Differential sensitivity of the Response Bias Scale (RBS) and MMPI-2 validity scales to memory complaints

The MMPI-2 Response Bias Scale (RBS) is designed to detect response bias in forensic neuropsychological and disability assessment settings. Validation studies have demonstrated that the scale is sensitive to cognitive response bias as determined by failure on the Word Memory Test (WMT) and other symptom validity tests. Exaggerated memory complaints are a common feature of cognitive response bias. The present study was undertaken to determine the extent to which the RBS is sensitive to memory complaints and how it compares in this regard to other MMPI-2 validity scales and indices. This archival study used MMPI-2 and Memory Complaints Inventory (MCI) data from 1550 consecutive non-head-injury disability-related referrals to the first author's private practice. ANOVA results indicated significant increases in memory complaints across increasing RBS score ranges with large effect sizes. Regression analyses indicated that the RBS was a better predictor of the mean memory complaints score than the F, F_B, and F_P validity scales and the FBS. There was no correlation between the RBS and the CVLT, an objective measure of verbal memory. These findings suggest that elevated scores on the RBS are associated with over-reporting of memory problems, which provides further external validation of the RBS as a sensitive measure of cognitive response bias. Interpretive guidelines for the RBS are provided.     

Seven Essential Strategies for Promoting and Sustaining Systemic Cultural Competence

Racial and ethnic disparities are disturbing facets of the American healthcare system that document the reality of unequal treatment. Research consistently shows that patients of color experience poorer quality of care and health outcomes contributing to increased risks and accelerated mortality rates relative to their white counterparts. While initially conceptualized as an approach for increasing the responsiveness of children’s behavioral health care, cultural competence has been adopted as a key strategy for eliminating racial and ethnic health disparities across the healthcare system. However, cultural competence research and practices largely focus on improving provider competencies, while agency and system level approaches for meeting the service needs of diverse populations are given less attention. In this article we offer seven essential strategies for promoting and sustaining organizational and systemic cultural competence. These strategies are to: (1) Provide executive level support and accountability, (2) Foster patient, community and stakeholder participation and partnerships, (3) Conduct organizational cultural competence assessments, (4) Develop incremental and realistic cultural competence action plans, (5) Ensure linguistic competence, (6) Diversify, develop, and retain a culturally competent workforce, and (7) Develop an agency or system strategy for managing staff and patient grievances. For each strategy we offer several recommendations for implementation.     

Alterations in cerebral oxygen metabolism after traumatic brain injury in children

Traumatic brain injury (TBI) is the most common cause of acquired disability in children. Metabolic defects, and in particular mitochondrial dysfunction, are important contributors to brain injury after TBI. Studies of metabolic dysfunction are limited, but magnetic resonance methods suitable for use in children are overcoming this limitation. We performed noninvasive measurements of cerebral blood flow and oxygen metabolic index (OMI) to assess metabolic dysfunction in children with severe TBI. Cerebral blood flow is variable after TBI but hypoperfusion and low OMI are predominant, supporting metabolic dysfunction. This finding is consistent with preclinical and adult clinical studies of brain metabolism and mitochondrial dysfunction after TBI.     

Endogenous Angiotensin II‐induced p44/42 Mitogen‐Activated Protein Kinase Activation Mediates Sodium Appetite but not Thirst or Neurohypophysial Secretion in Male Rats

The renin–angiotensin–aldosterone system makes a critical contribution to body fluid homeostasis, and abnormalities in this endocrine system have been implicated in certain forms of hypertension. The peptide hormone angiotensin II (AngII) regulates hydromineral homeostasis and blood pressure by acting on both peripheral and brain targets. In the brain, AngII binds to the angiotensin type 1 receptor (AT1R) to stimulate thirst, sodium appetite and both arginine vasopressin (AVP) and oxytocin (OT) secretion. The present study used an experimental model of endogenous AngII to examine the role of p44/42 mitogen‐activated protein kinase (MAPK) as a signalling mechanism to mediate these responses. Animals were given a combined treatment of furosemide and a low dose of captopril (furo/cap), comprising a diuretic and an angiotensin‐converting enzyme inhibitor, respectively, to elevate endogenous AngII levels in the brain. Furo/cap induced p44/42 MAPK activation in key brain areas that express AT1R, and this effect was reduced with either a centrally administered AT1R antagonist (irbesartan) or a p44/42 MAPK inhibitor (U0126). Additionally, furo/cap treatment elicited water and sodium intake, and irbesartan markedly reduced both of these behaviours. Central injection of U0126 markedly attenuated furo/cap‐induced sodium intake but not water intake. Furthermore, p44/42 MAPK signalling was not necessary for either furo/cap‐ or exogenous AngII‐induced AVP or OT release. Taken together, these results indicate that p44/42 MAPK is required for AngII‐induced sodium appetite but not thirst or neurohypophysial secretion. This result may allow for the discovery of more specific downstream targets of p44/42 MAPK to curb sodium appetite, known to exacerbate hypertension, at the same time as leaving thirst and neurohypophysial hormone secretion undisturbed.     

PET imaging of acetylcholinesterase inhibitor‐induced effects on α4β2 nicotinic acetylcholine receptor binding

Acetylcholinesterase inhibitors (AChEIs) are drugs that increase synaptic acetylcholine (ACh) concentrations and are under investigation as treatments for symptoms accompanying Alzheimer's disease. The goal of this work was to use PET imaging to evaluate alterations of in vivo α4β2 nicotinic acetylcholine receptor (nAChR) binding induced by the AChEIs physostigmine (PHY) and galanthamine (GAL). The α4β2 nAChR‐specific radioligand [¹⁸F]nifene was used to examine the effects of 0.1–0.2 mg/kg PHY, 5 mg/kg GAL, and saline in three separate experiments all performed on each of two rat subjects. A 60‐min bolus‐infusion protocol was used with drug administered after 30 min. Data from the thalamus and cortex were analyzed with a graphical model accounting for neurotransmitter activation using the cerebellum as a reference region to test for transient competition with bound [¹⁸F]nifene. Significant [¹⁸F]nifene displacement was detected in both regions during one PHY and both GAL studies, while no significant competition was observed in both saline studies. This preliminary work indicates the viability of [¹⁸F]nifene in detecting increases in synaptic ACh induced by AChEIs. Synapse 67:882–886, 2013. © 2013 Wiley Periodicals, Inc.     

Chronic ethanol and withdrawal differentially modulate pre- and postsynaptic function at glutamatergic synapses in rat basolateral amygdala

Withdrawal anxiety is a significant factor contributing to continued alcohol abuse in alcoholics. This anxiety is long-lasting, can manifest well after the overt physical symptoms of withdrawal, and is frequently associated with relapse in recovering alcoholics. The neurobiological mechanisms governing these withdrawal-associated increases in anxiety are currently unknown. The basolateral amygdala (BLA) is a major emotional center in the brain and regulates the expression of both learned fear and anxiety. Neurotransmitter system alterations within this brain region may therefore contribute to withdrawal-associated anxiety. Because evidence suggests that glutamate-gated neurotransmitter receptors are sensitive to acute ethanol exposure, we examined the effect of chronic intermittent ethanol (CIE) and withdrawal (WD) on glutamatergic synaptic transmission in the BLA. We found that slices prepared from CIE and WD animals had significantly increased contributions by synaptic NMDA receptors. In addition, CIE increased the amplitude of AMPA-receptor-mediated spontaneous excitatory postsynaptic currents (sEPSCs), whereas only WD altered the amplitude and kinetics of tetrodotoxin-resistant spontaneous events (mEPSCs). Similarly, the frequency of sEPSCs was increased in both CIE and WD neurons, although only WD increased the frequency of mEPSCs. These data suggest that CIE and WD differentially alter both pre- and postsynaptic properties of BLA glutamatergic synapses. Finally, we show that microinjection of the AMPA-receptor antagonist, DNQX, can attenuate withdrawal-related anxiety-like behavior. Together, our results suggest that increased glutamatergic function may contribute to anxiety expressed during withdrawal from chronic ethanol.