Silent brain infarct in migraine: Systematic review and meta-analysis.

BACKGROUND: While migraine, particularly migraine with aura, is a recognized risk factor for ischemic stroke, the association of migraine with silent brain infarction is a matter of debate, as studies on this topic have yielded conflicting results. METHODS: A systematic review of the literature was conducted of studies reporting migraine and silent brain infarction, assessed by magnetic resonance imaging, between January 1980 and April 2022, by consulting Medline and Embase databases. Studies with a control group were included in a meta-analysis of population-based studies. An exploratory meta-analysis of both population-based and clinical-based studies was further performed to test the association between migraine with aura and silent brain infarction. RESULTS: A total of 2,408 articles were identified, among which 24 were included in the systematic review and 10 in the meta-analysis. The meta-analysis of population-based studies showed no association of migraine with silent brain infarction (odds ratio (OR)=1.32 [95% CI 0.92;1.90], P=0.13) and migraine with aura with silent brain infarction (OR=1.56 [0.74;3.30], P=0.24). However, in the exploratory meta-analysis of population-based and clinical-based studies, migraine with aura was significantly associated with silent brain infarction (OR=1.91 [1.02;3.59], P=0.04) and to silent cerebellar infarcts (OR=2.57 [1.01;6.56], P=0.05). CONCLUSION: In this updated systematic review and meta-analysis of population-based studies, migraine and migraine with aura were not associated with silent brain infarction.

Interhemispheric distribution of amyloid and small vessel disease burden in cerebral amyloid angiopathy-related intracerebral hemorrhage.

BACKGROUND AND PURPOSE: Intracerebral hemorrhage (ICH) is a devastating presentation of cerebral amyloid angiopathy (CAA), but the mechanisms leading from vascular amyloid deposition to ICH are not well known. Whether amyloid burden and magnetic resonance imaging (MRI) markers of small vessel disease (SVD) are increased in the ICH-affected hemisphere compared to the ICH-free hemisphere in patients with a symptomatic CAA-related ICH was investigated. METHODS: Eighteen patients with CAA-related ICH and 18 controls with deep ICH who underwent brain MRI and amyloid positron emission tomography using 18 F-florbetapir were prospectively enrolled. In each hemisphere amyloid uptake using the standardized uptake value ratio and the burden of MRI markers of SVD including cerebral microbleeds, chronic ICH, cortical superficial siderosis, white matter hyperintensities and lacunes were evaluated. Interhemispheric comparisons were assessed by non-parametric matched-pair tests within each patient group. RESULTS: Amyloid burden was similarly distributed across the brain hemispheres in patients with CAA-related ICH (standardized uptake value ratio 1.11 vs. 1.12; P = 0.74). Cortical superficial siderosis tended to be more common in the ICH-affected hemisphere compared to the ICH-free hemisphere (61% vs. 33%; P = 0.063). Other MRI markers of SVD did not differ across brain hemispheres. In controls with deep ICH, no interhemispheric difference was observed either for amyloid burden or for MRI markers of SVD. CONCLUSIONS: Brain hemorrhage does not appear to be directly linked to amyloid burden in patients with CAA-related ICH. These findings provide new insights into the mechanisms leading to hemorrhage in CAA.

Acute ischaemic lesions are associated with cortical superficial siderosis in spontaneous intracerebral hemorrhage.

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.

Cortical superficial siderosis and acute convexity subarachnoid hemorrhage in cerebral amyloid angiopathy.

BACKGROUND AND PURPOSE: Acute convexity subarachnoid hemorrhage (cSAH) and cortical superficial siderosis (cSS) are neuroimaging markers of cerebral amyloid angiopathy (CAA) that may arise through similar mechanisms. The prevalence of cSS in patients with CAA presenting with acute cSAH versus lobar intracerebral hemorrhage (ICH) was compared and the physiopathology of cSS was explored by examining neuroimaging associations. METHODS: Data from 116 consecutive patients with probable CAA (mean age, 77.4 ± 7.3 years) presenting with acute cSAH (n = 45) or acute lobar ICH (n = 71) were retrospectively analyzed. Magnetic resonance imaging scans were analyzed for cSS and other imaging markers. The two groups' clinical and imaging data were compared and the associations between cSAH and cSS were explored. RESULTS: Patients with cSAH presented mostly with transient focal neurological episodes. The prevalence of cSS was higher amongst cSAH patients than amongst ICH patients (88.9% vs. 57.7%; P < 0.001). In multivariable logistic regression analysis, focal [odds ratio (OR) 6.73; 95% confidence interval (CI) 1.75-25.81; P = 0.005] and disseminated (OR 11.68; 95% CI 3.55-38.35; P < 0.001) cSS were independently associated with acute cSAH, whereas older age (OR 0.93; 95% CI 0.87-0.99; P = 0.025) and chronic lobar ICH count (OR 0.45; 95% CI 0.25-0.80; P = 0.007) were associated with acute lobar ICH. CONCLUSIONS: 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.

Migraine with aura and silent brain infarcts lack of mediation of patent foramen ovale.

BACKGROUND AND PURPOSE: Population-based studies have shown a heightened prevalence of clinically silent brain infarcts in subjects who have migraine with aura (MA). We sought to determine whether this association could be confirmed in young patients with cryptogenic ischemic stroke, and explored the role of patent foramen ovale (PFO) as a potential underlying mechanism. METHODS: Patients were selected from a registry of young patients consecutively treated for ischemic stroke in a tertiary university hospital among those without definite cause of stroke. Patients with PFO were matched for age and gender with patients with normal atrial septum. Migraine and MA were evaluated after patient selection and matching. Silent brain infarcts were independently evaluated on MRI. RESULTS: We included 100 patients [60 men; mean age (SD), 44.8 years (8.3)], 50 patients with PFO. We found silent brain infarcts in 36 patients and MA in 13 patients. MA was more frequent in patients with silent brain infarcts than in patients without silent brain infarcts (25.0% vs. 6.3%; OR, 5; 95% CI, 1.4-17.6; P = 0.01). Traditional cardiovascular risk factors were not associated with silent brain infarcts. PFO was neither associated with MA (OR, 1.7; 95% CI, 0.5-5.3) nor silent brain infarcts (OR, 0.7; 95% CI, 0.3-1.5). The association of MA with silent brain infarcts was not altered after adjustment for PFO. CONCLUSION: Findings suggest that silent brain infarcts in young patients with cryptogenic stroke is associated with MA. We found no evidence for a mediating effect of PFO on this association.

Etiologic investigation of ischemic stroke in young adults.

OBJECTIVES: We attempted to classify causes of ischemic stroke in young adults using a progressive diagnostic algorithm and the ASCO (atherosclerosis, small-vessel disease, cardiac source, other cause) classification system. METHODS: Patients aged 16-54 years consecutively treated for acute ischemic stroke in a tertiary stroke unit were included in this retrospective analysis. Causes of stroke were classified using the ASCO system, which assigns a graded level of likelihood to each potential cause in individual patients. The initial etiologic workup included brain imaging, magnetic resonance or CT angiography of cerebral and cervical vessels, EKG, and routine blood studies. Patients without a definite cause of ischemic stroke after initial evaluation underwent transesophageal echocardiography. RESULTS: We included 318 patients (195 men and 123 women); 131 patients were aged 16-44 years, and 187 were aged 45-54 years. A definite cause of stroke (ASCO grade 1) could be identified in 145 patients (45.5%). An uncertain cause of stroke (ASCO grade 2) was found in 59 (18.5%) further patients. Most (130 of 145) definite causes were identified by initial evaluation. The 2 major definite or uncertain causes of stroke were patent foramen ovale associated with atrial septal aneurysm (PFO-ASA) (20 of 131 [15.3%]) and dissection of the cervical or cerebral artery (19 of 131 [14.5%]) in patients aged 16-44 years and large-vessel atherosclerosis (37 of 187 [19.8%]) and PFO-ASA (23 of 187 [12.3%]) in patients aged 45-54 years. CONCLUSIONS: Our findings suggest that PFO-ASA may be a major cause of ischemic stroke in young adults.

Cortical subarachnoid haemorrhage in the elderly: a recurrent event probably related to cerebral amyloid angiopathy.

OBJECTIVE: Isolated, non-traumatic, cortical subarachnoid haemorrhage (cSAH) is a rare type of cerebrovascular disease caused by various disorders. In a few cases, especially in the elderly, no apparent cause can be identified. We report a case series of patients without apparent cause of cSAH. We aimed to determine whether cerebral amyloid angiopathy (CAA) could be a common cause of cSAH. METHODS: We retrospectively analysed clinical and radiological data of consecutive patients admitted to a tertiary stroke unit with cSAH. All patients had brain MRI as a part of their initial evaluation and a repeat examination during follow-up. RESULTS: Amongst 25 patients with cSAH, 10 patients had no apparent cause of cSAH (six men and four women; mean age ± SD: 73.8 ± 8.5 years). All patients with no apparent cause presented with single or recurrent focal transient neurological symptoms of short duration. Only one patient experienced headache. cSAH was limited to one or two sulci, mostly the central sulcus. MRI showed the evidence of prior asymptomatic bleeding in 9/10 patients: cortical hemosiderosis (9/10), lobar intracerebral haemorrhage (ICH) (6/10) and cortical microbleeds (9/10). Eight of ten patients met the Boston criteria for probable CAA and 2/10 for possible CAA. During follow-up, three patients had recurrent bleeding: cSAH (2) and lobar ICH (1). CONCLUSIONS: Our findings suggest that CAA could be a common cause of cSAH in the elderly with a fairly uniform clinical presentation. In addition to prior cortical bleeding (ICH, MBs), most patients from the present series had evidence of focal cortical hemosiderosis likely corresponding with prior unrecognized cSAH and suggesting that cSAH was a recurrent event.

Unruptured intracranial aneurysm as a cause of cerebral ischemia.

BACKGROUND: Unruptured intracranial artery aneurysms (IAs) can be revealed by cerebral ischemia. Little is known on the clinical course and outcome of patients with this condition. We report our findings in a consecutive series of 15 such patients. METHODS: We retrospectively analyzed patients with ischemic stroke (IS) or transient ischemic attack (TIA), unruptured IA on the symptomatic cerebral artery, and no other potential cause of cerebral ischemia consecutively treated in a tertiary stroke unit. RESULTS: Fifteen patients (ten women, and five men) were identified. Their mean age was 49.7 years (range, 37-80 years). Ten patients presented with IS, and five with TIA. The median diameter of IA was 7.5mm (range, 2.5-23 mm). Aneurysm thrombosis was found on imaging in 9/10 patient with IS, and 1/5 patients with TIA (p=0.017). Thirteen patients were given an antiplatelet agent. Mean follow-up until last visit or treatment of aneurysm was 393 days (median 182 days; range, 6-1825 days). There was no ischemic recurrence. Partial or complete recanalization of aneurysm thrombosis occurred in 7/10 patients. Two patients, both with initial aneurysmal thrombosis and on antiplatelet therapy, experienced aneurysm rupture. CONCLUSION: Unruptured IA is a rare cause of IS/TIA. IS is associated with aneurysm thrombosis. Our findings suggest that aneurysm thrombosis is a dynamic process which is associated with a low rate of ischemic recurrence on antiplatelet therapy but may be followed by subarachnoid hemorrhage.

[Value of CT perfusion for the diagnosis of early middle cerebral artery stroke]. / Intérêt de la TDM de perfusion dans le diagnostic d'un AVC ischémique sylvien à la phase précoce.

The need for early diagnosis of stroke at the acute phase has increased with the validation of intravenous thrombolysis therapy. The purpose of this article was to determine the accuracy of CT perfusion for the diagnosis of acute MCA stroke. We have retrospectively compared the results on CT perfusion obtained at acute presentation with follow-up imaging in 30 non consecutive patients admitted for suspected stroke that did not undergo thrombolysis. In our series, the sensitivity of CT perfusion for the diagnosis of MCA infarction was 84%. CT perfusion was poor for the diagnosis of lacunar and strictly cortical infarcts with a sensitivity of 20%. CT perfusion can easily and routinely be performed for the diagnosis of acute stroke, especially in centers where MRI may not be readily available.

Isolated acute nontraumatic cortical subarachnoid hemorrhage.

Our aim was to review the etiologic background of isolated acute nontraumatic cSAH. While SAH located in the basal cisterns originates from a ruptured aneurysm in approximately 85% of cases, a broad spectrum of vascular and even nonvascular pathologies can cause acute nontraumatic SAH along the convexity. Arteriovenous malformations or fistulas, cortical venous and/or dural sinus thrombosis, and distal and proximal arteriopathies (RCVS, vasculitides, mycotic aneurysms, Moyamoya, or severe atherosclerotic carotid disease) should be sought by noninvasive imaging methods or/and conventional angiography. Additionally, PRES may also be a source of acute cSAH. In elderly patients, cSAH might be attributed to CAA if numerous hemorrhages are demonstrated by GRE T2 images. Finally, cSAH is rarely observed in nonvascular disorders, such as abscess and primitive or secondary brain tumors.

[Clinical course and outcome in French adults with Moyamoya disease]. / Aspects cliniques et évolutifs de la maladie de Moyamoya chez des adultes français.

BACKGROUND AND PURPOSE: Moyamoya disease is rare among non-Asian populations and its clinical features are ill-defined. We report 12 new cases of Moyamoya disease in French, non-Asian adults. METHODS: We identified adults with Moyamoya disease managed at a French University Hospital from 1998 through 2006. We reviewed baseline clinical and radiological data and collected follow-up data between March and June 2008. The risk of recurrent stroke was determined using the Kaplan-Meier method. RESULTS: Twelve patients, 10 women and two men, were included. The mean age at baseline was 31.1 years. The initial clinical manifestation was ischemic stroke in 10 patients. The disease was clinically asymptomatic in two patients. The mean follow-up in the 10 symptomatic patients was 52.4 months. Only one patient was surgically treated. The one and five-year risk of recurrent stroke were both 50%. At the end of the follow-up, one patient was dead, four patients had no functional impairment (grade 0-1 on the Rankin scale), and seven patients had moderate functional impairment (grade 2-3 on the Rankin scale). A cognitive dysfunction as identified by failure on the Trail Making Test part B was found in six of ten patients evaluated. CONCLUSION: Moyamoya disease in this cohort of French, non-Asian adults was associated with high rates of both recurrent stroke and cognitive impairment. The findings suggest that Moyamoya disease in non-Asian adults is a potentially severe disease.