Background and Purpose-Internal carotid artery dissection (ICAD) is a frequent cause of ischemic stroke in young patients. Whether cerebral ischemia is of embolic or hemodynamic origin remains to be determined. Heparin is often administered in ICAD; however, a drug trial can hardly be conducted because of the low recurrence rate after the acute stage. Therefore, the best therapeutic approach should be determined on the basis of the presumed mechanism of cerebral ischemia. One way to approach the mechanism of stroke in ICAD is to determine stroke patterns. We postulated that most cortical and large subcortical infarcts (Ն15 mm) are of embolic origin and that small subcortical infarcts (Ͻ15 mm) and junctional infarcts are not. The aim of our study was to determine the stroke patterns in 40 consecutive patients with ICAD. Methods-The patients (26 women and 14 men; mean age, 42.8 years) had a total of 65 ICADs. Seventeen patients were free of any vascular risk factor. CT scans, MRI scans, and angiographic features were analyzed by observers who were blinded to the clinical findings. Results-We found 34 cortical infarcts, 25 large subcortical infarcts, 1 small subcortical infarct, and 5 junctional infarcts. Conclusions-Most infarcts related to ICAD are cortical infarcts or large subcortical infarcts; small subcortical infarcts and junctional infarcts are infrequent. Therefore, these findings suggest that most infarcts occurring in carotid artery dissection (CAD) are probably embolic rather than hemodynamic in origin. According to this presumed mechanism, anticoagulation seems a logical treatment at the early stage of CAD.
The purpose of this study was to estimate the frequency of various risk factors, courses and outcome of infarct subtypes in a large hospital-based stroke registry. Methods: From 1987 to 1994, 1,776 stroke patients with a first-ever infarction were included in the Besançon Stroke Registry. All patients were evaluated by a standard protocol (risk factors, stroke onset, stroke courses, clinical characteristics, neuroimaging, Doppler ultrasonography and cardiac investigations). Outcome was evaluated at 30 days using the Rankin scale. Results: There were 1,012 men (mean age 67.2 ± 13.7 years) and 764 women (mean age 71.4 ± 15.6 years). At least two neuroimaging examinations were performed in 81.4% (n = 1,446) of the patients and an infarct was visible in 80.9% (n = 1,436). The second neuroimaging examination (CT or MRI) was performed after 8.2 ± 1.6 days. 85.4% of patients were admitted on the first day of the stroke: 28.3% within 3 h and 48.4% within 6 h. In addition, stroke severity was well correlated with the short time interval between stroke onset and admission. Past medical history of hypertension was the major risk factor occurring in 57.5% of all types of infarction. While diabetes was more frequently found in small deep infarct, atrial fibrillation and history of heart failure were found in anterior circulation infarcts. The distribution of clinical presentations was conventional. Hemorrhagic transformation was found in 14.9% of the patients, especially in MCA and PCA infarcts. In all patients, logistic regression analysis determined independent predictive factors for death: clinical deterioration at the 48th hour (OR 7.5, 95% CI 4.9–11.3), initial loss of consciousness (OR 3.3, 95% CI 2.1–4.9), age (OR 1.05, 95% CI 1.03–1.06), complete motor deficit (OR 2.6, 95% CI 1.7–3.8), history of heart failure (OR 1.9, 95% CI 1.3–3.0), lacunar syndrome (OR 0.25, 95% CI 0.10–0.60) and regressive stroke onset (OR 0.24, 95% CI 0.10–0.52). However, the outcome was clearly correlated with the infarct location. The in-hospital mortality rate was lowest in patients with small deep infarct (2.9%) or border zone infarcts (3.4%) and the highest in patients with total middle cerebral artery infarct (47.4%) or multiple infarcts (27.6%). Conclusion: Our registry appears to be a useful tool to understand the course and outcome of a large group of nonselected patients with subtypes of infarction. It can also help to analyze the influence of specific stroke management in the different categories of stroke types.
During the first hours after acute ischemic stroke, the CT usually shows no abnormalities. Therapeutic trials of ischemia in the middle cerebral artery (MCA) territory involves decision-making when the CT may not show obvious ischemic changes. We reviewed 100 consecutive patients, admitted within 14 hours after a first stroke. Selective criteria were clinical presentation with MCA ischemia and at least two CTs (1 initial and 1 control). All CTs were retrospectively analyzed by at least two physicians blinded to the patient's status. On the first CT, early signs were hyperdense MCA sign (HMCAS), early parenchymatous signs (attenuation of the lentiform nucleus [ALN], loss of the insular ribbon [LIR], and hemispheric sulcus effacement [HSE]), midline shift, and early infarction. Subsequent infarct locations were classified according to total, partial superficial (superior or inferior), deep, or multiple MCA territories. Clinical features, etiology, and Rankin scale were collected. There were 52 women (mean age 70.8). The CTs were performed at mean 6.4 hours (1 to 14 hours) and before the sixth hour in 62% of the patients. Early CT was abnormal in 94% of the cases, and the abnormalities found were an HMCAS in 22 patients, ALN in 48, LIR in 59, HSE in 69, midline shift in 5, and early infarct in 7. CT was normal in six patients where it was performed earliest (mean 4.5 hours) and in the oldest patients (mean age 80.1). Early parenchymatous CT signs were significantly associated with subsequent MCA infarct location and extension: ALN and deep infarct, HSE and superficial infarct, LIR and large infarct. HMCAS was never found in isolation and was always associated with the three other signs in extended MCA infarct. The presence of two or three signs (ALN, LIR, or HSE) was associated with extended MCA infarct (p < 0.001) and poor outcome (p < 0.001). Our findings suggest that CT frequently discloses parenchymal abnormalities during the first hours of ischemic stroke. Early signs allow the prediction of subsequent infarct locations; CT may provide a simple tool in evaluating the early prognosis of MCA infarction and thus may be useful in selecting better treatments.
The purpose of this study was to estimate the frequency of various risk factors, courses and outcome of stroke subtypes in a large hospital-based stroke registry. The Centre Hospitalier Universitaire of Besançon is the only public hospital with a neurological department in the county to admit any unselected patient with an acute stroke. A prospective hospital-based registry using systematic computer coding of data was conducted. All patients were evaluated by standard testing (neuroimaging, Doppler ultrasonography and cardiac investigations). From 1987 to 1994, 2,500 stroke patients with a first-ever stroke were included in the Besançon Stroke Registry. There were 1,425 men (mean age 66.1 years) and 1,075 women (mean age 70.6 years). Ischemic stroke was present in 84% of the patients (cerebral infarction in 84.5% and transient ischemic attacks in 15.5%), primary intracerebral hemorrhage (PIH) in 14.2% and cerebral venous thrombosis in 1.8%. On the 1st day of the stroke 79.7% of the patients were admitted, 47.1% within 6 h. In addition, stroke severity was well correlated with the time of the patient''s admission. Past medical history of hypertension was the major risk factor occurring in 55.8% of all patients, followed by smoking, atrial fibrillation, ischemic heart disease, hypercholesterolemia and diabetes mellitus. Clinical presentation was distributed according to classical patterns. The in-hospital mortality rate was 13.6% and was higher in patients with infarcts (13.7%) or PIH (25.6%). Logistic regression analysis determined independent predictive factors for death: deterioration at 48 h [odds ratio (OR) 10.1, 95% confidence interval (CI) 7.0-14.5], initial loss of consciousness (OR 4.5, 95% CI 3.1-6.4), age <70 (OR 2.6, 95% CI 1.8-3.8), complete motor deficit (OR 1.9, 95% CI 1.3-2.8), major cognitive syndrome (OR 1.5, 95% CI 1.1-2.3), hyperglycemia at admission (OR 1.007, 95% CI 1.004-1.01), female gender (OR 0.7, 95% CI 0.5-0.9) and regressive stroke onset (OR 0.2, 95% CI 0.1-0.5). The Besançon Stroke Registry is a useful tool for the study of the risk factors, clinical features, and the course of strokes in an early phase.
The rate of recurrent stroke after cervical artery dissection (CAD) remains unknown. The aim of this study was to evaluate the rate of recurrent stroke in the same territory in patients who were discharged alive after CAD. The secondary aims were to evaluate the rate of death, any stroke or transient ischemic attacks (TIA), recurrent CAD, reopening and residual headache or cervical pain. We contacted 110 consecutive patients with angiographically proven CAD who were discharged alive after CAD. Five of the 110 patients (4.5%) were lost to follow-up. The 105 remaining patients shared a total of 110 CAD (67 carotid, 43 vertebral). The median duration of follow-up was 36 months. Ninety-two patients had no event and 5 died 1–7 years after CAD. Two patients had a recurrent stroke and 3 had TIA in the territory of the previously dissected vessel; 3 had a recurrent dissection of the same vessel, revealed by TIA in 1 and isolated cervical pain in 2. Twenty-one patients had residual headache or cervical pain. In 90 patients who underwent a second angiography, reopening occurred in 52 (partial in 2) and an aneurysm in 5. The risk of recurrent stroke remains low in patients discharged alive after CAD. One of the most frequent sequelae is residual headache.
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