Neuroplasticity and rehabilitation Flashcards
Neuroplasticity
the brain’s capacity to change following experience; “experience-dependent change”
Neuroplasticity: new wiring for old jobs (RICH CLUB VS POOR CLUB)
- The brain has ~80 million neurons, and more connections between them than necessary
- “Rich club” (some neurons are highly connected) vs “poor club” (others make relatively little connections) regions & neurons, MEANING an amount of unused potential - more ways that these neurons can connect with one another
“Neurons that fire together wire together”
Two neurons activated at the same time will strengthen their neurons together, opposed to ones that activate at different times
Mechanisms of neuroplasticity (3)
- Functional plasticity
- Structural plasticity
- Neurogenesis
Functional plasticity
Mechanisms of neuroplasticity
- Strengthening or weakening synapses (long-term potentiation vs long-term depression)
- Modified gene expression & protein synthesis
- Increased or decreased connectivity between distant brain areas
- Reorganization of firing patterns within brain areas
Structural plasticity
Mechanisms of neuroplasticity
- Changes in dendritic spine density and morphology
- Axonal sprouting
- Up- or down-regulation of synaptic pruning
Neurogenesis
Birth of new neurons
Age-dependent plasticity can be seen in humans: cataracts in children
- Some children are born with cataracts which obstruct vision in one eye (clouding of lens in eye)
- The brain reorganizes to favour input from the other eye (amblyopia)
- If not addressed in time, 3D vision remains poor (unable to use both eyes together to see things in 3D) even with cataract removal due to this pathological reorganization
Age-dependent plasticity can be seen in humans: cataracts in adults
- Not the case for adults (less plasticity)
- Their 3D vision is typically fine, as there’s no plasticity to favour the good eye
Age-dependent plasticity: primary visual cortex in children born blind
- In children who are born blind, primary visual cortex assumes non-visual functions
- Asking “what does your visual cortex do?”
- Takes on other functions - “brain hates to leave a neuron without a job”
Charles Bonnet Syndrome
- In adults who lose vision, without neuroplastic reorganization, the visual cortex neurons can begin to fire on their own in the absence of environmentally-relevant sensory input
- EX: While relaxing at home in the living room, “the cattle [would] stare at [me] while quietly munching away at the grass” (Jacob et al., 2004)
- Individuals know that this is not real - not similar to schizophrenia
Area-dependent plasticity
idea that plasticity is not equal across every part of the nervous system, but rather area dependent
Area-dependent plasticity - Rats given amphetamine showed…
That amphetamine can cause different plastic changes in different parts of the brain (EX: two different parts of the PFC - increase vs decreases in spine densities)
Cortical maps - how can we measure plasticity?
- Somatosensory and motor homunculi are a convenient way to measure plasticity
- Organized in the homunculi - and use the way this “map” is organized to locate particular plastic changes
Cortical maps - OVERUSE of a body part is called…
- Focal dystonia: disorder involving involuntary muscle movements and postures of an overused body part
- EX: in musicians - those who do repetitive finger movements
Cortical maps after injury: The Phantom Limb
- How does the brain deal with a sudden loss of input to a limb? i.e., the leftover area of the brain/homunculi
- Most likely related to the cortical map reorganization
- Essentially trying to reprovide the missing input (EX: using a mirror) to restore boundaries
Interventions targeting neuroplasticity: Antidepressants and psychedelics - GLUTAMATE RECEPTORS
AMPARs + NMDARs = glutamate receptors
Interventions targeting neuroplasticity: Antidepressants and psychedelics - GLUTAMATE AFTER ANTIDEPRESSANT INTERVENTIONS
- Glutamate receptors can go under a number of changes after antidepressant interventions
- When NMDARs and AMPARs are activated by glutamate, they produce calcium signalling within the post-synaptic
- This upregulates the production of BDNF - which stimulates back to the post-synaptic cell (called Track B)
- Track B changes the expressions of neurotransmitters on the post-synaptic
Interventions targeting neuroplasticity: Antidepressants and psychedelics
- Psychedelics and anti-depressants (psilocybin or ketamin) can induce juvenile-like periods of plasticity
- Essentially taking an older neuron and making it younger, inducing plasticity; drugs do so by making cells more receptive to BDNF
Interventions targeting neuroplasticity: Antidepressants and psychedelics - BDNF ARE ONLY RECEPTIVE TO WHAT TYPE OF NEURONS?
- BDNF is only released by active neurons - meaning that an antidepressant won’t make every cell in the brain more plastic
- Therefore, these drugs make the brain more sensitive to environmental experience (possibly good and bad); antidepressants + therapy = best effect
Interventions targeting neuroplasticity: rTMS
- repeated Transcranial Magnetic Stimulation (rTMS) has the potential to impact plasticity at several levels: circuit, neural, and synapse
- Particularly acts upon BDNF
- Early studies in patients with depression (who show low BDNF), addiction, schizophrenia, OCD
- Traditional ECT (electroconvulsive therapy) does this too! Highly effective & fast-acting for severe depression, but can carry a lot of stigma
Plasticity & pain
- Neuropathic pain is caused by a lesion or disease of the somatosensory nervous system (NOT AN ACTUAL, PHYSICAL INJURY)
- Many causes including: spinal cord injury, diabetic neuropathy, MS, cancer, trigeminal neuralgia…
- Affects 7-10% of the adult population
What is Central sensitization?
is a plastic change in pain processing in the central nervous system resulting in:
- Allodynia
- Primary Hyperalgesia
- Secondary Hyperalgesia
Allodynia
Central sensitization
- Pain in response to usually non-painful stimuli
- EX: sunburn
