Acute ischaemic stroke represents the most common cause of new sudden neurological deficit, but other diseases mimicking stroke happen in about one-third of the cases. Magnetic resonance imaging (MRI) is the best technique to identify those ‘stroke mimics’. In this article, we propose a diagnostic approach of those stroke mimics on MRI according to an algorithm based on diffusion-weighted imaging (DWI), which can be abnormal or normal, followed by the results of other common additional MRI sequences, such as T2 with gradient recalled echo weighted imaging (T2-GRE) and fluid-attenuated inversion recovery (FLAIR). Analysis of the signal intensity of the parenchyma, the intracranial arteries and, overall, of the veins, is crucial on T2-GRE, while anatomic distribution of the parenchymal lesions is essential on FLAIR. Among stroke mimics with abnormal DWI, T2-GRE demonstrates obvious abnormalities in case of intracerebral haemorrhage or cerebral amyloid angiopathy, but this sequence also allows to propose alternative diagnoses when DWI is negative, such as in migraine aura or headaches with associated neurological deficits and lymphocytosis (HaNDL), in which cortical venous prominence is observed at the acute phase on T2-GRE. FLAIR is also of major interest when DWI is positive by better showing evocative distribution of cerebral lesions in case of seizure (involving the hippocampus, pulvinar and cortex), hypoglycaemia (bilateral lesions in the posterior limb of the internal capsules, corona radiata, striata or splenium of the corpus callosum) or in posterior reversible encephalopathy syndrome (PRES). Other real stroke mimics such as mitochondrial myopathy, encephalopathy, lactic acidosis, stroke-like episodes (MELAS), Susac’s syndrome, brain tumour, demyelinating diseases and herpes simplex encephalitis are also included in our detailed and practical algorithm.Key points • About 30% of sudden neurological deficits are due to non-ischaemic causes. • MRI is the best technique to identify stroke mimics. • Our practical illustrated algorithm based on DWI helps to recognise stroke mimics.

Amongst patients with CAA, cSS is independently associated with acute cSAH. These findings suggest that cSAH may be involved in the pathogenesis of the cSS observed in CAA. Longitudinal studies are warranted to assess this potential causal relationship.

Background and purpose Diffusion‐weighted imaging (DWI) commonly detects acute ischaemic lesions in patients with acute intracerebral hemorrhage (ICH), especially with cerebral amyloid angiopathy (CAA). We investigated the relationship between cortical superficial siderosis (cSS), a neuroimaging marker of CAA, and DWI lesions in patients with acute ICH. Methods We conducted a retrospective analysis of prospectively collected data from consecutive patients with acute supratentorial ICH who underwent brain magnetic resonance imaging within 10 days after symptom onset. Magnetic resonance imaging scans were analyzed for DWI lesions, cSS and other markers for small‐vessel disease. Univariate and multivariate analyses were performed to assess the association between cSS and DWI lesions. Results Among 246 ICH survivors (mean age 71.4 ± 12.6 years) who were enrolled, 126 had lobar ICH and 120 had deep ICH. Overall, DWI lesions were observed in 38 (15.4%) patients and were more common in patients with lobar ICH than deep ICH (22.2% vs. 8.3%; P = 0.003). In multivariate logistic regression analysis, the extent of white matter hyperintensities [odds ratio (OR), 1.29; 95% confidence interval (CI), 1.05–1.58; P = 0.02] and cSS severity (focal cSS: OR, 3.54; 95% CI, 1.28–9.84; disseminated cSS: OR, 4.41; 95% CI, 1.78–10.97; P = 0.001) were independently associated with the presence of DWI lesions. Conclusions Diffusion‐weighted imaging lesions are more frequently observed in patients with acute lobar ICH than in those with deep ICH. cSS severity and white matter hyperintensity extent are independent predictors for the presence of DWI lesions, suggesting that CAA may be involved in the pathogenesis of DWI lesions associated with acute ICH.

Background In Moyamoya Angioplasty (MMA), increased apparent diffusion coefficient (ADC) in frontal white matter (WM) with a normal appearance has been associated with frontal hypoperfusion and executive dysfunction. Multiple burr-hole surgery enables the revascularization of large frontal areas. Goal: To assess the effect of multiple burr-hole surgery on the ADC and cognitive functions in adults with MMA. Methods ADC was measured in 26 brain hemispheres of 14 consecutive adults with MMA (9 women, mean age ± SD: 38.1 ± 10.7 years) prior to and 6 months after burr-hole surgery. ADC was obtained from regions of interest located in frontal and posterior (temporo-occipital) normal-appearing WM. Ten patients had neuropsychological assessment that focused on executive and attentional functions before and after surgery. Results Anterior and posterior ADC values did not differ before surgery (815.8 ± 60.1 vs. 812.1 ± 35.3 mm2/s, p = 0.88). After surgery, frontal ADC was lower than prior to surgery (789.9 ± 64.5 vs. 815.8 ± 60.1 mm2/s; p <0.001) whereas no change occurred in posterior ADC (p = 0.31). Trail-making test part B median z-score increased from − 1.47 to − 0.21 (p = 0.018), suggesting improved cognitive flexibility. Conclusion In adults with MMA, indirect revascularization with burr-hole is followed by a decrease of ADC in normal-appearing frontal WM and may have improved some executive functions in the flexibility process. Change in ADC may reflect the improvement in cerebral perfusion after surgery. The measuring of ADC may be a promising tool in exploring potentially reversible microstructural WM damage related to hypoperfusion and cognitive change in MMA.

Background: Convexity subarachnoid hemorrhage (cSAH) or subdural Hematoma (SDH) are occasionally described on CT or MRI in the area of acute lobar intracerebral hematoma (ICH). The prevalence and the etiologic significance of this association are not well known. Hypothesis: We hypothesized that cSAH and SDH were more frequent in Cerebral Amyloid Angiopathy (CCA)-related lobar ICH. Methods: Using our electronic database, we retrospectively reviewed the clinical and MRI characteristics of 165 consecutive patients (mean age 70 ± 13 years) admitted for acute lobar ICH. The presence of cSAH and SDH was assessed by 2 reviewers on a brain MRI performed within 10 days after ICH onset. Results: SDH and cSAH were present in respectively 28.5 and 54.5 % of all patients. Among patients with acute lobar ICH meeting the modified Boston criteria for probable CAA, the frequency was 37.5 % (27/72) for SDH and 73 % (53/72) for cSAH, which is significantly higher than among patients with hematoma of other causes ( 21.5 and 39.8 %; p=0.03 and p<0.001 respectively). The association remained significant considering patients meeting the modified Boston criteria for probable or possible CAA versus others causes. Conclusions: Using MRI for evaluation of acute lobar ICH, cSAH and SDH were very frequent and associated with CCA. This is consistent with the involvement of leptomeningeal arteries in this disease. The presence of subarachnoid or subdural hemorrhage should be systematically assessed and could be added to diagnostic criteria for CAA.