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.ABBREVIATIONS: CAA ϭ cerebral amyloid angiopathy; cSAH ϭ cortical subarachnoid hemorrhage; CTA ϭ CT angiography; CTV ϭ CT venography; CVT ϭ cerebral venous thrombosis; DSA ϭ digital subtraction angiography; DWI ϭ diffusion-weighted imaging; FLAIR ϭ fluid-attenuated inversion recovery; Gd ϭ gadolinium; GRE T2 ϭ gradient echo T2-weighted imaging; MRA ϭ MR angiography; MRV ϭ MR venography; PRES ϭ posterior reversible encephalopathy syndrome; RCVS ϭ reversible cerebral vasoconstriction syndrome; SAH ϭ subarachnoid hemorrhage; SWI ϭ susceptibility-weighted imaging; TIA ϭ transient ischemic attack; TOF ϭ time of flight N ontraumatic (spontaneous) SAH arises in approximately 85% of cases from rupture of a saccular aneurysm at the base of the brain. Nonaneurysmal perimesencephalic hemorrhages account for another 10%.
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.
This article reviews the most relevant state-of-the-art magnetic resonance (MR) techniques, which are clinically available to investigate brain diseases. MR acquisition techniques addressed include notably diffusion imaging (diffusion-weighted imaging (DWI), diffusion tensor imaging (DTI), and diffusion kurtosis imaging (DKI)) as well as perfusion imaging (dynamic susceptibility contrast (DSC), arterial spin labeling (ASL), and dynamic contrast enhanced (DCE)). The underlying models used to process these images are described, as well as the theoretic underpinnings of quantitative diffusion and perfusion MR imaging-based methods. The technical requirements and how they may help to understand, classify, or follow-up neurological pathologies are briefly summarized. Techniques, principles, advantages but also intrinsic limitations, typical artifacts, and alternative solutions developed to overcome them are discussed. In this article, we also review routinely available three-dimensional (3D) techniques in neuro MRI, including state-of-the-art and emerging angiography sequences, and briefly introduce more recently proposed 3D quantitative neuro-anatomy sequences, and new technology, such as multi-slice and multi-transmit imaging.
BackgroundWhite matter hyperintensities (WMH) lesions on T2/FLAIR brain MRI are frequently seen in healthy elderly people. Whether these radiological lesions correspond to irreversible histological changes is still a matter of debate. We report the radiologic-histopathologic concordance between T2/FLAIR WMHs and neuropathologically confirmed demyelination in the periventricular, perivascular and deep white matter (WM) areas.ResultsInter-rater reliability was substantial-almost perfect between neuropathologists (kappa 0.71 - 0.79) and fair-moderate between radiologists (kappa 0.34 - 0.42). Discriminating low versus high lesion scores, radiologic compared to neuropathologic evaluation had sensitivity / specificity of 0.83 / 0.47 for periventricular and 0.44 / 0.88 for deep white matter lesions. T2/FLAIR WMHs overestimate neuropathologically confirmed demyelination in the periventricular (p < 0.001) areas but underestimates it in the deep WM (0 < 0.05). In a subset of 14 cases with prominent perivascular WMH, no corresponding demyelination was found in 12 cases.ConclusionsMRI T2/FLAIR overestimates periventricular and perivascular lesions compared to histopathologically confirmed demyelination. The relatively high concentration of interstitial water in the periventricular / perivascular regions due to increasing blood–brain-barrier permeability and plasma leakage in brain aging may evoke T2/FLAIR WMH despite relatively mild demyelination.
Our data provide in situ evidence that PML-IRIS brain lesions are enriched in cytotoxic CD8+ T cells that engage JCV-infected oligodendrocytes. This leads to a better control of JCV dissemination, but at the cost of oligodendrocyte cell death and demyelination.
International audienceBackground: Toxoplasmic encephalitis associated with immune reconstitution inflammatory syndrome (TE-IRIS) is rarely described. Methods: To identify TE-IRIS cases, we performed a retrospective study of all HIV-infected patients diagnosed with TE in our unit between January 2000 and June 2009, and a review of published cases. Results: Three patients out of our 65 TE cases, together with six from the literature, fulfilled unmasking TE-IRIS definition. None fulfilled paradoxical TE-IRIS definition. TE occurred within a median time of 48.5 days [IQ25-75 21-56] after starting antiretroviral therapy. Cases did not have distinctive clinical nor neuroimaging features from TE occurring without immune reconstitution. However: i) Cases occurred at a median CD4 lymphocytes count of 222/µL [IQ25-75 160-280], ii) TE occurred in five patients who were supposed to take an effective chemoprophylaxis, iii) Two patients had a brain biopsy showing an intense angiocentric inflammatory infiltrates with predominantly CD8 lymphocytes, iv) In one patient, the abnormal length of evolution under treatment might be due to the heightened immune response. Conclusion: Although rare, unmasking TE-IRIS exists and might occur despite effective prophylaxis and an unusually high CD4 lymphocytes count. IRIS does not modify TE diagnosis and treatment but might extend its clinical course
3D T1 SPACE sequence offers similar information with its 2D counterpart, in a shorter acquisition time and larger coverage area.
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