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Spinal Cord Function After Injury

Spinal Cord Function After Injury. spinal cord structure in relation to vertebrae types of lesions fibre tracts in spinal cord sensory loss motor loss reflexes and spinal shock neuropathic pain. Orientation of spinal cord and spinal roots with respect to vertebrae. Posterior.

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Spinal Cord Function After Injury

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  1. Spinal Cord Function After Injury • spinal cord structure in relation to vertebrae • types of lesions • fibre tracts in spinal cord • sensory loss • motor loss • reflexes and spinal shock • neuropathic pain

  2. Orientation of spinal cord and spinal roots with respect to vertebrae Posterior

  3. Collapse of disc space Disc prolapse Slippage of vertebra over disc

  4. Collapsed vertebra in patient with severe osteoporosis

  5. Arrows indicate S3-S4 disc prolapse Arrow indicates L4-L5 disc prolapse

  6. Arrow indicates compression fracture at C5 Arrow indicates fracture-dislocation at C6/C7

  7. Head and neck Diaphragm Deltiods, Biceps Wrist extenders Triceps Hand Chest muscles (T1-T7) Abdominal muscles (T7-T12) Leg muscles Bowel, bladder Sexual function

  8. Paralysis of the lower half of the body is called paraplegia. Paralysis of both arms and legs is called quadriplegia (or tetraplegia).

  9. Posterior Sensory fiber tracts Dorsal columns Cuneate funiculus Gracile funiculus Dorsal root ganglion Upper trunk, arm, neck, head Leg, Lower trunk Touch, vibration, pressure, Proprioception Aα, Aβ Pain, temperature, crude touch Aδ, C Ventrolateral spinothalamic Anterior

  10. Posterior Motor fiber tracts Lateral corticospinal anterior horn cells for limbs anterior horn cells for trunk Anterior horn cells Medial corticospinal Aα motor neuron Anterior

  11. Dorsal columns dorsal and ventral horns Lateral Corticospinal, Anterior horn cells motor pain, temperature vibration, proprioception, touch Ventrolateral spinothalamic

  12. medulla upper limbs Aα, Aβ(touch, vib,propriocep) Aδ, C (pain, temp.) Aα motor lower limbs

  13. Examples The diagrams that follow indicate the motor and sensory loss as a consequence of one of the following lesions. Identify the lesion in each case and indicate on the spinal cord and spinal cord section the site, level and side of the lesion. Lesions: Anterior cord syndrome Posterior cord syndrome Central cord syndrome Transverse cord Hemicord (Brown-Sequard)

  14. Central cord syndrome (small lesion) – cape distribution Eg. Spinal cord contusion (bruise causing bleeding in spinal column), spinal cord tumors Anterior cord syndrome Eg. Trauma, multiple sclerosis, anterior spinal artery infarct cervical T8/T9 Damage to spinothalamic fibers as cross anterior commissure

  15. Hemicord lesion Brown-Sequard Eg. Penetrating injuries, lateral compression from tumors, multiple sclerosis E D Transverse cord lesion Eg. Trauma, tumors, multiple sclerosis (demyelination) C Posterior cord Syndrome Eg. Trauma, extrinsic compression from posterior tumors, multiple sclerosis T8/T9 T8/T9 T8/T9

  16. Signs and symptoms of UMN versus LMN lesions UMN lesionLMN lesion Yes Weakness Yes No (yes, disuse) Atrophy Yes No Fasciculations Yes Increased* Reflexes Decreased Increased* Muscle tone Decreased *except decreased during spinal shock

  17. Spinal Shock • Initially hyporeflexia (spinal shock) (24hrs up to ~2months) Loss of descending excitation (bleeding, oedema, inflammation, cell hypoxia, cell death, demyelination) • Followed by return of reflexes Denervation hypersensitivity (increased neurotransmitter release, increased responsiveness to neurotransmitter) • Followed by hyperreflexia Axonal and soma regrowth (neural plasticity) with denervation hypersensitivty

  18. Neuropathic pain Treat early to prevent wind-up (hyperalgesia) Drugs: opioids, antiepileptics (block Na+ channels), Tricyclic antidepressants (serotonin and NA reuptake inhibitors) Surgery: nerve root ablation Descending inhibition - Enkephalin Opioids Inhibitory interneuron + Serotonin NA Aδ, C + Glutamate SCI → Wind-up Denervation hypersensitivity, increased neurotansmitter release, increased responsiveness to neurotransmitter, neural plasticity

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