Download Child and Adolescent Psychopathology

Behavioral Inhibition
as a Temperamental
Vulnerability to
Psychopathology
Chapter 7
Jerome Kagan
HISTORICAL CONTEXT
 Eighteenth and 19th centuries restricted the referent for
psychopathology to a small number of deviant profiles who were
regarded as biologically distinct from the rest of the population.
 Freud explained that anxiety was between the biology that was
presumed to be the primary foundation of symptoms and the
individual’s thoughts, behaviors, and emotions. He insisted that
the child’s early experiences, especially those within the family,
made an important contribution to psychological symptoms.
 Presently, the emergence of psychopathology requires a
biological vulnerability, usually but not always inherited,
combined with an acute trauma, chronic stress, or disadvantaged
position in society.
CONCEPTUAL ISSUES
 Four conceptual issues penetrate research on the
conditions that lead to pathology:
 The number and exact nature of biological vulnerabilities
(diatheses)
 The number and types of experiential risks (stressors)
encountered
 The most fruitful categories for psychopathology
 Evidence used to infer the constructs for risk and
pathology
THE ETIOLOGICAL ROLE OF
TEMPERAMENTS
Genes, Neurochemistry, and Temperaments
Molecules that, along with the density and locations of their
receptors, have the potential to influence the feelings and
behaviors that define human temperaments including:
•
•
•
•
•
Norepinephrine
Dopamine
Pinephrine
Serotonin
Corticotropin releasing
hormone (CRH)
• Glutamate
• Gamma aminobutyric acid
(GABA)
•
•
•
•
•
•
Opioids
Vasopressin
Oxytocin
Prolactin
Monoamine oxidase (MAO)
Sex hormones androgen and
estrogen
THE ETIOLOGICAL ROLE OF
TEMPERAMENTS
 Reactions to the Unexpected or Unfamiliar
 Two biases that have been studied more extensively than
others are:
• Behaviorally inhibited: Children who show restrained, cautious,
avoidant reactions to unfamiliar objects, people, or settings.
• Uninhibited: Children displaying spontaneous approach to the same
events.
 High- and Low-Reactive Infants
 Child and early adolescent evaluations
 Age 18 assessments
THE ETIOLOGICAL ROLE OF
TEMPERAMENTS
 Particular genetic polymorphisms make small
contributions to behavioral inhibition, especially when
combined with particular experiences.
• Possession of the short allele of the 5-HTTLPR gene, combined
with the experience of stress during childhood, especially severe
maltreatment, increases by a small amount the risk for persistent
adult depression (Karg, Burmeister, Shedden & Sen, 2011; Uher et al.,
2011).
THE ETIOLOGICAL ROLE OF
TEMPERAMENTS
 Adults with 2 or 5 rather than 7 repeats in the DRD4 receptor gene
are high in novelty seeking but, surprisingly, individuals from
economically disadvantaged backgrounds with the same
polymorphisms are not (Eley et al., 2004; Caspi et al., 2003; Kaufman et al.,
2004; Lahti et al., 2006).
 High- and Low-Reactive Infants
 Primary functions of the amygdala are to respond to all
unfamiliar or unexpected events and to generate an initial
state of vigilance and preparation for action when the
event poses a threat (Fitzgerald et al., 2006).
 Infants with excitable amygdalae should be more likely
than others to become inhibited children.
THE ETIOLOGICAL ROLE OF
TEMPERAMENTS
 Longitudinal study to discover patterns of infant behaviors that might
predict the inhibited and uninhibited profiles that appear later in life:
 High reactive: 20% of the infants showed a pattern that combined high levels of limb
activity, back arching, and crying.
 Low Reactive: 40% percent showed a pattern of minimal motor activity, few arches,
and little crying.
 Child and early adolescent evaluations
• High-reactives assessed at 14 and 21 months were significantly
more avoidant of and fearful to a series of unfamiliar social and
nonsocial incentives than low reactives. However, about 20% of the
high reactives were not highly fearful at both ages because, we
presume, their experiences allowed them to gain some control of
the public expression of signs of fear.
THE ETIOLOGICAL ROLE OF
TEMPERAMENTS
 Child and early adolescent evaluations
• At age 7 years about half of the high reactives possessed fears of
animals, the dark, thunder storms, and/or unfamiliar people and
places, compared with fewer than 10% of low reactives.
• At 11 and 15 years high reactives were not only quieter and
emotionally more subdued, but they also showed few spontaneous
smiles during laboratory sessions designed to measure four
biological reactions that are indirect signs of a more excitable
amygdala.
• More high- than low reactives showed a larger brain stem auditory
evoked response from the inferior colliculus at both 11 and 15
years.
THE ETIOLOGICAL ROLE OF
TEMPERAMENTS
 Age 18 assessments
 The high- and low reactives differed significantly on three
biological measures:
High reactives had a thicker cortex in a small region in the ventromedial prefrontal
cortex (vmPFC) of the right hemisphere.
 High reactives showed a larger surge of blood flow (the BOLD signal) to the right
amygdala the first time they saw a set of angry faces they did not expect.
 High reactives showed a shallower slope of habituation of the BOLD signal to the
left amygdala to repeated presentations of ecologically invalid scenes.

 Significantly higher prevalence of depression, social phobia, and/or
general anxiety disorder among high reactives than low-reactives
SYNTHESIS
 Investigators should be sensitive to the contexts of
observation, a requirement that applies to the source
of evidence used for inferences.
 Investigators should base their inferences on patterns
of variables, not single measures.
 Hyping Biology
 The current emphasis on the biological contribution has
considerable value. But it has two serious disadvantages.
• It fails to raise public consciousness over the contributions of the many
adults and peers whose interactions with a particular child can place
that youth at risk for pathology.
• It motivates a single-minded approach to finding risk genes and drug
cures for all disorders and fails to motivate clinicians to consider
combining medicines with strategies that might alter the child’s
circumstances.