Treatment Patterns of Anxiety and Posttraumatic Stress Disorder Following Traumatic Brain Injury.

OBJECTIVE: Symptoms of mental disorders are common, are underrecognized, and contribute to worse outcomes after traumatic brain injury (TBI). Post-TBI, prevalence of anxiety disorders and prevalence of posttraumatic stress disorder (PTSD) are comparable with that of depression, but evidence-based treatment guidelines are lacking. The investigators examined psychotropic medication use and psychotherapy patterns among individuals diagnosed with anxiety disorders and PTSD post-TBI. METHODS: Administrative claims data were used to compare the prevalence and patterns of pharmacotherapy and psychotherapy utilization among individuals diagnosed with an anxiety disorder or PTSD post-TBI. RESULTS: Among 207,354 adults with TBI, prevalence of anxiety disorders was 20.5%, and prevalence of PTSD was 0.6% post-TBI. Receipt of pharmacotherapy pre- and post-TBI (anxiety: pre-TBI=58.4%, post-TBI=76.2%; PTSD: pre-TBI=53.7%, post-TBI=75.2%) was considerably more common than receipt of psychotherapy (anxiety: pre-TBI=5.8%, post-TBI=19.1%; PTSD: pre-TBI=11.2%, post-TBI=36.0%). Individuals diagnosed with anxiety were 66% less likely to receive psychotherapy compared with individuals diagnosed with PTSD, although engagement in psychotherapy decreased faster over time among those with PTSD. Overall, psychotropic medication use and rates of antidepressant prescription use in the anxiety group were higher compared with those in the PTSD group. Benzodiazepines were the second most commonly prescribed medication class in the anxiety group, even though judicious use is warranted post-TBI. CONCLUSIONS: Further exploration of differences and risks associated with pharmacotherapy for anxiety and PTSD post-TBI is warranted to refine treatment guidelines. The low level of psychotherapy engagement suggests that barriers and facilitators to psychotherapy utilization post-TBI should be examined in future studies.

Lack of association between cognitive impairment and systemic inflammation in asymptomatic carotid stenosis.

BACKGROUND: Asymptomatic carotid atherosclerotic stenosis (ACAS) is associated with cognitive impairment. Systemic inflammation occurs in patients with systemic atherosclerosis and is also associated with cognitive impairment. The goal of this study was to determine if cognitive impairment in patients with ACAS is the result of systemic inflammation. METHODS: A cross-sectional analysis of 104 patients (63 patients with ACAS, 41 controls) with cognitive function and inflammatory biomarker assessments was performed. Venous blood was assayed for proinflammatory biomarkers (IL-1ß, IL-6, IL-6R, IL-8, IL-17, tumor necrosis factor-α, matrix metalloproteinase [MMP]-1, MMP-2, MMP-7, MMP-9, vascular cell adhesion molecule, and high-sensitivity C-reactive protein). The patients also underwent comprehensive cognitive testing to compute five domain-specific cognitive scores per patient. We first assessed the associations between carotid stenosis and cognitive function, and between carotid stenosis and systemic inflammation in separate regression models. We then determined whether cognitive impairments persisted in patients with carotid stenosis after accounting for inflammation by adjusting for inflammatory biomarker levels in a combined model. RESULTS: Patients with ACAS and control patients differed in age, race, coronary artery disease prevalence, and education. Stenosis patients had worse cognitive scores in two domains: learning and memory (P = .05) and motor and processing speed (P = .002). Despite adjusting for inflammatory biomarker levels, patients with ACAS still demonstrated deficits in the domains of learning and memory and motor and processing speed. CONCLUSIONS: Although systemic atherosclerosis-induced inflammation is a well-recognized cause for cognitive impairment, our data suggest that it is not the primary underlying mechanism behind cognitive impairments seen in ACAS. Cognitive impairments in learning and memory and motor and processing speed seen in patients with ACAS persist after adjusting for systemic inflammation. Thus, alternative mechanisms should be explored to account for the observed functional impairments.

Integration of Neuropsychological Services in a VA HIV Primary Care Clinic.

The Department of Veteran Affairs (VA) is the largest health care provider for individuals with human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS), with >28,000 Veterans with HIV/AIDS enrolled in care. Advances in medical treatment have improved the life-limiting effects of the disease, though many chronic symptoms persist. Comprehensive care is critical to manage the diverse constellation of symptoms. However, many patients face challenges to receiving optimal care due to limited resources, mistrust of health care providers, and/or co-occurring medical, psychiatric, and substance use disorders. The VA is a leader in developing integrated models of care to address these barriers. The inclusion of subspecialty mental health and substance abuse treatment in HIV care has been implemented across many VAs, with evidence of improved patient outcomes. However, neuropsychology has not traditionally been included, despite the fact that cognitive dysfunction represents one of the most ubiquitous complications of HIV/AIDS. Cognitive impairment is associated with myriad negative outcomes including medication non-adherence, reduced quality of life, and increased mortality. We contend that neuropsychologists are uniquely equipped to contribute to the comprehensive care of patients with HIV/AIDS. Neuropsychologists understand the range of factors that can impact cognition and have the requisite knowledge and skills to assess and treat cognitive dysfunction. Although we focus on HIV/AIDS, neuropsychologists often play critical roles in the provision of care for other infectious diseases (e.g., hepatitis C).

Asymptomatic carotid stenosis is associated with cognitive impairment.

BACKGROUND: Cerebrovascular risk factors (eg, hypertension, coronary artery disease) and stroke can lead to vascular cognitive impairment. The Asymptomatic Carotid Stenosis and Cognitive Function study evaluated the isolated impact of asymptomatic carotid stenosis (no prior ipsilateral or contralateral stroke or transient ischemic attack) on cognitive function. Cerebrovascular hemodynamic and carotid plaque characteristics were analyzed to elucidate potential mechanisms affecting cognition. METHODS: There were 82 patients with ≥50% asymptomatic carotid stenosis and 62 controls without stenosis but matched for vascular comorbidities who underwent neurologic, National Institutes of Health Stroke Scale, and comprehensive neuropsychological examination. Overall cognitive function and five domain-specific scores were computed. Duplex ultrasound with Doppler waveform and B-mode imaging defined the degree of stenosis, least luminal diameter, plaque area, and plaque gray-scale median. Breath-holding index (BHI) and microembolization were measured using transcranial Doppler. We assessed cognitive differences between stenosis patients and control patients and of stenosis patients with low vs high BHI and correlated cognitive function with microembolic counts and plaque characteristics. RESULTS: Stenosis and control patients did not differ in vascular risk factors, education, estimated intelligence, or depressive symptoms. Stenosis patients had worse composite cognitive scores (P = .02; Cohen's d = 0.43) and domain-specific scores for learning/memory (P = .02; d = 0.42) and motor/processing speed (P = .01; d = 0.65), whereas scores for executive function were numerically lower (P = .08). Approximately 49.4% of all stenosis patients were impaired in at least two cognitive domains. Precisely 50% of stenosis patients demonstrated a reduced BHI. Stenosis patients with reduced BHI performed worse on the overall composite cognitive score (t = -2.1; P = .02; d = 0.53) and tests for learning/memory (t = -2.7; P = .01; d = 0.66). Cognitive function did not correlate with measures of plaque burden (degree of stenosis, least luminal diameter, and plaque area) or with plaque gray-scale median. CONCLUSIONS: Asymptomatic carotid stenosis is associated with cognitive impairment independent of known vascular risk factors for vascular cognitive impairment. Approximately 49.4% of these patients demonstrate impairment in at least two neuropsychological domains. The deficit is driven primarily by reduced motor/processing speed and learning/memory and is mild to moderate in severity. The mechanism for impairment is likely to be hemodynamic as evidenced by reduced cerebrovascular reserve and the likely result of hypoperfusion from a pressure drop across the stenosis in the presence of inadequate collateralization.

The moderating role of negative affect on objective verbal memory performance and subjective memory complaints in healthy older adults.

Subjective memory complaints (SMCs) are part of the diagnostic criteria for Mild Cognitive Impairment (MCI), yet little is known about their etiology. In some previous studies, no direct relation has been found between SMCs and objective memory performance, yet significant correlations have been identified between SMCs and psychological factors such as depression and anxiety. In the current study, we examined whether negative affect moderated the relation between objective memory functioning and SMCs in a sample of healthy, non-demented participants aged 65 and older. As predicted, several negative affect measures moderated the relationship between objective cognitive functioning and SMCs. In the absence of objective memory impairment as indexed by the Rey Auditory Verbal Learning Test (RAVLT) and the Dementia Rating Scale-2nd Edition (DRS-2), higher levels of negative affect were associated with increased levels of SMCs. Moreover, a lower order negative affect factor, anxiety sensitivity, significantly moderated the relation between objective memory functioning and SMCs, after controlling for higher order measures of general negative affectivity. Findings suggest that negative affect, particularly anxiety sensitivity, distorts the subjective appraisal of one's own memory, such that people high on negative affect factors report more episodes of forgetting, even in the absence of objective cognitive impairments.