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Fetal alcohol spectrum disorder

2007 Schools Wikipedia Selection. Related subjects: Health and medicine

   Fetal alcohol spectrum disorder (FASD) describes a spectrum of
   permanent and often devastating birth-defect syndromes caused by
   maternal consumption of alcohol during pregnancy. The main effect of
   fetal alcohol exposure is brain damage. This can be caused during any
   trimester, because the fetus's brain continues to develop throughout
   the entire pregnancy. The brain damage is often accompanied by, and
   reflected in, distinctive facial stigmata, as seen in the photograph on
   the right.

   There are a number of subtypes, including standard fetal alcohol
   syndrome (FAS), and the less noticeable, but sometimes equally serious,
   possible fetal alcohol effects (PFAE). The latter is also known as
   prenatal exposure to alcohol (PEA) or alcohol-related
   neurodevelopmental disorder (ARND).

   Features of FASD may include facial deformities, stunted physical and
   emotional development, memory and attention deficits, a tendency to
   impulsive behaviour, inability to reason from cause to effect, a
   failure to comprehend the concept of time, difficulty telling fantasy
   from reality, inability to control sexual impulses, and an apparent
   lack of remorse. Secondary disabilities such as mental illness and drug
   addiction are also likely to develop. Unlike the primary disabilities,
   these do not reflect the central nervous system damage, but instead
   develop because the child has difficulty adapting to his environment.

   Fetal alcohol exposure is regarded by researchers as the leading known
   cause of mental retardation in the Western world. In the United States
   alone, it is estimated that, every year, one in 750 babies born suffers
   from FAS, and 40,000 from PFAE. The lifetime medical and welfare costs
   of each child are estimated by some to be as high as US$5 million.

Naming of the syndrome

   Fetal alcohol syndrome was named in 1973 by two dysmorphologists,
   Kenneth Lyons Jones and David W. Smith of the University of Washington
   Medical School in Seattle. They identified a pattern of "craniofacial,
   limb, and cardiovascular defects associated with prenatal onset growth
   deficiency and developmental delay" in eight unrelated children of
   three ethnic groups, all born to mothers who were alcoholics. The
   pattern of malformations indicated that the damage was prenatal. News
   of the discovery was shocked some, while others were skeptical of the
   findings."

   Dr. Paul Lemoine of Nantes, France had already published a study in a
   French medical journal in 1968 about children with distinctive features
   whose mothers were alcoholics, and in the U.S., Christy Ulleland and
   colleagues at the University of Washington Medical School had conducted
   an 18-month study in 1968-1969 documenting the risk of maternal alcohol
   consumption among the offspring of 11 alcoholic mothers. The Washington
   and Nantes findings were confirmed by a research group in Gothenburg,
   Sweden in 1979.

   Researchers in France, Sweden, and the United States were struck by how
   similar these children looked, though they were not related, and how
   they behaved in the same unfocused and hyperactive manner.

   Within four years of the Washington discovery, animal studies,
   including non-human primate studies carried out at the University of
   Washington Primate Centre by Dr Sterling Clarren, had confirmed that
   alcohol was a teratogen. By 1978, 245 cases of FAS had been reported by
   medical researchers, and the syndrome began to be described as the most
   frequent known cause of mental retardation.

Brain damage and facial defects

   Craniofacial abnormalities are visible in children with FAS, though not
   in children with FAE. Generally, children with FAS have a smaller head
   circumference and low birth weight, and they may fail to thrive. Their
   facial features are distinctive and diagnostically significant, in that
   they are a sign of brain damage, although there may be brain damage
   without the visible facial effects.

   Common findings are mild to moderate microcephaly; small palpebral
   fissure lengths (palpebral fissures are the opening of the eyelids,
   measured from between the exocanthion and endocanthion of each eye); a
   thin upper lip; smooth philtrum (the vertical "divot" or groove between
   the nose and upper lip); flattened cheekbones; and a short nose.

   Sterling Clarren of the University of Washington's Fetal Alcohol and
   Drug Unit told a conference in 2002:

     I have never seen anybody with this whole face who doesn't have some
     brain damage. In fact in studies, as the face is more FAS-like, the
     brain is more likely to be abnormal. The only face that you would
     want to counsel people or predict the future about is the full FAS
     face. But the risk of brain damage increases as the eyes get
     smaller, as the philtrum gets flatter, and the lip gets thinner. The
     risk goes up but not the diagnosis.

     At one-month gestation, the top end of your body is a brain, and at
     the very front end of that early brain, there is tissue that has
     been brain tissue. It stops being brain and gets ready to be your
     face ... Your eyeball is also brain tissue. It's an extension of the
     second part of the brain. It started as brain and "popped out." So
     if you are going to look at parts of the brain from alcohol damage,
     or any kind of damage during pregnancy, eye malformations and
     midline facial malformations are going to be very actively related
     to the brain across syndromes ... and they certainly are with FAS.

   As of 2002, there were 25 reports of autopsies on babies known to have
   been suffering from FASD. The first was in 1973 on a baby who died
   shortly after birth. The examination revealed extensive brain damage,
   including microcephaly, migration anomalies, callosal dysgenesis, and a
   massive neuroglial, leptomeningeal heterotopia covering the left
   hemisphere.

   Sterling Clarren described a second baby born in 1977, whose mother was
   a binge drinker. The baby died ten days after birth. The autopsy showed
   severe hydrocephalus, abnormal neuronal migration, and a small corpus
   callosum (which connects the two hemispheres) and cerebellum (ibid).

   Since then, FASD has also been linked to brainstem and cerebellar
   changes, agenesis of the corpus callosum and anterior commissure,
   migration errors, absent olfactory bulbs, meningomyelocele, and
   porencephaly (ibid, p. 11).

Diagnostic criteria

   Although clinicians agree on the definition of full-blown fetal alcohol
   syndrome, there is no agreement on the clinical criteria or names for
   lesser forms of it. This has led to some confusion for clinicians and
   patients. The following definitions are used in the clinic of Dr.
   Sterling Clarren (Clarren in Streissguth and Kanter 2002, p. 46):
     * FAS with a confirmed history of fetal alcohol exposure

   The definition of FAS is much the same as when the syndrome was first
   named. Diagnostic criteria include growth deficiency, the
   characteristic set of facial anomalies described above, and evidence of
   organic brain damage including structural, neurological, or functional
   stigmata.
     * FAS without a confirmed history of fetal alcohol exposure

   Clarren writes that he has never seen a patient with the same findings
   as above who has confirmed negative for prenatal alcohol exposure.
   However, his clinic does see patients who fit the diagnosis for whom no
   early history is available. Prenatal exposure is therefore not regarded
   as part of the diagnostic criteria, but will tend only to confirm it.
     * Atypical FAS or Possible FAS (PFAS)

   These patients have almost all the findings, and a confirmed history of
   alcohol exposure, but may lack growth deficiency or the full facial
   stigmata.
     * Fetal alcohol effect (FAE), possible fetal alcohol effect (PFAE)

   This term was used in research studies to describe humans and animals
   in whom teratogenic effects were seen after confirmed fetal alcohol
   exposure, but without obvious physical anomalies (Clarren and Smith
   1978). Because alcohol could not be regarded with certainty as the only
   cause of the effects, the term "possible fetal alcohol effects" was
   proposed for clinical use. This term has fallen out of favour with
   clinicians because it was being regarded by the public as a final
   diagnosis rather than a tentative one, and because it seemed to
   overstate the relationship between the possible cause and the perceived
   effects.
     * Alcohol-related birth defect

   This was proposed as an alternative to FAE and PFAE, but it has fallen
   out of favour, according to Clarren.
     * Alcohol-related neurodevelopmental disorder

   This was suggested by Stratton, Howe, and Battaglia in 1996 to replace
   FAE and PFAE, but Clarren regards the term as begging the question
   regarding the extent to which alcohol may have played a role, when the
   damage in some patients is minimal and hard to evaluate in terms of
   causation.

When the brain damage occurs

   During the first trimester, according to Sterling Clarren and Ann
   Streissguth of the University of Washington, alcohol interferes with
   the migration and organization of brain cells (Journal of Pediatrics,
   92(1):64-67).

   Most of the clinical features of FAS (the facial and other visible
   deformities) are believed to be caused mainly during the 10th and 20th
   week (Early Human Development; 1983 Jul Vol. 8(2) 99-111).

   During the third trimester, damage can be caused to the hippocampus,
   which plays a role in memory, learning, and emotion, leading to
   difficulty encoding visual and auditory information (Neurotoxicology
   and Teratology, 13:357-367, 1991).

Other physical effects

     * Growth — Pre- and postnatal onset growth retardation.
     * Performance — The I.Q. may be in the low or very low range, though
       this depends on the severity of the condition. Poor eye-hand
       coordination. Fine motor dysfunction manifested by a weak grasp.
     * Skeletal — Joint anomalies including abnormal position and
       function, altered palmar crease patterns. Small distal phalanges
       and small fifth fingernails.
     * Cardiac — A heart murmur that frequently disappears by one year of
       age. Ventricular septal defect most commonly seen, followed by an
       atrial septal defect.
     * Occasional abnormalities — Ptosis of the eyelid. Microophthalmia,
       cleft lip with or without a cleft palate, webbed neck, short neck,
       Tetralogy of Fallot, coarctation of the aorta, Spina bifida, and
       hydrocephalus.

Prevention

   Alcohol is a teratogen, and the only certain way to prevent FASD is to
   avoid drinking alcohol during pregnancy. Some studies have shown that
   small amounts of alcohol during pregnancy might not pose a risk to the
   fetus (for example, Abel, 1996; Day, 1992; du Florey et al., 1992;
   Forrest and du Florey, 1991; Goodlett and Peterson, 1995; Polygenis et
   al., 1998; Streissguth et al., 1994; Wilkie, 1997), although no amount
   of alcohol during pregnancy can be guaranteed to be absolutely safe. In
   the United States, the Surgeon General recommended in 1981 that women
   not drink while pregnant or while planning a pregnancy, the latter to
   avoid damage in the earliest stages of a pregnancy while the woman may
   not be aware that she has conceived. Congress passed legislation in
   1989 that requires warning labels be placed on all alcoholic beverage
   containers.
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