Table 1.
Key Health Risk Factors | Possible Mechanism | Key Intervention/Prevention Strategy |
---|---|---|
Smoking during pregnancy | Nicotine and carbon monoxide impairment of the noradrenergic system, decreased dopamine and Serotonin Impaired basal ganglia, cerebral cortex and cerebellar cortex; reduction in brain glucose; retardation in brain growth, structural deficits to the corpus callosum |
Assess smoking status of all expecting or prospective mothers; individual smoking cessation counseling, such as Quit Works, a counseling and referral service used in Massachusetts; pharmacotherapy, such as nicotine patch, gum, inhalers, sprays (Centers For Disease Control and Prevention, 2006); early prevention programs in schools focused on dealing with peer pressure to smoke and building self-esteem (Botvin et al., 1995). |
Birth complications (preeclampsia, preterm birth, gestational diabetes) | Direct brain injury (e.g. forceps delivery) Indirect brain damage due to hypoxia (e.g., cord compression) with anoxia and selective damage to the hippocampus Perinatal asphyxia leads to damage in the brainstem, thalamus, basla ganglia, parasagittal areas, and hippocampus as well as impaired intellectual abilities, slower academic progress, and poorer visual-motor integration |
Prenatal care, prenatal vitamins, ultrasound, patient education |
Alcohol, drug abuse during pregnancy | Structural deficits in the corpus callosum Brain growth retardation |
Screening prospective and expecting mothers for drug use/abuse, abuse cessation education, referral for treatment and support, drug counseling, group counseling (National Institute on Drug Abuse, 2009), early prevention programs in schools focused on dealing with peer pressure to take drugs, and building self- esteem (Botvin et al., 1995) |
Teenage pregnancy | Decreased family stability Increased risk of poverty Increased risk of child abuse Increased risk of poor school performance |
Education of parents, children and teachers aimed at improving social outcomes (academic achievement, resisting peer pressure, developing positive alternatives) and strengthening children’s support system (Hawkins et al., 1999) |
Maternal Depression | Decreased responsiveness to children Increased risk of affective and behavioral problems, such as hostility, lack of warmth, and disengagement from the child (Gelfand et al., 1990) |
Screening and follow-up, such as community-based support programs (Knitzer, 2008); education and awareness promotion; family support. |
Malnutrition | Reduction in brain cells Disturbed neurochemistry function (altered neurotransmitter regulation with decreased serotonin and dopamine, altered hormone regulation) Exacerbation of neurotoxins |
Nutritional screening for diagnosis, nutritional intake, and anthropometric measures (child weight, height, head circumference, with values charted at each follow-up); referral to dietician, primary care provider, or speech/language therapist (for swallowing, chewing difficulty) as needed; education on adequate nutrition; food intake diary (McCarthy et al., 2008; Royal College of Nursing, 2006) |
Lead exposure | Neurotoxicity Decrease in Prefrontal Cortex gray matter volume Alterations in neurotransmitters Inhibition of NMDA receptor |
Blood lead level (BLL) screening, lead risk assessment of home, education, information on sources of lead, follow-up with healthcare provider (Wisconsin Council on Families and Children, 2000) nutrition intervention |
Head injury | Release of inflammatory mediators that contribute to cell-death cascades or post-synaptic receptor modifications Release of free radicals Excessive glutamate, excitotoxicity from calcium and zinc influx into neurons, dysfunctional mitochondria, separation of axons from cell body, microcirculatory derangements, break-down of blood-brain barrier due to astrocyte foot process swelling (Park et al., 2008), degenerative brain changes (Boll and Barth, 1983 as cited by Bijur, 1990) Damage to prefrontal region that normally controls and regulates reactions generated by limbic system Injuries are associated with sensory and motor deficits, language difficulties, and memory and attention dysfunctions. |
Follow-up care with healthcare provider, educate on prevention in the home (by use of bicycle helmets, car seats or booster seats, gates on stairways and doors, window guards, no wheeled baby walkers) (Schutzman, 2008; Park et al., 2008) |
Child abuse | Traumatic brain injury (e.g., shaken baby syndrome), which can result in diffuse axonal injury, subdural and/or subarachnoid hemorrhage Hypoxic/ischemic damage that can lead to cerebral edema and then cerebral atrophy and/or infarction, chronic extra-axial fluid collection, cystic encephalomalacia (Kairys et al., 2001) Low family functioning, poor stability, and security within the family |
Education on child development and discipline, social services assistance, screening and treatment of alcohol, drug abuse and psychological problems, family planning, accessible healthcare (Bethea, 1999) |
Maternal stress | Increased cortisol, which can affect the expression of thousands of genes in fetal brain cells, so elevated levels of maternal cortisol may impact fetal brain development Down regulation in placental 11β-HSD2, increasing fetal exposure to cortisol (Glover et al., 2009; O’Donnell et al., 2009 Mairesse et al., 2007) Reductions in measured PI (pulsatility index) value in the middle cerebral artery and a higher measured PI value in the umbilical artery of the fetus, which is considered a sign of fetal hypoxia (Sjostrom et al., 1997) HPA axis regulation of the fetus; changes in HPA axis activity are associated with physical and mental disorders (Entringer et al. 2009) |
Minimize stress, including seeking psychological therapy is needed; seek support from friends and family to reduce stress during pregnancy; consume adequate protein (in pregnant rats, a 50% reduction in protein intake was associated with a 33% drop in placental 11β-HSD2 activity) |