A short presentation on spinal shock which occurs following spinal cord injury.

1. Presented by – NAMITA KAUSHIK
MPT (NEUROLOGY)

2. Spinal shock
Following a spinal cord injury
 A transient period of areflexia
 Abrupt withdrawl of connection between
higher centres and spinal cord
 Below the level of lesion loss of sensory,
motor and reflexes.

3. Characteristic effects
 Motor – paraplegia , quadriplegia
 Tone – flaccid
 Sensory – loss below the lesion
 Reflexes – loss below the lesion
 Autonomic changes – bradyarrhythmia,
av block and hypotension

5. Phase 1:
A complete loss or weakening of all reflexes
below
the level of spinal cord injury
Spinal concussion caused the neurons
involved in various reflex arcs and the neural
input from the
brain become hyperpolarized and unresponsive.

6. Phase 2
Characterized by the return of some reflexes.
The first reflexes to reappear is the
bulbocavernosus reflex
The reason reflexes return is the hypersensitivity
of reflex muscles following denervation; more
receptors for neurotransmitters are expressed and
are therefore they are easier to stimulate.

7. Phases 3 and 4
Characterized by hyperreflexia
Neurons below the injury attempt to reestablish
the synapses

13. CLINICAL IMPLICATIONS OF SPINAL SHOCK
• Formation of new synapses could lead to both
desirable and undesirable clinical effects.
• With significant sparing of descending motor inputs,
descending axons can sprout, resulting in motor
recovery.
•With minimal sparing, growth of segmental reflexes
inputs leads to spasticity, neuropathic pain and less
voluntary motor recovery.

14. Interventions
 Coordinating active exercise and functional
training to enhance the underlying synapse
growth
 Selected activity and electric activation may
lead to selected desired synaptic growth.
 Exercise can increase NT synthesis and could
be molecular signal for activity dependant
recovery.
 Functional electrical stimulation is alternative
tool.
 Gait training may promote synapse formation
in the CPG.

15.  Additional intervention to enhance synapse
formation-
1. Medications to increase excitability of spinal
neurons (5-HTP, clonidine, TRH, Theophylline)
2. Stimulants of axonal growth (inosine)
3. Stimulants of axonal synthesis (clenbutorol)
4. Inhibition of Glutamate Toxicity (dizocilpine)
5. Cell Replacement Strategies

16. References
 Spinal shock revisited: a four phase model
International spinal cord society, march 2010
 Rossignol S. Neural control of stereotypic limb
movements. In: Rowell LB, Sheperd JT (eds.)
Handbook of Physiology. Oxford University Press:
New York, 1996, pp 173–216
 Skup M, Dwornik A, Macias M, Sulejczak D, Wiater
M, Czarkowska-Bauch J. Long-term locomotor
training upregulates TrkB(FL) receptor-like proteins,
brain-derived neurotrophic factor, and neurotrophin 4
with different topographies of expression in
oligodendroglia and neurons in the spinal cord. Exp
Neurol 2002; 176: 289–307.
 Sussan o sullivan , sixth edition

17. THANK
YOU