Alexithymia, an impairment of affective and cognitive emotional processing, is often associated with human immunodeficiency virus (HIV) and may reflect effects of the virus on brain areas that are also important for multiple cognitive functions, such as the prefrontal and anterior cingulate cortices. We hypothesized that there would be a correlation between extent of alexithymia and cognitive performance associated with these brain areas, including attention, executive function, and visuospatial processing. Thirty-four asymptomatic HIV+ participants and 34 matched healthy HIV− volunteers were administered the Toronto Alexithymia Scale, a series of neuropsychological tests, and measures of apathy, depression, and quality of life (QoL). The HIV+ participants had significantly higher levels of alexithymia, depression and apathy than the HIV− group. The extent of alexithymia and two of its processing components (Difficulty Describing Feelings [DDF] and Externally Oriented Thinking), but not depression, correlated with performance on measures of executive and visuospatial abilities, consistent with dysfunction of the frontostriatal circuits and their cortical projections. Apathy was related to alexithymia and two processing components (Difficulty Identifying Feelings and DDF) but to only one cognitive measure. The higher rate of alexithymia, as well as cognitive dysfunction, in HIV may be a consequence of the infection on the frontostriatal system and its cortical connections. Our findings also demonstrated a dissociation of apathy and alexithymia in HIV, pointing to overlapping but distinct neural substrates within frontostriatal circuits. Alexithymia correlated strongly with QoL ratings, underscoring the importance of assessment and treatment of HIV-associated emotional and cognitive processing deficits.
Infection with human immunodeficiency virus (HIV) is associated with deficits in cognition and emotion, but the relation between them is not understood. This study explores the association between alexithymia and cognition in individuals with HIV in its early asymptomatic stage.
HIV affects frontostriatal thalamocortical circuits (Everall et al., 1999) early in the course of the disease (Avison et al., 2004, Berger and Nath, 1997, Chang et al., 2001, Chang et al., 2004, Ernst et al., 2002 and Gray, 1996). Structural magnetic resonance imaging (MRI) has shown that HIV infection is associated with reduced volumes of frontal cortex, thalamus, hippocampus, and caudate (Jernigan et al., 1993), as well as with tissue loss in frontal and parietal areas (Thompson et al., 2005). Neuroimaging studies of asymptomatic HIV+ patients have documented reduced brain volume (Aylward et al., 1993), cerebral metabolic asymmetry (left or right) in prefrontal and specifically orbitofrontal areas (Pascal et al., 1991), and differences in signal changes in lateral frontal and posterior parietal areas (Castelo, Sherman, Courtney, Melrose, & Stern, 2006).
Neuropsychological studies of cognition in HIV have shown that asymptomatic HIV+ individuals exhibit cognitive deficits consistent with dysfunction of frontostriatal circuits (Bogdanova et al., 2008, Castelo et al., 2007 and Heaton
