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.

Both PTSD and TBI commonly occur in the general population, both share some pathophysiological characteristics and both are associated with cognitive impairment and sleep disruption. PTSD and TBI present with a number of overlapping symptoms, which can lead to over-diagnosis or misdiagnosis. Both conditions are associated with co-morbidities important in diagnosis and treatment planning. More research is needed to elucidate what treatments are effective in PTSD and TBI co-morbidity and on factors predictive of treatment success.

Background: Links between dissociation and functional neurological disorder (FND)/conversion disorder are well-established, yet the pathophysiology of dissociation remains poorly understood. This MRI study investigated structural alterations associated with somatoform and psychological dissociation in FND. We hypothesized that multimodal, paralimbic cingulo-insular regions would relate to the severity of somatoform dissociation in patients with FND. Methods: FreeSurfer cortical thickness and subcortical volumetric analyses were performed in 26 patients with motor FND and 27 matched healthy controls. Patients with high dissociation as measured by the Somatoform Dissociation Questionnaire-20 (SDQ) or Dissociative Experiences Scale (DES) were compared to controls in stratified analyses. Within-group analyses were also performed with SDQ and DES scores in patients with FND. All cortical thickness analyses were whole-brain corrected at the cluster-wise level. somatoform dissociation (SDQ > 35) showed reduced left caudal anterior cingulate cortex (ACC) cortical thickness compared to controls. In within-group analyses, SDQ scores inversely correlated with left caudal ACC cortical thickness in patients with FND. Depersonalization/derealization scores positively correlated with right lateral occipital cortical thickness. Both within-group findings remained statistically significant controlling for trait anxiety/depression, borderline personality disorder and posttraumatic stress disorder, adverse life events, and motor FND subtypes in post-hoc analyses. Conclusion: Using complementary between-group and within-group analyses, an inverse association between somatoform dissociation and left caudal ACC cortical thickness was observed in patients with FND. A positive relationship was also appreciated between depersonalization/derealization severity and cortical thickness in visual association areas. These findings advance our neuropathobiological understanding of dissociation in FND. Hum Brain Mapp 39:428-439, 2018.V C 2017 Wiley Periodicals, Inc.

Head pain is the fifth most common reason for emergency department (ED) visits. It is second only to focal weakness as the most common reason for neurological consultation in the ED. This manuscript reviews how patients with migraine, the most common primary headache disorder for which patients seek medical treatment, are managed in the ED. We discuss existing guidelines for head imaging in patients with migraine, recommended pharmacologic treatments, and current treatment trends. We also review studies evaluating the discharge care of migraine patients in the ED. With the goal of standardizing, streamlining, and optimizing ED-based migraine care, we offer ideas for future research to improve the evaluation, treatment, and discharge care of patients who present to an ED with acute migraine.

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Background Levodopa is the most efficacious drug in the symptomatic therapy of motor symptoms in Parkinson's disease (PD); however, long‐term treatment is often complicated by troublesome levodopa‐induced dyskinesia (LID). Recent evidence suggests that LID might be related to increased cortical gamma oscillations. Objective The objective of this study was to test the hypothesis that cortical high‐gamma network activity relates to LID in the 6‐hydroxydopamine model and to identify new biomarkers for adaptive deep brain stimulation (DBS) therapy in PD. Methods We recorded and analyzed primary motor cortex (M1) electrocorticogram data and motor behavior in freely moving 6‐OHDA lesioned rats before and during a daily treatment with levodopa for 3 weeks. The results were correlated with the abnormal involuntary movement score (AIMS) and used for generalized linear modeling (GLM). Results Levodopa reverted motor impairment, suppressed beta activity, and, with repeated administration, led to a progressive enhancement of LID. Concurrently, we observed a highly significant stepwise amplitude increase in finely tuned gamma (FTG) activity and gamma centroid frequency. Whereas AIMS and FTG reached their maximum after the 4th injection and remained on a stable plateau thereafter, the centroid frequency of the FTG power continued to increase thereafter. Among the analyzed gamma activity parameters, the fraction of longest gamma bursts showed the strongest correlation with AIMS. Using a GLM, it was possible to accurately predict AIMS from cortical recordings. Conclusions FTG activity is tightly linked to LID and should be studied as a biomarker for adaptive DBS. © 2020 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society

Traumatic brain injury (TBI) is a serious health risk for older adults, and the consequences of TBI range from full recovery to death. For many who survive, there is a legacy of cognitive, physical, and emotional disability. Falls are the major cause of head injury in older adults. There are many risk factors including pre-existing brain disease, other diseases, and, sometimes, iatrogenic factors. Efforts directed at prevention are of great importance. Outcome studies indicate that outcome is generally worse for older people than for younger people with similar injuries, but older individuals also deserve aggressive rehabilitation directed at the best possible recovery. This review will discuss the symptoms and syndromes that commonly result from TBI with comments about treatment.

Neurobiologic, psychologic, and social factors interact jointly to create and perpetuate the symptoms of post-traumatic stress disorder (PTSD). The fear conditioning paradigm in animal research helped researchers gather preclinical evidence for the possible contribution of several brain areas to PTSD symptoms. In the past 10 years, highly sophisticated neuroimaging techniques made it possible for researchers to look at the brain of patients with PTSD and draw conclusions about the neurocircuitry underlying PTSD symptoms. In this article, the author will review the evidence from neuroimaging studies for the involvement of the following brain areas in PTSD neurocircuitry: the amygdala, the anterior cingulate cortex and subcallosal gyrus, the inferior frontal gyrus, the posterior cingulate cortex, and the hippocampus. Neuroimaging studies have shown these areas as altered in structure or function in patients with PTSD. The author also presents the normal functions that these areas subserve and, whenever possible based on the evidence, infer how their dysfunction may contribute importantly to the symptomatology of PTSD.