What is abuse-induced brain trauma?
- people have long known that children who had been deprived of normal nurturing environments early in life exhibit significant and apparently irreversible deficits (especially social maladjustment) in later life
- from stories of “wild children”, to more recent studies of the institutional scale neglect of children reared in impoverished orphanages, to the emerging prevalence of intitutional sexual abuse in Australia, there is clear recognition that early life experiences are critical to normal adult social functioning
- experiments in the 1950s by Harlow and other replicated (some would say unnecessarily) the effect of early maternal deprivation on subsequent social and cognitive behaviour in monkeys
- why is child abuse in various forms (neflect, physical abuse, sexual abuse) so harmful? what damage does it do? why are these wounds so deep?
What evidence exists of the impact of abuse-induced brain trauma?
A. time spent in orphanages with conditions of social deprivation correlates with incidence of neurocognitive impairment
B. MRI tractography showing abnormally sparse connections in a socially deprived child
C. fearful, timid withdrawn: a monkey who was reared in isolation from its mother is incapable of normal social and exploratory behviour
What is the critical period?
- critical period for normal adult social behaviours not when these behaviours are taught or modelled or even seen
- the systems mediating adult social cognition requires activation of tactile-based attachment and nurturing experiences
- similar critical periods have been characterised in perceptual development
- visual perception requires experience of learning, it is the “learnt present”
How was visual input organisation discovered?
- radioactive amino acids injected in eye (often leucine)
- transypatic transport through the LGN terminates in layer 4 of the primary visual cortex
- terminations are visible as bright bands on the autoradiogram
- protein transfers across the synapse so can be seen in the projections to visual cortex as well
What is the consequence of having two forward facing eyes?
- binocular vision
- allows fine visual motor tasks
What is the distribution of inputs in a normal adult (cat) in the visual cortex?
- 25 neurons get inputs only from contralateral eye
- same for ipsilateral eye
- most cells responded, at least to some extent, to both
- some totally equal some favoured one more than the other
What happens if you block one eye for about 2.5 months after birth?
- all cells respond only to ipsilateral eye
- none respond to input from contralateral eye
- no stereoscopic vision
- some cells nonresponsive
(contralateral is one that was closed)
What happens when you have open for first 12 months and then close one eye?
- almost same as adult
- most cells driven by both eyes
- some contralateral only, some ipsilateral only
So what determines failure of development of stereoscopic vision?
- deprivation early in life rather than late in life
- just six days of covering one eye just before one month of age resulted in complete failure of responding to that eye
- three days, slightly more normal but still abnormal pattern
How does monocular deprivation affect neuronal architecture?
short-term during critical period
- deprived eye: weird looking
- sparse
- don’t have as much complexity
- same in long term
What is seen in the visual cortex of someone/cat with a lazy eye?
- have far fewer cells driven by both eyes
- no stereostopic vision
What do you see if you add an eye to a frog?
- starts to compete with normal eye and forms banding patterns in visual cortex
- seems to be intrinsic property of neurons to start to separate out
What is occuring during critial period?
- competition between left and right eye to act as inputs onto neuron
- higher input will out-compete weak inputs
- enhanced - grow bigger and more synapses
- permanent change in synaptic efficacy
- involves transcription of factors that cause the presynaptic cell to elaborate more terminals
- e.g. BDNF (superstar molecule), involved in plasticity
- can work fairly locally
- pre synaptic neuron that takes it up will be encouraged to create more and bigger synapses
What are critical periods and molecular regulators for some neural systems?
- neuromuscular junction: mouse, prior to day 12, Ach
- cerebellum
- LGN
- ocular dominance
- orientation bias
- somatosensory map
- tonotopic map
- absolute pitch:
- taste, olfaction
- imprinting
- stress, anxiety
- slow-wave sleep
- sound localisation
- birdsong
- language
What is the critical period in the stress response?
- possibly related to abuse
- amygdala
- coordinated autonomic response
- effect on cognition
- also has a potent activation over piuitary/hypothalamus
What is the current theory for what might be going wrong when a child or animals is abused?
- fear, anxiety, the “stress (HPA) axis” and its feedback modulated by cortisol receptors in the hippocampus
- could severe childhood stress, damage brain regions mediating cortisol feedback, resulting in a faulty HPA axis?
- child abuse greatly increases the risk of developing mood and anxiety disorders
- animal models of neglect reveal the critical importance of mono/indol-amine system activity
- HPA over activity is a common finding in depressed patients
- push/pull activation of stress axis
- cortisol provides a means of coping with physiological stressors
- high levels of cortisol receptors on hippocampus (negative feedback)
- hippocampus thereby inhibits HPA releasing cortisol
- cortisol lipid soluble
- amygdala activates release of cortisol
- stress axis seems to be broken
- hippocampal neurons sensitive to over-excitation
- reduced hippocampal volumes in abused patients
- childhood maltreatment is associated with reduced volume in the hippocampal subfields CA3, dentate gyrus, and subiculum
- reduced medial prefrontal cortex volume in adults reporting childhood emotional maltreatment
- interaction of childhood stress with hippocampus and prefrontal cortex volume reduction in major depression
- the relationship between levels of harm or neglect or enrichment and the neurodevelopmental outcome is known best at the extremes: severe abuse, and complete neglect (and absolute experimental sensory restriction) produced marked and possibly irreversible deficits
- what is not so clear is whether the relationship is linear and monotonic or whether there is a threshold above which development is normal
- and if abuse occurs and produces abnormal development, to what extent can it be reversed?
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