A Quantitative Meta-analysis of Olfactory Dysfunction in Epilepsy.

Olfactory dysfunction in epilepsy is well-documented in several olfactory domains. However, the clinical specificity of these deficits remains unknown. The aim of this systematic meta-analysis was to determine which domains of olfactory ability were most impaired in individuals with epilepsy, and to assess moderating factors affecting olfactory ability. Extant peer-reviewed literature on olfaction in epilepsy were identified via a computerized literature search using PubMed, MEDLINE, PsycInfo, and Google Scholar databases. Twenty-one articles met inclusion criteria. These studies included a total of 912 patients with epilepsy and 794 healthy comparison subjects. Included studies measured olfaction using tests of odor identification, discrimination, memory, and detection threshold in patients with different types of epilepsy, including temporal lobe epilepsy (TLE), mixed frontal epilepsy (M-F), and mixed epilepsy (MIX). Olfactory deficits were robust in patients with epilepsy when compared to healthy individuals, with effect sizes in the moderate to large range for several olfactory domains, including odor identification (d = -1.59), memory (d = -1.10), discrimination (d = -1.04), and detection threshold (d = -0.58). Olfactory deficits were most prominent in patients with TLE and M-F epilepsy. Amongst patients with epilepsy, sex, age, smoking status, education, handedness, and age of illness onset were significantly related to olfactory performance. Overall, these meta-analytic findings indicate that the olfactory system is compromised in epilepsy and suggest that detailed neurobiological investigations of the olfactory system may provide further insight into this disorder.

HIV-associated neurocognitive disorders: the relationship of HIV infection with physical and social comorbidities.

The prevalence of HIV (human immunodeficiency virus) associated neurocognitive disorders (HAND) will undoubtedly increase with the improved longevity of HIV-infected persons. HIV infection, itself, as well as multiple physiologic and psychosocial factors can contribute to cognitive impairment and neurologic complications. These comorbidities confound the diagnosis, assessment, and interventions for neurocognitive disorders. In this review, we discuss the role of several key comorbid factors that may contribute significantly to the development and progression of HIV-related neurocognitive impairment, as well as the current status of diagnostic strategies aimed at identifying HIV-infected individuals with impaired cognition and future research priorities and challenges.

The contribution of the rat prelimbic-infralimbic areas to different forms of task switching.

The experiments examined the effects of prelimbic-infralimbic inactivation in rats on the acquisition and reversal learning of different discrimination tasks: 2- or 4-choice odor discrimination in Experiments 1 and 2, the shift from 2-choice odor discrimination to 2-choice place discrimination in Experiment 3, and the shift from 2-choice place to 2-choice odor discrimination in Experiment 4. Infusions of 2% bupivacaine did not impair performance in the odor discrimination tests. Prelimbic-infralimbic inactivation did not impair acquisition but did impair the shift from an odor to a place discrimination and vice versa. Analysis of the errors revealed that the deficit was due to perseveration of the previously learned strategy. The selective deficits observed in the odor-place tests suggest that the prelimbic-infralimbic areas enable behavioral flexibility when conditions demand inhibiting the use of one type of attribute information and learning a new type of attribute information.