Collaborative initiative on fetal alcohol spectrum disorders: methodology of clinical projects

Mattson, Sarah N.; Foroud, Tatiana; Sowell, Elizabeth R.; Jones, Kenneth Lyons; Coles, Claire D.; Fagerlund, Åse; Autti‐Rämö, Ilona; May, Philip A.; Adnams, Colleen M.; Konovalova, Valentina; Wetherill, Leah; Arenson, Andrew D.; Barnett, William K.; Riley, Edward P.

doi:10.1016/j.alcohol.2009.08.005

Cited by 87 publications

(149 citation statements)

References 13 publications

(8 reference statements)

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“…A diagnosis of Fetal Alcohol Syndrome (FAS) was sufficient to meet study criteria for inclusion in the AE group. FAS diagnosis was based on the presence of two or more key facial features (short palpebral fissures, smooth philtrum, and thin vermilion border of the upper lip) and either evidence of growth deficiency (height and/or weight ≤ 10th percentile) or microcephaly (head circumference ≤ 10th percentile) (for details, see Jones et al, 2006; Mattson et al, 2010a). Three subjects in the AE group met these criteria for a diagnosis of FAS.…”

Section: Methodsmentioning

confidence: 99%

Altered functional connectivity during spatial working memory in children with heavy prenatal alcohol exposure

Infante

Moore

Bischoff‐Grethe

et al. 2017

Alcohol

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Individuals prenatally exposed to alcohol often have impaired spatial working memory (SWM). This study examines functional connections of frontal and parietal regions that support SWM in children with and without prenatal alcohol exposure. Children ages 10 to 16 with histories of heavy prenatal alcohol exposure (AE group; n = 18) and controls (CON group; n = 19) underwent functional magnetic resonance imaging while performing a SWM task. Whole brain task-related functional connectivity of bilateral dorsolateral prefrontal cortex (DLPFC) and posterior parietal cortex (PPC) seed regions were estimated for each participant using a psychophysiological interaction approach. Children in the AE group were less accurate than children in the CON group when performing the SWM task (p = .008). Positive coupling between bilateral DLPFC seeds and regions within the fronto-parietal network was observed in the CON group, whereas the AE group showed negative connectivity. In contrast to the CON group, the AE group showed positive connectivity between PPC seeds and frontal lobe regions. Across seeds, decreased negative coupling with regions outside the fronto-parietal network (e.g., left middle occipital gyrus) were observed in the AE group relative to the CON group. Functional data clusters were considered significant at p < .05. Overall findings suggest that localized alterations in neural activity, aberrant fronto-parietal network synchrony, and poor coordination of neural responses with regions outside of this network may help explain SWM deficits in individuals with a history of heavy prenatal alcohol exposure.

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Section: Methodsmentioning

confidence: 99%

Altered functional connectivity during spatial working memory in children with heavy prenatal alcohol exposure

Infante

Moore

Bischoff‐Grethe

et al. 2017

Alcohol

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“…Based on criteria outlined previously (Kenneth Lyons Jones et al, 2006; Sarah N. Mattson et al, 2010), the evaluation resulted in a determination of 1) Fetal Alcohol Syndrome (FAS); 2) non-FAS; or 3) a “deferred” status due to some criteria being met, but not enough to diagnose FAS. FAS was diagnosed on the basis of two or more of the following key facial features: thin vermillion border, smooth philtrum, and short palpebral fissure length – together with either microcephaly (occipital-frontal circumference ≤ 10%) or growth deficiency (height or weight ≤ 10%) or both.…”

Section: Methodsmentioning

confidence: 99%

Functional connectivity abnormalities and associated cognitive deficits in fetal alcohol Spectrum disorders (FASD)

Wozniak

Mueller

Mattson

et al. 2016

Brain Imaging and Behavior

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Objectives Consistent with well-documented structural and microstructural abnormalities in prenatal alcohol exposure (PAE), recent studies suggest that functional connectivity (FC) may also be disrupted. We evaluated whole-brain FC in a large multi-site sample, examined its cognitive correlates, and explored its potential to objectively identify neurodevelopmental abnormality in individuals without definitive dysmorphic features. Experimental Design Included were 75 children with PAE and 68 controls from four sites. All participants had documented heavy prenatal alcohol exposure. All underwent a formal evaluation of physical anomalies and dysmorphic facial features. MRI data were collected using modified matched protocols on three platforms (Siemens, GE, and Philips). Resting-state FC was examined using whole-brain graph theory metrics to characterize each individual's connectivity. Principal Observations Although whole-brain FC metrics did not discriminate prenatally-exposed from unexposed overall, atypical FC (> 1 standard deviation from the grand mean) was significantly more common (2.7 times) in the PAE group vs. controls. In a subset of 55 individuals (PAE and controls) whose dysmorphology examination could not definitively characterize them as either Fetal Alcohol Syndrome (FAS) or non-FAS, atypical FC was seen in 27% of the PAE group, but 0% of controls. Across participants, a 1% difference in local network efficiency was associated with a 36 point difference in global cognitive functioning. Conclusions Whole-brain FC metrics have potential to identify individuals with objective neurodevelopmental abnormalities from prenatal alcohol exposure. When applied to individuals unable to be classified as FAS or non-FAS from dysmorphology alone, these measures separate prenatally-exposed from non-exposed with high specificity.

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“…The CIFASD is supported by the National Institute on Alcohol Abuse and Alcoholism and is a multidisciplinary initiative conducted in several countries throughout the world (www.CIFASD.org). This randomized trial of prenatal micronutrient supplementation has been described elsewhere in detail (Chambers et al, 2014; Coles et al, 2015; Mattson et al, 2010). Briefly, all women who presented to one of two centralized prenatal care facilities in western Ukraine between April 2008 through August 2012 were eligible for screening.…”

Section: Methodsmentioning

confidence: 99%

Assessing the Independent and Joint Effects of Unmedicated Prenatal Depressive Symptoms and Alcohol Consumption in Pregnancy and Infant Neurodevelopmental Outcomes

Bandoli

Coles

Kable

et al. 2016

Alcoholism Clin & Exp Res

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Background Prenatal alcohol exposure (PAE) is an established risk factor for neurodevelopmental deficits in the offspring. Prenatal depression has been associated with neurodevelopmental deficits in the offspring, although investigations into un-medicated prenatal depression have been inconsistent. We hypothesized that un-medicated prenatal depressive symptoms would independently and jointly with PAE predict neurodevelopmental outcomes in infant offspring. Methods We studied 344 participants from a randomized clinical trial of multivitamin supplements in pregnant women in Ukraine. Women were recruited based upon peri-conceptional alcohol use and followed up to 12 months postpartum. Prenatal depressive symptoms were assessed at approximately 32 weeks of gestation using the Beck Depression Scale. Neurodevelopment was assessed with the Bayley Scales for Infant Development II Mental Development Index (MDI) and Psychomotor Development Index (PDI) at 6 and 12 months postpartum. Generalized linear regression models were constructed to assess the independent and joint effects of prenatal depressive symptoms and PAE in models adjusted for sociodemographic and pregnancy characteristics. Results PAE was independently associated with deficits in neurodevelopmental outcomes at 6 and 12 months, however, level of prenatal depressive symptoms was not. We found marginal evidence of synergism of depressive symptoms and PAE, with larger deficits in those with both exposures observed for the PDI-6 months (p=0.05) and MDI-12 months (p=0.09). Additionally, there was a suggestion of sexual dimorphism; females had stronger deficits from joint exposures than males (depressive symptom (MDI-6 months) female: −8.28, 95% CI −13.06, −3.49; male: 0.68, 95% CI −4.58, 5.94; p for interaction 0.04). While not statistically significant for the MDI or PDI at 12 months, the trend persisted. Conclusion Infants exposed to PAE and prenatal depression may be at an increased risk of neurodevelopmental deficits. Healthcare providers should be aware of this possible synergism in their efforts to mitigate the neurodevelopmental effects of these co-occurring exposures.

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Collaborative initiative on fetal alcohol spectrum disorders: methodology of clinical projects

Cited by 87 publications

References 13 publications

Altered functional connectivity during spatial working memory in children with heavy prenatal alcohol exposure

Altered functional connectivity during spatial working memory in children with heavy prenatal alcohol exposure

Functional connectivity abnormalities and associated cognitive deficits in fetal alcohol Spectrum disorders (FASD)

Assessing the Independent and Joint Effects of Unmedicated Prenatal Depressive Symptoms and Alcohol Consumption in Pregnancy and Infant Neurodevelopmental Outcomes

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