出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/07/12 13:58:00」(JST)
| Fetal alcohol spectrum disorders | |
|---|---|
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Baby with fetal alcohol syndrome.
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| 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 (FASD) 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, poor coordination, low intelligence, behavior problems, and problems with hearing or seeing.[1] Those affected more commonly have trouble in school, have trouble with law enforcement, are frequently jailed, are involved in high risk sexual activity, and have trouble with alcohol or other drugs.[2] The most severe form of the condition is known as fetal alcohol syndrome (FAS).[1] Other types including partial fetal alcohol syndrome (pFAS), alcohol-related neurodevelopmental disorder (ARND) and alcohol-related birth defects (ARBD).[1][3]
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 in the last month and 20% to 30% drank at some point during the pregnancy.[4] About 4% of women who are pregnant have alcohol use disorder.[5] The risk of problems depends on the amount, frequency, and when during pregnancy alcohol is consumed.[4] Other risk factors include an older mother, smoking, and a mother who has poor nutrition.[4] There is no known safe amount or safe time to drink during pregnancy.[1] While small amounts of alcohol do not cause an abnormal appearance it may cause behavioral issues.[5] Alcohol crosses the blood brain barrier and both directly and indirectly affects a developing baby.[6] Diagnosis is based on a person's signs and symptoms.[1]
Fetal alcohol spectrum disorders are preventable by avoiding alcohol.[7] Medical organizations recommend no alcohol during pregnancy for this reason.[8][9][10] While the condition is permanent treatment can improve outcomes.[1] This may include parent-child interaction therapy, efforts to modify behavior, and possibly medications.[11]
FASD is estimated to affect between 2% and 5% of people in the United States and Western Europe.[12] FAS is believed to occur in between 0.2 and 9 per 1000 live births in the United States.[12] In South Africa some populations have rates as high as 9%.[3] The negative effects of alcohol have been described since ancient times.[3] The lifetime cost of an individual with FAS were estimated to be two million USD in 2002.[12] The term fetal alcohol syndrome was first used in 1973.[3]
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.
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.[13] Deficiencies are documented when height or weight falls at or below the 10th percentile of standardized growth charts appropriate to the population.[14]
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),[9] while the CDC and Canadian guidelines use the 10th percentile as a cut-off to determine growth deficiency.[15][16] 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.[13] 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:"[13]
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.[citation needed] 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.[9]
Several characteristic craniofacial abnormalities are often visible in individuals with FAS.[17] 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.[18]
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.[19][20] 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,[21] a 5-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.[22]
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:[13][23]
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.[9][24] 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.[9] 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.[13][15] The "4-Digit Diagnostic Code" also allows for an FASD diagnosis when only two functional domains are measured at two standard deviations or worse.[13] The "4-Digit Diagnostic Code" further elaborates the degree of CNS damage according to four ranks:
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).[9]
Microcephaly is determined by comparing head circumference (often called occipitofrontal circumference, or OFC) to appropriate OFC growth charts.[14] 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.[9][13][15][16]
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.[25] 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.[26]
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.[27] The examination revealed extensive brain damage, including microcephaly, migration anomalies, callosal dysgenesis, and a massive neuroglial, leptomeningeal heterotopia covering the left hemisphere.[28]
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.[28] 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.[28]
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.[9][13][15][16]
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.
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.[9][13][15][16] 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[9] and only CDC guidelines label developmental delays as such,[15] 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:
Other conditions may commonly co-occur with FAS, stemming from prenatal alcohol exposure. However, these conditions are considered alcohol-related birth defects[9] and not diagnostic criteria for FAS.
Fetal alcohol syndrome usually occurs when a pregnant women has more than four standard drinks per day.[30] Milder symptoms have been found with two drinks per day during the early part of pregnancy.[30][31] Among those who are alcoholic about a third of children have FAS.[30]
Evidence of harm from less than two drinks per day or 10 drinks per week is not clear.[30][32] While small amounts of alcohol do not cause an abnormal appearance it may cause behavioral issues.[5] There is conflicting evidence regarding whether drinking by fathers before conception can cause FAS.[30]
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.[33]
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.[34]
A human fetus appears to be at triple risk from maternal alcohol consumption:[35][36]
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.[citation needed]
The original description of fetal alcohol syndrome (FAS) was published in 1973. 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.[9] 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.[16]
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.
The following criteria must be fully met for an FAS diagnosis:[9][13][15][16]
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.[37] 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 (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:[9][13][16]
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.[38] Smith (1981) described FAE as an "extremely important concept" to highlight the debilitating effects of brain damage, regardless of the growth or facial features.[39] 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.[40]
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.[41] 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.[41][42]
The following criteria must be fully met for a diagnosis of ARND or static encephalopathy:[9][13][16]
Alcohol-related birth defects (ARBD), formerly known as possible fetal alcohol effect (PFAE),[38] was a term proposed as an alternative to FAE and PFAE[43] The IOM presents ARBD as a list of congenital anomalies that are linked to maternal alcohol use but have no key features of FASD.[9] 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.[41] The Canadian guidelines recommend that ARBD should not be used as an umbrella term or diagnostic category for FASD.
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:
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.[9] 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.[44]
"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.[13]
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.[15] 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 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.[13][15]
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.[37]
The proposed Ten Brain Domains include:[37]
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.[45]
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:[15]
The only certain way to prevent FAS is to avoid drinking alcohol during pregnancy.[41] 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.[8] 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.[46] 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.[47]
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.
Psychoactive drugs are frequently tried on those with FAS as many FAS symptoms are mistaken for or overlap with other disorders, most notably ADHD.[48]
Behavioral interventions are based on the learning theory, which is the basis for many parenting and professional strategies and interventions.[42] 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.
Because the "learning system" of a person with FAS is damaged, however, behavioral interventions are not always successful, or not successful in the long run, especially because overlapping disorders frequently stem from or are exacerbated by FAS.[42] Kohn (1999) suggests that a rewards-punishment system in general may work somewhat in the short term but is unsuccessful in the long term because that approach fails to consider content (i.e., things "worth" learning), community (i.e., safe, cooperative learning environments), and choice (i.e., making choices versus following directions).[49] While these elements are important to consider when working with FAS and have some usefulness in treatment, they are not alone sufficient to promote better outcomes.[42] Kohn's minority challenge to behavioral interventions does illustrate the importance of factors beyond learning theory when trying to promote improved outcomes for FAS, and supports a more multi-model approach that can be found in varying degrees within the advocacy model and neurobehavioral approach.
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,[50] 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.[50]
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.[50] 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.[citation needed]
The advocacy model takes the point of view that someone is needed to actively mediate between the environment and the person with FAS.[41] 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.[41]
The advocacy model is often recommended, for example, when developing an Individualized Education Program (IEP) for the person's progress at school.[48]
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.[51]
Treating FAS at the public health and public policy level promotes FAS prevention and diversion of public resources to assist those with FAS.[41] 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.[51]
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.[52] Often, primary disabilities are mistaken as behavior problems, but the underlying CNS damage is the originating source of a functional difficulty,[53] 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.[41] Representative examples include:
Functional difficulties may result from CNS damage in more than one domain, but common functional difficulties by domain include:[41][42][50][53] Note that this is not an exhaustive list of difficulties.
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.[52]
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):[41][52]
Two additional secondary disabilities exist for adults:[41][52]
Eight factors were identified in the same study as universal protective factors that reduced the incidence rate of the secondary disabilities:[41][52]
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:[42]
FASD is estimated to affect between 2% and 5% of people in the United States and Western Europe.[12] FAS is believed to occur in between 0.2 and 9 per 1000 live births in the United States.[12] The lifetime cost of an individual with FAS were estimated to be two million USD in 2002.[12]
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.[27] 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.[57] 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.[41] A case study by Henry H. Goddard of the Kallikak family — popular in the early 1900s — represents this earlier perspective,[58] though later researchers have suggested that the Kallikaks almost certainly had FAS.[59] General studies and discussions on alcoholism throughout the mid-1900s were typically based on a heredity argument.[60]
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.[41]
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.[61] The pattern of malformations indicated that the damage was prenatal. News of the discovery shocked some, while others were skeptical of the findings.[62]
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,[63] 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.[64] The Washington and Nantes findings were confirmed by a research group in Gothenburg, Sweden in 1979.[65] 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.[65]
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.[66] 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.[66] Nobody was aware of the full range of possible birth defects from FAS or its prevalence rate at that time,[66] but admission of alcohol use during pregnancy can feel stigmatizing to birth mothers and complicate diagnostic efforts[15] of a syndrome with its preventable cause in the name.
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.[66] Currently, FAS[9][38][61] 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.
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| リンク元 | 「胎児性アルコール作用」「FAEs」 |
| 関連記事 | 「effect」「fetal」「alcohol」 |
胎児アルコール影響障害 : 12 件 胎児アルコール効果 : 8 件 胎児アルコール作用 : 0 件 胎児アルコール影響障害 : 12 件 胎児アルコール兆候 : 0 件 胎児性アルコール影響障害 : 2 件 胎児性アルコール効果 : 29 件 胎児性アルコール作用 : 38 件 胎児性アルコール影響障害 : 2 件 胎児性アルコール兆候 : 5 件 胎児アルコール影響障害 FAE : 3 件 胎児アルコール効果 FAE : 6 件 胎児アルコール作用 FAE : 0 件 胎児アルコール影響障害 FAE : 3 件 胎児アルコール兆候 FAE : 0 件 胎児性アルコール影響障害 FAE : 0 件 胎児性アルコール効果 FAE : 16 件 胎児性アルコール作用 FAE : 51 件 胎児性アルコール影響障害 FAE : 0 件 胎児性アルコール兆候 FAE : 4 件
[★] 胎児性アルコール作用 fetal alcohol effects