Foetal Alcohol Spectrum Disorders

Foetal Alcohol Spectrum Disorders

1. 1. BRAIN DEVELOPMENT

   • Neurogenesis; cell proliferation; migration; differentiation; synaptic pruning
   • Teratogens: any disease/drug/substance that can harm developing fetus. CNS defects include:Agenesis, dysgenesis and are either focal or diffuse.
   • Risk factors: Prenatal & Postnatal factors
     • Prenatal: Maternal stress/age; maternal health; nutrition; maternal drug/alcohol use; enviro toxins
     • Postnatal: birth complications; nutrition; enviro toxins; cerebral infections; environment/experience (nature vs. nurture)
   • Plasticity: Kennard principle- negative linear relationship between age damage acquired and outcome expectancy. Optimal window for recovery; differences between child/adult brain
   • Anderson's model: Primary damage-- Neuro and psychosocial impairment-- influences development--further abnormal development--further neuro/psycho impairments--generalised impairment

2. 2. PRENATAL ALCOHOL EXPOSURE:

   • Mechanisms of alcohol exposure- prospective vs. retrospective data
   • Levels of prenatal alcohol exposure: Binge drinking (4 drinks per session). Continuous alcohol exposure (light-moderate-heavy exposure)
   • Biomarkers vs. Biobehavioural markers
     • Biomarker of exposure= biological marker EG fatty acid ethyl ester (FAEE) in meconium- can validate maternal report of drinking; does not indicate degree of impairment
     • Biobehavioural marker of effect- behavioural outcome linked to FASD with neural substrates have been identified and examined directly. Used to indicate degree of impairment, improve diagnosis/treatment EG eyeblink conditioning & magnitude comparison.

3. 3. FASD

   • FAS>PFAS>ARND>ARBD
     • FAS: 3 main diagnostic criteria in combo with confirmed history of PAE: (1) deficits in CNS development/functioning; (2) deficient growth patterns; (3) craniofacial irregularities
     • PFAS: confirmed history of PAE; some of the facial features; either CNS OR cog/behavioural impairments OR physical growth symptoms
     • ARBD: confirmed PAE; congenital physical abnormalities. ARND: confirmation of PAE; deficits in CNS development/ functioning (IE cog/behavioural difficulties)
   • Facial features assoc. with heavy alcohol exposure during 1st trimester: 1. microcephaly; 2. epicanthal folds; 3. low nasal bridge; 4. short palpebral fissures; 5. minor ear abnormalities; 6. flat midface; 7. short nose; 8. indistinct philtrum; 9. thin upper lip; 10. micrognathia
     • Diagnosed by dysmorophologists. Look-alike disorders (phenocopies)= Williams and Fetal Hydantoin Syndrome

4. 4. BRAIN DEVELOPMENT IN FASD

   • Overall reduction in brain size (inferior parietal, frontal, perisylvian areas); decreased white matter integrity
   • Cerebellum: reduction in cerebellar volume esp. anterior vermis; displacement of anterior vermis; eyeblink conditioning implicated here
   • Corpus Callosum: agenesis (rare); volume reduced; displacement related to learning difficulties/ impaired info processing
   • Basal ganglia: volume reduced; caudate nucleus esp. vulnerable
   • Hippocampus & amygdala: structural abnormalities; links to subcortical-limbic system

5. 5. FUNCTIONAL IMAGING STUDIES

   • Structural abnormalities assoc. with abnormal neural activations both cortical & sub; wider networks to complete tasks

6. 6. DEVELOPMENTAL TRAJECTORY

   • Abnormal developmental trajectory reported in longitudinal studies: eg delayed white matter development in frontal association

7. 7. COGNITIVE & BEHAVIOURAL OUTCOMES

   • Cognitive outcomes: IQ; attention; learning & memory'; EFs; social emotional processing; number processing
   • Behavioural outcomes: increased internalising/externalizing behaviours; secondary disabilities risk; delinquent behaviourss; persist into adulthood