About FASD — The Overlooked Disorder

It is now well established in literature that spans 40 years that alcohol is a teratogen that can cause extensive damage to the unborn child during pregnancy. This damage involves the brain, which develops throughout the full nine months of gestation. In general, the more prenatal exposure to alcohol, the more extensive the brain damage. However, we also know that even small amounts of alcohol on a regular basis or occasional binge drinking during pregnancy can affect brain development and related cognitive-behavioral functioning. Thus, non-alcoholic mothers who drink only in the first weeks of pregnancy before they learn they are pregnant may expose their unborn children to the damaging effects of alcohol just like mothers who binge-drink and/or drink regularly throughout pregnancy. Some drugs can cause cognitive-behavioral dysfunction as well (e.g., cocaine). Most women with histories of drug use typically drink alcohol along with their drug use.

FASD conditions generally involve a complex combination of abnormalities that can have profound and lifelong effects on an individual’s ability to function in an effective and pro-social manner. Research has established that if FASD conditions are not diagnosed early in childhood and appropriately treated, a significant percentage of affected individuals will display adverse outcomes ("Secondary Disabilities") in adolescence and adulthood. One of these adverse outcomes is criminal behavior.

Nature of the task and context are critical factors with respect to executive function capacity and corresponding adaptive behavior in FASD. In FASD, prenatal exposure damages brain structures throughout the brain, including the prefrontal cortex and networks between the prefrontal cortex and the limbic system. Because the location of brain damage in FASD depends on many factors, including developmental processes occurring in the fetal brain at the time of exposure, those with FASD tend to produce variable results on neuropsychological test batteries. Often, such variability can even be seen within a single IQ test because the multiple subdomains assessed in IQ tests such as the Wechsler involve different kinds of intellectual processing. In particular, task complexity significantly affects performance in FASD. Although this population does not show difficulty in simple tests of executive organization and control, they exhibit impairments in complex tasks requiring rapid decision-making, conscious mental effort, or organizing multiple cognitive skills (Kodituwakku, 2009). Consequently, IQ tasks that rely most heavily on complex executive processing such as working memory or processing speed may be more affected in FASD than tasks involving well-learned verbal material or simple nonverbal skills (e.g., verbal comprehension, perceptual reasoning).

FASD is the only neurodevelopmental condition known to produce a significant discrepancy or “disconnect" between full-scale IQ and adaptive functioning. While those with autism spectrum disorder (ASD) exhibit significant social dysfunction, this population does not exhibit the pervasive adaptive dysfunction found in FASD (DSM-5). In addition, many people with ASD do not exhibit the disconnect between full-scale IQ and adaptive functioning found in FASD (DSM-5). The reason FASD seems to stand alone with respect to this IQ/adaptive behavior disconnect is executive dysfunction. Although traumatic brain injury (TBI) in the prefrontal cortex may produce the same kind of executive function impairments and associated adaptive dysfunction found in FASD, including the disconnect between full-scale IQ and adaptive behavior, unlike FASD TBIs are time-specific and do not affect an individual’s adaptive functioning prior to the injury.

Context also is a critical component in adaptive behavior in FASD. For example, adding emotional elements such as stress to cognitive tasks decreases performance in this population. Consequently, when those with FASD are left to their own devices in complex social situations involving stress and the need for independent decision-making and impulse control, adaptive behavior is even more impaired than it might appear in structured and well-controlled test settings. As much of everyday behavior involves some degree of stress and frequent novelty, and interpersonal relationships always involve complexity, it is not surprising that adaptive functioning in FASD falls well below performance on IQ tests, which is assessed in highly structured test settings.

Fetal alcohol syndrome (FAS) was first identified in the United States by researchers at the University of Washington in Seattle and published in peer-reviewed publications published in 1973. From that early beginning, diagnostic criteria for FAS have always involved for three basic diagnostic criteria: facial abnormalities or “dysmorphology,” growth deficits, and central nervous system abnormalities. Until the late 1990s, individuals with prenatal alcohol exposure (PAE) who displayed central nervous system dysfunction but did not show outward physical manifestations of FAS were diagnosed with fetal alcohol effect (FAE) or static encephalopathy, alcohol exposed (i.e., brain damage due to PAE).

Terminology began changing in the 1990s to accommodate the somewhat confusing FAE designations. In 1996, the Institute of Medicine (IOM) tried to clarify the terminology confusion by listing five specific diagnostic conditions under the Fetal Alcohol Spectrum Disorders (FASD) umbrella:

Type 1: Fetal Alcohol Syndrome (FAS) with confirmed maternal alcohol exposure
Type 2: FAS without confirmed maternal alcohol exposure
Type 3: Partial FAS with confirmed maternal alcohol exposure
Type 4: Alcohol-related birth defects (ARBD)
Type 5: Alcohol-related neurodevelopmental disorder (ARND)

In 1997, the Washington State FAS Diagnostic and Prevention Network published a comprehensive method for diagnosing the full FASD spectrum of conditions for patients with prenatal alcohol exposure. This diagnostic method, called the 4-Digit Diagnostic Code, involves quantitative, objective measurement scales as well as specific condition definitions. The four digits in the Code (i.e., 1, 2, 3, 4) reflect the magnitude of expression of the four key diagnostic features of FAS in terms of growth deficiency, FAS facial features, central nervous system damage/dysfunction, and prenatal alcohol exposure. The magnitude of expression of each feature is ranked, with “1” reflecting complete absence of the FAS feature and “4” reflecting strong or classic presence of the FAS feature.

In 2004, the Centers for Disease Control (CDC) clarified Type 1 FAS and added specific instructions for diagnosing each of the four criteria required for this condition: facial abnormalities, growth problems, Central Nervous System abnormalities, and prenatal alcohol exposure.

In clinical settings in the United States, the IOM, CDC, and 4-Digit Code are used either individually or together.

As of mid-2013 with the publication of the new DSM-5, FASD was recognized as a neurodevelopmental disorder (i.e., Neurodevelopmental Disorder associated with Prenatal Alcohol Exposure, or ND-PAE). Criteria for ND-PAE, which are provided in the DSM-5 under a section entitled "Neurobehavioral Disorder associated with Prenatal Alcohol Exposure," are generally consistent with the IOM and CDC. The DSM-5 indicates there is no difference in terms of diagnostic classification (i.e., name) or criteria between dysmorphic FASD conditions (i.e., Fetal Alcohol Syndrome) and non-dysmorphic conditions (i.e., Alcohol Related Neurodevelopmental Disorder).

Unfortunately, there are very few specialists in the United States who are trained to diagnose and treat these conditions because education about FASD is not part of the standard curriculum in any medical school or graduate psychology program. As a result, most medical doctors and psychologists enter the workforce with limited knowledge about a condition that can involve significant and permanent brain damage. Because the observable physical manifestations of FAS (i.e., facial abnormalities and growth deficits) become more difficult to detect in adolescence and adulthood, FASD conditions are challenging to identify post-puberty, even for physicians trained in dysmorphology. Consequently, it is generally accepted in the field that accurate diagnosis of individuals in high-stakes forensic contexts, regardless of age but especially in the teens and adult years, should involve multidisciplinary analysis from multiple perspectives, with emphasis necessarily on neurological and cognitive-behavioral symptoms of FASD in lieu of observable facial dysmorphology and growth deficits.