17740698 Ashleigh Fordham

Neuroplasticity: Rehabilitation after Spinal Cord Injury

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17740698 Ashleigh Fordham

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Neuroplasticity: Rehabilitation after Spinal Cord Injury
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  1. NEUROPLASTICITY:

    Slide 1 - NEUROPLASTICITY:

    • Rehabilitation after Spinal Cord Injury
    • Ashleigh Fordham
    • 17740698
  2. OUTLINE

    Slide 2 - OUTLINE

    • OUTLINE
    • 1. What is Neuroplasticity?
    • Definition
    • Purpose
    • 2. Animal Studies
    • Rodents
    • Cats
    • 3. Human Studies
    • Body Weight Support (BWS)
    • Mechanisms
  3. 1. DEFINITION

    Slide 3 - 1. DEFINITION

    • Neuroplasticity: The ability of the Central Nervous System to form new neural connections and strengthen or weaken current connections based on the required functions of the individual.
    • Learning
    • Behaviour
    • Environment
    • Development
    • Damage
    • Emotion
  4. Where does this Happen?

    Slide 4 - Where does this Happen?

    • Each day new neurons are minted in the Hippocampus and integrated into the learning circuits. Minute-by-minute new circuits are built, strengthened and altered. Each night unnecessary circuits are pruned.
    • (Fenner et al., 2015)
  5. 1. PURPOSE

    Slide 5 - 1. PURPOSE

    • Neuronal activity promotes new connections-
    • Rehabilitation therapy attempts to stimulate particular neurons that have not been active for some time.
    • To promote selective self-repair and reorganization through specific motor activity.
    • Practice makes Perfect-
    • “constraint-induced movement-based therapy”
    • Essential for Locomotion Rehabilitation: Helps your brain form and strengthen the connections necessary for that movement.
  6. 1. MECHANISMS

    Slide 6 - 1. MECHANISMS

    • Signal Size
    • AMPA and NMDA
    • Calcium Influx.
    • Dendritic Length
    • BDNF
    • Post Synaptic Density
    • Interlocking Proteins
  7. 1. Signal Size

    Slide 7 - 1. Signal Size

    • Pre synaptic neurons release glutamate and another neurotransmitters such as glycine. This release must trigger two different postsynaptic receptors- AMPA and NMDA.
    • When both the AMPA and NMDA receptors are triggered, the NMDA receptor opens and calcium rushes in. This calcium influx triggers the manufacture of more AMPA receptors.
    • AMPA receptors are then placed in the synapse: increasing the size of the signals.
    • More calcium = more AMPA receptors = increase in the signal called long term potentiation.
    • Long Term Potentiation: Neuroplasticity associated with conscious memory and learning.
    • (Jon Lieff, M.D., 2013)
  8. (Jon Lieff, M.D., 2013)

    Slide 8 - (Jon Lieff, M.D., 2013)

  9. 1. Dendritic Length

    Slide 9 - 1. Dendritic Length

    • Dendrites change length: This increases the ability to rapidly receive information as well as making the connections more stable. Spine alterations are influenced by: BDNF and oestrogen etc.
    • Stress stimulates this type of neuroplasticity: Reducing the size of the hippocampus and increasing the amygdala.
    • These alterations are influenced by environment, seasonal changes, and age.
    • (Jon Lieff, M.D., 2013)
  10. Slide 10

    • Brain derived Neurotrophic Factor (BDNF): Belongs to the growth factor family, involved in promoting synaptic efficacy, neuronal connectivity and neuroplasticity. (Informahealthcare.com, 2015)
    • (Ebi.ac.uk, 2015)
    • (Grande et al., 2010)
  11. 1. Post Synaptic Density

    Slide 11 - 1. Post Synaptic Density

    • Post Synaptic Region: Found in the Post Synaptic Cell the PSD region includes over 1000 different proteins. This dense area of proteins has recently been discovered and appear to be variable in size and composition. Participate in the regulation of synaptic adhesion, transmitter receptor clustering, and modulation of receptor. Sensitivity (Jon Lieff, M.D., 2013)
  12. (Jon Lieff, M.D., 2013)

    Slide 12 - (Jon Lieff, M.D., 2013)

  13. Slide 13

    • 2. Animal Studies
    • Animal based evidence regarding Neuroplasticity provides a basis for the treatment of humans post Spinal Cord Injury.
  14. 2. RODENTS

    Slide 14 - 2. RODENTS

    • EXPERIMENT
    • Electrochemical Neuro-Prosthetic and Robotic Postural Interface
    • Electrical Frequency- Applied to L2 and S1
    • spinal
    • Segments
    • 40-50Hz
    • 1-4V
    • Agonists Injected
    • Serotonin (5HT1A/7 and 5HT2A/C)
    • Dopamine (D1)
    • Lateral Support
    • Ventral Support
  15. Slide 15

    • Restoring Voluntary Control of Locomotion after Paralysing Spinal Cord Injury
  16. (Van den Brand et al., 2012)

    Slide 16 - (Van den Brand et al., 2012)

  17. 2. RESULTS

    Slide 17 - 2. RESULTS

    • Voluntary Movement:
    • Overground training increases the number of labelled neurons
    • in intermediate and ventral laminae of the T8/T9 segments of the spinal cord compared to non-trained and treadmill trained.
  18. 2. CATS

    Slide 18 - 2. CATS

    • EXPERIMENT
    • Hip Position
    • Load
  19. Vibration of the hip flexor muscle of SCI cats during stance lead to an earlier onset of the swing phase while walking.Enabling the cats to walk more efficiently, since the vibration stimulated the primary and secondary nerve endings of muscle spindles in hip flexor muscles which simulated the stretch.

    Slide 19 - Vibration of the hip flexor muscle of SCI cats during stance lead to an earlier onset of the swing phase while walking.Enabling the cats to walk more efficiently, since the vibration stimulated the primary and secondary nerve endings of muscle spindles in hip flexor muscles which simulated the stretch.

    • 2. CATS-Hip Position
  20. 2. CATS- Load

    Slide 20 - 2. CATS- Load

    • Load is relayed by the Golgi tendon organs (lb) in the ankle extensor muscle during walking.
    • By gradually increasing the load applied to the Achilles tendon, both amplitude and duration of the rhythmic EMG bursts of the ankle extensors in cats increased.
  21. 3. Human Rehabilitation

    Slide 21 - 3. Human Rehabilitation

    • Neuroplasticity after spinal cord injury is a potential rehabilitation technique. It encourages therapists to shift their methodology from ‘compensation to recovery’, to promote Neuroplasticity in areas of learning to move the muscles required to walk, rather than teaching patients to manoeuvre a wheelchair. (Behrman, Bowden and Nair, 2006)
  22. 3. BODY WEIGHT SUPPORT SYSTEM

    Slide 22 - 3. BODY WEIGHT SUPPORT SYSTEM

    • Hugues Barbeau was a physical therapist and neuroscientist.
    • He used a ‘Body Weight Support System’ (BWS) over a treadmill with the aim of providing the sensory experience of walking for patients post SCI. Once a patient develops the capacity to step, balance and the maintenance of posture, this skill must be practiced without a treadmill.
    • (Rehab.research.va.gov, 2015)
  23. 3. Supplemental Video

    Slide 23 - 3. Supplemental Video

  24. (Behrman, Bowden and Nair, 2006)

    Slide 24 - (Behrman, Bowden and Nair, 2006)

  25. 3. RESULTS

    Slide 25 - 3. RESULTS

    • Evidence proves the Benefits of the BWS systems. For example; a patient who started Locomotion Therapy (BWS and Treadmill) 5 months after incomplete Spinal Cord Injury:
    • Improved Walking speed from 0.19 to 1.01 m/s.
    • Walking activity increased to 3,924 (+/- 1,629)steps/day.
    • The patient is able to use an ambulator at home and a cane in public.
  26. Combined animal and human based evidence proves by stimulating the existing motor neurons in a variety of rehabilitation exercises, basic motor functions can be performed.

    Slide 26 - Combined animal and human based evidence proves by stimulating the existing motor neurons in a variety of rehabilitation exercises, basic motor functions can be performed.

    • An ‘voluntary’ function can be regained after practice.
    • With Neuroplasticity in mind; partnerships between neuroscientists and physicians have the potential to create an era of greater recovery after Spinal Cord Injury. (Behrman, Bowden and Nair, 2006)
    • CONCLUSION
  27. REFERENCES

    Slide 27 - REFERENCES

    • Ebi.ac.uk, (2015). [online] Available at: http://www.ebi.ac.uk/pdbe/entry/pdb/1bnd [Accessed 29 Apr. 2015].
    • Fenner, J., Fellows, M., Cobb, D., Savastio, R., Smith, M., Ukinski, T. and Smith, M. (2015). Blood Sugar Levels May Affect Hippocampus, Says Study. [online] Guardian Liberty Voice. Available at: http://guardianlv.com/2013/10/blood-sugar-levels-may-affect-hippocampus-and-memory-says-study/ [Accessed 29 Apr. 2015].
    • Grande, I., Fries, G., Kunz, M. and Kapczinski, F. (2010). The Role of BDNF as a Mediator of Neuroplasticity in Bipolar Disorder. Psychiatry Investigation, 7(4), p.243.
    • Informahealthcare.com, (2015). Brain-derived neurotrophic factor and neuroplasticity in bipolar disorder, Expert Review of Neurotherapeutics, Informa Healthcare. [online] Available at: http://informahealthcare.com/doi/abs/10.1586/14737175.8.7.1101?journalCode=ern [Accessed 29 Apr. 2015].
    • Jon Lieff, M.D., (2013). Another Form of Neuroplasticity by Switching Glutamate NMDA Subunits. [online] Available at: http://jonlieffmd.com/blog/another-form-of-neuroplasticity-by-switching-glutamate-nmda-subunits#sthash.QArwvc9y.dpuf [Accessed 29 Apr. 2015].
    • Rehab.research.va.gov, (2015). [online] Available at: http://www.rehab.research.va.gov/jour/00/37/6/images/COLO-F02.GIF [Accessed 29 Apr. 2015].
    • van den Brand, R., Heutschi, J., Barraud, Q., DiGiovanna, J., Bartholdi, K., Huerlimann, M., Friedli, L., Vollenweider, I., Moraud, E., Duis, S., Dominici, N., Micera, S., Musienko, P. and Courtine, G. (2012). Restoring Voluntary Control of Locomotion after Paralyzing Spinal Cord Injury. Science, 336(6085), pp.1182-1185.