Transection of the spinal cord

 Complete Transection  Incomplete Transection  Hemi section

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

Clinical stages
 Stage of spinal shock  Stage of reflex activity,  Stage of reflex failure

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

Spinal Shock
In 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.

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

Complete lesions above T1 will therefore eliminate all sympathetic outflow. Lesions between T1 and T6 will preserve sympathetic tone in the head and upper extremities but deny it to the adrenals and the lower extremities. Lesions between T6 and the lumbar cord will preserve adrenal innervation but denervate the lower extremities.

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

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

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

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.

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.

Stage of Reflex Activity
 Flexor reflexes return first reflex(sign) positive.

Babiski’s

 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

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

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.

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 )

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

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

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 tract lesion)

Upper Motor Neuron (UMN) vs. Lower Motor Neuron (LMN) Syndrome
UMN syndrome LMN Syndrome

Type of Paralysis

Spastic Paresis

Flaccid Paralysis

Atrophy

No (Disuse) Atrophy
Increase

Severe Atrophy
Absent DTR Absent Present Could be Present

Deep Tendon Reflex

Pathological Reflex Positive Babinski Sign Superficial Reflex Absent Fasciculation and Fibrillation Absent

Syringomyelia, Hematomyelia
Lesion

- central canal of spinal cord - gradually extended to peripheral part of the cord Symptom - initial symptom is bilateral loss of pain (compression of anterior white commissure) - variety of symptoms appear according to the lesion extended from central canal

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.

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

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

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.

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.

Neural Control of Blood Pressure and
Blood Flow

Complete lesions above T1 will therefore eliminate all sympathetic outflow. Lesions between T1 and T6 will preserve sympathetic tone in the head and upper extremities but deny it to the adrenals and the lower extremities. Lesions between T6 and the lumbar cord will preserve adrenal innervation but denervate the lower extremities.

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