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Spinal shock Physiology
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Spinal shock Physiology

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  • 1. Transection of the spinal cord Complete Transection Incomplete Transection Hemi section
  • 2. Complete transection of spinalcord Common causes of Complete transection are Gunshot injuries, Dislocation of spine, Occlusion of the blood vessels. Common site of involvement is at mid thoracic level
  • 3. Clinical stages Stage of spinal shock Stage of reflex activity, Stage of reflex failure
  • 4. Stage of spinal shock Effects depends on site of injury Complete transection in cervical region (above c5) is fatal paralysis of respiratory muscles In quick trasection of spinal cord patient feel as it has been cut in to two portions, upper portion is unaffected and in lower part all the motor activity sensations are lost
  • 5. Spinal ShockIn all vertebrates, transection of the spinal cordis followed by a period of spinal shock duringwhich all spinal reflex responses are profoundlydepressed. Subsequently, reflex responsesreturn and become hyperactive. The duration ofspinal shock is proportionate to the degree ofencephalization of motor function in the variousspecies. In frogs and rats it lasts for minutes; indogs and cats it lasts for 1 to 2 h; in monkeys itlasts for days; and in humans it usually lasts for aminimum of 2 wk.
  • 6. Characteristic effects of spinal shock Motor Effects Paraplegia,Quadriplegia Loss of tone Muscles become flaccid A reflexia All the superficial and deep reflexeses are lost Sensory Effects All Sensations are lost below the level of transection
  • 7. Complete lesions above T1 will therefore eliminate allsympathetic outflow.Lesions between T1 and T6 will preserve sympathetic tone inthe head and upper extremities but deny it to the adrenals andthe lower extremities.Lesions between T6 and the lumbar cord will preserveadrenal innervation but denervate the lower extremities.
  • 8. Vasomotor Effects Sympathetic fibers leave the spinal cord between T1 and L2 Transection at the level of T1 Sharp fall in blood pressure(MBP 40mmhg) Cold and cyanosed extremities Skin become s red ,dry and scaly and bed sores may develops
  • 9. Stage of reflex activity If the patient survives the stage of spinal shock, some developments occurs in chronological orders(after 3 weeks period) smooth muscles regain functional activity first of all automatic evacuation of urinary bladder and bowel Sympathetic tone of blood vessels is regained BP is restored to normal In skin sweating starts, bed sores heal up
  • 10. Stage of reflex activity Skeleton muscle tone than recovers slowelyafter 3-4 weeks Tone of flexor muscle s return first leading to PARAPLEGIA IN FLEXION(both lower limbs are in state of flexion) Reflex activity begins to return after few weeks of recovery of muscle tone
  • 11. The recovery of reflex excitability may be due tothe development of denervation hypersensitivityto the mediators released by the remainingspinal excitatory endings. Another possibility forwhich there is some evidence is the sprouting ofcollaterals from existing neurons, with theformation of additional excitatory endings oninterneurons and motor neurons.
  • 12. The first reflex response to appear as spinal shockwears off in humans is often a slight contraction ofthe leg flexors and adductors in response to anoxious stimulus. In some patients, the knee jerkreflex recovers first. The interval between cordtransection and the return of reflex activity is about2 weeks in the absence of any complications, but ifcomplications are present it is much longer. It is notknown why infection, malnutrition, and othercomplications of SCI inhibit spinal reflex activity.Once the spinal reflexes begin to reappear afterspinal shock, their threshold steadily drops.
  • 13. Stage of Reflex Activity  Flexor reflexes return first Babiski’s reflex(sign) positive.  Extensor reflexes return after a variable period of 1-5 weeks of appearance of flexor reflexes  Initially knee jerk appears,then ankle jerk may return
  • 14. Stage of Reflex Activity Mass reflex can be elicited in some cases Scratching of the skin over the lower limbs or the anterior abdominal wall Spasm of flexor muscles of both the limbs, evacuation of bowel and bladder and profuse sweating below the level of lesion
  • 15. Stage of Reflex Failure The failure of reflex activity may occur when general condition of the patient starts deteriorating due to malnutrition ,infections Reflexes become more difficult to elicit The threshold for stimulus increases. Mass reflex is abolished, and The muscles become extremely flaccid and undergo wasting.
  • 16. Incomplete trasection ofspinal cord Spinal cord is gravely injured but doesnt suffer from complete transection(i.e. few tracts are intact) Clinical stages Stage of spinal shock(same as complete transection ) Stage of reflex activity(differ remarkably) Stage of reflex failure(same as complete transection )
  • 17. Stage of Reflex Activity Tone appears in extensor muscle first(c.f. complete transection in which tone appears in flexor muscle first) Paraplegia in extension (c.f. complete transection in which paraplegia in flexion is seen) Because some of the descending tract(vestibulospinal and reticulospinal tracts) may escape injury activity in extensor motor neurons
  • 18. Stage of Reflex Activity Extension reflexes(strech reflexes) return first(c.f. complete transection in which flexor reflexes return first) Reflexes which can be elicited Phillipson reflex Extensor thrust reflex Crossed extensor reflex Mass reflex is not elicited
  • 19. Brown-Sequard syndrome (spinal cord hemisection)Major Symptoms 1. ipsilateral UMN syndrome below the level of lesion 2. ipsilateral LMN syndrome at the level of lesion 3. ipsilateral loss of discriminative touch sensation and conscious proprioception below the level of lesion (posterior white column lesion) 4. contralateral loss of pain and temperature sensation below the level of lesion (spinothalamic tractlesion)
  • 20. Upper Motor Neuron (UMN) vs. Lower Motor Neuron (LMN) Syndrome UMN syndrome LMN SyndromeType of Paralysis Spastic Paresis Flaccid ParalysisAtrophy No (Disuse) Atrophy Severe AtrophyDeep Tendon Reflex Increase Absent DTRPathological Reflex Positive Babinski Sign AbsentSuperficial Reflex Absent PresentFasciculation and Absent Could beFibrillation Present
  • 21. Syringomyelia, Hematomyelia Lesion - central canal of spinal cord - gradually extended to peripheral part ofthe cord Symptom - initial symptom is bilateral loss of pain (compression of anterior whitecommissure) - variety of symptoms appear according to the lesion extended fromcentral canal
  • 22. syringomyelia Cause: Extensive growth of neuroglial tissue around the central canal of the spinal cord with cavity formation Common site: cervical region sign and symptoms in hand and arms. Loss of pain and temperature.(dissociated anaesthesia) Touch is retained (as it has double pathway) At the level of lesion: initially flaccid paralysis of the muscle(usually of the hands) Later spastic paralysis of the legs.
  • 23. •Tabes Dorsalis - common variety of neurosyphilis - posterior column and spinal posterior rootlesion - loss of discriminative touch sensation andconscious proprioception below the level of lesion - posterior column ataxia - lancinating pain (a stabbing or piercingsensation)due to stimulation of pain fibers - loss of deep tendon reflex (DTR)
  • 24. •Tabes Dorsalis - perforating ulcers at pressure points.Anesthesia round the anus,over legs, upper chestand hands(due to involvement of dorsal nerve rootsin lumbosacral and cervicothoracic region) -loss of position sense and vibration sense.
  • 25. The cause of spinal shock is uncertain. Cessation oftonic bombardment of spinal neurons by excitatoryimpulses in descending pathways undoubtedly plays arole, but the subsequent return of reflexes and theireventual hyperactivity also have to be explained. Therecovery of reflex excitability may be due to thedevelopment of denervation hypersensitivity to themediators released by the remaining spinal excitatoryendings. Another possibility for which there is someevidence is the sprouting of collaterals from existingneurons, with the formation of additional excitatoryendings on interneurons and motor neurons.
  • 26. The first reflex response to appear as spinal shockwears off in humans is often a slight contraction ofthe leg flexors and adductors in response to anoxious stimulus. In some patients, the knee jerkreflex recovers first. The interval between cordtransection and the return of reflex activity is about2 weeks in the absence of any complications, but ifcomplications are present it is much longer. It is notknown why infection, malnutrition, and othercomplications of SCI inhibit spinal reflex activity.Once the spinal reflexes begin to reappear afterspinal shock, their threshold steadily drops.
  • 27. Neural Control of Blood Pressure and Blood FlowComplete lesions above T1 will therefore eliminate allsympathetic outflow.Lesions between T1 and T6 will preserve sympathetic tone inthe head and upper extremities but deny it to the adrenals andthe lower extremities.Lesions between T6 and the lumbar cord will preserveadrenal innervation but denervate the lower extremities.

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