up of relapsing‐remitting multiple sclerosis patients was performed in order to study the relationship of immune changes with the clinical course of the disease. Twenty patients were monitored monthly during a mean time of nine months for peripheral blood lymphocyte subsets (CD3, CD4, CD8, CD19), including the immunoregulatory subsets CD4CD29 (helper‐inducer), and CD4CD45RA (suppressor‐inducer) and activated T helper cells (CD4CD25) by flow cytometry. A total of 14 untreated relapses was included. The most significant observations were a decrease in T suppressor‐inducer CD4+ CD45RA+ subset during clinical relapses (P= 0.028) that was also detectable one month before (P= 0.020) and the lack of changes in CD4+ CD29+ and CD8+ T cells. In addition, variations in the percentage of CD4+CD25+ activated T helper cells were not associated with clinical exacerbations. These results indicate the existence of a temporal association of immune changes in peripheral blood, but not activation, with the clinical manifestations of multiple sclerosis.