ALDS 3604 Lecture Notes - Lecture 2: Diffusion Mri, Prosodic Unit, N100

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Harjeenna Sivapatham Wednesday, January, 13th, 2016
ALDS 3604 – Brain Imaging Techniques, Learning, and Neuroplasticity
Learning Objectives: students will
- Review basic understanding of neuron structure
- Understand basic neural correlates of learning, neuroplasticity & (re)habilitation
- Understand basic features of most currently used brain imaging techniques
- Understand role that these techniques play in furthering knowledge of language learning
& communication disorders
The Neuron: *diagram in lecture slide*
Basic Concepts/Terms:
- Neurons (dendrites; cell bodies (gray matter); axons (white matter/fibre tracts – 1mm to
1m); myelin sheath/Nodes of Ranvier
- PNS – Schwann cells control myelination; CNS – Oligodendrocytes control myelination
- Electrochemical signals/action potentials/neurotransmitters/synapses
- Afferent/efferent nerves; inhibition/excitation
- Cerebrum (hemispheres; lobes)
- Diencephalon (thalamus, hypothalamus)
- Brain stem – reticular formulation (alertness, consciousness)
- Cerebellum (coordination of movement, motor learning, posture)
- Neural circuits
Neural Development Versus Neuroplasticity:
- Neural Development:
oMediated by genetics
oNewborn neurons develop mostly prior to birth (location & connectivity
determined in utero)
oContinuous after birth as well
- Neuroplasticity:
oNeural changes due to external stimuli (sensory)
oChanges due to internal reorganization
Prenatal and Neonatal Periods:
- Most neurons developed by 25th gestational week (possible neurogenesis later in
hippocampus, olfactory region & cerebellum)
- Neural tube differentiates into various parts of brain (cerebrum, brain stem, spinal cord,
- Great increase in surface area & folding of cerebral cortex
- 350% increase in brain size in 1st 2 yrs
- Mostly glial cells, synaptic growth, myelination result in brain growth postnatally
- Neurons migrate to various regions & then growth cones guide axons to synapse w/ other
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- Pruning (preprogrammed cell death/apoptosis)
- Less efficient or redundant pathways die off
Following damage, what actually is happening post-injury?
- Is damaged region repairing itself?
- Are other areas of brain compensating for the damaged area?
- Are higher level executive functions improved in order to facilitate more adaptive
behaviours or skills? E.g. improved self-monitoring, attentional skills, etc.
- Are compensatory strategies in environment accounting for change (but no endogenous
change in brain)?
Specific Neural Processes Post-injury:
- Damage can occur to both cell body & axons
- Swelling in damaged tissue due to impaired blood-brain barrier
- Infiltration of infection-fighting cells (Neutrophils)
- After 1 week, swelling starts to reduce
- Microglia travels to sit of lesion & engulfs debris (even as soon as 24 hrs post injury)
- Astrocutes form scar tissue around smaller lesions
- Axonal regeneration (better in PNS than CNS, maybe due growth protein present in PNS
but not in CNS; no Schwann cells in CNS, etc.)
- Still adjacent neuronal tissue may take on new functions or reorganization of may occur
across hemispheres
Learning and Neuroplasticity:
- Neurogenesis
- Neuronal migration
- Dendritic arborisation
- Axon & dendritic growth
- Myelination
- Synaptogenesis
- Pruning
- Development of neuronal circuits: “Neurons that fire together, wire together” (Donald
Hebb, 1940s and 50s)
- Establishment/modification of cortical fields/circuits
Factors Affecting Plasticity and Learning:
- Genetics
- Pre-injury learning
- Sensory & motor experience
- Hormones
- Drugs (nicotine, other stimulants)
- Neurotrophic factors, esp BDNF
- Rewards
- Aging, Stress. Diet
- Magnetic/electrical stimulation
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- Single most replicable finding:
oGreat improvement & change in adults in stimulating & complex environments
oMay not hold for children, esp those w/ ASD
Plasticity and Sensitive Periods:
- Prior to 1980s: Thought no new neural architecture developed past early childhood
- Clear that there are certain sensitive periods e.g. Kuhl & speech perception, imprinting,
- Neuroplastic changes can occur passively during childhood
- Later in life
oSmaller scale changes still occur
oUsually in response to strong stimuli (need to work harder to get results)
oRequire conscious attention
Following brain injury (CVAs, TBIs, etc.):
- Improved skills associated w/ increased recruitment of regions in damaged hemisphere
- Reorganization may also include complementary tissue in contralateral hemisphere
- Considerable variability of cortical changes across victims
oExtent of regions that are recruited
o# of individuals who recruit only affected hemisphere compared to those who
recruit contralateral hemisphere as well
Cognitive Reserve:
- Repeatedly found: not always direct relationship b/w brain damage &
clinical/behavioural presentation
- Two possibilities:
oBrain reserve capacity:
Physical attributes such as brain size, # of synapses
oCognitive reserve:
Neural reserve i.e. brain networks present pre-injury
Neural compensation i.e. utilisation of other circuits not usually used to
take on new functions
- Likely, both possibilities work together
- Regardless, individuals w/ higher IQ, educational attainment, reading skills, occupational
attainment, etc. do better w/ similar brain insult compared to those w/ lower levels on
these measures
Implications for Rehabilitation:
- Early intervention most effective
- Intensive training most effective
- Intervention still effective past “critical periods”
- Neuroplasticity still in effect into advanced age but usually require conscious effort &
more work – therefore support for intervention, even in older adults
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