Fetal alcohol spectrum disorder

"FASD" redirects here. For other uses, see FASD (disambiguation).
Fetal alcohol spectrum disorders

Baby with fetal alcohol syndrome.
Classification and external resources
Specialty Pediatrics, toxicology
ICD-10 Q86.0
ICD-9-CM 760.71
DiseasesDB 32957
MedlinePlus 000911
eMedicine ped/767
MeSH D005310

Fetal alcohol spectrum disorders (FASDs) are a group of conditions that can occur in a person whose mother drank alcohol during pregnancy.[1] Problems may include an abnormal appearance, short height, low body weight, small head size, poor coordination, low intelligence, behavior problems, and problems with hearing or seeing.[1][2] Those affected are more likely to have trouble in school, legal problems, participate in high-risk behaviors, and have trouble with alcohol or other drugs.[3] The most severe form of the condition is known as fetal alcohol syndrome (FAS).[1] Other types include partial fetal alcohol syndrome (pFAS), alcohol-related neurodevelopmental disorder (ARND) and alcohol-related birth defects (ARBD).[1][4]

Fetal alcohol spectrum disorders are caused by drinking alcohol during pregnancy.[1] Surveys from the United States have found about 10% of pregnant women have drunk alcohol in the last month, and 20% to 30% drank at some point during the pregnancy.[5] About 4.7% of North American women who are pregnant have alcoholism.[6] The risk of problems depends on the amount consumed and the frequency of consumption as well as when during pregnancy the alcohol is consumed.[5] Other risk factors include an older mother, smoking, and poor diet.[5] There is no known safe amount or safe time to drink during pregnancy.[1][7] While drinking small amounts of alcohol does not cause abnormalities in the face, it may cause behavioral issues.[6] Alcohol crosses the blood brain barrier and both directly and indirectly affects a developing baby.[8] Diagnosis is based on signs and symptoms in the person.[1]

Fetal alcohol spectrum disorders are preventable by avoiding alcohol.[9] Medical organizations recommend no alcohol during pregnancy for this reason.[10][11][12] While the condition is permanent, treatment can improve outcomes.[1] Interventions may include parent-child interaction therapy, efforts to modify child behavior, and possibly medications.[13]

FASD is estimated to affect between 2% and 5% of people in the United States and Western Europe.[14] FAS is believed to occur in between 0.2 and 9 per 1000 live births in the United States.[14] In South Africa, some populations have rates as high as 9%.[4] The negative effects of alcohol have been described since ancient times.[4] The lifetime cost per child with FAS was $2,000,000 in 2002.[14] The term fetal alcohol syndrome was first used in 1973.[4]

Types

FASDs encompass a range of physical and neurodevelopmental problems that can result from prenatal alcohol exposure.[1] The most severe condition is called fetal alcohol syndrome (FAS),[1] which refers to individuals who have a specific set of birth defects and neurodevelopmental disorders characteristic of the diagnosis.[15] Partial fetal alcohol syndrome (pFAS) refers to individuals with a known, or highly suspected, history of prenatal alcohol exposure who have alcohol-related physical and neuroldevelopmental deficits that don’t meet the full criteria for FAS.[15] The subtypes of pFAS are alcohol-related neurodevelopmental disorder (ARND) and alcohol-related birth defects (ARBD).[15] In addition to FAS, pFAS, ARND, and ARBD, any other conditions believed to be related to prenatal alcohol exposure, such as spontaneous abortion and sudden infant death syndrome (SIDS), are also considered to be on the spectrum of related disorders.[15]

Signs and symptoms

Facial characteristics of a child with FAS

The key of FASD can vary between individuals exposed to alcohol during pregnancy. While consensus exists for the definition and diagnosis of FAS, minor variations among the systems lead to differences in definitions and diagnostic cut-off criteria for other diagnoses across the FASD continuum. (The central nervous system (CNS) damage criteria particularly lack clear consensus.) A working knowledge of the key features is helpful in understanding FASD diagnoses and conditions, and each are reviewed with attention to similarities and differences across the four diagnostic systems.

Growth

In terms of FASD, growth deficiency is defined as significantly below average height, weight or both due to prenatal alcohol exposure, and can be assessed at any point in the lifespan. Growth measurements must be adjusted for parental height, gestational age (for a premature infant), and other postnatal insults (e.g., poor nutrition), although birth height and weight are the preferred measurements.[16] Deficiencies are documented when height or weight falls at or below the 10th percentile of standardized growth charts appropriate to the population.[17]

Criteria for FASD are least specific in the IOM diagnostic system ("low birth weight..., decelerating weight not due to nutrition..., [or] disproportional low weight to height" p. 4 of executive summary),[11] while the CDC and Canadian guidelines use the 10th percentile as a cut-off to determine growth deficiency.[18][2] The "4-Digit Diagnostic Code" allows for mid-range gradations in growth deficiency (between the 3rd and 10th percentiles) and severe growth deficiency at or below the 3rd percentile.[16] Growth deficiency (at severe, moderate, or mild levels) contributes to diagnoses of FAS and pFAS, but not ARND or static encephalopathy.

Growth deficiency is ranked as follows by the "4-Digit Diagnostic Code":[16]

In the initial studies that discovered FAS, growth deficiency was a requirement for inclusion in the studies; thus, all the original people with FAS had growth deficiency as an artifact of sampling characteristics used to establish criteria for the syndrome. That is, growth deficiency is a key feature of FASD because growth deficiency was a criterion for inclusion in the original study that determined the definition of FAS. This reinforces assertions that growth deficiency and FAS facial features are less critical for understanding the disability's of FASD than the neurobehavioral sequelae to the brain damage.[11]

Facial features

Several characteristic craniofacial abnormalities are often visible in individuals with FAS.[19] The presence of FAS facial features indicates brain damage, though brain damage may also exist in their absence. FAS facial features (and most other visible, but non-diagnostic, deformities) are believed to be caused mainly during the 10th and 20th week of gestation.[20]

Refinements in diagnostic criteria since 1975 have yielded three distinctive and diagnostically significant facial features known to result from prenatal alcohol exposure and distinguishes FAS from other disorders with partially overlapping characteristics.[21][22] The three FAS facial features are:

Measurement of FAS facial features uses criteria developed by the University of Washington. The lip and philtrum are measured by a trained physician with the Lip-Philtrum Guide,[23] a five-point Likert Scale with representative photographs of lip and philtrum combinations ranging from normal (ranked 1) to severe (ranked 5). Palpebral fissure length (PFL) is measured in millimeters with either calipers or a clear ruler and then compared to a PFL growth chart, also developed by the University of Washington.[24]

Ranking FAS facial features is complicated because the three separate facial features can be affected independently by prenatal alcohol. A summary of the criteria follows:[16][25]

Central nervous system

Central nervous system (CNS) damage is the primary key feature of any FASD diagnosis. Prenatal alcohol exposure, which is classified as a teratogen, can damage the brain across a continuum of gross to subtle impairments, depending on the amount, timing, and frequency of the exposure as well as genetic predispositions of the fetus and mother.[11][26] While functional abnormalities are the behavioral and cognitive expressions of the FASD disability, CNS damage can be assessed in three areas: structural, neurological, and functional impairments.

All four diagnostic systems allow for assessment of CNS damage in these areas, but criteria vary. The IOM system requires structural or neurological impairment for a diagnosis of FAS, but also allows a "complex pattern" of functional anomalies for diagnosing PFAS and ARND.[11] The "4-Digit Diagnostic Code" and CDC guidelines allow for a positive CNS finding in any of the three areas for any FASD diagnosis, but functional anomalies must measure at two standard deviations or worse in three or more functional domains for a diagnoses of FAS, PFAS, and ARND.[16][18] The "4-Digit Diagnostic Code" also allows for an FASD diagnosis when only two functional domains are measured at two standard deviations or worse.[16] The "4-Digit Diagnostic Code" further elaborates the degree of CNS damage according to four ranks:

Structural

Structural abnormalities of the brain are observable, physical damage to the brain or brain structures caused by prenatal alcohol exposure. Structural impairments may include microcephaly (small head size) of two or more standard deviations below the average, or other abnormalities in brain structure (e.g., agenesis of the corpus callosum, cerebellar hypoplasia).[11]

Microcephaly is determined by comparing head circumference (often called occipitofrontal circumference, or OFC) to appropriate OFC growth charts.[17] Other structural impairments must be observed through medical imaging techniques by a trained physician. Because imaging procedures are expensive and relatively inaccessible to most people, diagnosis of FAS is not frequently made via structural impairments, except for microcephaly.

Evidence of a CNS structural impairment due to prenatal alcohol exposure will result in a diagnosis of FAS, and neurological and functional impairments are highly likely.[11][16][18][2]

During the first trimester of pregnancy, alcohol interferes with the migration and organization of brain cells, which can create structural deformities or deficits within the brain.[27] During the third trimester, damage can be caused to the hippocampus, which plays a role in memory, learning, emotion, and encoding visual and auditory information, all of which can create neurological and functional CNS impairments as well.[28]

As of 2002, there were 25 reports of autopsies on infants known to have FAS. The first was in 1973, on an infant who died shortly after birth.[29] The examination revealed extensive brain damage, including microcephaly, migration anomalies, callosal dysgenesis, and a massive neuroglial, leptomeningeal heterotopia covering the left hemisphere.[30]

In 1977, Dr. Clarren described a second infant whose mother was a binge drinker. The infant died ten days after birth. The autopsy showed severe hydrocephalus, abnormal neuronal migration, and a small corpus callosum (which connects the two brain hemispheres) and cerebellum.[30] FAS has also been linked to brainstem and cerebellar changes, agenesis of the corpus callosum and anterior commissure, neuronal migration errors, absent olfactory bulbs, meningomyelocele, and porencephaly.[30]

Neurological

When structural impairments are not observable or do not exist, neurological impairments are assessed. In the context of FASD, neurological impairments are caused by prenatal alcohol exposure which causes general neurological damage to the central nervous system (CNS), the peripheral nervous system, or the autonomic nervous system. A determination of a neurological problem must be made by a trained physician, and must not be due to a postnatal insult, such as a high fever, concussion, traumatic brain injury, etc.

All four diagnostic systems show virtual agreement on their criteria for CNS damage at the neurological level, and evidence of a CNS neurological impairment due to prenatal alcohol exposure will result in a diagnosis of FAS or pFAS, and functional impairments are highly likely.[11][16][18][2]

Neurological problems are expressed as either hard signs, or diagnosable disorders, such as epilepsy or other seizure disorders, or soft signs. Soft signs are broader, nonspecific neurological impairments, or symptoms, such as impaired fine motor skills, neurosensory hearing loss, poor gait, clumsiness, poor eye-hand coordination. Many soft signs have norm-referenced criteria, while others are determined through clinical judgment. "Clinical judgment" is only as good as the clinician, and soft signs should be assessed by either a pediatric neurologist, a pediatric neuropsychologist, or both. Those affected have mild retardation.

Functional

When structural or neurological impairments are not observed, all four diagnostic systems allow CNS damage due to prenatal alcohol exposure to be assessed in terms of functional impairments.[11][16][18][2] Functional impairments are deficits, problems, delays, or abnormalities due to prenatal alcohol exposure (rather than hereditary causes or postnatal insults) in observable and measurable domains related to daily functioning, often referred to as developmental disabilities. There is no consensus on a specific pattern of functional impairments due to prenatal alcohol exposure[11] and only CDC guidelines label developmental delays as such,[18] so criteria (and FASD diagnoses) vary somewhat across diagnostic systems.

The four diagnostic systems list various CNS domains that can qualify for functional impairment that can determine an FASD diagnosis:

Related signs

Other conditions may commonly co-occur with FAS, stemming from prenatal alcohol exposure. However, these conditions are considered alcohol-related birth defects[11] and not diagnostic criteria for FAS.

Cause

Fetal alcohol syndrome usually occurs when a pregnant woman has more than four standard drinks per day.[32] Milder symptoms have been found with two drinks per day during the early part of pregnancy.[32][33] Among those who are alcoholic about a third of children have FAS.[32]

Evidence of harm from less than two drinks per day or 10 drinks per week is not clear.[32][34] While small amounts of alcohol do not cause an abnormal appearance it may cause behavioral issues.[6] There is conflicting evidence regarding whether drinking by fathers before conception can cause FAS.[32]

Mechanism

Despite intense research efforts, it has not been possible to identify a single clear-cut mechanism for development of FAS or FASD. On the contrary, clinical and animal studies have identified a broad spectrum of pathways through which maternal alcohol can negatively affect the outcome of a pregnancy. Clear conclusions with universal validity are difficult to draw, since different ethnic groups show considerable genetic polymorphism for the hepatic enzymes responsible for ethanol detoxification.[35]

Genetic examinations have revealed a continuum of long-lasting molecular effects that are not only timing specific but are also dosage specific; with even moderate amounts being able to cause alterations.[36]

A human fetus appears to be at triple risk from maternal alcohol consumption:[37][38]

  1. The placenta allows free entry of ethanol and toxic metabolites like acetaldehyde into the fetal compartment. The so-called placental barrier is no barrier with respect to ethanol.
  2. The developing fetal nervous system appears particularly sensitive to ethanol toxicity. The latter impacts negatively on proliferation, differentiation, neuronal migration, axonic outgrowth, integration and fine tuning of the synaptic network. In short, all major processes in the developing central nervous system appear compromised.
  3. Fetal tissues are quite different from adult tissues in function and purpose. For example, the main detoxicating organ in adults is the liver, whereas fetal liver is incapable of detoxicating ethanol as the ADH and ALDH enzymes have not yet been brought to expression at this early stage. Up to term, fetal tissues do not have significant capacity for the detoxification of ethanol, and the fetus remains exposed to ethanol in the amniotic fluid for periods far longer than the decay time of ethanol in the maternal circulation.

Generally, fetal tissues have far less antioxidant protection than adult tissues as they express no significant quantities ADH or ALDH, and far less antioxidant enzymes like SOD, glutathion transferases or glutathion peroxidases.

Diagnosis

Because admission of alcohol use during pregnancy can stigmatize birth mothers, many are reluctant to admit drinking or to provide an accurate report of the quantity they drank. This complicates diagnosis and treatment [18] of the syndrome. As a result, diagnosis of the severity of FASD relies on protocols of observation of the child's physiology and behavior rather than maternal self-reporting. Presently, four FASD diagnostic systems that diagnose FAS and other FASD conditions have been developed in North America:

Each diagnostic system requires that a complete FASD evaluation includes an assessment of the four key features of FASD, described below. A positive finding on all four features is required for a diagnosis of FAS. However, prenatal alcohol exposure and central nervous system damage are the critical elements of the spectrum of FASD, and a positive finding in these two features is sufficient for an FASD diagnosis that is not "full-blown FAS".

While the four diagnostic systems essentially agree on criteria for fetal alcohol syndrome (FAS), there are still differences when full criteria for FAS are not met. This has resulted in differing and evolving nomenclature for other conditions across the spectrum of FASD, which may account for such a wide variety of terminology. Most individuals with deficits resulting from prenatal alcohol exposure do not express all features of FAS and fall into other FASD conditions.[11] The Canadian guidelines recommend the assessment and descriptive approach of the "4-Digit Diagnostic Code" for each key feature of FASD and the terminology of the IOM in diagnostic categories, excepting ARBD.[2]

Thus, other FASD conditions are partial expressions of FAS. However, these other FASD conditions may create disabilities similar to FAS if the key area of central nervous system damage shows clinical deficits in two or more of ten domains of brain functioning. Essentially, even though growth deficiency and/or FAS facial features may be mild or nonexistent in other FASD conditions, yet clinically significant brain damage of the central nervous system is present. In these other FASD conditions, an individual may be at greater risk for adverse outcomes because brain damage is present without associated visual cues of poor growth or the "FAS face" that might ordinarily trigger an FASD evaluation. Such individuals may be misdiagnosed with primary mental health disorders such as ADHD or oppositional defiance disorder without appreciation that brain damage is the underlying cause of these disorders, which requires a different treatment paradigm than typical mental health disorders. While other FASD conditions may not yet be included as an ICD or DSM-IV-TR diagnosis, they nonetheless pose significant impairment in functional behavior because of underlying brain damage.

Fetal alcohol syndrome

The following criteria must be fully met for an FAS diagnosis:[11][16][18][2]

  1. Growth deficiency: Prenatal or postnatal height or weight (or both) at or below the 10th percentile[17]
  2. FAS facial features: All three FAS facial features present[24]
  3. Central nervous system damage: Clinically significant structural neurological, or functional impairment
  4. Prenatal alcohol exposure: Confirmed or Unknown prenatal alcohol exposure

Fetal alcohol syndrome (FAS) is the first diagnosable condition of FASD that was discovered. FAS is the only expression of FASD that has garnered consensus among experts to become an official ICD-9 and ICD-10 diagnosis. To make this diagnosis or determine any FASD condition, a multi-disciplinary evaluation is necessary to assess each of the four key features for assessment. Generally, a trained physician will determine growth deficiency and FAS facial features. While a qualified physician may also assess central nervous system structural abnormalities and/or neurological problems, usually central nervous system damage is determined through psychological, speech-language, and occupational therapy assessments to ascertain clinically significant impairments in three or more of the Ten Brain Domains.[39] Prenatal alcohol exposure risk may be assessed by a qualified physician, psychologist, social worker, or chemical health counselor. These professionals work together as a team to assess and interpret data of each key feature for assessment and develop an integrative, multi-disciplinary report to diagnose FAS (or other FASD conditions) in an individual.

Partial FAS

Partial FAS (pFAS), previously known as atypical FAS in the 1997 edition of the "4-Digit Diagnostic Code". People with pFAS have a confirmed history of prenatal alcohol exposure, but may lack growth deficiency or the complete facial stigmata. Central nervous system damage is present at the same level as FAS. These individuals have the same functional disabilities but "look" less like FAS.

The following criteria must be fully met for a diagnosis of Partial FAS:[11][16][2]

  1. Growth deficiency: Growth or height may range from normal to deficient[17]
  2. FAS facial features: Two or three FAS facial features present[24]
  3. Central nervous system damage: Clinically significant structural, neurological, or functional impairment in three or more of the Ten Brain Domains[39]
  4. Prenatal alcohol exposure: Confirmed prenatal alcohol exposure

Fetal alcohol effects

Fetal alcohol effects (FAE) is a previous term for alcohol-related neurodevelopmental disorder and alcohol-related birth defects.[1] It was initially used in research studies to describe humans and animals in whom teratogenic effects were seen after confirmed prenatal alcohol exposure (or unknown exposure for humans), but without obvious physical anomalies.[40] Smith (1981) described FAE as an "extremely important concept" to highlight the debilitating effects of brain damage, regardless of the growth or facial features.[41] This term has fallen out of favor with clinicians because it was often regarded by the public as a less severe disability than FAS, when in fact its effects can be just as detrimental.[42]

Alcohol-related neurodevelopmental disorder

Alcohol-related neurodevelopmental disorder (ARND) was initially suggested by the Institute of Medicine to replace the term FAE and focus on central nervous system damage, rather than growth deficiency or FAS facial features. The Canadian guidelines also use this diagnosis and the same criteria. While the "4-Digit Diagnostic Code" includes these criteria for three of its diagnostic categories, it refers to this condition as static encephalopathy. The behavioral effects of ARND are not necessarily unique to alcohol however, so use of the term must be within the context of confirmed prenatal alcohol exposure.[43] ARND may be gaining acceptance over the terms FAE and ARBD to describe FASD conditions with central nervous system abnormalities or behavioral or cognitive abnormalities or both due to prenatal alcohol exposure without regard to growth deficiency or FAS facial features.[43][44]

The following criteria must be fully met for a diagnosis of ARND or static encephalopathy:[11][16][2]

  1. Growth deficiency: Growth or height may range from normal to minimally deficient[17]
  2. FAS facial features: Minimal or no FAS facial features present[24]
  3. Central nervous system damage: Clinically significant structural, neurological, or functional impairment in three or more of the Ten Brain Domains[39]
  4. Prenatal alcohol exposure: Confirmed prenatal alcohol exposure;0

Alcohol-related birth defects

Alcohol-related birth defects (ARBD), formerly known as possible fetal alcohol effect (PFAE),[40] was a term proposed as an alternative to FAE and PFAE[45] The IOM presents ARBD as a list of congenital anomalies that are linked to maternal alcohol use but have no key features of FASD.[11] PFAE and ARBD have fallen out of favor because these anomalies are not necessarily specific to maternal alcohol consumption and are not criteria for diagnosis of FASD.[43] The Canadian guidelines recommend that ARBD should not be used as an umbrella term or diagnostic category for FASD.

Exposure

Prenatal alcohol exposure is determined by interview of the biological mother or other family members knowledgeable of the mother's alcohol use during the pregnancy (if available), prenatal health records (if available), and review of available birth records, court records (if applicable), chemical dependency treatment records (if applicable), or other reliable sources.

Exposure level is assessed as confirmed exposure, unknown exposure, and confirmed absence of exposure by the IOM, CDC and Canadian diagnostic systems. The "4-Digit Diagnostic Code" further distinguishes confirmed exposure as High Risk and Some Risk:

Confirmed exposure

Amount, frequency, and timing of prenatal alcohol use can dramatically impact the other three key features of FASD. While consensus exists that alcohol is a teratogen, there is no clear consensus as to what level of exposure is toxic.[11] The CDC guidelines are silent on these elements diagnostically. The IOM and Canadian guidelines explore this further, acknowledging the importance of significant alcohol exposure from regular or heavy episodic alcohol consumption in determining, but offer no standard for diagnosis. Canadian guidelines discuss this lack of clarity and parenthetically point out that "heavy alcohol use" is defined by the National Institute on Alcohol Abuse and Alcoholism as five or more drinks per episode on five or more days during a 30-day period.[46]

"The 4-Digit Diagnostic Code" ranking system distinguishes between levels of prenatal alcohol exposure as high risk and some risk. It operationalizes high risk exposure as a blood alcohol concentration (BAC) greater than 100 mg/dL delivered at least weekly in early pregnancy. This BAC level is typically reached by a 55 kg female drinking six to eight beers in one sitting.[16]

Unknown exposure

For many adopted or adults and children in foster care, records or other reliable sources may not be available for review. Reporting alcohol use during pregnancy can also be stigmatizing to birth mothers, especially if alcohol use is ongoing.[18] In these cases, all diagnostic systems use an unknown prenatal alcohol exposure designation. A diagnosis of FAS is still possible with an unknown exposure level if other key features of FASD are present at clinical levels.

Confirmed absence of exposure

Confirmed absence of exposure would apply to planned pregnancies in which no alcohol was used or pregnancies of women who do not use alcohol or report no use during the pregnancy. This designation is relatively rare, as most people presenting for an FASD evaluation are at least suspected to have had a prenatal alcohol exposure due to presence of other key features of FASD.[16][18]

Ten brain domains

A recent effort to standardize assessment of functional CNS damage has been suggested by an experienced FASD diagnostic team in Minnesota. The proposed framework attempts to harmonize IOM, 4-Digit Diagnostic Code, CDC, and Canadian guidelines for measuring CNS damage vis-à-vis FASD evaluations and diagnosis. The standardized approach is referred to as the Ten Brain Domains and encompasses aspects of all four diagnostic systems' recommendations for assessing CNS damage due to prenatal alcohol exposure. The framework provides clear definitions of brain dysfunction, specifies empirical data needed for accurate diagnosis, and defines intervention considerations that address the complex nature of FASD with the intention to avoid common secondary disabilities.[39]

The proposed Ten Brain Domains include:[39]

The Fetal Alcohol Diagnostic Program (FADP) uses unpublished Minnesota state criteria of performance at 1.5 or more standard deviations on standardized testing in three or more of the Ten Brain Domains to determine CNS damage. However, the Ten Brain Domains are easily incorporated into any of the four diagnostic systems' CNS damage criteria, as the framework only proposes the domains, rather than the cut-off criteria for FASD.[47]

Differential diagnosis

The CDC reviewed nine syndromes that have overlapping features with FAS; however, none of these syndromes include all three FAS facial features, and none are the result of prenatal alcohol exposure:[18]

Prevention

The only certain way to prevent FAS is to avoid drinking alcohol during pregnancy.[43] In the United States, the Surgeon General recommended in 1981, and again in 2005, that women abstain from alcohol use while pregnant or while planning a pregnancy, the latter to avoid damage even in the earliest stages (even weeks) of a pregnancy, as the woman may not be aware that she has conceived.[10] In the United States, federal legislation has required that warning labels be placed on all alcoholic beverage containers since 1988 under the Alcoholic Beverage Labeling Act.

There is some controversy surrounding the "zero-tolerance" approach taken by many countries when it comes to alcohol consumption during pregnancy. The assertion that moderate drinking causes FAS is said to lack strong evidence and, in fact, the practice of equating a responsible level of drinking with potential harm to the fetus may have negative social, legal, and health impacts.[48] In addition, special care should be taken when considering statistics on this disease, as prevalence and causation is often linked with FASD, which is more common and causes less harm, as opposed to FAS.[49]

Treatment

There is no cure for FASD, but treatment is possible. Because CNS damage, symptoms, secondary disabilities, and needs vary widely by individual, there is no one treatment type that works for everyone.

Medication

Psychoactive drugs are frequently tried on those with FASD as many FASD symptoms are mistaken for or overlap with other disorders, most notably ADHD.[50]

Behavioral interventions

Behavioral interventions are based on the learning theory, which is the basis for many parenting and professional strategies and interventions.[44] Along with ordinary parenting styles, such strategies are frequently used by default for treating those with FAS, as the diagnoses oppositional defiance disorder (ODD), conduct disorder, reactive attachment disorder (RAD) often overlap with FAS (along with ADHD), and these are sometimes thought to benefit from behavioral interventions. Frequently, a person's poor academic achievement results in special education services, which also utilizes principles of learning theory, behavior modification, and outcome-based education.

Developmental framework

Many books and handouts on FAS recommend a developmental approach, based on developmental psychology, even though most do not specify it as such and provide little theoretical background. Optimal human development generally occurs in identifiable stages (e.g., Jean Piaget's theory of cognitive development, Erik Erikson's stages of psychosocial development, John Bowlby's attachment framework, and other developmental stage theories). FAS interferes with normal development,[51] which may cause stages to be delayed, skipped, or immaturely developed. Over time, an unaffected child can negotiate the increasing demands of life by progressing through stages of development normally, but not so for a child with FAS.[51]

By knowing what developmental stages and tasks children follow, treatment and interventions for FAS can be tailored to helping a person meet developmental tasks and demands successfully.[51] If a person is delayed in the adaptive behavior domain, for instance, then interventions would be recommended to target specific delays through additional education and practice (e.g., practiced instruction on tying shoelaces), giving reminders, or making accommodations (e.g., using slip-on shoes) to support the desired functioning level. This approach is an advance over behavioral interventions, because it takes the person's developmental context into account while developing interventions.

Advocacy model

The advocacy model takes the point of view that someone is needed to actively mediate between the environment and the person with FAS.[43] Advocacy activities are conducted by an advocate (for example, a family member, friend, or case manager) and fall into three basic categories. An advocate for FAS: (1) interprets FAS and the disabilities that arise from it and explains it to the environment in which the person operates, (2) engenders change or accommodation on behalf of the person, and (3) assists the person in developing and reaching attainable goals.[43]

The advocacy model is often recommended, for example, when developing an Individualized Education Program (IEP) for the person's progress at school.[50]

An understanding of the developmental framework would presumably inform and enhance the advocacy model, but advocacy also implies interventions at a systems level as well, such as educating schools, social workers, and so forth on best practices for FAS. However, several organizations devoted to FAS also use the advocacy model at a community practice level as well.[52]

Public health and policy

Treating FAS at the public health and public policy level promotes FAS prevention and diversion of public resources to assist those with FAS.[43] It is related to the advocacy model but promoted at a systems level (rather than with the individual or family), such as developing community education and supports, state or province level prevention efforts (e.g., screening for maternal alcohol use during OB/GYN or prenatal medical care visits), or national awareness programs. Several organizations and state agencies in the U.S. are dedicated to this type of intervention.[52]

Prognosis

Primary disabilities

The primary disabilities of FAS are the functional difficulties with which the child is born as a result of CNS damage due to prenatal alcohol exposure.[53] Often, primary disabilities are mistaken as behavior problems, but the underlying CNS damage is the originating source of a functional difficulty,[54] rather than a mental health condition, which is considered a secondary disability.

The exact mechanisms for functional problems of primary disabilities are not always fully understood, but animal studies have begun to shed light on some correlates between functional problems and brain structures damaged by prenatal alcohol exposure.[43] Representative examples include:

Functional difficulties may result from CNS damage in more than one domain, but common functional difficulties by domain include:[43][44][51][54] Note that this is not an exhaustive list of difficulties.

Secondary disabilities

The secondary disabilities of FAS are those that arise later in life secondary to CNS damage. These disabilities often emerge over time due to a mismatch between the primary disabilities and environmental expectations; secondary disabilities can be ameliorated with early interventions and appropriate supportive services.[53]

Six main secondary disabilities were identified in a University of Washington research study of 473 subjects diagnosed with FAS, PFAS (partial fetal alcohol syndrome), and ARND (alcohol-related neurodevelopmental disorder):[43][53]

Two additional secondary disabilities exist for adults:[43][53]

Protective factors and strengths

Eight factors were identified in the same study as universal protective factors that reduced the incidence rate of the secondary disabilities:[43][53]

Malbin (2002) has identified the following areas of interests and talents as strengths that often stand out for those with FASD and should be utilized, like any strength, in treatment planning:[44]

Epidemiology

FASD is estimated to affect between 2% and 5% of people in the United States and Western Europe.[14] FAS is believed to occur in between 0.2 and 9 per 1000 live births in the United States.[14] The lifetime cost of an individual with FAS were estimated to be two million USD in 2002.[14]

Australia

FASD among Australian youth is more common in indigenous Australians.[58] The only states that have registered birth defects in Australian youth are Western Australia, New South Wales, Victoria and South Australia.[59] In Australia only 12% of Australian health professionals are aware of the diagnostics and symptoms of FASD.[58] In Western Australia, the rate of births resulting in FASD is 0.02 per 1000 births for non-Indigenous Australians, however among indigenous births the rate is 2.76 per 1000 births.[59] In Victoria, there have been no registered FASD related births for indigenous Australians, but the rate for the general population in Victoria is 0.01-0.03 per 1000 births.[59] There have been no dedicated FASD clinics within Western Australia, but there are also no nationally supported diagnostic criteria anywhere in Australia.[60] Passive surveillance is a prevention technique used within Australia to assist in monitoring and establishing detectable defects during pregnancy and childhood.[59]

History

From the 1960s to the 1980s, alcohol was commonly used as a tocolytic, a method to stop preterm labor. The method originated with Dr. Fritz Fuchs, the chairman of the department of obstetrics and gynecology at Cornell University Medical College.[61][62] Doctors recommended a small amount of alcohol to calm the uterus during contractions in early pregnancy or Braxton Hix contractions. In later stages of pregnancy, the alcohol was administered intravenously and often in large amounts. "Women experienced similar effects as occur with oral ingestion, including intoxication, nausea and vomiting, and potential alcohol poisoning, followed by hangovers when the alcohol was discontinued."[63] Vomiting put the mother at a high risk for aspiration and was "a brutal procedure for all involved." [61] Because the alcohol was being given intravenously, the doctor could continue giving the treatment to the mother long after she had passed out, resulting in her being more intoxicated than would otherwise be possible. Such heavy intoxication is highly likely to contribute to FASD.[61]

Historical references

Anecdotal accounts of prohibitions against maternal alcohol use from Biblical, ancient Greek, and ancient Roman sources imply a historical awareness of links between maternal alcohol use and negative child outcomes.[29] In Gaelic Scotland, the mother and nurse were not allowed to consume ale during pregnancy and breastfeeding (Martin Martin).

The earliest recorded observation of possible links between maternal alcohol use and fetal damage was made in 1899 by Dr. William Sullivan, a Liverpool prison physician who noted higher rates of stillbirth for 120 alcoholic female prisoners than their sober female relatives; he suggested the causal agent to be alcohol use.[64] This contradicted the predominating belief at the time that heredity caused intellectual disability, poverty, and criminal behavior, which contemporary studies on the subjects usually concluded.[43] A case study by Henry H. Goddard of the Kallikak family—popular in the early 1900s—represents this earlier perspective,[65] though later researchers have suggested that the Kallikaks almost certainly had FAS.[66] General studies and discussions on alcoholism throughout the mid-1900s were typically based on a heredity argument.[67]

Prior to fetal alcohol syndrome being specifically identified and named in 1973, a few studies had noted differences between the children of mothers who used alcohol during pregnancy or breast-feeding and those who did not, but identified alcohol use as a possible contributing factor rather than heredity.[43]

Recognition as a syndrome

Fetal Alcohol Syndrome was named in 1973 by two dysmorphologists, Drs. Kenneth Lyons Jones and David Weyhe Smith of the University of Washington Medical School in Seattle, United States. 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.[68] The pattern of malformations indicated that the damage was prenatal. News of the discovery shocked some, while others were skeptical of the findings.[69]

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,[70] 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.[71] The Washington and Nantes findings were confirmed by a research group in Gothenburg, Sweden in 1979.[72] 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.[72]

Within nine years of the Washington discovery, animal studies, including non-human monkey studies carried out at the University of Washington Primate Center 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 intellectual disability.

While many syndromes are eponymous, i.e. named after the physician first reporting the association of symptoms, Dr. Smith named FAS after the causal agent of the symptoms.[73] He reasoned that doing so would encourage prevention, believing that if people knew maternal alcohol consumption caused the syndrome, then abstinence during pregnancy would follow from patient education and public awareness.[73] At the time, nobody was aware of the full range of possible birth defects from FAS or its rate of prevalence.[73] Over time, as subsequent research and clinical experience suggested that a range of effects (including physical, behavioral, and cognitive) could arise from prenatal alcohol exposure, the term Fetal Alcohol Spectrum Disorder (FASD) was developed to include FAS as well as other conditions resulting from prenatal alcohol exposure.[73] Currently, FAS[11][40][68] is the only expression of prenatal alcohol exposure defined by the International Statistical Classification of Diseases and Related Health Problems and assigned ICD-9 and diagnoses.

References

  1. 1 2 3 4 5 6 7 8 9 10 11 "Facts about FASDs". April 16, 2015. Retrieved 10 June 2015.
  2. 1 2 3 4 5 6 7 8 9 10 Chudley; et al. (2005), "Fetal alcohol spectrum disorder: Canadian guidelines for diagnosis", CMAJ 172 (5 Suppl): S1–S21, doi:10.1503/cmaj.1040302, PMC 557121, PMID 15738468, retrieved 16 Apr 16 Check date values in: |access-date= (help)
  3. ↑ Coriale, G; Fiorentino, D; Di Lauro, F; Marchitelli, R; Scalese, B; Fiore, M; Maviglia, M; Ceccanti, M (2013). "Fetal Alcohol Spectrum Disorder (FASD): neurobehavioral profile, indications for diagnosis and treatment.". Rivista di psichiatria 48 (5): 359–69. doi:10.1708/1356.15062. PMID 24326748.
  4. 1 2 3 4 Riley, EP; Infante, MA; Warren, KR (June 2011). "Fetal alcohol spectrum disorders: an overview.". Neuropsychology review 21 (2): 73–80. doi:10.1007/s11065-011-9166-x. PMID 21499711.
  5. 1 2 3 "Fetal Alcohol Exposure". April 2015. Retrieved 10 June 2015.
  6. 1 2 3 McHugh, RK; Wigderson, S; Greenfield, SF (June 2014). "Epidemiology of substance use in reproductive-age women.". Obstetrics and gynecology clinics of North America 41 (2): 177–89. doi:10.1016/j.ogc.2014.02.001. PMID 24845483.
  7. ↑ Williams, J. F.; Smith, V. C. (19 October 2015). "Fetal Alcohol Spectrum Disorders". Pediatrics 136 (5): e1395–e1406. doi:10.1542/peds.2015-3113.
  8. ↑ Fetal Alcohol Spectrum Disorder: Management and Policy Perspectives of FASD. John Wiley & Sons. 2011. pp. 73–75. ISBN 9783527632565.
  9. ↑ "Alcohol Use in Pregnancy". April 17, 2014. Retrieved 10 June 2015.
  10. 1 2 Vice Admiral Richard H. Carmona (2005). "A 2005 Message to Women from the U.S. Surgeon General" (PDF). Retrieved 12 June 2015.
  11. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 Committee to Study Fetal Alcohol Syndrome, Division of Biobehavioral Sciences and Mental Disorders, Institute of Medicine (1995). Fetal alcohol syndrome : diagnosis, epidemiology, prevention, and treatment. Washington, D.C.: National Academy Press. ISBN 0-309-05292-0.
  12. ↑ "Australian Government National Health and Medical Research Council". Retrieved 4 November 2012.
  13. ↑ Roszel, EL (13 April 2015). "Central nervous system deficits in fetal alcohol spectrum disorder.". The Nurse practitioner 40 (4): 24–33. doi:10.1097/01.npr.0000444650.10142.4f. PMID 25774812.
  14. 1 2 3 4 5 6 "Data & Statistics Prevalence of FASDs". Center for Disease Control and Prevention. April 16, 2015. Retrieved 10 June 2015.
  15. 1 2 3 4 Kingdon; et al. (2016), "Research Review: Executive function deficits in fetal alcohol spectrum disorders and attention-deficit/hyperactivity disorder – a meta-analysis", Journal of Child Psychology and Psychiatry 57 (2): 116-131, doi:10.1111/jcpp.12451
  16. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 Astley, S.J. (2004). Diagnostic Guide for Fetal Alcohol Spectrum Disorders: The 4-Digit Diagnostic Code. Seattle: University of Washington. PDF available at FAS Diagnostic and Prevention Network. Retrieved on 2007-04-11.
  17. 1 2 3 4 5 Clinical growth charts. National Center for Growth Statistics. Retrieved on 2007-04-10
  18. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 Fetal Alcohol Syndrome: Guidelines for Referral and Diagnosis (PDF). CDC (July 2004). Retrieved on 2009-09-22
  19. ↑ Jones K, Smith D (1975). "The fetal alcohol syndrome". Teratology 12 (1): 1–10. doi:10.1002/tera.1420120102. PMID 1162620.
  20. ↑ Renwick J, Asker R (1983). "Ethanol-sensitive times for the human conceptus". Early Hum Dev 8 (2): 99–111. doi:10.1016/0378-3782(83)90065-8. PMID 6884260.
  21. ↑ Astley SJ, Clarren SK (1996). "Most FAS children have a smaller brain then other children "A case definition and photographic screening tool for the facial phenotype of fetal alcohol syndrome"". Journal of Pediatrics 129 (1): 33–41. doi:10.1016/s0022-3476(96)70187-7. PMID 8757560.
  22. ↑ Astley SJ, Stachowiak J, Clarren SK, Clausen C (2002). "Application of the fetal alcohol syndrome facial photographic screening tool in a foster care population". Journal of Pediatrics 141 (5): 712–717. doi:10.1067/mpd.2002.129030. PMID 12410204.
  23. ↑ Lip-philtrum guides. FAS Diagnostic and Prevention Network, University of Washington. Retrieved on 2007-04-10.
  24. 1 2 3 4 FAS facial features. FAS Diagnostic and Prevention Network, University of Washington. Retrieved on 2007-04-10
  25. ↑ Astley, Susan. Backside of Lip-Philtrum Guides (2004) (PDF). University of Washington, Fetal Alcohol Syndrome Diagnostic and Prevention Network. Retrieved on 2007-04-11
  26. ↑ West, J.R. (Ed.) (1986). Alcohol and Brain Development. New York: Oxford University Press.
  27. ↑ Clarren S, Alvord E, Sumi S, Streissguth A, Smith D (1978). "Brain malformations related to prenatal exposure to ethanol". J Pediatr 92 (1): 64–7. doi:10.1016/S0022-3476(78)80072-9. PMID 619080.
  28. ↑ Coles C, Brown R, Smith I, Platzman K, Erickson S, Falek A (1991). "Effects of prenatal alcohol exposure at school age. I. Physical and cognitive development". Neurotoxicol Teratol 13 (4): 357–67. doi:10.1016/0892-0362(91)90084-A. PMID 1921915.
  29. 1 2 Jones K.L., Smith D.W. (1973). "Recognition of the fetal alcohol syndrome in early infancy". Lancet 2: 999–1001. doi:10.1016/s0140-6736(73)91092-1. PMID 4127281.
  30. 1 2 3 Mattson, S.N., & Riley, E.P. (2002). "Neurobehavioral and Neuroanatomical Effects of Heavy Prenatal Exposure to Alcohol," in Streissguth and Kantor. (2002). p. 10.
  31. ↑ Strömland K, Pinazo-Durán M (2002). "Ophthalmic involvement in the fetal alcohol syndrome: clinical and animal model studies". Alcohol Alcohol 37 (1): 2–8. doi:10.1093/alcalc/37.1.2. PMID 11825849.
  32. 1 2 3 4 5 Yaffe, Sumner J. (2011). Drugs in pregnancy and lactation : a reference guide to fetal and neonatal risk (9 ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 527. ISBN 9781608317080.
  33. ↑ "Pregnancy and alcohol: occasional, light drinking may be safe.". Prescrire Int. 124 (21): 44–50. Feb 2012. PMID 22413723.
  34. ↑ Henderson, J; Gray, R; Brocklehurst, P (March 2007). "Systematic review of effects of low-moderate prenatal alcohol exposure on pregnancy outcome.". BJOG : an international journal of obstetrics and gynaecology 114 (3): 243–52. doi:10.1111/j.1471-0528.2006.01163.x. PMID 17233797.
  35. ↑ Warren K., Li T-K (2005). "Genetic polymorphisms: Impact on the risk of fetal alcohol spectrum disorders". Birth Defect Res A 73: 195–203. doi:10.1002/bdra.20125.
  36. ↑ Laufer BI, Mantha K, Kleiber ML, Diehl EJ, Addison SM, Singh SM (July 2013). "Long-lasting alterations to DNA methylation and ncRNAs could underlie the effects of fetal alcohol exposure in mice". Disease Models & Mechanisms 6 (4): 977–92. doi:10.1242/dmm.010975. PMC 3701217. PMID 23580197.
  37. ↑ Brien J.; et al. (1983). "Disposition of ethanol in human maternal venous blood and amniotic fluid". Am J Obstet Gynecol 146: 181–186.
  38. ↑ Nava-Ocampo A.; et al. (2004). "Elimination kinetics of ethanol in pregnant women". Reproduct Toxicol 18: 613–617.
  39. 1 2 3 4 5 6 Lang, Jeannette (2006). "Ten Brain Domains: A Proposal for Functional Central Nervous System Parameters for Fetal Alcohol Spectrum Disorder Diagnosis and Follow-up" (PDF). Journal of the FAS Institute 4: 1–11.
  40. 1 2 3 Clarren S.K., Smith D.W. (1978). "Fetal alcohol syndrome". New England Journal of Medicine 298: 1063–1067. doi:10.1056/NEJM197805112981906. PMID 347295.
  41. ↑ Smith D.W. (1981). "Fetal alcohol syndrome and fetal alcohol effects". Neurobehavioral Toxicology and Teratology 3: 127.
  42. ↑ Aase J.M., Jones K.L., Clarren S.K. (1995). "Do we need the term FAE?". Pediatrics 95 (3): 428–430. PMID 7862486.
  43. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 Streissguth, A. (1997). Fetal Alcohol Syndrome: A Guide for Families and Communities. Baltimore: Brookes Publishing. ISBN 1-55766-283-5.
  44. 1 2 3 4 Malbin, D. (2002). Fetal Alcohol Spectrum Disorders: Trying Differently Rather Than Harder. Portland, OR: FASCETS, Inc. ISBN 0-9729532-0-5.
  45. ↑ Sokol R.J., Clarren S.K. (1989). "Guidelines for use of terminology describing the impact of prenatal alcohol on the offspring". Alcoholism: Clinical and Experimental Research 13 (4): 597–598. doi:10.1111/j.1530-0277.1989.tb00384.x.
  46. ↑ U.S. Department of Health and Human Services. (2000). National Institute on Alcohol Abuse and Alcoholism. Tenth special report to the U.S Congress on alcohol and health: Highlights frfom current research. Washington, DC: The Institute.
  47. ↑ FADP – Fetal Alcohol Diagnostic Program
  48. ↑ http://alcalc.oxfordjournals.org/content/35/3/276.full
  49. ↑ http://www.cdc.gov/ncbddd/fasd/data.html
  50. 1 2 Buxton, B. (2005). Damaged Angels: An Adoptive Mother Discovers the Tragic Toll of Alcohol in Pregnancy. New York: Carroll & Graf. ISBN 0-7867-1550-2.
  51. 1 2 3 4 McCreight, B. (1997). Recognizing and Managing Children with Fetal Alcohol Syndrome/Fetal Alcohol Effects: A Guidebook. Washington, DC: CWLA. ISBN 0-87868-607-X.
  52. 1 2 National Organization on Fetal Alcohol Syndrome, Minnesota Organization on Fetal Alcohol Syndrome. Retrieved on 2007-04-11
  53. 1 2 3 4 5 Streissguth, A.P., Barr, H.M., Kogan, J., & Bookstein, F.L. (1996). Understanding the occurrence of secondary disabilities in clients with fetal alcohol syndrome (FAS) and fetal alcohol effects (FAE): Final report to the Centers for Disease Control and Prevention on Grant No. RO4/CCR008515 (Tech. Report No. 96-06). Seattle: University of Washington, Fetal Alcohol and Drug Unit.
  54. 1 2 Malbin, D. (1993). Fetal Alcohol Syndrome, Fetal Alcohol Effects: Strategies for Professionals. Center City, MN: Hazelden. ISBN 0-89486-951-5
  55. ↑ Abel EL, Jacobson S, Sherwin BT (1983). "In utero alcohol exposure: Functional and structural brain damage". Neurobehavioral Toxicology and Teratology 5: 363–366. PMID 6877477.
  56. ↑ Meyer L, Kotch L, Riley E (1990). "Neonatal ethanol exposure: functional alterations associated with cerebellar growth retardation". Neurotoxicol Teratol 12 (1): 15–22. doi:10.1016/0892-0362(90)90107-N. PMID 2314357.
  57. ↑ Zimmerberg B, Mickus LA (1990). "Sex differences in corpus callosum: Influence of prenatal alcohol exposure and maternal undernutrition". Brain Research 537: 115–122. doi:10.1016/0006-8993(90)90347-e. PMID 2085766.
  58. 1 2 Elliot, E. J; Payne, J; Hann, E; Bower, C (2006). "Diagnosis of fetal alcohol syndrome and alcohol use in pregnancy: A survey of Paediatricians' knowledge, attitudes and practice". Journal of Paediatrics and Child Health 42 (1): 698–703. doi:10.1111/j.1440-1754.2006.00954.x.
  59. 1 2 3 4 Burns, L; Breen, C; Bower, C; O'Leary, C; Elliiot, E. J (2015). "Counting fetal alcohol spectrum disorders in Australia:The evidence and the challenges". Drugs and Alcohol Review 32 (5): 461–467. doi:10.1111/dar.12047.
  60. ↑ Mutch, R. C; Watkins, R; Bower, C (2014). "Fetal alcohol spectrum disorders: Notifications to Western Australian register of developmental anomalies". Journal of Paediatrics and Child Health 51 (4): 433–436. doi:10.1111/jpc.12746.
  61. 1 2 3 Armstrong, E. M. (2003). Conceiving risk, bearing responsibility: Fetal alcohol syndrome & the diagnosis of moral disorder. Baltimore: The Johns Hopkins University Press.
  62. ↑ http://www.nytimes.com/1995/03/04/obituaries/dr-fritz-fuchs-76-who-advanced-obstetrics.html
  63. ↑ King, T. L., & Brucker, M. C. (2011). Pharmacology for women's health. Sudbury, MA: Jones and Bartlett.
  64. ↑ Sullivan W.C. (1899). "A note on the influence of maternal inebriety on the offspring". Journal of Mental Science 45: 489–503. doi:10.1192/bjp.45.190.489.
  65. ↑ Goddard, H.H. (1912). The Kallikak Family: A Study in the Heredity of Feeble-Mindedness. New York: Macmillan.
  66. ↑ Karp R.J., Qazi Q.H., Moller K.A., Angelo W.A., Davis J.M. (1995). "Fetal alcohol syndrome at the turn of the century: An unexpected explanation of the Kallikak family". Archives of Pediatrics and Adolescent Medicine 149 (1): 45–48. doi:10.1001/archpedi.1995.02170130047010. PMID 7827659.
  67. ↑ Haggard, H.W., & Jellinek, E.M. (1942). Alcohol Explored. New York: Doubleday.
  68. 1 2 Jones K.L., Smith D.W, Ulleland C.N., Streissguth A.P. (1973). "Pattern of malformation in offspring of chronic alcoholic mothers". Lancet 1: 1267–1271. doi:10.1016/S0140-6736(73)91291-9. PMID 4126070.
  69. ↑ Streissguth, A.P. (2002). In A. Streissguth, & J. Kanter (Eds.), The Challenge in Fetal Alcohol Syndrome: Overcoming Secondary Disabilities. Seattle: University of WA Press. ISBN 0-295-97650-0.
  70. ↑ Lemoine P., Harousseau H., Borteyru J.B., Menuet J.C. (1968). "Les enfants de parents alcooliques. Anomalies observées, à propos de 127 cas". Quest Medical 21: 476–482. PMID 12657907.
  71. ↑ Ulleland C.N. (1972). "The offspring of alcoholic mothers". Annals of the New York Academy of Sciences 197: 167–169. doi:10.1111/j.1749-6632.1972.tb28142.x. PMID 4504588.
  72. 1 2 Olegard R., Sabel K.G., Aronsson M. Sandin, Johannsson P.R., Carlsson C., Kyllerman M., Iversen K., Hrbek A. (1979). "Effects on the child of alcohol abuse during pregnancy". Acta Paediatrica Scandinavica 275: 112–121. PMID 291283.
  73. 1 2 3 4 Clarren, S.K. (2005). A thirty year journey from tragedy to hope. Foreword to Buxton, B. (2005). Damaged Angels: An Adoptive Mother Discovers the Tragic Toll of Alcohol in Pregnancy. New York: Carroll & Graf. ISBN 0-7867-1550-2.

External links

Wikimedia Commons has media related to Fetal alcohol syndrome.
This article is issued from Wikipedia - version of the Saturday, May 07, 2016. The text is available under the Creative Commons Attribution/Share Alike but additional terms may apply for the media files.