Module 3 GQ's

• Neural response to central nervous system injury

  1. Brain or spinal cord can be injured acutely by physical trauma

  2. Lack of oxygen created by locally diminished blood flow or ischemia secondary to a vascular occlusion or local bleeding that occurs in persons who sustained a stroke

  3. Neurodegenerative diseases (Alzheimer's & Parkinson's disease)
• Sequence of physical degeneration of the axon

  1. Nerve terminal begins to degenerate & distal stump separates from cell body & undergoes Wallerian degeneration

  2. Fragmentation of myelin & lesion site is invaded by phagocytic cells

  3. Cell body of the damaged neuron swells & the nucleus moves to an eccentric position

  4. Withdrawal of synaptic terminals in contact with damaged neurons occurs & synaptic clef is invaded by glial cells

  5. Atrophy & degeneration occurs in the adjacent input & target neurons of the injured neurons which is called retrograde & anterograde transneuronal degeneration

  6. Loss of a neuron at the site of injury has a cascading effect resulting in degeneration along neuronal pathways which increases the extent of neuronal disruption
• Excitotoxicity


  • Leads to cell death in postsynaptic neuron
  • Contributes to neuronal damage in persons with stroke, TBI, neurogenerative disease, spinal cord injury & acquired immunodeficiency syndrome
• Diaschisis


  • Transient functional changes in brain structures connected to white matter tracts at a remote distance from the site of focal brain damage
  • Can be due to decrease in blood flow and/or metabolism
• Cerebral edema


  • Can produce functional depression in brain tissue that may be not a part of the primary injury (ex. Local edema)
  • Accumulation of intracellular fluid & swelling occurs in cytotoxic cerebral edema
  • Increase permeability of capillary endothelial cells with leakage of proteins and fluid from damaged blood vessels into the extracellular space results in vasogenic edema which can effect white matter long axons
• Recovery of synaptic effectiveness

  • Occurs with reduction of local edema that interferes with action potential conduction
  • Decreased pressure on presynaptic neurons restores normal cellular function, allowing for synthesis and transport of neurotransmitters to resume
• Denervation hypersensitivity


  • Occurs after destruction of presynaptic neurons deprives postsynaptic neurons of an adequate supply of neurotransmitter
  • Postsynaptic neurons develop new receptors at the remaining terminals results in an increased response to neurotransmitters released from other nearby axons
• Synaptic hypereffectiveness


  • Occurs after some presynaptic terminals are lost
  • Neurotransmitter accumulates in the undamaged axon terminals, resulting in excessive release of transmitter at the remaining terminals
• Unmasking of silent synapses


  Activation of silent synapses occurs in response to injury
• Collateral sprouting of axons

  • AKA reactive synaptogenesis
  • Occurs when neighboring normal axons spout to innervate synaptic sites that were previously activated by the injured axons
• Neurogenesis


  Process by which new neurons are formed in the brain
• Cortical reorganization


  • Occurs after a peripheral injury such as amputation or central nervous system injury such as a stroke or traumatic brain injury
  • Cortical neuron function is restructured in adults following nervous system injury
• Changes in cortical maps after acquired & degenerative nervous system lesions

  • Focal damage to the central nervous system can increase the capacity for structural and functional changes within the central nervous system
  • Motor recovery following damage to primary motor cortex may be mediated by other cortical areas in the damaged hemisphere, through the use of either redundant pathways or new regions that take over the function of the damaged axons
  • Contralesionally motor pathway has been shown to be active during hand movements on the paretic side but their role in recovery of function is not clear
  • Cerebellar hemisphere opposite to the damaged corticospinal tract can contribute to motor recovery via establishment of automatic motor skills
• Neural plasticity


  • The ability of neurons to change their function, chemical profile & structure
  • Involved in learning & the creation of new memories
• Experience-dependent neural plasticity


  Process of repair & remodeling is responsive to the experience of the patient following injury
• Adaptive plasticity


  Promoting recovery of lost function
• Drivers of adaptive plasticity


  Begins with active movement
• 'Use it or lose it'


  Failure to drive specific brain function can lead to functional degradation
• 'Use it and improve it'


  Training that drives a specific brain function can lead to an enhancement of that function
• Specificity


  The nature of the training experience dictates the nature of the plasticity
• Repetition matters


  Induction of plasticity requires sufficient repetition
• Intensity matters


  Induction of plasticity requires sufficient training intensity
• Time matters


  Different forms of plasticity occur at different times during training
• Salience matters


  The training experience must be sufficiently salient to induce plasticity
• Age matters


  Training-induced plasticity occurs more readily in younger brains
• Transference


  Plasticity in response to one training experience can enhance the acquisition of similar behaviors
• Interference


  Plasticity in response to one experience can interfere with the acquisition of other behaviors
• Maladaptive plasticity


  Prevents recovery of lost function
• Maladaptive plasticity (big picture)

  Targets synaptogenesis in contralateral hemisphere, expansion of the motor maps in these regions, & facilitates abnormal interhemispheric inhibition
• Substitution and compensatory movement strategies

  • Use of motor patterns that incorporate trunk displacement & rotation, scapular elevation, shoulder abduction, & internal rotation to assist arm and hand transport and aid in hand positioning, orientation for grasping
• Learned non-use


  Patients fails to use paretic limb even though spontaneous recovery has occurred & the paretic limb has greater movement ability and function
• Recovery of function


  Reacquisition of movement skills lost through injury
• Spontaneous recovery


  Initial or early recovery that occurs independent of external interventions
• Activity-induced recovery


  Improvements related to specific activities & training
• Motor recovery at the level of the health condition (neuronal)


  • Restoring function in neural tissue that was initially lost after injury
  • Reactivation in brain areas previously inactivated by the circulatory event
• Motor recovery at the level of body structure and function (performance)


  Restoring the ability to perform a movement in the same manner as it was performed prior to the injury occurrence
• Motor recovery at the level of activity (functional)


  Occurs when using limbs or end effectors to perform a task typically used in persons w/o nervous system injury
• Motor compensation at the level of health condition (neuronal)


  • Neural tissue acquires a function that it did not have prior to injury
  • May be seen as activation in alternative brain areas not normally observed in individuals without disability
• Motor compensation at the level of body structure and function (performance)


  Restoring the ability to perform a movement in the same manner as it was performed before injury
• Motor compensation at the level of activity (functional)


  Successful task accomplishment using alternate limbs or end effectors