Objective: To identify and compare clinical and neuroimaging predictors of primary lobar intracerebral hemorrhage (ICH) recurrence, assessing their relative contributions to recurrent ICH.Methods: Subjects were consecutive survivors of primary ICH drawn from a single-center prospective cohort study. Baseline clinical, imaging, and laboratory data were collected. Survivors were followed prospectively for recurrent ICH and intercurrent aspirin and warfarin use, including duration of exposure. Cox proportional hazards models were used to identify predictors of recurrence stratified by ICH location, with aspirin and warfarin exposures as time-dependent variables adjusting for potential confounders.Results: A total of 104 primary lobar ICH survivors were enrolled. Recurrence of lobar ICH was associated with previous ICH before index event (hazard ratio [HR] 7.7, 95% confidence interval [CI] 1.4 -15.7), number of lobar microbleeds (HR 2.93 with 2-4 microbleeds present, 95% CI 1.3-4.0; HR ϭ 4.12 when Ն5 microbleeds present, 95% CI 1.6 -9.3), and presence of CTdefined white matter hypodensity in the posterior region (HR 4.11, 95% CI 1.01-12.2). Although aspirin after ICH was not associated with lobar ICH recurrence in univariate analyses, in multivariate analyses adjusting for baseline clinical predictors, it independently increased the risk of ICH recurrence (HR 3.95, 95% CI 1.6 -8.3, p ϭ 0.021). Conclusions:Recurrence of lobar ICH is associated with previous microbleeds or macrobleeds and posterior CT white matter hypodensity, which may be markers of severity for underlying cerebral amyloid angiopathy. Use of an antiplatelet agent following lobar ICH may also increase recurrence risk. Neurology ® 2010;75:693-698 GLOSSARY CAA ϭ cerebral amyloid angiopathy; CI ϭ confidence interval; CT-WMH ϭ CT-defined white matter hypodensity; HR ϭ hazard ratio; ICH ϭ intracerebral hemorrhage; VIF ϭ variance inflation factor.Intracerebral hemorrhage (ICH), although accounting for only 15% of acute strokes in the United States, 1 carries the worst prognosis of all acute cerebrovascular diseases. 2,3 Lobar ICH location (selective involvement of the cerebral cortex and underlying white matter) is associated with greater risk for recurrence than deep ICH location [4][5][6] and is associated with different clinical features and risk factors. 7,8 Nonfamilial cerebral amyloid angiopathy (CAA), caused by ␤-amyloid deposition in cerebral arteries and arterioles, is a major cause of lobar ICH but not deep ICH, as shown by autopsy investigations, 9 as well as studies linking lobar ICH with several hallmarks of CAA, such as the APOE ⑀2 and ⑀4 alleles, 5,9,10 asymptomatic microbleeds detected on gradient-echo MRI, 11,12 and white matter lesions. 13 Based on recent evidence, there is some suggestion that asymptomatic CAA may be highly prevalent in the elderly. 14,15 Although several predictors of lobar ICH recurrence have been described, little is known regarding the relative contribution or interaction of each of these predictors. For examp...

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The physiological consequences of acute and chronic stress on a range of organ systems have been well documented after the pioneering work of Hans Selye more than 70 years ago. More recently, an association between exposure to stressful life events and the development of later-life cognitive dysfunction has been proposed. Several plausible neurohormonal pathways and genetic mechanisms exist to support such an association. However, many logistical and methodological barriers must be overcome before a defined causal linkage can be firmly established. Here the authors review recent studies of the long-term cognitive consequences of exposures to cumulative ordinary life stressors as well as extraordinary traumatic events leading to posttraumatic stress disorder. Suggestive effects have been demonstrated for the role of life stress in general, and posttraumatic stress disorder in particular, on a range of negative cognitive outcomes, including worse than normal changes with aging, Alzheimer's disease, and vascular dementia. However, given the magnitude of the issue, well-controlled studies are relatively few in number, and the effects they have revealed are modest in size. Moreover, the effects have typically only been demonstrated on a selective subset of measures and outcomes. Potentially confounding factors abound and complicate causal relationships despite efforts to contain them. More well-controlled, carefully executed longitudinal studies are needed to confirm the apparent association between stress and dementia, clarify causal relationships, develop reliable antemortem markers, and delineate distinct patterns of risk in subsets of individuals.

Adult patients with significant childhood and current symptoms of attention-deficit hyperactivity disorder (ADHD), but whose ADHD had not been previously recognized, were evaluated by three clinical consultants working with diverse referral populations. These 60 adults shared common characteristics of physical and mental restlessness, impulsivity, disabling distractibility, low self-esteem, self-loathing, and a gnawing sense of underachievement. Specific learning or behavior problems were often present. These patients were chronically disaffected. The diagnosis of ADHD appeared to be missed because these individuals presented with atypical symptoms or had found ways to compensate for their deficits. Descriptive generalizations are offered concerning their coping strategies. These adults had sought previous psychiatric care for non-ADHD symptoms but had numerous unsuccessful treatment attempts. Most patients had been treated for mood or anxiety disorders. Traditional defense analysis had little beneficial effect and aggravated problems of self-esteem; modifications of the psychotherapeutic process are recommended. In open clinical trials without formal measures, the majority of such patients appeared to respond to low doses of antidepressants (i.e., desipramine 10-30 mg daily) and seemed to lose the therapeutic effect at higher antidepressant doses.