This document discusses neuroplasticity and recovery after spinal cord injury. It classifies spinal cord injuries and explains that neuroplasticity refers to the brain's ability to form new neural connections. It provides examples of cortical reorganization and plasticity in the brain after injuries like amputation or spinal cord injury. The document also discusses how sensory feedback training and treadmill training can enhance neuroplasticity and promote recovery of locomotion through reorganization of spared pathways in the spinal cord.

1. Neuroplasticity
Key to recovery after
spinal cord injury
Presented by : Dr. Shamim Khan
RMO, Medical Care Services
CRP, SAVAR

2. Classification of SCI
 According to cause :
– Traumatic
• Fall from height
• Fall while carrying heavy
load
• Fall of heavy object
• RTA, assault etc.
– Nontraumatic
• Tubercular spondylitis
• Pyogenic spondylitis
• Spinal cord tumour
• Transverse myelitis
• GBS
 According to site of injury :
– Cervical (tetraplegia)
– Dorsolumber (paraplegia)

3. Classification of SCI (cont.)
 According to ASIA impairment scale
Complete (A) Incomplete (B to E)

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. 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. 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. 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. Cortical map
of a normal person

9. Cortical map
of a Drummer

10. Cortical map of a
Football player

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. 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. 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. 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. Cortical plasticity in paraplegic
patients (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. Cortical plasticity
 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.
Is it desirable or degradable ?

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. 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. 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. 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. Strategies to enhance
recovery of locomotion
 Body weight supported treadmill training
(BWST).
 Pharmacological interventions.
 Biotechnology to regenerate spinal connectivity.

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. BWST !! Light at the end of tunnel
 Of acutely injured paitents 92% who used wheelchairs became
independent walkers after treadmill training.
Researcher No. of
subjects
Durationof
injury
Training
period
Result
%improved Extent
Dr. Anton
Wernig(1995)
44 6 months
– 18 yrs
3 – 20 wks 36 indepen
dent
Dr. A. L.
Hicks(2005)
14 1.2 – 24
yrs
12 – 15
months
Dr. Marcus
Wirz (2005)
20 2-17 yrs 8 wks

24. Pharmacological intervention
to improve stepping after SCI
 Clonidine, a noradrenergic agonist.
 Bicuculline, a GABA antagonist.
 Strychnine, a glycinergic receptor
antagonist.
 Cyproheptadine, a serotonergic
antagonist.

25. Molecular Biology and Biotechnology
to 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. 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.