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Neuroanatomy & -physiology > 12 Neuroplasticity in Response to Stress and Injury > Flashcards

12 Neuroplasticity in Response to Stress and Injury Flashcards

1
Q

What is neuroplasticity?

A

Capacity of neurons and neural networks in the brain to change their connections and behaviour in response to new information, sensory stimulation, development, damage, or dysfunction

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2
Q

What are the 2 functions of neuroplasticity

A
  • learning or enhancing cognitive capacities
  • strengthening areas where function is lost or damaged
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3
Q

What are the 4 types of neuroplasticity?

A
  • homologous area adaptation
  • cross-modal reassignment
  • map extension
  • compensatory masquerade
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4
Q

How does homologous area adaptation work?

A

cognitive process taken over by homologous region in opposite hemisphere

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5
Q

What is cross-modal reassignment (cross-modal plasticity)?

A
  • reorganization and functional change of brain structures as response to sensory loss / to compensate for sensory deficit
  • varying effects depending on: timing of sensory deprivation, sensory experience, damaged brain regions, etc.
  • cross-modal recruitment: recruitment of deprived sensory cortex by remaining senses
  • compensatory plasticity: functional refinement of spared sensory cortices
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6
Q

What is map expansion?

A
  • enlargement of functional brain region based on performance
  • size of cortical map devoted to particular function may enlarge with skilled practice or frequent exposure to stimulus
  • in adult owl monkeys, after amputation of 1-2 digits adjacent digit representations expanded topographically
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7
Q

What is compensatory masquerade?

A

allocation of new specific cognitive process to perform task

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8
Q

Are all sensory and motor body representations contralateral in the brain?

A
  • no, auditory processing is ipsilateral
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9
Q

Cross-modal recruitment in blind people

A
  • visual cortex active for processing somatosensory information, V1 & V2 active while reading Braille
  • TMS of occipital cortex leads to error rate increase with Braille and roman embossed letters (distorted tactile experience: phantom dots or extra dots, not for sighted - sensorimotor cortex)
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10
Q

compensatory plasticity in blind people

A
  • better in tactile grating detection task (independent of Braille reading ability or blindness onset)
  • more precise at localizing and focusing on sounds in periphery (both in congenitally and late blind)
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11
Q

cross-modal recruitment in deaf people

A
  • primary auditory cortex activated by visual stimuli and sign language
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12
Q

compensatory plasticity in deaf people

A
  • hearing loss leading to enhancement in some vision related tasks
  • not general enhancement but in specific abilities
  • motion processing, visual stimulus onset dection
  • spatial attention to peripheral visual field (not found in hearing signers)
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13
Q

Neural correlates of cross-modal reassignment

A

changes in subcortical connectivity
- tracing studies in blind mole rats
- alteration in projection from inferior colliculus to thalamus
- not only to auditory, but also to non-degenerated visual thalamus
- recruitment of occipital cortex by auditory stimulus
indirect cortical connections through multisensory cortical areas
- feedback from parietal cortex as source of crossmodal rearrangement
Sensory loss leading to circuit adaptation that favors feedforward processing in the spared cortices while promoting intracortical processing in deprived cortex

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14
Q

6 neocortical layers and their connectivity patterns

A
  • layer 1: no neural cell bodies, only axons and dendrites
  • layer 2: input mainly from other cortical areas, dfficult to distinguish from layer 3
  • layer 3: output mainly to other cortical areas
  • layer 4: input mainly from thalamus (non-cortical sources)
  • layer 5: output mainly to basal ganglia and spinal cord (non-cortical targets)
  • layer 6: output mainly to thalamus
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15
Q

What are sensory substitution devices (SSDs)?

A
  • non-invasive human-machine interfaces
  • transform stimuli characteristic of one sensory modality into stimuli of another sensory modality
  • e.g. visual-to-tactile SSD: “Seeing with touch”
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16
Q

What are the 3 components of SSDs?

A
  • sensor : collects information from external environment (e.g. camera, sonic, infrared sensors)
  • coupling system: signal transduction
  • stimulator: relayed onto receptors of sensory organ (e.g. tongue, back, hand, ears)
17
Q

What are shortcomings of SSDs?

A
  • limited attentional capacity and sensory overload
  • interference with other perceptual functions or daily tasks (tradeoff between acuity and usability)
  • active training and assessment
18
Q

first SSDs by Paul Bach-y-rita

A

Tactile vision substitution system (TVSS)
- In 1969, first experimental evidence for sensory substitution
- conducted with congenitally blind
- Brightness of pixel => tactile stimulation on 20x20 grid
- Object recognition even when obscured, person identification, batting a ball + reports of 3D vision, distal attribution
- Recruitment of brain areas considered purely visual (Kupers et al., 2003; Ptito et al., 2005)

19
Q

case of Cheryl Schiltz

A

bilateral vestibular damage as side effects of antibiotics
- feeling of perpetually falling, oscillopsia, vertigo
- tactile-vestibular SSD with tongue display unit (TDU)
- tactile information encoding direction of head
- prolonged residual effect with training -> complete removal of device

20
Q

basics of synaptic plasticity

A
  • number of synapses increases steeply during first year of life, then steadily declines
  • increased use of given pathway leads to consolidation of circuitry (sprouting of new synapses, stronger response to stimuli)
  • decreased use weakens circuitry
  • past synaptic activity modifies future synaptic activity (= synaptic plasticity)
21
Q

What is phantom limb pain?

A
  • pain sensation to a limb, organ or other tissue after amputation and/or nerve injury
  • sometimes hard to distinguish with post-operative pain
  • clinical problem: existence of pain in a non-existent limb, seems inherently untreatable
  • complex phenomenology, age-dependent, which body part amputated
22
Q

Causes of Phantom limb pain

A
  • wishful thinking, frayed nerve endings (neuromas) fool higher brain regions, or cortical remapping and expansion
  • change in cortical maps (homunculi) in amputees
  • motor commands to missing limb are also received by somatosensory cortices, dissonance between motor and sensory areas involved in body image might cause pain
    other factors:
  • errors in pain modulation from descending pathways and local interactions in peripheral nervous system (loss of inhibitory control in dorsal horn => increased sensitivity => allodynia)
  • proprioceptive memory
  • visual dissociation with proprioception
23
Q

How can cortical maps change rapidly in response to amputation?

A
  • sprouting of axonal collaterals into neighboring regions (gradual)
  • redundancy of nonfunctional connections that are now activated (immediate)
24
Q

Neuromatrix Theory of pain

A
  • most explanations ascribed to it
  • pain is produced by patterns of neural impulses
  • widely distributed neural network called body-self neuromatrix actively generating subjective experience based on memory, biological and sensory influences (modified by life experience)
  • body representations (possibly poorly rewired in cortical maps) remain intact without sensory input/life experience to update them
  • incongruence enhanced with lack of visual feeback can lead to excessive pain
25
Q

mirror therapy

A
  • PLP increases when visual feedback mismatches with body image
  • mirror therapy: visual feedback can resolve paralyzed feeling and subsequent pain
  • proof that body-self matrix is adaptable and may subsequently affect brain structure by life experience
26
Q

pharmacological treatment

A
  • aim: ease symptoms
  • NSAIDs, pain killers, anti-seizure medications, muscle relaxers, antidepressants
  • electrical impulses to nervous system may also reduce symptoms (deep brain stimulation, spinal cord stimulation, transcutaneous electrical nerve stimulation (TENS)
27
Q

VR Therapy

A
  • control sensory experiences and implement mirror therapy
  • modify neurosignature (abnormal reorganization) of matrix with systemic approach
  • significant reduction of pain after VR session, pre-session pain levels also decreased
28
Q

Neuromatrix of Pain - limitations

A
  • phantom pain never fully eliminated in patients
  • poorly explains how sensations can rapidly appear (perhaps result of activation of dormant networks)
  • no explanation why some patients never experience PLP
  • objectively hard to empirically study (or bayesian inference, predictive coding, synthetic sensory input)

Neuroanatomy & -physiology (14 decks)

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