Systematic Review and Meta-Analysis of the Association Between Appearance of Lesions on Diffusion-Weighted Imaging and Poor Outcomes Among Patients with Intracerebral Hemorrhage.

OBJECTIVE: Some patients with intracerebral hemorrhage show lesions on diffusion-weighted magnetic resonance imaging, and such lesions have been associated with a greater risk of worse prognosis. Here we meta-analyzed the available evidence for such an association. METHODS: Studies that reported the presence or absence of lesions on diffusion-weighted imaging (DWI) after intracerebral hemorrhage as well as clinical or radiological outcomes were systematically reviewed and meta-analyzed. Clinical outcome was defined as a score of modified Rankin scale (mRS) at admission to 90 days. RESULTS: Ten studies involving 3575 patients were included in the meta-analysis, and the incidence of DWI lesions ranged from 11.1% to 49.6%. Lesions were associated with a significantly higher risk of poor outcome (mRS scores 3-6) across 6 studies (odds ratio: 2.91; 95% confidence interval: 1.62-5.23; P < 0.001). In subgroup analysis, mRS scores 4-6 were associated with the presence of lesions on DWI (odds ratio: 2.18; 95% confidence interval: 1.31-3.60; P = 0.003). We observed similar results using 3 different definitions of lesions on DWI. Some studies have reported that recurrence of intracerebral hemorrhage was also related with DWI lesions. But there was controversy on the relationship between mortality, ischemic stroke, and hematoma volume and DWI lesions. CONCLUSIONS: Lesions on DWI after intracerebral hemorrhage were associated with a higher risk of poor outcome, but large longitudinal studies are needed to verify this association.

HMGB1/TLR4 axis promotes pyroptosis after ICH by activating the NLRP3 inflammasome.

BACKGROUND: We previously reported that the HMGB1/TLR4 axis promoted inflammation during the acute phase of intracerebral hemorrhage. Given that this phase is known to involve neuronal pyroptosis and neuroinflammation, here we explore whether HMGB1/TLR signaling activate inflammasome and pyroptosis after intracerebral hemorrhage. METHODS: Autologous blood was injected into Sprague-Dawley rats to induce intracerebral hemorrhage. Neurological deficits were assessed using a modified neurological severity score. These expression and localization of NLRP1 and NLRP3 inflammasomes, as well as the levels of pyroptosis and pyroptosis-associated proteins were assessed using Western blot or immunocytochemistry. These experiments were repeated in animals that received treatment with short interfering RNAs against NLRP1 or NLRP3, with HMGB1 inhibitor ethyl pyruvate or TLR4 inhibitor TAK-242. RESULTS: Intracerebral hemorrhage upregulated NLRP1 and NLRP3 in the ipsilateral striatum and increased the proportions of these cells that were pyroptosis-positive. Additionally, the levels of caspase protein family (e.g., pro-caspase-1 and caspase-1), apoptosis-associated speck-like protein (ASC), pro-interleukin-1ß (IL-1ß), and IL-1ß were also elevated. These effects on pyroptosis and associated neurological deficit, were partially reversed by knockdown of NLRP1 or NLRP3, or by inhibition of HMGB1 or TLR4. Inhibition of HMGB1 or TLR4 resulted in the downregulation NLRP3 but not NLRP1. CONCLUSIONS: The HMGB1/TLR4 signaling may activate the NLRP3 inflammasome during the acute phase of intracerebral hemorrhage, resulting in the inflammatory process known as pyroptosis. These insights suggest potential therapeutic targets for the mitigation tissue injury and associated neurological deficits following hemorrhagic stroke.

A Case of Cerebral Large-Vessel Vasculitis Concomitant Fahr Syndrome in Systemic Lupus Erythematosus.

INTRODUCTION: Systemic lupus erythematosus (SLE) is a heterogenous, devastating autoimmune inflammatory disease with multiorgan involvement. A variety of neurological and psychiatric symptoms may be caused by nervous system involvement, termed neuropsychiatric systemic lupus erythematosus. CASE REPORT: We describe a young man newly diagnosed with SLE who had a stroke as an initial symptom and was found to have cerebral large-vessel vasculitis and Fahr syndrome. CONCLUSIONS: The novelties of this report are the extensive cerebral calcification demonstrated on head computerized tomography in a patient with SLE, and the depiction of an underlying vasculitis on high-resolution magnetic resonance vessel wall imaging. It is our aim to describe this atypical form of neuropsychiatric systemic lupus erythematosus onset and to make known the usefulness of the new magnetic resonance imaging techniques for the diagnosis of cerebral large-vessel vasculitis.

Association Between Silent Brain Infarcts and Cognitive Function: A Systematic Review and Meta-Analysis.

BACKGROUND AND PURPOSE: Silent brain infarct (SBI), which has traditionally been considered clinically silent, has been proposed as a subclinical risk marker for future cognitive function decline. METHODS: We conducted a systematic review of literature in the Cochrane Library, MEDLINE, EMBASE, and the China National Knowledge Infrastructure database. RESULTS: In the end, 19 case-control studies, comprising 6712 participants, and 3 prospective cohort studies comprising 4433 participants, met all inclusion criteria and were included in the systematic review. Meta-analysis of 9 studies showed that SBI was an important factor in cognitive function decline (Mini-Mental State score) (standardized mean difference -.47, 95% confidence interval; -.72 to -.22). Another meta-analysis of 4 studies reported the SBI was an independent factor in cognitive dysfunction (Montreal Cognitive Assessment Scale) (standardized mean difference -3.36, 95% confidence interval; -5.90 to -.82). Ten studies further reported that SBI was associated with decreases in specific areas of cognitive function. CONCLUSIONS: These results suggest that rather than being clinically silent, SBI might be a factor inducing cognitive dysfunction.