Neurodevelopmental functioning in children with FAS, pFAS, and ARND

Children's Research Triangle, Chicago, IL, USA.
Journal of developmental and behavioral pediatrics: JDBP (Impact Factor: 2.13). 04/2010; 31(3):192-201. DOI: 10.1097/DBP.0b013e3181d5a4e2
Source: PubMed


The purpose of this article is to compare the neurodevelopmental profiles of 78 foster and adopted children with fetal alcohol syndrome (FAS), partial FAS (pFAS), or alcohol-related neurodevelopmental disorder (ARND).
Seventy-eight foster and adopted children underwent a comprehensive diagnostic evaluation. By using criteria more stringent than those required by current guidelines, the children were placed in 1 of 3 diagnostic categories: FAS, pFAS, or ARND. Each child was evaluated across the domains of neuropsychological functioning most frequently affected by prenatal exposure to alcohol. Multivariate analyses of variance were conducted to examine differences in neuropsychological functioning between the 3 diagnostic groups. Descriptive discriminant analyses were performed in follow-up to the multivariate analyses of variance.
The children in the 3 diagnostic categories were similar for descriptive and child welfare variables. Children with FAS had significantly decreased mean weight, height, and head circumference. Children with FAS exhibited the most impaired level of general intelligence, significantly worse language-based memory compared with children with ARND, and significantly poorer functional communication skills than children with pFAS. On executive functioning, the FAS group of children performed significantly worse on sequencing and shift than either the pFAS or ARND groups. Children with pFAS and ARND were similar in all neurodevelopmental domains that were tested.
The children who met tightly defined physical criteria for a diagnosis of FAS demonstrated significantly poorer neurodevelopmental functioning than children with pFAS and ARND. Children in these latter 2 groups were similar in all neurodevelopmental domains that were tested.

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Available from: Anne Wells, Apr 22, 2014
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    • "Fetal alcohol spectrum disorders (FASD) encompass a constellation of physical and cognitive abnormalities that result from prenatal alcohol exposure in humans (Chasnoff, Wells, Telford, Schmidt, & Messer, 2010; Jones, 2011; Mattson, Crocker, & Nguyen, 2011). Afflicted individuals may exhibit a variety of structural and functional neurological deficits, including impaired executive function, attention, and learning and memory (Mattson et al., 2011; Niccols, 2007). "
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    ABSTRACT: In rodents, ethanol exposure in early postnatal life is known to induce structural and functional impairments throughout the brain, including the hippocampus. Herein, rat pups were administered one of three ethanol doses over postnatal days (PD) 4-9, a period of brain development comparable to the third trimester of human pregnancy. As adults, control and ethanol rats were trained and tested in a variant of hippocampal-dependent one-trial context fear conditioning. In Experiment 1, subjects were placed into a novel context and presented with an immediate footshock (i.e., within ∼8 sec). When re-exposed to the same context 24 hr later low levels of conditioned freezing were observed. Context pre-exposure 24 hr prior to the immediate shock reversed the deficit in sham-intubated and unintubated control rats, enhancing freezing behavior during the context retention test. Even with context pre-exposure, however, significant dose-dependent reductions in contextual freezing were seen in ethanol rats. In Experiment 2, the interval between context pre-exposure and the immediate shock was shortened to 2 hr, in addition to the standard 24 hr. Ethanol rats trained with the 2 hr, but not 24 hr, interval displayed retention test freezing levels roughly equal to controls. Results suggest the ethanol rats can encode a short-term context memory and associate it with the aversive footshock 2 hr later. In the 24 hr ethanol rats the short-term context memory is poorly transferred or consolidated into long-term memory, we propose, impeding the memory's subsequent retrieval and association with shock. © 2014 Wiley Periodicals, Inc. Dev Psychobiol.
    Developmental Psychobiology 03/2014; 56(6). DOI:10.1002/dev.21210 · 3.31 Impact Factor
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    • "It is considered the leading preventable cause of congenital defects and mental impairment [11]. Patients with fetal alcohol syndrome often develop persistent attention deficit hyperactivity disorder, in all of its subtypes [4] [12] [13] [14] [15] [16] [17] [18] [19] (62% of all children with fetal alcohol syndrome in the study of Landgren et al.) [16]. Although some studies have compared cerebral cortical thickness by means of structural brain magnetic resonance imaging between patients with fetal alcohol spectrum disorders or fetal alcohol syndrome and control subjects, and between patients with attention deficit hyperactivity disorder and control subjects, to the best of our knowledge, no studies have compared control subjects with patients manifesting attention deficit hyperactivity disorder and fetal alcohol syndrome or patients without attention deficit hyperactivity disorder, even though attention deficit hyperactivity disorder is such a common comorbidity [15-20]. "
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    ABSTRACT: Introduction Tuberous sclerosis complex (TSC) is one of the most frequent neurocutaneous disorders. Cortical tubers are the most common pathological changes in TSC and they are directly related to the disease's main clinical manifestations: seizures, mental retardation, and autistic behaviour. Objective The aim of this study is to establish a correlation between tuber size and the severity of clinical features in TSC. Material and methods We performed a retrospective study of the clinical and imaging findings from 45 TSC patients (22 females and 23 males) and compared the clinical features with the location, size, and number of the cortical tubers in each patient. Results Four patients had voluminous tubers located in 1 or both cerebral hemispheres. All of these patients had intractable seizures and severe mental retardation; 3 of these cases also presented with autistic behaviour, despite tubers having been resected in all 4 patients. Thirteen patients had tubers of large-to-average size, and all patients in this group showed intractable seizures and mental retardation. Nine patients who had experienced infantile spasms during the first year of life presented autistic behaviour. Multiple tubers of small to average size were found in 28 patients. In general, this group had seizures that responded well to antiepileptic drugs and a low prevalence of autism. In 3 patients who all presented good seizure control and normal intelligence, single cortical/subcortical tubers were located in the frontal or occipital lobes. Of the total of 45 patients, 13 had cerebellar as well as cerebral tubers; these were generally present in cases with more severe clinical features. Conclusions Although large tubers are less common than small to medium-sized ones, they are much more likely to be accompanied by severe clinical symptoms (seizures, mental retardation and autistic behaviour), even when the smaller tubers are quite numerous.
    Neurologia (Barcelona, Spain) 11/2013; 28(9):550–557. DOI:10.1016/j.nrl.2012.11.002 · 1.38 Impact Factor
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    • "afflicted children along the FASD continuum are diagnosed with FAS, which has a birth prevalence of 2–7 per 1000 births in the United States [4]. At the opposite end of the spectrum, alcoholrelated neurodevelopmental disorder (ARND) refers to children that express the mental but not physical abnormalities associated with early alcohol exposure [5]. In fact, the estimated number of FASD children may be up to 10 times higher than reported due to difficulties in diagnosing ARND children in the absence of physical dysmorphology [6] [7]. "
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    ABSTRACT: Binge-like postnatal ethanol exposure produces significant damage throughout the brain in rats, including the cerebellum and hippocampus. In the current study, cue- and context-mediated Pavlovian conditioning were assessed in adult rats exposed to moderately low (3E; 3g/kg/day) or high (5E; 5g/kg/day) doses of ethanol across postnatal days 4 to 9. Ethanol-exposed and control groups were presented with 8 sessions of trace eyeblink conditioning followed by another 8 sessions of delay eyeblink conditioning, with an altered context presented over the last two sessions. Both forms of conditioning rely on the brainstem and cerebellum, while the more difficult trace conditioning also requires the hippocampus. The hippocampus is also needed to gate or modulate expression of the eyeblink conditioned response (CR) based on contextual cues. Results indicate that the ethanol-exposed rats were not significantly impaired in trace EBC relative to control subjects. In terms of CR topography, peak amplitude was significantly reduced by both doses of alcohol, whereas onset latency but not peak latency was significantly lengthened in the 5E rats across the latter half of delay EBC in the original training context. Neither dosage resulted in significant impairment in the contextual gating of the behavioral response, as revealed by similar decreases in CR production across all four treatment groups following introduction of the novel context. Results suggest ethanol-induced brainstem-cerebellar damage can account for the present results, independent of the putative disruption in hippocampal development and function proposed to occur following postnatal ethanol exposure.
    Behavioural brain research 12/2012; 242(1). DOI:10.1016/j.bbr.2012.12.030 · 3.03 Impact Factor
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