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96 Cards in this Set

  • Front
  • Back
Principles of Growth
1. Development is directional
-cephalocaudal: head to foot
-proximodistal: center of body outward
2. Development proceeds from basic to specialized
3. Development proceeds in order of importance
4. Canalization
-development tends to follow and return to a normative course
Prenatal growth
Reflected as weight per gestational age
-AGA: weight b/w 10-90% for GA
-SGA: weight below 10% for GA
-LGA: weight above 90% for GA

Mediated by maternal nutrition and growth factors
Intrauterine growth restriction (IUGR)
Failure of the fetus to attain its pre-determined growth potential (similar to SGA)

-affects 1-3% of pregnancies
-poor maternal nutrition, lack of adequate oxygen to fetus
Asymmetric IUGR
Restriction of weight, followed by length

-head develops at normal rate (head sparing)
-usually develops later in pregnancy
Symmetric IUGR
Restriction of overall growth- no head sparing

-less common and higher risk
-usually begins in early pregnancy
Baker/Thrifty hypothesis
IUGR and/or low birth weight is associated with increased risk of later health problems via prenatal programming
Infant growth
Period of rapid, decelerating physical growth

-1st 2 years infants have a "catch-up" or "catch-down" to est. growth
-growth over 1st 12 months is related to nutrition
Childhood growth
Rate of growth slows from infancy to early childhood

-"steady" growth
-dependent on growth hormones and thyroid hormones
- bones undergo remodeling
-minimal sex differences in growth until onset of puberty
Puberty
Period when an individual becomes capable of sexually reproducing

-rapid growth in height and weight
-changes in body composition
-development of primary sex characteristics
-development of secondary sex characteristics
-changes in circulatory and respiratory systems
-muscle grows faster in boys
-body fat increases in girls
-growth spurt slows after puberty- flattens at 20 for boys, 16-18 for girls
Endocrine system
Composed of glands that produce and secrete hormones

Regulates body energy levels, reproduction, growth/development and maintains homeostasis
Hypothalamus and pituitary
Hypothalamus links the nervous system to the endocrine system via the pituitary gland (not part of the brain)

-pit. is inhibited or stimulated by the hypot.
-when levels of hormones rise above/fall below a set point, secretion decreases/increases; "feedback loop"
HPT Axis
Hypothalamic-pituitary-thyroid axis

Thyroid
-controls how quickly the body uses energy, makes proteins and how sensitive the body is to other hormones

Thyroid hormones
-control cell migration and layering pattern prenatally
-contributes to dentritic development
-contributes to myleination
-essential for development of skeletal, muscular and nervous systems
HPT Axis- Congenital hypothyroidism
Thyroid hormone deficiency at birth, resulting in problems in physical growth and brain development, including mental retardation

-iodine deficiency during pregnancy or unknown cause
-treated with daily dose of thyroid hormones

Symtoms
-excessive sleeping
-reduced feeding
-jaundice
-low or hoarse cry
-low body temp
HPS/Growth Axis
Hypothalamic-pituitary-somatotrope axis

Somatotropes
-cells in the anterior (front) pituitary that produce growth hormone; secretes in a pulsatile (spiked) manner (usually at night)

Growth hormone
-anabolic effect on tissues of the body
-increases linear height
-increases insulin-like growth factor production --> bone growth
-important for growth of all body tissues EXCEPT CNS and genitals
-increased levels during puberty
HPS Axis- Short stature
Height 2 deviations below what is expected for age and sex

Causes:
Achondroplasia (dwarfism)
-autosomal dominant genetic disorder or sporadic mutation resulting in disproportionate growth
-mutation in growth factor receptor, causing abnormal cartilage formation

Growth hormone deficiency
-insufficient growth hormone produced
-tiny overall, still proportionate
-caused by many factors
-can be treated with Human Growth Hormone; used as a "catch-up"
-those without a deficiency, but still use HGH, can cause headaches/broken bones (unaware of later consequences still); societal influences!
HPS Axis- Gigantism
Excessive growth and height above average, caused by over-production of growth hormone in childhood
HPG Axis
Hypothalamic-pituitary-gonadal axis

Gonads
-testes, ovaries; release sex hormones
-important for pubertal development and maintaining bone balance/peak mass

Androgens: males > females
Estrogens: females > males

Gonadarche
-increasing HPG activity, ending with the attainment of reproductive competence

GnRH neurons in the hypothalamus have pulsatile activity
-minimal in pre-puberty
-responsible for primary and secondary sex characteristic changes
-influence reproductive behavior
HPG Axis- Disorders
Kallmann syndrome
-GnRH deficiency, resulting in failure to start or complete puberty

Precocious puberty
-puberty occurring at an early age; can be cause by early GnRH activity
HPA Axis
Hypothalamic-pituitary-adreanal axis

Adrenals
-the adrenal gland releases hormones in response to stress and also produces androgens

Adrenarche
-maturation of the adrenal glands
-starts earlier than gonadarche
-stimulates development of secondary sex characteristics
-increases responsitivity to stress
Sleep
A state that the brain actively produces
-reduced motor activity
-reduced response to stimulation
-stereotypic posture
-relatively easy reversibility

Polysomnography
-sleep study which monitors the brain, eye movements, muscle activity, heart rhythm, etc
Sleep- Stage 1
"Drowsy sleep"

What?
-transition into sleep from quiet wakefulness

Body?
-lose some muscle tone; lose most conscious awareness of external movement; hypnic jerks present

EEG?
-transition from alpha (awake) to theta (S1) waves
Sleep- Stage 2
"Light sleep"

What?
-transition into light sleep

Body?
-muscular activity decreases; conscious awareness of external movement disappears

EEG?
-theta waves; K-Complex & Sleep Spindle
Sleep- Stage 3
"Deep/slow-wave sleep"

What?
-slow-wave sleep

Body?
-slow heart rate and breathing rate; difficult to awaken

EEG?
-slow, large amplitude delta waves

Stage where sleep-walking can occur
-arise from slow-wave sleep to perform activity
-1 out of 4 people
-dont usually have memory of event

Sleep Inertia
-decline in motor activity and feeling of grogginess following an abrupt wakening; most intense in this stage
Fatal Familial Insomnia
Rare autosomal dominant inherited disease in which individuals eventually cannot go past S1 sleep during sleep cycle

-eats away at thalamus
-"jams" at awake position
-inability to sleep
-develops suddenly
-no treatment
Rem vs NREM sleep
REM
-periods characterized by rapid eye movements during sleep
-EEG waves are irregular, looks like alpha waves during awake stage
-most muscles are paralyzed
-harder to arouse
-brain activity increases to waking levels
-most memorable dreams occur
-increases in neuronal activity in reticular formation/limbic system
-decrease activity in dorsolateral prefrontal cortex

NREM
-stages S1-S3; all other but REM
Sleep cycle
S1-->S2-->S3-->S2-->REM

-more slow-wave sleep earlier in the night
-more REM sleep in cycles before waking

Transition into sleep results from changes in activity of thalamocortical neurons
-filter sensory input
Circadian rhythm
Biological rhythm which has

1. a specific period: 24 hours
2. Endogenous: persists in the absence of external cues
3. Entrainable: can be adjusted to match local time
4. is maintained over a range of temps

Zeitgeber
-any stimulus that can reset the circadian rhythm
Kleine-Levin syndrome
Neurological disorder characterized by recurring periods of excessive amounts of sleep and eatings

-more than 2 months
-"sleeping beauty syndrome"
-wide spread dysfunction
Suprachiasmatic nucleus
Part of the anterior hypothalamus and the main control center of the circadian rhythms for sleep

-located above the optic chiasm
-SCN cells fire in a rhythmic pattern
-damage to the SCN causes less consistent body rhythms that are no longer synchronized to environmental patterns of light and dark

-light resets the SCN via the retinohypothalamic path
Retinohypothalamic path
Important for tracking environmental cues in the SCN

Comes from retinal ganglion cells called ipRGC's
-contain their own photopigment called melanopsin
-respond directly to light, no input from rods or cones
-axons travel directly from retina to SCN
Pineal gland and melatonin
The pineal gland secretes melatonin, which is synthesized from serotonin to increase sleepiness
-SCN regulates waking/sleeping by controlling activity in the pineal gland (endocrine gland; posterior to the thalamus)
-peaks at night
Non-24 hour sleep-wake syndrome
Period of peak alertness moves around the clock from day to day
-out-of-sync body clock; disrupted circadian rhythm
-occurs in about 1/2 of all blind people, due not non-syncronizing of external light cues
Adenosine
Neurotransmitter that inhibits many processes associated with wakefulness
-increase over the day and accumulate in specific brain regions during wakefulness
-high levels = sleepiness
-decline during periods of sleep
-caffeine blocks adenosine receptors in the CNS
REM behavior sleep disorder
Abnormal behavior during REM sleep, involving acting out dreams
-partner is at risk of injury
-cant control movements
-common in older people
-treatment with melatonin
Arousal systems
1. Reticular formation
-activity increases REM-off neurons
2. Posterior (back) hypothalamus
-histamine activates cortical neurons

Orexin
-also called hypocretin
-neurotransmitter released from lateral nucleus of the hypothalamus that is responsible for staying awake
Narcolepsy
Destruction of orexin producing neurons

1. severe daytime sleepiness
2. loss of muscle tone during wakefulness (cataplexy)
3. sleep paralysis
4. dream-like hallucinations

-big risk of injury
-no warning
-treatment includes CNS stimulant or scheduled naps
Theories of sleep
Recuperation theory
-being awake disrupts the homeostasis of the body and sleep is required to restore it

Adaptation theory
-sleep is not a reaction to the disruptive effect of being awake, but the result of an internal 24 hour timing mechanism
Delayed phase shift disorder
Chronic inability to fall asleep and wake at desired clock time
-consistency in late fall asleep time, due to preference in sleep time shifting over adolescence
-excessive daytime sleepiness
-impaired functioning related to sleep disturbance
-occurs in adolescence
Sleep deprivation effects
Moderate sleep
-increased sleepiness
-negative affect of mood
-poor vigilance performance

REM sleep
-rebound

Long-term
-more efficient sleep, more time in slow-wave sleep
What is emotion?
1. Appraisal
-assessment of the nature of a situation that may elicit emotion

2. Physiological response
-bodily sensations associated with arousal state

3. Action tendencies
-motivation to prepare motor actions

4. Expression
-outward facial, body and vocal signs that signal emotional reaction and future intentions

5. Feelings
-one's own subjective experience of the emotional state

Used for:
communication, social affiliation, attention, learning and memory
Views on emotion
1. Universal emotion
-6 basic categories: angry, scared, surprised, disgusted, happy and sad
-culturally universal, although expressions may not be identical

2. Emotion as a continuum
-2 dimensions: valence (pleasant to unpleasant) & arousal (mild to intense)

3. Somatic marker hypothesis
-emotion as a navigational aid in decision-making
-marker of valence and intensity
-conscious awareness of emotion follows from the physiological response
-gut feelings
Amygdala lesions
Later/adult lesions
-lack of fear response to threatening stimuli and increase social affiliation

Earlier/child lesions
-lack of fear response to threatening stimuli and increased fear in social affiliations
Connections between amygdala and treatment
Less amygdala reactivity and larger anterior cingulate gyrus activity --> better treatment success

Higher white matter connectivity between amygdala and ventral prefrontal cortex --> lowest anxiety
Phineas Gage
Injury to his orbitofrontal cortex led to behavioral disinhibition
-emotional outbursts, rudeness, profanity, illogical

Damage to the ventromedial prefrontal cortex (center of the orbiotofrontal cortex) results in a lack of physiological responses to emotional stimuli & their subjective psychological responses
Frontal leukotomy (lobotomy)
Disconnects the inferior frontal cortex from communication with other brain regions, including the amygdala
-results in reduced emotionality, including complete lack of emotion in some cases
-apathy, no sensation of emotion, no facial expression- despite all knowledge that they should have an emotion!
Psychopathy
Personality disorder characterized by:
1. callousness
2. proneness to boredom
3. poor behavioral control (impulsivity)
4. antisosical behavior (theft, arson, bullying)

-often charming and sociable, but have difficulty maintaining relationships due to manipulative, cruel behavior
-commit a disproportionate amount of crime, lack loyalty, are undisturbed by confrontation, fail societal obligations
-due to disruptions of orbitofrontal and amygdala functions
Psychopathy and reward
Wisconsin card sorting
-difficulty changing to a new rule; perseverate

Show more errors when switching rules (set shifting), associated with the orbitofrontal cortex

Also show perseveration of high risk choices in gambling games; impulsivity

Increased dopamine activity
Childhood psychopathy
Psychopathic tendencies include:

1. antisocial behavior/impulsivity
-quick to anger, hostile attribution bias, risk-taking
2. callous/unemotional behavior
-bullying, intimidation, cruelty to animals, fights, manipulative
Autism
Pervasive developmental disorder characterized by:
1. deficits in language
2. presence of stereotypical or repetitive behaviors
3. social impairments

-infants lack social smiling
-impaired eye contact
-limited imitation
-lack of pretend play
-lack of empathy- unable to understand
Mirror neurons
Neurons that fire when we perform a specific action or watch someone else perform an action
-involved with imitating others, empathy and perception of other's intentions
Mu wave activity in Autism
Activity is suppressed when PERFORMING a motor action
-true for BOTH typical and autistic kids

Children with Autism DO NOT suppress activity when OBSERVING an action, suggesting dysfunction of mirror neurons
Stress
Homeostasis
-physiological functions such as temp, oxygenation and glucose level are close to ideal

Stressor
-something in the environment that tilts our system out of homeostasis

Stress response
-series of physiological and metabolic processes that occur in attempt to establish homeostasis
-alters/transfers hormone and energy levels
SAM system
Sympathetic-adrenomedullary system

Fast pathway; adrenaline rush; prepares body for sudden burst of activity

1. brain (hypothalamus) sends a neural message though the spinal cord
2. sympathetic system of the spinal cord is activated to stimulate the adrenal gland
3. adrenal medulla (inside) releases epinephrine into the circulatory system
4. epinephrine activates the body's cells, endocrine glands and brain
HPA system
Hypothalamic-pituitary-adrenocortical system

Slow pathway; glucocorticoids; prepares body for longer-lasting adaptations and restoration of cells

1. hypothalamus releases CRH into the pituitary gland
2. pituitary gland releases ACTH, which acts on the adrenal gland
3. adrenal cortex (outside) releases cortisol into the circulatory system
4. cortisol activates the body's cells, endocrine glands and brain
Effects of epinephrine (adrenaline)
Immediate
-reduced pain sensitivity
-increased blood clotting
-increased blow flow to muscles
-increased oxygen intake
-increased arousal or alerting

Chronic
-increased blood pressure, damage to vessels/hardening of arteries
Effects of cortisol
Immediate
-reduced digestion
-reduced insulin
-reduced activity to reproductive organs
-inhibition of immune system

Chronic
-immune suppression
-abnormal responsiveness of cortisol system (circadian rhythm)
-increased abdominal fat, loss of muscle and bone
Ending a stress response
Normally, stress responses are short-lived

Feedback loops shut it off

Signals from the hippocampus may be important for signaling hypothalamus to stop

Normal stress is good; challenges our body to deal with stressor

If stress is chronic, then effects of HPA may be prolonged, causing cell death, damage to brain/organs and lower hippocampal volume
Daily cortisol rhythm
Follows a circadian rhythm

Linked to sleep/wake cycle and light/dark cycle

Peaks just after waking (7 am) with a minimum around night time
Stress in early rodent development
Hypo-responsive period
-period when the pup is highly buffered from stress, controlled by stimulation from the mother

Disturbing the nest in ways the enhance maternal behavior results in stress resilient offspring (short-term stress)
-high threshold for perceiving threat, sensitive to safety cues, optimistic, confident

Disturbing the nest in ways that disorganize maternal behavior results in stress vulnerable offspring (prolonged stress)
-low threshold for perceiving threat, vigilant, sensitive to danger cues, defensive, worry
Stress and child care
Higher cortisol levels = low sensitive/responsive babysitters

Preschool stress
-morning stress levels are the same at home and school
-afternoon levels are elevated at school
-toddlers show biggest effect; not shutting off during the day

Higher quality daycare = lower cortisol levels
Immune system
Functions to protect us from infection by pathogens; constantly active

Cells are derived from white blood cells called leukocytes
-produced and stored in bone marrow then travel to the spleen and thymus gland (all known as lymphoid organs)

Clumps of tissue that house white blood cells are called lymph nodes
Phagocytes
White blood cells that ingest and destroy bacteria, foreign particles and other cells
-if someone has an infection, there would be an increase of phagocytes in the blood
Lymphocytes
White blood cells that function by recognizing and deactivating foreign substances
-remember previous invaders, and send out counteractive measures
-types include T & B lymphocytes
Innate immune response
1. first line of defense
2. fast acting (minutes)
3. non-sepcific
4. no memory for past pathogens
5. Phagocytes are activated to identify and ingest pathogens

Uses physical and chemical barriers for 1st line of defense
-skin, mucous membranes
-provide a physical barrier and a high level of acidity

Other defenses include body temp, fevers and inflammation (widening of blood vessels)
Adaptive immune response
1. second line of defense (advanced/higher level)
2. slow to respond (days)
3. responds to each pathogen differently
4. remembers past pathogens

Chemically mediated (humoral)
-bone marrow lymphocytes (B-lymphocytes) releases chemical antibodies that bind to specific pathogens
-common process for fighting bacteria

Cell mediated
-thymus gland lymphocytes (T-lymphocytes) attack and destroy pathogens
-common process for fighting viruses and removing altered cells (cancer)
Antigens
Unique proteins on the surface of a pathogen

1. phagocytes detect these antigens and will try to remove the pathogen
2. these detectors will signal lymphocytes to get involved
3. B-lymphocytes start to produce antibodies that are specific to the pathogen
4. once the antibodies are present, T-cells can destroy the pathogen
Immune system development
Immune cells form around 5 weeks gestation
-system is stimulated by germs during and after birth
-at 1 yr age, infants will show adult levels of immunity

Passive immunity
-infant receives antibodies from mom from breast milk and in utero
-last a few months

Passive inoculation
-receiving antibodies from someone who is immune, while you are sick, and can aid recovery process
Vaccinations
Expose us to antigens without making us ill
-live vaccines have low does of the true pathogen
-other vaccines have inactivated versions (flu) of the pathogen, but allow our bodies to get the antigens so our body learns to produce the antibody

MMR
-live, attenuated doses of the diseases
-Measles: could led to mental retardation or death
-Mumps: sterility in adolescent males
-Rubella: congenital birth defects
Primary immune deficiencies
Condition in which a part of the immune system is missing or not functioning properly
-symptoms may not appear immediately

IgA deficiency
-most common
-produce too little IgA (antibody in saliva and fluids)
-increased susceptibility to colds and respiratory infections

22q11.2 deletion syndrome
-associated with poor T-cell immunity due to undeveloped thymus gland
-highly susceptible to infection
Acquired immune deficiency
Caused by a virus or infection, or induced by a medication

HIV
-most common
-attacks the immune system by wiping out certain T-cells
-without these cells, highly susceptible to normally harmless organisms
-contact with infected blood or fluids

Organ transplant medications are also immunosuppressants
Chemotherapy drugs also attack the immune system
Autoimmune diseases
Immune system mistakenly attack the body's own cells as if they were foreign

Lupus
-most common
-immune system attacks cells throughout the body
-inflammation of the joints, skin and body organs
-periods of illness and periods of wellness

Rheumatoid arthritis
-affects joints (fingers, toes, knees, elbows, wrists, ankles, hips, shoulders)
Allergic disorders
Immune system overreacts to exposure to antigens in the environment

Allergies
-result in swelling, inflammation and irritation of membranes
-can lead to anaphylaxis (life threatening heart response)

Asthma
-breathing tubes in the lungs become swollen and narrowed, leading to breathing and wheezing difficulties

Other
-food, drug, seasonal, environmental allergies
Maltreatment stats
Maltreatment is common
-younger kids are more likely to be maltreated, goes down with age
-majority of maltreatment is due to neglect or multiple types (neglect & physical abuse)
-most abuse related deaths come from fathers/other males
-most neglect related deaths come from mothers
Maltreatment outcomes
Show higher incidence of behavioral and emotional problems, including anxiety, PTSD and conduct problems

Childhood maltreatment history predicts adult psychiatric problems like major depression and anxiety
-equifinality: different risk factors result in same outcome
-multifinality: single risk factor results in multiple outcomes

Age, duration, type/severity of abuse, identity of abuser, protective factors, genetic risk are factors for outcome also
Types of maltreatment
Errors of commission
-actions against the child that can interfere with development (adding)
-abuse (physical, sexual and emotional)

Errors of omission
-actions of failed care that can interfere with development
-neglect (witnessing family violence)
Maltreatment- Shaken baby syndrome
Form of child abuse in which the infant is held by the torso and shaken violently, causing whiplash due to rapid acceleration and deceleration
-2nd most common cause of infant death under 1 year of age

Associated with axonal shearing (rip/cuts in white fibers)
-most severe along the midline of the brain
-retinal hemorrhages is another symptom
Maltreatment- Malnutrition
Lack of sufficient nutrients necessary for normal functioning
-nutritional neglect is the most common neglect

Failure to thrive
-occurs when children are unable to take in, retain or utilize calories to grow as expected

Iron deficiency
-most common single nutrient deficiency
-critical for brain myelination; leads to hypomyelination in animals
Maltreatment and stress response
Maltreated children show significantly lower levels of morning cortisol
-greater severity of physical neglect
-chronic stress

Maltreated children with high levels of morning cortisol had greater severity of emotional abuse
-acute stress
Pituitary and adrenal effects of maltreatment
Normally, there is a pituitary response when injected with CRH
-women who were abused show a HYPERACTIVE pituitary response to CRH and dump out more ACTH

Normally, there is a cortisol response from the adrenal gland when injected with ACTH
-women who were abused show a BLUNTED cortisol response, suggesting adrenal insufficiency
Stress & hippocampus/prefrontal cortex
Hippocampal dendritic branching (and volume) is decreased in studies of chronic immobilization stress
Stress & amygdala/orbitofrontal cortex
Chronic immobilization stress results in increased volume and dendritic branching in the amygdala
Maltreatment- Total brain volume and stress
Maltreated children show:

1. smaller overall brain volume
2. slightly larger ventricles
3. no difference in overall gray/white matter ratios
4. significantly reduced corpus callosum volume
5. overall smaller orbitofrontal cortex

Differences in the limbic system (hippocampus and amygdala) for adults, but not necessarily for children

Women who experienced abuse AND developed PTSD related to that abuse showed smaller hippocampal volume
Maltreatment- Emotion recognition
Neglected children
-poorer at emotion recognition overall

Physically abused children
-better than control children at detecting anger
-show a bias to call faces angry (false positives for anger)
-perceived angry faces at an earlier age than control children
-required more info to perceive sad expressions
-show a broader, more inclusive, category for anger
Maltreatment- ERP response to emotional faces
Show larger responses for maltreated children when attending to angry faces than control children (devoting more attention to angry faces)
-infants show greater activity in frontal sites to angry faces
-early abuse alters ERP responses to emotional faces early in life
Maltreatment- Psychopathology as adaptation
Set of physiological responses and behaviors may develop as an adaptation to one context, but create problems in another context
Deprivation stats- Orphanages
Deprivation in orphanages includes:
1. failure to meet basic health/nutritional needs
2. inadequate sensory and/or cognitive stimulation
3. inadequate social stimulation
4. lack of consistent, responsive caregiving relationship**

-10,000-20,000 kids are adopted internationally each year
-75-85% come from institutionalized care
-most are female
-most are less than 2 years old
-most go to well-resourced families
Deprivation- Canalization of growth- Adoptees
Development tends to follow and return to a normative course
-loss of 1 month of growth/2-3 months in orphanage (cortisol inhibits growth hormone)

Catch-up growth
-occurs at 1-1.5 times the normal rate, after adoption
Deprivation- Precocious puberty- Adoptees
Continued institutionalization will delay puberty onset

Precocious puberty
-puberty occurring at an early age; can be caused by early GnRH neuron activity (HPG axis)
-specific to girls?
-early deprivation with growth stunting and rapid catch-up growth is associated with precocious puberty
Outcomes for deprivation
"Post-institutional syndrome"
1. low IQ or developmental delay
2. quasi-autistic behavior (atypical social interaction)
3. inattention/overactivity (ADHD-like)
4. attachement disorders

Internalizing and externalizing disorders are equivalent rates to that of non-adopted children in childhood, but INCREASE during adolescence
Deprivation and stress response
Lack of daily patterning in cortisol production while in orphanage context

Higher cortisol levels across the day 6.5 years post-adoption
-levels are highest for children with the most growth stunting at adoption
-most stress=more stunting=more HPA problems
Brain effects of early deprivation
Prefrontal cortex volume
-both earlier and later adopted post-institutionalized children have smaller prefrontal cortex volumes

Amygdala volume
-studies of post-institutionalized children found enlarged amygdala volume

Hippocampal volume
-later adopted post-institutionalized children have the largest reduction in hippocampal volume

White matter connectivity
-decreased white matter connectivity in the uncinate fasiculus, a tract that connects the limbic system (hippocampus, amygdala) and frontal cortex
-low white matter in this area is associated with longer duration of institutional care and increased symptoms of hyperactivity
Executive function in post-institutionalized children
Rodents
-chronic immobilization stress reduces dendritic branching in the prefrontal cortex
-also impairs set-shifting behavior

Newly adopted children
-EF performance is impaired 1 year after adoption in 2.5-4 year old post-institutionalized children

Adolescents with a history of adoption
-EF performance is normal in earlier adopted children, but remains impaired in later adoptees
Resilience
Adaptive systems within the child, family and community that function to help children achieve appropriate development despite risk and adversity
Deprivation- protective factors
Differential susceptibility
-post-institutionalized children with a Met allele of the BDNF gene are more sensitive to environmental influences
-high age at adoption (with Met allele) showed most ADHD like symptoms, and low adoption age showed lowest symptoms

Enriched environment
-animals exposed to prolonged maternal separation who grow up in an enriched environment show:
1. normal cortisol response to restraint stress
2. no evidence of anxiety on open field test
Intervention foster care
Children in foster care show low AM cortisol

Intervention foster care
-parents who receive training and support in sensitive caregiving, enriched environments
-these children showed similar cortisol levels to the control (normal) group after 6 months
Differences and similarities between maltreatment and deprivation
Early deprivation in the form of institutional care is a significant risk factor for atypical physical, cognitive and socioemotional development

LIKE maltreatment:
-poor institutional care is a form of chronic, traumatic stress

UNLIKE maltreatment:
-institutional care is limited to an early life period, followed by environmental enrichment via adoption into a highly resourced family (intervention)