BOLD Response During Spatial Working Memory in Youth With Heavy Prenatal Alcohol Exposure

Autor: Sarah N. Mattson, Andrea D. Spadoni, Susan F. Tapert, Edward P. Riley, Susanna L. Fryer, Alissa Bazinet
Rok vydání: 2009
Předmět:
Zdroj: Alcoholism: Clinical and Experimental Research. 33:2067-2076
ISSN: 1530-0277
0145-6008
Popis: The negative effects of prenatal alcohol exposure on the developing embryo and fetus are well documented and include a wide range of physical anomalies and neurocognitive deficits. The diagnosis of fetal alcohol syndrome (FAS) requires a triad of characteristics: (1) pre- or post-natal growth deficiency, (2) cranio-facial abnormalities (e.g. indistinct philtrum, thin upper vermillion, small palpebral fissures) and (3) evidence of central nervous system (CNS) dysfunction (Jones and Smith, 1973; Jones et al., 1973). While FAS is considered to be at the most severe end of the outcome spectrum, it is recognized that prenatal alcohol exposure is associated with cognitive and behavioral deficits even in the absence of the facial features and growth deficiency required to make a diagnosis of FAS. Consequently, the National Task Force on Fetal Alcohol Syndrome and Fetal Alcohol Effects has adopted the non-diagnostic umbrella term Fetal Alcohol Spectrum Disorders (FASDs) to describe the range of effects resulting from gestational alcohol exposure (Bertrand et al., 2005). The incidence of FASDs has been estimated at 10 per 1,000 live births (May and Gossage, 2001) and impairments in general intelligence, attention, learning, memory, language, and several related domains have been demonstrated in such individuals (Mattson and Riley, 1998; Vaurio et al., 2008). Neuropsychological studies have suggested that individuals with FASDs have visuospatial cognitive deficits (Coles et al., 1991; Hamilton et al., 2003; Kaemingk et al., 2002; Mattson and Riley, 1998; Mattson et al., 1996; Olson et al., 1998; Streissguth et al., 1989; Uecker and Nadel, 1996; Willford et al., 2004) and exhibit poor working memory abilities (Jacobson et al., 1998; Olson et al., 1998; Streissguth et al., 1990). These reports demonstrated impaired learning and recall for both simple and complex figures (Mattson and Roebuck, 2002), locations (Hamilton et al., 2003; Kaemingk et al., 2002; Uecker and Nadel, 1996) and digit span backwards (Jacobson et al., 1998; Olson et al., 1998; Streissguth et al., 1989). Evidence of poor visuospatial cognition and working memory suggests that spatial working memory (SWM), or the maintenance of the spatial location of a remembered visual stimulus (Constantinidis and Wang, 2004), may also be impaired in individuals with prenatal alcohol exposure. Structural brain abnormalities observed in regions supporting SWM may contribute to observed deficits in visuospatial functioning in youth with FASDs. For example, alterations in the size and structure of frontal, parietal, and temporal cortices have been reported (Archibald et al., 2001; Sowell et al., 2001b; Sowell et al., 2002a; Sowell et al., 2002b). Disproportionate reduction in white matter relative to gray matter volumes in the parietal regions (Archibald et al., 2001), increased gray matter density in lateral temporal and inferior parietal lobes (Archibald et al., 2001; Sowell et al., 2001b; Sowell et al., 2002a), and abnormal glial cell metabolism (Fagerlund et al., 2006) suggest that white matter may be particularly vulnerable to alcohol-induced pathology. Observed increases in cortical thickness, that may reflect an abnormality in the process of white matter deposition or synaptic pruning (Sowell et al., 2008a), and reduced fiber integrity in the corpus callosum (Ma et al., 2005; Wozniak et al., 2006) suggest that microstructural abnormalities may contribute to poorer cognitive abilities in many alcohol-exposed individuals (Fryer et al., 2008; Sowell et al., 2008a). Thus, altered white matter integrity in regions important for SWM may contribute to the behavioral deficits observed in this population. Patterns of brain response to cognitive demands in youth with FASDs may elucidate the neural mechanisms (perhaps stemming from structural abnormalities) of cognitive deficits. Functional neuroimaging (fMRI) studies have revealed altered patterns of BOLD response in alcohol-exposed individuals during cognitive task performance. In controlled comparisons, greater blood oxygen level dependent (BOLD) response during inhibition and verbal learning has been observed in prefrontal regions of youth with FASDs (Sowell et al., 2007a), while reduced response has been demonstrated in the right caudate during inhibition (Fryer et al., 2007) and in medial and posterior temporal cortices during verbal encoding and retrieval (Sowell et al., 2007). A previous fMRI study of BOLD response during a SWM task reported increased functional activity of inferior middle frontal brain regions in children and adults with FASDs, but relatively decreased brain response in superior frontal and superior parietal areas (Malisza et al., 2005). Due to the very small body of functional neuroimaging evidence in alcohol-exposed populations and limited overlap of the cognitive domains sampled, the neural mechanisms of cognitive deficits in this population remain speculative. In light of alcohol-exposed individuals’ documented deficits in the component processes of SWM and evidence of structural and functional abnormalities in brain regions underlying SWM, we examined functional brain response to SWM demands in youth with FASDs. In the current study, age- and sex-matched youths performed a task that alternated between 2-back location matching (SWM) and baseline (vigilance) conditions during fMRI. Despite differences in task demands, greater prefrontal brain activation has been reported across the three previous fMRI studies of youth with FASDs (Fryer et al., 2007b; Malisza et al., 2005; Sowell et al., 2007). Therefore, we anticipated that alcohol-exposed individuals would have comparatively increased BOLD response in prefrontal brain regions during SWM relative to vigilance conditions. Any observed group differences in BOLD response during SWM might provide insight into the underpinnings of impaired cognitive function in youth with FASDs.
Databáze: OpenAIRE
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