Neuroplasticity

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Neuroplasticity

  1. 1. Neuroplasticity Key to recovery after spinal cord injuryPresented by : Dr. Shamim Khan RMO, Medical Care Services CRP, SAVAR
  2. 2. Classification of SCI According to cause :  According to site of injury : – Traumatic – Cervical (tetraplegia) • Fall from height – Dorsolumber (paraplegia) • Fall while carrying heavy load • Fall of heavy object • RTA, assault etc. – Nontraumatic • Tubercular spondylitis • Pyogenic spondylitis • Spinal cord tumour • Transverse myelitis • GBS
  3. 3. Classification of SCI (cont.) According to ASIA impairment scale Complete (A) Incomplete (B to E)
  4. 4. Spinal shock This is a time period after the transection of the spinal cord during which all the spinal reflex responses are profoundly depressed. Duration : Minimum 2 weeks Bulbocavernous reflex : First reflex to appear following recovery of spinal shock.
  5. 5. Cellular mechanism of SCI Primary injury : – Membrane dysruption – Vascular damage – Heamorrhage & edema. – Ischemia (lack of O2) Secondary injury : – Chemical mediators released by activated macrophage and glial cells – Prolonged inflammation and scarring. – Neural cell death and neurological damage.
  6. 6. Why SCI is an irreversible lesion? Once injured, CNS neurons cannot regenerate their axons, because : – Lack of NGF. – Inhibition of growth by Oligodendrocytes. – Clean up activities of lymphocytes and Microglia. – Increased GABAergic and Glycinergic inhibition of spinal networks.
  7. 7. Neuroplasticity The ability of the neurons to change their function, chemical profile ( amount and types of neurotransmitters produced) or structure is referred to as neuroplasticity. The plastic changes in neuron can occur – Physiologically according to activity and skill. – Pathologically due to injury or disease of CNS.
  8. 8. Cortical mapof a normal person
  9. 9. Cortical mapof a Drummer
  10. 10. Cortical map of a Football player
  11. 11. Mechanism of Neuroplasticity in CNS after an injury Acute reorganization – Unmasking of previously present latent synapses. Chronic reorganization – Changes in synaptic efficacy. – Growth of new synapses by axonal sprouting. These plasticity changes in CNS can occur at multiple levels like cerebral cortex, brain stem and spinal cord.
  12. 12. Cortical Plasticity Structural and functional reorganization of cortical representation following injury is known as cortical plasticity. Cortical plasticity can occur after : – CNS injury (stroke, SCI) – Loss of a body part (amputation of limb or digit). Changes in cortical map depends on : – Spared connections available. – Post injury survival time.
  13. 13. Cortical plasticity after arm amputation In a person with a missing upper limb fMRI and TMS study on somatosensory cortex shows the hand area becomes reorganized for representation of the face.
  14. 14. Cortical plasticity in paraplegic patients In a complete paraplegic patient after six months or more, extensive use of hands with least or no leg movements results in plastic invasion of cortical hand area on the leg area. PET scan study demonstrated extension of cortical hand map into the cortical leg map.
  15. 15. Cortical plasticity in paraplegicpatients (cont.) By this way, the upper limb gain strength and lower limbs lose the chance of functional recovery. And the patient becomes wheelchair bound forever !!
  16. 16. Cortical plasticity Is it desirable or degradable ? It is desirable in a sense that, increased strength and function of the upperlimbs of paraplegic pt can compensate the weekness of lower limbs for locomotion, bed transfer etc. It is degradable, because it weakens the chance of lower limbs locomotor recovery.
  17. 17. Plasticity in transected spinal cord Reorganization of severed descending pathways of spinal cord can occur over time, and with the aid of regenerative strategies.1. Regeneration from the severed fibre to the original target.2. Regeneration through a haphazard pathway.3. Sprouting from neighbouring fibres onto the denervated target neuron.4. Enhanced intrinsic plasticity through sensory feedback training.
  18. 18. Plasticity in spinal pathways Role of sensory feedback training Studies of spinal reflex conditioning states that, repeated cutaneous or electrical stimulation on paralysed lower limbs can enhance motor response by changing synaptic efficacy along the spinal reflex arc.
  19. 19. Motor tasks can be learned by spinal cord after transection Can sensory feedback training help spinal cord to acquire the ability to perform complex motor activity, like walking or stepping? Several studies on complete thoracic spinal transected cat trained on treadmill for locomotion resulted full weight-bearing stepping. The spinal cord is able to integrate and adapt to sensory information during locomotor training and in response to sensory feedback, spinal neurons learn to generate stepping in absence of supraspinal input.
  20. 20. Can a complete spinal transected human walk again ? Studies states that, if only 10% of descending spinal tacts are spared, some voluntary control of locomotion can be recovered. Task specific locomotor training triggers spinal cord’s central pattern generator that can sustain lower-limb repetitive movement (walking), independent of direct brain control.
  21. 21. Strategies to enhance recovery of locomotion Body weight supported treadmill training (BWST). Pharmacological interventions. Biotechnology to regenerate spinal connectivity.
  22. 22. Body weight supported treadmill training (BWST) About 50% of patients body weight is suspended in a harness. Therapists manually assist his legs to step on a slowly moving treadmill. The aim is to gradually achieve full weight- bearing at increasing treadmill velocities.
  23. 23. BWST !! Light at the end of tunnel Of acutely injured paitents 92% who used wheelchairs became independent walkers after treadmill training.Researcher No. of Durationof Training Result subjects injury period %improved ExtentDr. Anton 44 6 months 3 – 20 wks 36 indepenWernig(1995) – 18 yrs dentDr. A. L. 14 1.2 – 24 12 – 15Hicks(2005) yrs monthsDr. Marcus 20 2-17 yrs 8 wksWirz (2005)
  24. 24. Pharmacological interventionto improve stepping after SCI Clonidine, a noradrenergic agonist. Bicuculline, a GABA antagonist. Strychnine, a glycinergic receptor antagonist. Cyproheptadine, a serotonergic antagonist.
  25. 25. Molecular Biology and Biotechnologyto regenerate spinal connectivity  Peripheral nerve grafting.  Transplantation of fetal nervous tissue.  Administration of antibodies that block growth inhibiting protein activity.  Implantation of engineered cells.
  26. 26. Role of Surgical Decompression and Stabilization Early decompression should be performed to remove the tissue debris, bone and disc that compress the spinal cord to alleviate pressure and to improve the circulation of blood and cerebrospinal fluid. Some Studies demonstrate that the longer compression of the spinal cord exists, the worse the prognosis for neurological recovery. Stabilization is obvious for discoligamentus unstable spinal fractures. Early stabilization allows early mobilization and locomotor training. Reduce chance of developing pressure sore, postural hypotension and local pain. Reduce hospital staying period, so reduced chance of acquired infections.

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