Alcohol Syndrome

Why do even the most effective, well-run programs have treatment failures with motivated patients? One reason may be due to a problem that is sometimes difficult to see: organic brain damage. People with central nervous system (CNS) dysfunction have difficulty processing information, which can have a significant impact on how they respond to treatment. Such individuals may appear normal during routine assessment, but once they begin participating in treatment, difficulties soon become apparent that set them apart from other patients. In particular, there may be problems linking cause with effect, memory deficits, or inability to think in abstract terms -- all of which are important for treatment efficacy. If a program's resources are to appropriately address the issues of such patients, CNS dysfunction must be addressed at intake, and services must be tailored to meet special needs.

One cause of CNS dysfunction is prenatal exposure to alcohol, estimated to affect approximately one to three per 1000 people in the United States.
(FAS) manifests in three primary symptom categories:

* Growth deficiency of prenatal onset (height or weight);
* Central nervous system (CNS) dysfunction, including microcephaly, delayed development, hyperactivity, attention deficits, learning disabilities and intellectual deficits; and
* A specific pattern of facial characteristics, including short palpebral fissures, thin upper lip and smooth and/or long philtrum. Individuals who are exposed to alcohol in utero and who display some, but not all, of these characteristics are often described ashaving possible fetal alcohol effects (FAE). The CNS dysfunction associated with FAS/FAE frequently causes attention problems, memory problems, affective problems and maladaptive behaviors such as poor impulse control.

Unless an individual exhibits the specific facial features and growth problems associated with prenatal alcohol exposure, it is often difficult to diagnose the disorder. Quite often, by adulthood, the normal maturation process has attenuated the characteristic facial features and growth anomalies. Consequently, only the cognitive and behavioral manifestations of FAS/FAE are left to serve as markers for the disorder. This situation not only makes diagnosis difficult, it seriously complicates treatment for impaired clients. Assessment procedures often address intellectual capacity, which can be determined by means of IQ testing. But assessing behavior is more complicated and more time consuming. However, if patients with FAS/FAE go unrecognized, treatment failure is almost certainly guaranteed. Such patients cannot deal easily with the concepts and abstractions that typically comprise most programs and often have difficulty following through on basic rules (e.g., abstinence) that are far more concrete.