Spinal shock Physiology

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Transcript of Spinal shock Physiology

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Transection of the spinal cordComplete Transection

Incomplete Transection

Hemi section

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Complete transection of spinal cord 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

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Clinical stages

Stage of spinal shock Stage of reflex activity, Stage of reflex failure

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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

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Spinal ShockIn all vertebrates, transection of the spinal cord is followed by a period of spinal shock during which all spinal reflex responses are profoundly depressed. Subsequently, reflex responses return and become hyperactive. The duration of spinal shock is proportionate to the degree of encephalization of motor function in the various species. In frogs and rats it lasts for minutes; in dogs and cats it lasts for 1 to 2 h; in monkeys it lasts for days; and in humans it usually lasts for a minimum of 2 wk.

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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

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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.

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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

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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

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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

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The recovery of reflex excitability may be due to the development of denervation hypersensitivity to the mediators released by the remaining spinal excitatory endings. Another possibility for which there is some evidence is the sprouting of collaterals from existing neurons, with the formation of additional excitatory endings on interneuron's and motor neurons.

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The first reflex response to appear as spinal shock wears off in humans is often a slight contraction of the leg flexors and adductors in response to a noxious stimulus. In some patients, the knee jerk reflex recovers first. The interval between cord transection and the return of reflex activity is about 2 weeks in the absence of any complications, but if complications are present it is much longer. It is not known why infection, malnutrition, and other complications of SCI inhibit spinal reflex activity. Once the spinal reflexes begin to reappear after spinal shock, their threshold steadily drops.

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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

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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

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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.

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Incomplete trasection of spinal cord Spinal cord is gravely injured but

doesn't 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 )

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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

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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

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Brown-Sequard syndromeBrown-Sequard syndrome (spinal cord (spinal cord hemisection)hemisection)

Major SymptomsMajor Symptoms 1. ipsilateral 1. ipsilateral UMN syndrome below UMN syndrome below the the

level of lesionlevel of lesion

2. ipsilateral 2. ipsilateral LMN syndrome LMN syndrome at at the level of the level of

lesionlesion

3. ipsilateral loss of 3. ipsilateral loss of discriminative touch discriminative touch

sensation sensation and and

conscious proprioceptionconscious proprioception belowbelow the the

level of lesionlevel of lesion

(posterior white column lesion)(posterior white column lesion)

4. 4. contralateralcontralateral loss of loss of pain and pain and

temperaturetemperature sensation sensation belowbelow the level of lesion the level of lesion (spinothalamic (spinothalamic

tract lesion)tract lesion)

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Type of Paralysis Type of Paralysis Spastic ParesisSpastic Paresis Flaccid Paralysis Flaccid Paralysis

Atrophy Atrophy No (Disuse) AtrophyNo (Disuse) Atrophy Severe Severe AtrophyAtrophy

Deep Tendon Reflex Deep Tendon Reflex Increase Increase Absent DTR Absent DTR

Pathological Reflex Pathological Reflex Positive Positive Babinski Babinski Sign Sign Absent Absent

Superficial Reflex Superficial Reflex AbsentAbsent PresentPresent

Fasciculation and Fasciculation and AbsentAbsent Could be Could beFibrillation Fibrillation PresentPresent

UMN syndrome UMN syndrome LMN LMN SyndromeSyndrome

Upper Motor Neuron (UMN) vs. Lower Motor Neuron (LMN) Upper Motor Neuron (UMN) vs. Lower Motor Neuron (LMN) SyndromeSyndrome

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Syringomyelia, Syringomyelia, HematomyeliaHematomyelia LesionLesion

- central canal of spinal cord- central canal of spinal cord - gradually extended to - gradually extended to peripheral part of the cordperipheral part of the cord

SymptomSymptom

- initial symptom is bilateral - initial symptom is bilateral

loss of painloss of pain (compression of anterior (compression of anterior white commissure)white commissure)

- variety of symptoms appear- variety of symptoms appear according to the lesion according to the lesion extended from central canalextended from central canal

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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.

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•Tabes DorsalisTabes Dorsalis - common variety of neurosyphilis- common variety of neurosyphilis - posterior column and spinal - posterior column and spinal posterior root lesionposterior root lesion - loss of discriminative touch - loss of discriminative touch sensation and conscioussensation and conscious proprioception below the level of proprioception below the level of lesionlesion - posterior column ataxia- posterior column ataxia - lancinating pain (- lancinating pain (a stabbing or a stabbing or piercing sensationpiercing sensation)due to stimulation of )due to stimulation of pain fiberspain fibers - loss of deep tendon reflex (DTR)- loss of deep tendon reflex (DTR)

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•Tabes DorsalisTabes Dorsalis - perforating ulcers at pressure - perforating ulcers at pressure points.points.Anesthesia round the anus,over legs, Anesthesia round the anus,over legs, upper chest and handsupper chest and hands(due to (due to involvement of dorsal nerve roots in involvement of dorsal nerve roots in lumbosacral and cervicothoracic regionlumbosacral and cervicothoracic region)) -loss of position sense and vibration -loss of position sense and vibration sense.sense.

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The cause of spinal shock is uncertain. Cessation of tonic bombardment of spinal neurons by excitatory impulses in descending pathways undoubtedly plays a role, but the subsequent return of reflexes and their eventual hyperactivity also have to be explained. The recovery of reflex excitability may be due to the development of denervation hypersensitivity to the mediators released by the remaining spinal excitatory endings. Another possibility for which there is some evidence is the sprouting of collaterals from existing neurons, with the formation of additional excitatory endings on interneurons and motor neurons.

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The first reflex response to appear as spinal shock wears off in humans is often a slight contraction of the leg flexors and adductors in response to a noxious stimulus. In some patients, the knee jerk reflex recovers first. The interval between cord transection and the return of reflex activity is about 2 weeks in the absence of any complications, but if complications are present it is much longer. It is not known why infection, malnutrition, and other complications of SCI inhibit spinal reflex activity. Once the spinal reflexes begin to reappear after spinal shock, their threshold steadily drops.

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Neural Control of Blood Pressure andBlood Flow

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.

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