Exposure to Teratogenic Agents as a Risk Factor for Psychopathology
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Transcript of Exposure to Teratogenic Agents as a Risk Factor for Psychopathology
Exposure to Teratogenic Agents
as a Risk Factor for Psychopathology
Child and Adolescent Psychopathology
General Points
Exposure might be inevitable because of pharmacological intervention
• e.g., seizure, depression
Exposure can occur prior to knowledge of pregnancy
Behavioral teratogens can cause changes in function
• e.g., cognitive, affective, sensorimotor, social
Environmental risk factors can moderate teratological effects
• Family placement (biological, foster, adoptive)• SES• Global intelligence
(Cont’d)
3 presenting symptoms:
1)Pre- and postnatal growth deficiency2)Dysmorphic facial features3)CNS dysfunction
incidence 9.1/1,000 live births for dysmorphic
and non-dysmorphic cases
incidence 1/1,000 per live births for FAS
Fetal Alcohol Spectrum Disorders (FASD)
Symptoms Of FASD:
o Stereotypies o Sleeping problems o Tics o Hand/body rocking o Peer-relationship difficulties o Phobias o Depression o Bipolar DO
*Psychiatric symptoms in children do not dissipate with time.
• ADHD, ODD, CD• Attention deficits
are useful markers of FASD
o Exposure amount and home placement moderate the
relationship between alcohol exposure and delinquency• biological and foster
homes => in delinquency
• adoptive homes => in delinquency
o Disruptive behavior disorders (associated with FASD):
*Possible mediational model: FASD attentional/impulse control problems conduct problems
o Mood Disorders (associated with FASD):
Mediational model #1 (O’Conner, 2001):
FASD negative infant affect depressive features at age 6
Mediational model #2 (O’Conner & Paley, 2006):
FASD quality of mother-child interaction
depression
Moderational model (O’Conner & Kasari, 2000):
FASD + gender + maternal depression + (FASD × gender) + (FASD × maternal depression)
depression
1)Girls depression
2) Maternal depression depression
o Mood Disorders (associated with FASD): (Cont’d)
Factors that affect pathway selection:
o Social skills deficits (after controlling for IQ)
o Many potential pathways suggest equifinality:
Pattern of infant withdrawal
(not discussed in book)
Timing (pregnancy stage, dosage, pattern of exposure, maternal characteristics, fetal genetic factors)
Conduct problems (controlling for genetic factors and parental antisocial behavior)
Antisocial behaviors
ADHD (controlling for SES, parental IQ, parental ADHD)
Moderational model:
DA transporter gene (DTG) + exposure + (DTG × exposure) ADHD/ODD
Higher rates of substance abuse and depression
Nicotine Exposure
Increased aggression in cocaine-exposed children
Gender and comorbid alcohol exposure moderate their relation
Other risk factors more predictive of psychopathology than cocaine exposure:
• caregiver’s recent drug use
• caregiver’s level of mental functioning
• caregiver’s depressive symptoms
Many potential pathways suggest equifinality:
• Factors that affect pathway selection -- gender and gestational age
• Disrupted balance between dopaminergically mediated and noradrenergically mediated arousal-regulating systems hyperarousal
Stimulant drugs
Neurobehavioral deficits
Prenatal and postnatal exposure (true for all drug exposure)
Delinquency and antisocial behavior (controlling for birth weight, parental IQ, quality of home environment, SES)
Methylmercury and Lead
Take careful prenatal exposure histories
Different response pattern to treatments
Stable, nurturing home buffers effects of alcohol
exposure
Clinical Implications
1)Cognitive: • confusion, poor concentration, inability to
follow directions or answer questions, amnesia, loss of consciousness
2)Medical: • headaches, nausea, vomiting
3)Sensory: • dizziness, poor coordination or loss of
balance, alterations in vision or hearing (seeing stars, ringing ears
4)Psychological: • irritability, changes in personality, emotions
inappropriate for context
Symptoms of closed head injuries:
Brain Injury as a Risk Factor for Psychopathology
Present : o Comparison with
baseline administration of standardized neuropsychological tests
Assessment of closed head injuries
Past: o Sideline
assessments of concussive symptoms
Low birth weightPrematurityPrenatal teratological exposureExposure to maternal cortisolRestricted blood flow through umbilical artery Nutritional differencesInsufficient oxygen supply
1) Nontraumatic brain injuries
Causes:
Equifinality and multifinality of outcomes
• Males• ADHD (and greater
severity)• Low SES• Poor parental
supervision(ADHD—> poor supervision—> brain
injury
injury)
Susceptibility
*Archives of Disease in Childhood, 2001
a. Small hemorrhages on overall surface of the brainb. Coup/contrecoup-rebound effect on opposite side
① Focal--translational force applied along brain’s linear axis
2) Traumatic brain injury (TBI)
a. Head strikes against broad object, diffusing force across the surface of the skullb. Shearing strain on brain, tearing axonal tissuec. Most common form of head injury, producing concussions
② Diffuse--rotational forces applied in angular movement around brain’s center of gravity
③ Head injuries are classified as mild, moderate, or severe using Glasgow Coma Scale
④ Mild injuries accumulated over time can be dangerous
a. Edema--swellingb. global tissue damage
⑤ Secondary injuries:
oToxic accumulation of calcium in cellsoApoptosis--programming death of neighboring
cellsoAccumulation of cell loss over weeks produces
behavioral deficitsoCommon complication of preterm infants oFactors related to hypoxia: developmental
maturation of neural tissue, duration and degree of hypoxic
exposure, degree of neuroprotective factors
Hypoxia--reduction in oxygen supply
o Sequence following hypoxia: cognition/behavior impairments, motor incoordination
o Ischemia (reduced blood supply to cell) potentiates hypoxia effects
o ADHD risk even in absence of marked neurological dysfunction
Role of genes in brain injury
1) E4 allele confers vulnerability for development of Alzheimer’s and TBI for adults but protection for children
2) Mediational model of schizophrenia:Genetic heightened sensitivity to hypoxic
event hypoxia schizophrenia 3) ADHD and schizophrenia: vulnerability of
dopaminergic system to hypoxic insult4) Female brains less vulnerable to ischemia/
hypoxia-induced damage5) Moderating variables: exacerbation of
preexisting pathology, reaction of child/family to loss of function, PTSD formation
6) High family functioning protects against the effects of brain injury (moderational model)
7) Ritalin less effective for hypoxia/TBI-induced ADHD
Fin