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Background and Purpose-T2*-weighted gradient-echo MRI is known to detect old microbleeds (MBs), considered indicative of microangiopathy. MBs might be a potential risk factor for early cerebral bleeding (CB) after ischemic stroke. Therefore, we assessed the impact of MBs on the occurrence of CB after cerebral infarction. Methods-We included prospectively stroke patients who had documented ischemic damage. The imaging protocol involved baseline CT scan, T2*-weighted gradient-echo MRI, diffusion-weighted imaging, T2-weighted imaging, and magnetic resonance angiography and had to be performed within 24 hours after symptom onset. The assessment of CB with T2*-weighted gradient-echo sequence necessitated a focal area of signal loss either within the ischemic area revealed by diffusion-weighted imaging or remote from it. Old MBs were defined on T2*-weighted images as homogeneous rounded areas of signal loss without surrounding edema. CT scan was systematically repeated within the first week to verify CB as diagnosed by the T2* weighted sequence. Results-One hundred patients (mean age, 60Ϯ13 years; range, 19 to 83 years; 58 men, 42 women) met the inclusion criteria. MBs were seen in 20 patients on T2*-weighted imaging. Multivariate logistic regression analysis revealed that age, diabetes, previous use of antithrombotic drugs, evidence of an atherothrombotic source of stroke, and lacunar infarct were significantly associated with MBs (PϽ0.0001). CB was diagnosed in 26 patients: at the acute stage by T2*-gradient echo sequence in 18 patients and with CT scan performed within the first week in 8 patients. Multivariate logistic regression analysis showed that baseline National Institutes of Health Stroke Scale score, diabetes, and MBs were considered significant and independent predictors of CB (PϽ0.001). Conclusions-Although the pathogenesis of CB after ischemic stroke is multifactorial, the increased observation of CB in patients with MBs suggests that the associated vascular vulnerability contributes to CB.

Pediatric CNS cavernomas still are diagnostically and therapeutically challenging lesions. With the help of magnetic resonance imaging, the natural history of cavernomas now guiding therapeutic strategies is well documented in adults but remains poorly known in the pediatric age group, since most previous studies dealt with adult and pediatric patients together. This paper focuses on clinical, imaging, and therapeutic features and differential diagnosis of CNS cavernomas with an emphasis on their specificities in the pediatric age group. It is based upon a critical review of the literature and our single-center experience with 36 children (35 with cerebral cavernomas and one with spinal cord cavernoma) operated on during the period of 1985-1999 as well as with seven additional unoperated pediatric cases. Our experience resembles that of other authors regarding the high hemorrhagic risk in children compared to adults. These angiographically occult vascular malformations are often revealed by the sudden onset of intracerebral hematoma with acute focal neurologic deficits, concomitant manifestations, and/or signs of raised intracranial pressure. True epilepsy is less common and may be related to chronic or recurrent microbleeding. Evocative imaging findings are also somewhat different in the two age groups, and we propose here an imaging classification of cerebral cavernomas based on both morphological and signal characteristics that is applicable to the pediatric age group. A sharply demarcated spherical intracerebral hematoma or heterogeneous lesion should always make one consider the hypothesis of a cavernoma. For symptomatic lesions and most rapidly growing asymptomatic lesions, the treatment of choice is complete microsurgical excision preceded by careful anatomical and functional evaluation. Improvements in surgical techniques and anesthesiology over recent years have brought good results in most operated children. The limited role of radiosurgery in the management of pediatric cerebral cavernomas is discussed. There is still a need for well-conducted specific evaluation of the natural history of these lesions in the pediatric age group to aid in systematic research, follow-up, and therapeutic strategies for asymptomatic cavernomas.

Background-Susceptibility-weighted (SW) MRI provides insight into the pathophysiology of acute stroke. We report on the use of SW imaging (SWI) sequences in clinical practice and highlight the future applications. Summary of Review-SWI exploits the magnetic susceptibility effects generated by local inhomogeneities of the magnetic field. The paramagnetic properties of deoxyhemoglobin support signal changes related to acute hemorrhage and the intravascular spontaneous blood oxygen level dependent (BOLD) effect. SWI allows the early detection of acute hemorrhage within 6 hours after symptom onset. SWI may also identify previous microbleeds in acute ischemia; however, the impact of these findings on thrombolytic therapy safety has not been definitely established. The diagnosis of arterial occlusion is usually performed by magnetic resonance angiography. SWI allows intravascular clot detection at the acute stage. Substantial experimental data suggest that spontaneous BOLD contrast may improve tissue viability assessment. The ratio of oxyhemoglobin to deoxyhemoglobin, measured by MRI in the capillary and venous compartments, reflects the oxygen extraction fraction (OEF) and the cerebral metabolic rate of oxygen. The combination of magnetic resonance (MR)-measured OEF and cerebral blood flow, via perfusion studies, may provide information about tissue viability. Conclusions-SWI offers a spectrum of current clinical applications and may improve our knowledge of the pathophysiology of acute stroke.

This article represents the update of ‘European Stroke Initiative Recommendations for Stroke Management’, first published in this Journal in 2000. The recommendations are endorsed by the 3 European societies which are represented in the European Stroke Initiative: the European Stroke Council, the European Neurological Society and the European Federation of Neurological Societies.

Background and Purpose— The relative merits of reperfusion versus recanalization to predict tissue and clinical outcomes in anterior circulation stroke have been previously assessed using data acquired >12 hours postonset. To avoid late-occurring confounders such as non-nutritional reperfusion, futile recanalization and no-reflow phenomenon, we performed ultraearly assessment of reperfusion and recanalization. Methods— From a multicenter prospective database, 46 patients with acute magnetic resonance angiography–visible occlusion and in whom both reperfusion and recanalization were assessed on follow-up magnetic resonance imaging ≤6 hours of symptom onset were identified. Multiple linear regressions modeled salvaged penumbra, diffusion-weighted imaging lesion growth, and final infarct at 1 month using baseline clinical and imaging parameters and acute reperfusion or recanalization. Best predictors were determined with the Akaike information criterion. Univariate and multivariate logistic regressions identified the clinical and imaging predictors of clinical outcome. Results— Admission magnetic resonance imaging showed M1 occlusion in 15 (33%) patients; median penumbra volume was 13.4 mL. Acute reperfusion was observed in 27 (59%) patients; 42% of nonrecanalized patients demonstrated reperfusion. The dichotomized classification of reperfusion and recanalization was discordant ( P =0.0002). Reperfusion ≤6 hours was a significant ( P <0.05) predictor of increased penumbra salvage, reduced lesion growth, and final infarct size. Recanalization did not improve model accuracy. Reperfusion, but not recanalization, was significantly associated with good clinical outcome in logistic regressions. Conclusions— Reperfusion ≤6 hours was consistently superior to recanalization in predicting tissue and clinical outcome. Reperfusion without recanalization was frequent and probably related to retrograde reperfusion through leptomeningeal collaterals. Acute reperfusion was the strongest predictor of, and may therefore, represent a reliable surrogate for, clinical outcome.

Because diffusion tensor imaging (DTI) is able to assess tissue integrity, we used diffusion to detect abnormalities in trigeminal nerves (TGN) in patients with trigeminal neuralgia (TN) caused by neurovascular compression (NVC). We also studied anatomical TGN parameters (cross-sectional area [CSA] and volume [V]). Using DTI sequencing in a 3-T magnetic resonance imaging (MRI) scanner, we measured the fraction of anisotropy (FA) and the apparent diffusion coefficient (ADC) of TGN in 10 patients selected as candidates to have microvascular decompression (MVD) for TN, and 6 normal control subjects. We compared data between the affected nerves of TN (ipsilateral TN), unaffected nerves of TN (contralateral TN), and both nerves in normal subjects (controls), and correlated these data with CSA and V. The FA of the ipsilateral TN (0.37±0.08) was significantly lower (P<.05) compared with the contralateral TN (0.48±0.08) and control values (0.52±0.04). The ADC of ipsilateral TN (5.6±0.89 mm(2)/s) was significantly higher (P<.05) compared with the contralateral TN (4.26±0.59 mm(2)/s) and control values (3.84±0.43 mm(2)/s). Ipsilateral TN had less V and CSA compared with contralateral TN and control values (P<.05). The Spearman correlation coefficient showed a strong positive correlation between loss of FA and loss of V (r=0.7576) and loss of CSA (r=0.9273) of affected nerves. The Spearman correlation coefficient showed a strong negative correlation between increase in ADC and loss of V (r=-0.7173) and loss of CSA (r=-0.7416) in affected nerves. DTI revealed alteration in the FA and ADC values of the affected TGN. These alterations were correlated with atrophic changes in patients with TN caused by NVC.

Background: Old asymptomatic microbleeds (MBs) visualized on T₂-weighted MRI are indicative of microangiopathy. They may be a marker of increased risk of intracerebral hemorrhage (ICH) following thrombolysis. However, data regarding this potential risk are limited. Methods: A retrospective analysis of pretreatment T₂-weighted MRI was performed in consecutive stroke patients who received intravenous tissue plasminogen activator (tPA). We aimed to assess the impact of MBs on the risk of cerebral bleeding. The frequency and location of MBs were assessed and compared with the location of ICH after thrombolysis. Results: Forty-four patients were studied. MBs were present on pretreatment MRI in 8 cases (18.2%). At day 1, symptomatic ICH occurred in none of 8 patients with MBs versus 1 of 36 patients without (NS). At day 1, ICH occurred in 3 of 8 patients with MBs versus 10 of 36 patients without (NS). At day 7, symptomatic ICH occurred in 1 of 8 patients with MBs versus 2 of 36 patients without (NS). At day 7, ICH occurred in 5 of 8 patients with MBs versus 12 of 36 patients without (NS). No ICH occurred at the site of an MB. ICH occurred within the ischemic area in all patients who bled. Conclusions: Our study suggests that stroke patients with a small number of MBs on pretreatment MRI could be treated safely with thrombolysis. Larger prospective studies are needed to address the predictive value of detection of MBs with regard to the risk of tPA-induced ICH.