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KHA452 > Week 10 - Neuroplasticity > Flashcards

Week 10 - Neuroplasticity Flashcards

1
Q

What was the first evidence of how memory formation results from molecular changes?

A

Eric Kandel, 1969

Memory formation results from molecular changes

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2
Q

What is long term potentiation?

A

The persistent strengthening of synapses based on recent patterns of activity

long lasting increases in the signalling between two neurons

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3
Q

Can plasticity be maladaptive?

A

yes, when associated with negative consequences such as a loss of unction or increased injury

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4
Q

What is metaplasticity?

A

Interactions between internally generated change and externally induced plasticity

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5
Q

When can maladaptive plasticity occur?

A

in response to treatment of neuropsychiatric disorders eg. tardive dyskinesia following antipsychotic drugs (dopamine antagonisys)

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6
Q

How does addiction effect plasticity?

A

maladaptive plasticity in the subcortical reward circuit

prefrontal regulation of subcortical limbic circuits re significantly reduces (loss of inhibitory modulation)

drug seeking/taking is then under control of evolutionarily older brain regions, with little control imposed by neo-cortex

Very resistant to reversal

Behaviours that override the drug seeking are hard to (re)establish

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7
Q

What is neurodegeneration?

A

Progressive declines in behaviour and neural function, often through a pathogenic process and maladaptive cycle

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8
Q

What does amyloid affect?

A

Synaptic plasticity and therefore cellular mechanisms for plastic changes in brain circuits

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9
Q

What declines with ageing?

A

processing speed

working memory

peripheral nervous system function

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10
Q

What are common themes in plasticity that emerge across diverse central nervous system conditions?

A

Experience dependence

Time sensitivity

Motivation and attention

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11
Q

What is a broad definition of neuroplasticity according to Cramer et al, 2011?

A

The ability of the nervous system to respond to intrinsic and extrinsic stimuli by reorganising its structure, function and connections

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12
Q

When can neuroplasticity occur?

A

during development

in response to the environment

in support of learning

in response to disease

in relation to therapy

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13
Q

When can plasticity be viewed as adaptive?

A

When associated with a gain in function

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14
Q

When can plasticity be viewed as maladaptive?

A

When associated with negative consequences such as loss of function or injury

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15
Q

What does it mean if there is a shift in inter-hemispheric balance towards the uninjured hemisphere?

A

Sign of a distressed system

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16
Q

The delayed onset of epilepsy after cerebral trauma suggests that…..?

A

Progressive changes in the brain, such as axonal sprouting and the formation of new connections, produce alterations in neural signalling and disinhibition that result in the induction of seizures

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17
Q

What are some examples of maladaptive neuroplasticity?

A

Delayed onset of epilepsy - Progressive changes in the brain, such as axonal sprouting and the formation of new connections, produce alterations in neural signalling and disinhibition that result in the induction of seizures

Chronic pain and allodynia following injury to a limb (eg. amputation) or to CNS

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18
Q

How do mental and addicitive disorders differ from stroke/trauma?

A

The onset of mental and addictive disorders is usually insidious

Course of the illness tends to be recurring/episodic

Reocvery in most of the disorders is slow when present

relapse rates are high

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19
Q

What areas are particularly noteworthy in relation to the clinical expression of neuropsychiatric disorders?

A

Prefrontal cortical association areas

20
Q

What does the kindling model suggest?

A

Heightened neural sensitivity to specific triggers reflects plasticity in N-Methyl-D-asparate receptor functioning in addiction and other neuropsychiatric disorders

21
Q

What control mechanisms are hijacked by subcortical reward systems in order to support drug-seeking behaviour?

A

Prefrontal control

22
Q

What receptors are critical for long term potentiation?

A

Perisynaptic metabotropic glutamate receptors

23
Q

What is cross-modal plasticity?

A

The ability of sensory maps to reorganise across afferent modalities when normal input is deprived

24
Q

How may maladaptive neuroplasticity affect a child who has optical problems?

A

Permanent visual deficits such as amblyopia

25
Q

What are critical modulators of plasticity?

A

Salience

Motivation

Attention

26
Q

What combination therapies have the potential to further drive Hebbian Plasticity?

A

Concomitant pharamacological

Peripheral nerve stimulation

27
Q

What interventions have the potential. to increase the efficacy of neuromodulation?

A

Imagery or behvaioural interventions

28
Q

The left temporoparietal cortex is one of several regions whose overactivity is associated with the perception of external voices in hallucinating patients. How would you use TMS to treat this?

A

Low freq stimulation of temporoparietal cortex has been used experimentally to inhibit cortical excitability and thereby quell severe, treatment-resistant auditory hallucinations with some success

29
Q

What are the two generally hypothesised mechanisms of deep brain stimulations?

A

Creates a functional lesion via inhibition within the stimulated region and, (immediate effects-meffects on motor function in parkinsons)

alternatively, the deep brain stimulation activates the neuronal network connected to the stimulated region, leading to modulation of pathological network activity (gradual effects - circuit retraining as seen in neuropsychiatric disorders)

30
Q

What brain areas have shown promise in treating depression with deep brain stimulation?

A

Subcallosal cortex and its adjacent white matter tracts, suggesting that disruption of the pathological limbic-cortical circuit may ameliorate treatment-resistant depression

Nucleus accumbens

anterior limb of the internal capsule

31
Q

How has deep brain stimulation shown promise for treating OCD?

A

Involve the overactivity of cortico-striatal-limbic circuits

Internal capsule extending into the ventral striatum

32
Q

What is a limitation of molecular mechanisms that support plasticity?

A

Pharmacological vulnerabilities

Behavioural gains induced by plasticity-promoting pharmacological interventions can be lost

33
Q

Emerging finctional conncectivity MRI methods provide what information related to neuroplasticity?

A

Strength of connections across multiple distributed networks such as emotion, motor and cognitive, in parallel

34
Q

What are some issues in the study of clinical neuroplasticity?

A

Disease can affect imaging biomarkers

Clinical trial design - crossover studies are not always possible

Selection bias

Impairments and limitations of those enrolled may not be representative of the overall disease population

Plasticity is time sensitive

Variability complicates generalisation

Translating neuroplasticity findings from animals to humans can be difficult

35
Q

What are the directions for future research regarding neuroplasticity?

A

Tailoring plasticity-based therapies based on individual patient measurements

High-throughput methods to screen potential plasticity-promoting interventions within specific networks

Examine therapies in combination

Animal models that replicate the complexity of disease mechanisms over time

More understanding of age effects on neuroplasticty

36
Q

What is EPSP?

A

Excitatory postsynaptic potential

Size of response, post synaptically

37
Q

What parts of the hippocampus are involved in long-term potentiation?

A

CA3 and CA1

38
Q

Following cerebral trauma, the brain may go through maladaptive changes in conjunction of adaptive changes, what is an example of this?

A

Epilepsy

39
Q

Chronic pain causes changes to the structure of the brain as well as causing reductions in cognitive ability. What are the two approaches to treating chronic pain?

A

Approach 1
Target the injury (bottom-up)

approach 2
Target the pain centrally - address the pain sensation “top down”

40
Q

Is it effective to treat chronic pain by targeting the injury?

A

This only addresses the nociceptive signals from the peripheral receptors

Very weak relationship between the extent of musculoskeletal damage and the extent of the pain

41
Q

What are the two ways to rehabilitate and reverse the abnormal changes to the CNS?

A

Treat the injury (bottom up)

Target the brain (top down)

42
Q

What is central sensitisation?

A

An amplification of neural signalling within the central nervous system eliciting pain hypersensitivity

considered a form on maladaptive plasticity

43
Q

What can changes in corticospinal excitability demonstrate?

A

Can reflect reorganisation at the cortical and spinal levels

44
Q

What happens if an individual modifies their motor strategies to control a joint?

A

Contribute to chronicity through maladaptive plasticity

45
Q

What changes cause people to modify their motor strategies to control a joint?

A

Changes in cortical maps or in the balance between inhibition and excitation may disrupt the facilitation of the muscles needed too execute a motor task, as well as the inhibition of other muscles for fine tuning movement

46
Q

How may clinicians examine sensorimotor changes in the clinic?

A

One option would be to evaluate how the joint is controlled by assessing how patients actively move their limb during a motor task

Looking for changes in

movement symmetry
appearance of compensations
Aberrant movements

Also assessment of cognitive-emotional factors
Workplace and sport activities

47
Q

What has been shown to improve motor performance and reduce clinical symptoms in patients with musculoskeletal disorders?

A

Sensorimotor or skill training

KHA452 (10 decks)

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