Neuroplasticity Notes

Neuroplasticity

Definition of Neuroplasticity

  • Etymology of "Plastic": The term derives from:
    • Greek: πλάσσω (plasso) - to form, mold, or shape.
    • Greek: πλαστικός (plastikós) - fit for molding.
    • Latin: plasticus - of or belonging to molding or modeling.
    • Prefix: plast-
    • Related terms: plaster, plastic, plasticine.
  • Neuroplasticity Definition: Dynamic structure, function, and organization of the nervous system.
  • Changes Include
    • In response to injury.
    • In response to environmental changes.
    • In response to experience.
    • Throughout the lifespan.
  • The nervous system can be 'molded' or 'shaped'.
  • Relevant Research Areas:
    • Brain Development
    • Cognitive-Brain Training
    • Sensation and Perception
    • Psychiatric and Neurological Treatments
    • Learning and Memory
    • Seasonal Behavior
    • Rehabilitation and Recovery Post-Injury
    • Drug Addiction
    • Brain-Computer Interfacing
    • Exercise
    • Epigenetics
    • Aging

Mechanism of Neuroplasticity

  • Long-Term Potentiation (LTP) and Depression (LTD): A key mechanism involves changes in 'synaptic strength'.
  • Neural function directly affects structure.
  • These changes can last a long time.
  • Long-Term Potentiation (LTP):
    • Pre-synaptic neuron fires frequently.
    • Post-synaptic cell increases the number of dendritic receptors.
    • Post-synaptic cell is easier to depolarize in the future.
  • Long-Term Depression (LTD):
    • Pre-synaptic neuron fires infrequently.
    • Post-synaptic cell decreases the number of dendritic receptors.
    • Post-synaptic cell is harder to depolarize in the future.

Changes in Response to Injury: The Case of Pedro Bach-y-Rita

  • Patient History:
    • Suffered a stroke at 65 years of age.
    • Experienced right-sided paralysis (hemiplegia).
    • Was unable to speak.
    • Underwent initial four-week rehabilitation.
    • Engaged in intensive 'home' therapy.
    • At 68 years of age, he had recovered enough to resume full-time work.
    • Died at 72 years of age.
    • Autopsy revealed that the lesion never healed.
  • Recovery:
    • Almost complete recovery.
    • Experienced slight clumsiness of right hand, evident when performing fine movements.
    • Autopsy revealed pathology limited to brain stem and spinal cord.
  • Pathology: The stroke affected the pons.
  • Corticospinal Tract Damage:
    • Degenerative changes in corticospinal (pyramidal) tract caudal to the pons.
    • Gliosis, demyelination, and atrophy were observed.
    • Tracts rostral to the pons were unaffected.
  • Basal Pons: Left basis pontis cystic infarct.
    • Thrombosis (blood clot) caused infarction (tissue starvation of oxygen) and necrosis (unregulated cell death).
    • No viable neural tissue remained in the centre of the left basis pontis.
    • Some longitudinal fiber bundles remained at the lateral and medial edges.
  • Medulla: Left medullary pyramid (above decussation) appeared shrunken and grey, showing degenerative changes.
    • Only sparsely scattered intact fibers remained.
  • Cervical Spinal Cord: Demyelination of the right lateral (contralateral) and left ventral (ipsilateral) corticospinal tracts.
    • Some widely disbursed myelinated axons remained.
  • Recap of Pedro Bach-y-Rita's Case: Suffered a stroke at 65 years with right hemiplegia, achieved almost complete functional recovery after intensive therapy, and autopsy 6 years post-stroke revealed structural damage to corticospinal tracts that had not healed. Thus, this is an example of functional neuroplasticity in the efferent CNS.

Evidence of Cortical Reorganization

  • Ward et al. (2003) Study: Studied 8 stroke patients with hemiparesis who received rehabilitation therapy.

    • Functional MRI scans were conducted while performing a hand grip task.
    • Longitudinal study with 6-10 scan sessions over 6 months post-stroke.
    • Lesions were in different parts of the motor circuits.
    • Patients 1, 4, and 7 had lesions in the pons, but none had language deficits.

  • Findings:

    • Early and widespread increase in task-related cortical activation.
    • Progressive reduction in this task-related recruitment over sessions that correlates with recovery scores.
    • These changes are mostly within the motor system.
    • Patients with greater initial deficit recruit more widely and to a greater extent, including non-motor regions.
    • Other modalities are increasingly utilized in those with greatest deficit to optimize task performance.