There are no medications to treat fetal alcohol syndrome specifically. But certain medicines can help with symptoms such as hyperactivity, inability to focus, or anxiety. It is also important for people to seek support if they drink alcohol excessively. Alcohol use disorder is a condition that has many different treatment options, including support groups, therapy, and medical help. These conditions affect infants’ physical, mental, and behavioral development, and the effects can last a lifetime. The primary disabilities of FASD are those that most directly reflect the underlying central nervous system damage caused by prenatal exposure to alcohol.
Glial Contributions to Brain Development
A reduction in neuritogenesis and neuronal survival was reported in naïve neurons co-cultured with astrocytes prepared from alcohol-exposed rats (Pascual and Guerri, 2007). In an earlier study, drunken baby syndrome neurons cultured in conditioned media from astrocytes exposed in culture to 100 mM alcohol for 4 days displayed reduced DNA content, neurite length, number of serotonin neurons and serotonin uptake (Lokhorst and Druse, 1993). Astrocytes also modulate the effect of alcohol on dendrite development in culture (Yanni et al., 2002). Astrocyte-specific expression of serum response factor in a ferret model of early alcohol exposure reverses alcohol-induced reductions in ocular dominance plasticity (Paul and Medina, 2012). FAS is characterized by prenatal alcohol exposure (PAE), craniofacial (head and face) differences, neurodevelopmental abnormalities (including behavioral issues), and growth impairment.
How can I help my child live with FASD?
- It’s also recommended that you not drink alcohol if you’re sexually active and not using effective birth control.
- Alcohol is broken down more slowly in the immature body of the fetus than in an adult’s body.
- As time progresses, babies with FASD may also be slower to reach developmental milestones than other infants.
Alcohol appears to affect astrocyte proliferation by inhibiting specific signal transduction pathways. Prenatal alcohol exposure has been reported to cause a decrease in astrocyte number (Miller and Potempa, 1990), an observation that supports the in vitro studies. During embryonic development in rodents, microglia appear in the activated state with an amoeboid shape and transition to a resting ramified morphology shortly after birth. Indeed, microglia phagocytize neural precursor cells, particularly during late stages of cortical neurogenesis therefore regulating the size of the neural precursor cell pool in the developing cortex (Cunningham et al., 2013).
- Agenesis (lack of formation) of the corpus callosum or anterior commissure, hypoplasia, volume reduction, heightened variability and displacement has been reported (Riley and McGee, 2005; Norman et al., 2009; Lebel et al., 2011).
- Treatment strategies for FAS include nonpharmacologic and pharmacologic interventions.
- In addition to the acute effects of withdrawal, babies often suffer the teratogenic (causing physical abnormalities) effects of alcohol.
- Sequelae include perturbations to affect regulation and cognition, as well as to physical appearance manifested via pathognomonic anomalies.
- The outlook for a child with fetal alcohol syndrome (FAS) depends on the severity of the condition, early intervention, and ongoing support.
Learning
Autopsies of infants born with FASD paint a grim picture of the effects of alcohol on the brain. In these, the most severe cases of FASD, damage is ubiquitous throughout the brain (Riley and McGee, 2005). A general CNS disorganization is observed, with errors in neuronal migration, neuroglial heterotopias, microcephaly, and abnormalities of the brainstem, cerebellum, basal ganglia, hippocampus and corpus callosum, pituitary gland and optic nerve (Jones et al., 1973).
Social and behavioral issues
Chondroitin sulfate proteoglycans (CSPGs) are inhibitors of neurite outgrowth. We found that alcohol upregulates the levels of CSPGs through the inhibition of the enzyme arulsulfatase B (ARSB). ARSB degrades the chondroitin sulfate moiety of CSPGs and leads to the extracellular proteolysis of the core-protein in astrocyte cultures in vitro and after neonatal alcohol exposure in vivo (Zhang et al., 2014). The formation of the corpus callosum is strongly affected by prenatal alcohol exposure (Riley and McGee, 2005; Norman et al., 2009; Lebel et al., 2011).
- A decrease in GFAP expression was confirmed in vivo after prenatal alcohol exposure in the brain of postnatal animals and was attributed to increased DNA methylation in the GFAP promoter region (Vallés et al., 1997).
- If people have any evidence that they may have been exposed to alcohol in the womb, they can present that to a doctor.
- It’s important to make an early diagnosis of fetal alcohol syndrome.
- There isn’t a direct test for FAS and pregnant people may not give a complete history of all alcohol intake during pregnancy.
What Causes Fetal Alcohol Spectrum Disorders and How Are They Prevented?
As children with FAS get older, they might develop behavioral problems, have problems learning and retaining information, or struggle with attention and hyperactivity, all of which may worsen as they mature. Fetal alcohol syndrome can also cause milestone (developmental) delays. The most effective treatments for fetal alcohol syndrome target your child’s specific issues.
Secondary
Given the range of cognitive impairments described above, it is not surprising that prenatal alcohol exposure is coincident with reduced academic performance and an increased frequency of learning disabilities (Howell et al., 2006). Indeed, attention deficit hyperactivity disorder (ADHD) is often diagnosed in FASD individuals with concordance rates ranging from 65–95% (Coles et al., 2002; Fryer et al., 2007; Rasmussen et al., 2010). Executive function is also impaired in individuals with FASD with deficits in response inhibition, concept formation, set shifting and planning (Guerri et al., 2009; Mattson et al., 2011).