L9 - Neuroplasticity Flashcards

1
Q

Explain how grey and white matter changes throughout development.

A
  • Almost all grey matter you are ever going to have is present at birth
  • By 10 years old, you have significantly less. Amount of grey matter decreases as you get older.
  • Laying down of synapses and white matter increases across development.
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2
Q

What is neuroplasticity?

A
  • Ability of nervous tissue to structurally reorganize as a response to experience, injury, sensory deprivation, or learning
  • Results in change in mapping of neural function to neural structure
  • Typically follows experience, trauma, cerebrovascular insult, or sensorimotor deprivation
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3
Q

What is the difference between exotropia and isotropia?

A
  • Exotropia: Strabismus where one eye points to the side

- Isotropia: Strabismus where one eye points to the midline

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4
Q

What is strabismus? How is it typically treated?

A
  • One eye points in different direction from other eye
  • Monocular vision even though vision in both eyes is intact: Brain doesn’t use signals from one eye
  • Corrected by patching good eye for a few months or an ophthalmologist will shorten one of the muscles to re-align the eyes
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5
Q

What is recovery of function?

A
  • Re-establishment of brain-behaviour relationships that are also affected by experience, cerebrovascular insult, trauma, or sensorimotor deprivation
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6
Q

What are the 9 principles of brain plasticity?

A
  1. Plasticity is common to all nervous systems and the principles are conserved across generations
  2. Plasticity can be analyzed at many different levels
  3. Two general types of plasticity
  4. Similar behavioural changes can correlate with different plastic changes
  5. Experience dependent changes interact
  6. Plasticity is age-dependent
  7. Plastic changes are time dependent
  8. Plasticity is related to experience
  9. Plasticity can be maladaptive
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7
Q

List 4 things that occur when the brain is injured.

A
  1. Ischemia (accumulation of fluid in tissue)
  2. Diaschisis (loss of function of distant brain region connected to area of damage)
  3. Changes in localized tissue / surrounding tissue
  4. Changes in cell metabolism
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8
Q

List the 6 steps of the metabolic cascade in order.

A
  1. Ionic changes (seconds to minutes)
  2. Second messengers (seconds to minutes)
  3. mRNA (seconds to minutes, hours to days)
  4. Proteins (seconds to minutes, hours to days)
  5. Inflammation (hours to days, weeks)
  6. Recovery (hours to days, weeks to months)
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9
Q

What are 6 examples of function restitution?

A
  1. Recovery from motor cortex damage
  2. Recovery from hemiplegia
  3. Return of reflexes
  4. Development of rigidity
  5. Grasping facilitated by other movements
  6. Development of voluntary grasping
  7. Recovery from aphasia
  8. Recovery from traumatic lesion
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10
Q

Explain the typical recovery of aphasics.

A
  • Head injured patients show the most rapid and complete recovery
  • Deficits the least severe in anomic patients and most severe in global aphasics
  • Rate of recovery similar in all patients
  • Progress to other stages with recovery but often stop in anomic phase
  • Most recovery occurs in first 3 months
  • Younger patients have better recovery
  • Language areas in RH most resistant to damage
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11
Q

What did Teuber find when examining veterans’ recovery after traumatic brain injury?

A
  • 50% did not recover at all
  • 43% recovered visual defects
  • 36% recovered from somatosensory defects
  • 24% recovered from dysphagia (abnormality of language)
  • 4% recovered from motor defects (likely had damage to brainstem)
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12
Q

Explain Mendel’s Second Law and the implications it has for neuroplasticity.

A
  • Law of independent assortment
  • During gamete formation, the formation of the segregation of the alleles of one allelic pair is independent of the segregation of the alleles of another allelic pair
  • Implication is that the brain cannot know about the characteristics of body parts as they were independently inherited
  • Ability to know this would be impossible without plastic brain – takes differences and creates a uniform model of control
  • Because your brain doesn’t know anything about your body, all the neural mechanisms for controlling and sensing your body have to be calibrated
  • Calibrating only once is not enough – must occur all the time
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13
Q

What is neuroplasticity?

A
  • The property of neural tissue that permits its reuse in response to changes in the environment and body
  • Dependent upon neural structural integrity
  • Clinical and experimental evidence from humans and animals
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14
Q

What are the 7 principles that allow us to infer neuroplasticity?

A
  1. Changes in behaviour
  2. Changes in brain anatomy
  3. Changes in functional brain maps
  4. Changes in synaptic organization
  5. Changes in physiological organization
  6. Changes in molecular structure
  7. Cellular mitosis
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15
Q

Explain how neurplasticity can be demonstrated through behavioural change.

A
  • Experience changes neural structure / function (learning and relearning)
  • Altered experience changes neural structure / function (e.g., distortion of vision; removal of somatosensory component; pinna shape changes)
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16
Q

Explain how neuroplasticity is demonstrated through changes to cortical brain maps.

A
  • Tonotopic areas in A1/A2 are found to be increased in musicians compared to non-musicians
  • Early blindness results in expansion of auditory areas of parietal and occipital lobes
  • Somatosensory cotica representation of digits adjacent to amputated digits invade the latter’s cortical area
  • Somatosensory cortical representation of digits sewn together also fuse into a single area
  • Surgery with webbed fingers: Initially, cortical representation of webbed fingers was a single area. Following the surgery, cortical area divided into two.
  • Braille readers have an expanded cortical representation of fingers used to read
17
Q

What is focal hand dystonia? How does it provide evidence that neuroplasticity isn’t always adaptive?

A
  • Loss of independent control of one or more of the fingers on a hand
  • Found in musicians and other occupations where long term, repetitive synchronous movements of the fingers are made
  • Results in expansion of corticomotor and corticosensory areas associated with each finger – analogous to functional fusion of two or more fingers
  • Thought to be caused by neural crosstalk amongst formerly segregated primary motor cortical areas
  • can be a career ending impairment for musicians
  • Treatments include retraining exercises to increase digit independence
  • Botulinum neurotoxin A
18
Q

Explain how neuroplasticity is demonstrated by changes in synaptic organization

A
  • Neuronal complexity may be related to the computational demands placed on the cell
  • Used golgi-type staining on post-mortem brain tissue to look at dendritic arborization and electron microscopy techniques to look at synaptic number and size
  • Took measurements from neurons in the trunk and finger regions of S1 and Wernicke’s area
  • Found that Wernicke’s area had most complex neurons, followed by the finger, then the trunk
  • Also found relationship between the complexity of dendritic arborization and the occupation of those whose brains were studied
19
Q

Explain how neuroplasticity is demonstrated through changes in physiological organization.

A
  • LTP: Repetitive electrical pulses applied to brain tissues have been shown to alter the efficiency of synaptic transmission
  • Under optimal conditions, electrical potentiation can result in long term changes in synaptic efficiency – believed by some to underlie memory consolidation
  • Kindling: The development of electrical seizure activity due to repeated exposure to an electrical pulse insufficient to generate seizure itself
  • Can be regarded as a form of learning (i.e., a semipermanent or permanent change in the physiological state of the brain in response to a stimulus)
20
Q

Explain how neuroplasticity is demonstrated through mitosis.

A
  • In adult brain, occurs in two regions: the hippocampus and olfactory bulb
  • No one knows why these two specific regions have adult neurogenesis and no one knows why the remainder of the brain does not
21
Q

What are Kertesz’s two stages of recovery from brain injury?

A
  • Stage 1: Acute recovery. Recovery from effects of metabolic and membrane failure, neurotransmission deficits, hemorrhage and edema. Some axonal regeneration occurs soon after injury with new synaptic connections.
  • Stage 2: Long-term brain reorganization. Axonal regeneration, collateral sprouting, reprogramming of cortical and subcortical processes.
22
Q

What is the kennard principle?

A
  • The earlier the patient suffers brain damage, the more functions are spared and the greater the chances of recovery for lost ones
  • There are some exceptions: Speech may be spared while syntax is not. This may be related to the equipotentiality hypothesis (brain can co-opt other areas to take over role of lost part. Reduction in efficiency of function is not related to what area was damaged, but how much damage to the brain was sustained as a whole).
23
Q

What are the 3 criteria for evaluating the degree of recovery from cortical damage?

A
  1. Cortical damage should be accompanied by loss of behaviours thought to be mediated by that cortical part. If behaviours re-appear, it isn’t necessarily because of recovery to that cortical part.
  2. Recovered behaviour must be same as what was previously lost.
  3. If treatment produces recovery then the recovery must be attributable to the treatment and would not have occurred without it
24
Q

What are the 3 theories that are used to explain recovery?

A
  • Artefact theories: A brain lesion may cause inhibition of other, remote structures (e.g., reduction in NT availability elsewhere). Accounts for symptoms that are due to changes in neural tissues from remote regions.
  • Anatomic reorganization theories: Functions of damaged tissues are taken up by other neural areas. Implausible due to the requirement that there is an inventory of spare tissue that can be marshalled for use.
  • Functional Adaptation theories: People can relearn some lost functions.