Background Both sensory and cognitive deficits have been associated with prenatal exposure to alcohol; however, very few studies have focused on sensory deficits in preschool aged children. Since sensory skills develop early, characterization of sensory deficits using novel imaging methods may reveal important neural markers of prenatal alcohol exposure. Materials and Methods Participants in this study were 10 children with a fetal alcohol spectrum disorder (FASD) and 15 healthy control children aged 3-6 years. All participants had normal hearing as determined by clinical screens. We measured their neurophysiological responses to auditory stimuli (1000 Hz, 72 dB tone) using magnetoencephalography (MEG). We used a multi-dipole spatio-temporal modeling technique (CSST – Ranken et al. 2002) to identify the location and timecourse of cortical activity in response to the auditory tones. The timing and amplitude of the left and right superior temporal gyrus sources associated with activation of left and right primary/secondary auditory cortices were compared across groups. Results There was a significant delay in M100 and M200 latencies for the FASD children relative to the HC children (p = 0.01), when including age as a covariate. The within-subjects effect of hemisphere was not significant. A comparable delay in M100 and M200 latencies was observed in children across the FASD subtypes. Discussion Auditory delay revealed by MEG in children with FASD may prove to be a useful neural marker of information processing difficulties in young children with prenatal alcohol exposure. The fact that delayed auditory responses were observed across the FASD spectrum suggests that it may be a sensitive measure of alcohol-induced brain damage. Therefore, this measure in conjunction with other clinical tools may prove useful for early identification of alcohol affected children, particularly those without dysmorphia.

The last two decades have witnessed a rapid growth of published data on the cognitive and behavioral functioning of children with fetal alcohol spectrum disorders (FASD). The main of aim of this paper is to review cognitive and behavioral data on FASD using a causal modeling framework originally proposed by Morton and Frith [1,2], according to which data pertinent to a neurodevelopmental disorder can be organized at three levels: neurobiology, cognition, and behavior. In this review, we confine ourselves to reviewing the studies of cognitive abilities and behavior in children with FASD. The studies of cognitive functions can be further divided into two groups: those of elementary functions (e.g., reflexive orienting responses) and those of complex functions (e.g., language, memory). There is evidence that children with FASD are slower at reflective orienting responses and exhibit deficits in associative learning. The pattern of results emerging from the studies of complex cognitive functions is that the FASD group shows performance decrements with increased task complexity. At the behavioral level, children with prenatal alcohol exposure are rated as showing deficient adaptive skills, particularly in the social domain. These children have also been observed to show deficits in executive functioning with notable behavioral and emotional regulatory problems. A broad range of risk factors including the alcohol's teratogenicity seem to interactively contribute to these cognitive and behavioral problems.

Since fetal alcohol syndrome was first described over 35 years ago, considerable progress has been made in the delineation of the neurocognitive profile in children with prenatal alcohol exposure. Preclinical investigators have made impressive strides in elucidating the mechanisms of alcohol teratogenesis and in testing the effectiveness of pharmacological agents and dietary supplementation in the amelioration of alcohol-induced deficits. Despite these advances, only limited progress has been made in the development of evidence-based comprehensive interventions for functional impairment in alcohol-exposed children. Having performed a search in PubMed and PsycINFO using key words, interventions, treatment, fetal alcohol syndrome, prenatal alcohol exposure, and fetal alcohol spectrum disorders, we found only 12 papers on empirically-based interventions. Only two of these interventions had been replicated and none met the criteria of "well-established," as defined by Chambless and Hollon (Journal of Consulting and Clinical Psychology 66(1):7-18, 1998). There has been only limited cross-fertilization of ideas between preclinical and clinical research with regard to the development of interventions. Therefore, we propose a framework that allows integrating data from preclinical and clinical investigations to develop comprehensive intervention programs for children with fetal alcohol spectrum disorders. This framework underscores the importance of multi-level evaluations and interventions.

Fetal alcohol spectrum disorders (FASD) are debilitating, with effects of prenatal alcohol exposure persisting into adolescence and adulthood. Complete characterization of FASD is crucial for the development of diagnostic tools and intervention techniques to decrease the high cost to individual families and society of this disorder. In this experiment we investigated visual system deficits in adolescents (12-21 years) diagnosed with an FASD by measuring the latency of patients’ primary visual M100 responses using MEG. We hypothesized that patients with FASD would demonstrate delayed primary visual responses compared to controls. M100 latencies were assessed both for FASD patients and age-matched healthy controls for stimuli presented at the fovea (central stimulus) and at the periphery (peripheral stimuli; left or right of the central stimulus) in a saccade task requiring participants to direct their attention and gaze to these stimuli. Source modeling was performed on visual responses to the central and peripheral stimuli and the latency of the first prominent peak (M100) in the occipital source timecourse was identified. The peak latency of the M100 responses were delayed in FASD patients for both stimulus types (central and peripheral), but the difference in latency of primary visual responses to central vs. peripheral stimuli was significant only in FASD patients, indicating that, while FASD patients’ visual systems are impaired in general, this impairment is more pronounced in the periphery. These results suggest that basic sensory deficits in this population may contribute to sensorimotor integration deficits described previously in this disorder.

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