This study aimed to describe children with moyamoya disease from an international multicenter stroke database, and explore risk factors for stroke recurrence. We reviewed data of children >28-days old with moyamoya disease enrolled in the International Pediatric Stroke Study from January 2003 to March 2013. A total of 174 children from 32 sites and 14 countries had moyamoya disease; median age 7.4 years, 49% male. Of these, 90% presented with ischemic stroke, 7.5% with transient ischemic attack, and 2.5% with hemorrhagic stroke. One-third of patients had moyamoya syndrome. Stroke recurrence was 20% over median follow-up of 13 months; 9% had multiple recurrences. Children treated with surgical revascularization were less likely to have stroke recurrence (P = .046). Moyamoya disease accounted for 8% of arterial strokes in this international pediatric stroke registry. One-third of pediatric patients with moyamoya disease have an underlying syndromic condition. Surgical revascularization is effective at reducing the incidence of stroke recurrence.

This population-based study assesses the long-term impact of childhood stroke on function and independence in young adults. We undertook a cross-sectional outcome study of patients with arterial ischemic stroke and cerebral sinovenous thrombosis, beyond 18 years of age. We studied 26 patients; 21 arterial stroke, 5 cerebral sinovenous thrombosis, with 16 females. Mean age at assessment was 21.5 years, and mean follow-up time was 10.8 years. According to the modified Rankin Scale, final outcomes were 37% normal, 42% mild, 8% moderate, and 15% severe deficits. Risk factors for abnormal functional outcome included arterial ischemic stroke, presence of arteriopathy, and 1-year poststroke Pediatric Stroke Outcome Measure score ≥ 2 (P < .05). Most (77-84%) were independent in driving, relationships, and employment. Functional status at 1 year poststroke strongly predicts long-term outcome. Mental illness in one-quarter of young adults surviving childhood stroke represents an important direction for research.

Although dysregulated stress biology is becoming increasingly recognized as a key driver of lifelong disparities in chronic disease, we presently have no validated biomarkers of toxic stress physiology; no biological, behavioral, or cognitive treatments specifically focused on normalizing toxic stress processes; and no agreed-upon guidelines for treating stress in the clinic or evaluating the efficacy of interventions that seek to reduce toxic stress and improve human functioning. We address these critical issues by (a) systematically describing key systems and mechanisms that are dysregulated by stress; (b) summarizing indicators, biomarkers, and instruments for assessing stress response systems; and (c) highlighting therapeutic approaches that can be used to normalize stress-related biopsychosocial functioning. We also present a novel multidisciplinary Stress Phenotyping Framework that can bring stress researchers and clinicians one step closer to realizing the goal of using precision medicine-based approaches to prevent and treat stress-associated health problems.