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 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
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 Severe Atrophy

Deep Tendon Reflex Increase Absent DTR

Pathological Reflex Positive Babinski Sign Absent

Superficial Reflex Absent Present

Fasciculation and Absent Could be

Fibrillation Present
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.