Lionel Calviere

Isolated Acute Nontraumatic Cortical Subarachnoid Hemorrhage

SUMMARY: 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.

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.

Executive dysfunction in adults with moyamoya disease is associated with increased diffusion in frontal white matter

Background and purpose Alteration of the cerebrovascular reserve (CVR) in the frontal lobes has been associated with cognitive dysfunction in adults with moyamoya disease (MMD). Elevation of the apparent diffusion coefficient (ADC) in normal-appearing white matter on conventional MRI may occur as a consequence of chronic haemodynamic failure. In the present study, the authors examined the relation of ADC with CVR and cognitive dysfunction in adults with MMD. Methods The authors measured ADC and CVR in the normal-appearing frontal white matter. CVR was calculated using dynamic susceptibility contrast-enhanced MRI and the acetazolamide challenge. A standardised and validated neuropsychological assessment test battery focusing on executive function was used. Results 14 patients, 9 women and 5 men (mean age 36.6±12.9 years), were included. The authors found executive dysfunction in 7 of 13 tested patients. ADC and CVR were negatively correlated (Spearman coefficient: −0.46; p=0.015). Elevation of ADC predicted executive dysfunction (area under receiver operating characteristic curve (95% CI): 0.85 (0.59 to 1.16); p=0.032). Conclusion Elevation of ADC in the normal-appearing frontal white matter of adults with MMD was associated with reduced CVR and executive dysfunction. This preliminary study suggests that measurement of ADC might be used to detect patients at risk for cerebral ischaemia and cognitive impairment.

Acute Convexity Subarachnoid Hemorrhage Related to Cerebral Amyloid Angiopathy: Clinicoradiological Features and Outcome

BACKGROUND The specificities of acute convexity subarachnoid hemorrhage (cSAH) related to cerebral amyloid angiopathy (CAA) and its evolution are not well known. We aimed to describe the clinicoradiological pattern, the magnetic resonance imaging (MRI) evolution, and the risk of recurrent bleeding in such patients. METHODS Among consecutive patients with an acute nontraumatic cSAH, subjects with available MRI who meet the modified Boston criteria for probable CAA were included. Review of medical records, MRI findings, and follow-up data was performed. RESULTS Twenty-three patients (14 women; mean age ± standard deviation: 75.9 ± 7.3 years) were included. cSAH was revealed by transient focal neurological episodes (TFNEs) in 18 of 23 (78.3%) patients. In all patients, acute cSAH appeared as a sulcal fluid-attenuated inversion recovery hyperintensity and GRE T2 hypointensity. Cortical superficial siderosis and cortical microbleeds, respectively, were observed in 21 (91.3%) and 20 (86.9%) patients. Twenty patients (87%) had available follow-up data with a mean duration of 29.8 ± 20.2 months. Recurrent TFNEs occurred in 40% of patients. Acute cSAH evolved into cortical superficial siderosis in all patients. New subarachnoid bleedings defined by recurrent acute cSAH (n = 8) or extension of siderosis (n = 14) were detected in 83.3% of the patients. Lobar intracerebral hemorrhage (ICH) occurred in 7 patients (35%). CONCLUSION CAA-related cSAH has a specific pattern defined by a high prevalence of TFNEs and cortical superficial siderosis, with a high risk of recurrent bleeding, either cSAH or lobar ICH. The systematic evolution from cSAH to focal cortical superficial siderosis reveals data on siderosis physiopathology.

Risk factor profile by etiological subtype of ischemic stroke in the young

BACKGROUND AND PURPOSE Studies of risk factors for ischemic stroke in the young have generally considered ischemic stroke as a whole. The purpose of the present study was to evaluate the association of traditional cardiovascular risk factors with etiological subtypes of ischemic stroke in young adults. METHODS Retrospective review of data from patients aged 16-54 years consecutively treated for first-ever ischemic stroke in an academic stroke unit. Definite causes of stroke were classified using the ASCO (A for atherothrombosis, S for small vessel disease, C for cardiac source, O for other cause) classification system. We used multinomial logistic regression analysis to evaluate associations of age, gender, smoking, hypertension, diabetes and blood lipids with each etiological subtype. RESULTS A total of 400 patients were included: 244 men (61.1%), 156 women (38.9%); mean age (SD) 44.5 (8.5) years. A definite cause of stroke could be identified in 202 (50.5%) patients. Definite causes of stroke included: atherothrombosis, 72 (18.0%) patients; cardioembolism, 37 (9.25%) patients; small vessel disease, 28 (7.0%) patients; other definite cause, 65 (16.25%) patients including 44 patients with carotid or vertebral artery dissection. Atherothrombosis was associated with age, smoking, diabetes, hypertension and low HDL-cholesterol. Small vessel disease was associated with age and hypertension. Cardioembolism was associated with age. CONCLUSION The risk factor profile differs between etiological subtypes of ischemic stroke in young adults. Our findings emphasize the impact of smoking, diabetes, hypertension and low HDL-cholesterol as risk factors for atherothrombosis, and of hypertension as a risk factor for small vessel disease in young adults.

Improvement in cognitive function and cerebral perfusion after bur hole surgery in an adult with moyamoya disease. Case report.

Recent studies have suggested that cognitive impairment may be a common complication in adults with moyamoya disease (MMD). However, the mechanisms of cognitive dysfunction have not been clarified. Whether cognitive impairment may occur as a consequence of cerebral hypoperfusion and may improve after revascularization surgery has not been determined. A 39-year-old West Indian woman with subacute dysexecutive cognitive syndrome and no history of stroke was diagnosed with MMD. Magnetic resonance imaging showed an old, small cerebral infarction in the left frontal white matter and no evidence of recent cerebral ischemia. Perfusion MR imaging with acetazolamide challenge demonstrated a reduced cerebrovascular reserve in both frontal lobes. Revascularization with bur hole surgery was performed, which resulted in complete regression of initial cognitive impairment. Improvement in cognitive function correlated with the development of transdural collaterals on angiography and improvement in cerebral perfusion on MR imaging. This case suggests a relationship between cognitive dysfunction and cerebral hypoperfusion in MMD. Cognitive impairment may be potentially reversible after bur hole surgery and cerebral perfusion improvement.

Cervical artery stenoses in sickle cell disease.

97.8%; A2Hb 2.2%, and AHb undetectable. Despite thrombolysis, blood transfusion exchanges, and anti-edematous treatment, the patient’s condition deteriorated. A decompressive craniectomy was performed on the 4th day. At 6 months, the patient remained hemiparetic and was unable to walk, but his dysphasia had markedly improved. The modified Ranking score was 4. Screening for thrombophilia (protein C and S, factor VII, antithrombin III and lipoprotein (a) plasma levels, search for antiphospholipid antibodies, factor V Dear Sir, Ischemic stroke is a common complication of sickle cell disease (SCD). Approximately 1 in10 patients with this disease has a stroke before the age of 20 years, and 20% have evidence of brain infarction on MRI [1–3] . It is the primary cause of stroke in children [2] . Ischemic stroke in these patients is usually associated with an intracranial internal carotid (IC) fork stenosis or occlusion. Here we report a patient with SCD, ischemic stroke and multiple stenoses of the extracranial carotid and vertebral arteries.

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.

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

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.

Magnetic Resonance Imaging and Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage: A Systematic Review and Meta-Analysis.

The prognosis of aneurysmal subarachnoid hemorrhage (aSAH) has improved during the past decades. However, a recent hospital-based study showed that 90-day case fatality is still 30%.1 Determinants of functional outcome after aSAH may include the severity of the initial hemorrhage, rebleeding of the aneurysm, and cerebral ischemia that can be distinguished into (1) acute ischemia at the time of bleeding when intracranial pressure rises and cerebral perfusion pressure drops, (2) procedure-related ischemia from endovascular or neurosurgical treatment of the aneurysm, and (3) delayed cerebral ischemia (DCI), which can occur between days 4 and 14 after the hemorrhage.2,3 Magnetic resonance diffusion weighted imaging (MRI-DWI) is increasingly used for the evaluation of ischemia after aSAH. The aims of the present review were to (1) analyze the proportion of patients with MRI-DWI lesions within 72 hours after aSAH, both before and after aneurysm treatment; (2) study determinants of MRI-DWI lesions within 72 hours after aSAH; (3) analyze the proportion of patients with MRI-DWI lesions between 72 hours and 21 days after aSAH; (4) investigate the predictive value of MRI-DWI lesions within 72 hours for the development of DCI; and 5) investigate whether MRI-DWI can be used for the diagnosis of DCI in patients with clinical deterioration. ### Search Strategy We searched the PUBMED, EMBASE, and Web of Science databases with the following combination of variables: MRI OR magnetic resonance AND subarachnoid hemorrhage OR SAH OR DCI OR delayed cerebral ischemia OR DIND. The last search was performed in June 28, 2016. Only studies published after January 1, 2000, were included to assure a similar degree of image quality, given the technical developments in MRI hardware and sequences. Both prospective and retrospective studies were included. Eligible articles were identified according to the PICO criteria. Type of patient population (P): (1) >95% of patients …