Lesions of Spinal Cord

7/29/2019 Lesions of Spinal Cord

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LESIONS OFSPINAL CORD:SECTION OF DORSAL NERVE ROOT:

If only 1 dorsal nerve root is cut noappreciable sensory loss. Why?


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Features of section ofdorsal nerve root: 1) ATONIA in muscles of affected area.

2) LOSS OF SUPERFICIAL & DEEP

REFLEXES. (reflex arc is broken).

3) movements of affected part are not

normal, because of loss of proprioceptive

impulses to parts of brain, which controlmovements.


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Section of ventral nerveroot: Ventral root of spinal nerve contains

somatic motor fibers & autonomic nerve

fibers. So in section, both of these fibersare cut.


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Features of section ofventral nerve root: 1) LOSS OF VOLUNTARY MOVEMENTS

(FLACCID PARALYSIS) in affected part, lossof muscle tone.

2) LOSS OF SUPERFICIAL & DEEPREFLEXES (reflex arc is broken).

These features are due to paralysis ofSOMATIC MOTOR FIBERS.

If lesion is in thoracic & lumbar segments ofspinal cord, then SYMPATHETIC NERVEFIBERS are damaged.


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Features of lesion ofsympathetic nerve fibers: 1) VASODILATATION: Due to loss of

vasomotor tone. (sympathetic tone on

blood vessels). 2) FALL IN PERIPHERAL RESISTANCE

& B.P:

3) LOSS OF SWEATING: in effectedpart, the skin becomes dry.


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SECTIONS OF SPINALCORD: A) COMPLETE TRANSECTION.

B) HEMISECTION OR BROWN

SEQUAARD SYNDROME.

C) INCOMPLETE TRANSECTION OF

SPINAL CORD.


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COMPLETE TRANSECTIONOF SPINAL CORD: CAUSES:

1) FRACTURE / DISLOCATION of

vertebral column due to stab wound orbullet wound.

2) due to expanding TUMOR.

3) ACCIDENT.


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When there is complete transaction,

features are divided in 3 stages:

1) STAGE OF FLACCIDITY (SPINALSHOCK).

2) STAGE OF REFLEX ACTIVITY.

3) STAGE OF FAILURE OF REFLEXACTIVITY.


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1) STAGE OF FLACCIDITY(SPINAL SHOCK): Immediately after the transaction, below

the level of transaction, there is:

COMPLETE FLACCID PARALYSIS. LOSS OF ALL SENSATIONS.

LOSS OF SKELETAL MUSCLE TONE.

LOSS OF SMOOTH MUSCLE TONE. LOSS OF TONE IN SPHINCTERS

URINARY & FECAL INCONTINENCE.


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IF TRANSECTION IS AT T1 OR ABOVE

LOSS OF VASOMOTOR TONE

FALL IN TPR & B.P LIMBS CLOD, BLUE & DRY.

BED SORES MAY APPEAR.


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CAUSE OF SPINALSHOCK: LOSS OF TONIC FACILITATORY

EFFECT OF HIGHER CENTRES ON

SPINAL CORD NEURONS, throughCorticospinal, Reticulospinal &

Vestibulospinal tracts.

Lasts for 2-3 weeks. Spinal cord neurons are functionless.


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2) STAGE OF REFLEXACTIVITY: * TONE RETURNS FIRST IN THE SMOOTH

MUSCLE & SPHINCTERS.

When tone appears in urinary & analsphincters retention of urine & feces.

Vasomotor tone may appear because SPINAL

CORD SYMPATHETIC PRE-GANGLIONIC

NEURONS learn to function without theexcitatory effect of higher centers.


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When vasomotor tone appears, then:

B.P increases

Blood flow to limbs improves.

Skin changes in the limbs recover.


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TONE also begins to appear in SKELETAL

MUSCLE.

It first appears in the FLEXORS, but tone is notequal to normal one, because, MYOTATIC

REFLEX (STRETCH REFLEX) is not normally

strong in the absence of excitatory effect from

higher centers. So legs are moderately flexed. THIS IS AN IMPORTANT FEATURE &

CALLED: PARAPLEGIA IN FLEXION.


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Muscles start contraction during reflex action.

There may be spontaneous involuntarycontractions involving mainly FLEXORS.

FLEXOR REFLEX / WITHDRAWAL REFLEXcan be elicited.

It is also accompanied by CROSSED

EXTENSOR REFLEX, but response is lessthan normal.

There is MASS REFLEX.


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MASS REFLEX: When skin over anterior abdominal wall or on the legs

is stretched or scratched RESPONSE:

CONTRACTION OF ANTERIOR ABDOMINAL WALL

MUSCLES. CONTRACTION OF FLEXORS IN THE LEGS.

EVACUATION OF URINARY BLADDER even if itcontains small amount of urine. This is due toincreased intra-vesical pressure resulting fromcontraction of anterior abdominal wall muscles.

Sweating also returns.


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In males erection can occur onphysical stimulation of genitalia.

Muscle tone returns in EXTENSORS. After months of transaction there is

UMN type of paralysis, below the level oflesion.

Sensory loss not recovered.

Muscles cant contract voluntarily.


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Automatic bladder & automatic defecation:because reflexes can be activated by highercenters.

When urine accumulates bladder reflexinitiated emptying of bladder but novoluntary control.

If patients skin is scratched around anus &bladder defecation & urination occurs.

Training is done.

Reflexes do not recover stage of failure ofreflex activity.


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3) STAGE OF FAILURE OFREFLEX ACTIVITY: Severe infection or toxemia condition

worsens.

Different reflexes

difficult to elicit. (elicited athigher intensity of stimuli).

Response during these reflexes is decreased.

Muscle tone decreases.

Bed sores appear.

Patient worse & worse.


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HEMISECTION OF SPINALCORD OR BROWN SEQUARDSYNDROME: CAUSES:

Fractures

Tumors accidents

FEATURES: 3 components:

1) above the level of hemisection. 2) at the level of hemisection.

3) below the level of hemisection.


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NO MOTOR LOSS, HYPERESTHESIA

LMN PARALYSIS,ANESTHESIA

UMN PARALYSIS

LOSS OF DCT

Sensations

(fine touch,

vibration,

proprioception,

tactile discrimination.

NO MOTOR LOSS

NO SENSORY LOSS

NO MOTOR LOSSNO SENSORY LOSS

NO MOTOR LOSS

LOSS OF STT Sensations(pain, temperature,

crude touch, tickle, itch)

LEFT HEMISECTION OF SPINAL CORD


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Above the level: No motor loss on same side & on

opposite side.

hyperesthesia: ipsilaterally, due toirritation of cut ends of sensory nerve

fibers.

No sensory loss on opposite side.


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NO MOTOR LOSS, HYPERESTHESIA

LMN PARALYSIS,ANESTHESIA

UMN PARALYSIS

LOSS OF DCT

Sensations

(fine touch,

vibration,

proprioception,

tactile discrimination.

NO MOTOR LOSS

NO SENSORY LOSS

NO MOTOR LOSSNO SENSORY LOSS

NO MOTOR LOSS

LOSS OF STT Sensations(pain, temperature,

crude touch, tickle, itch)

LEFT HEMISECTION OF SPINAL CORD


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At the level: Ipsilaterally, there is LMN type of

paralysis, due to damage to ventral horn

motor neurons (they are lower motorneurons).

Ipsilaterally, there is a band of anesthesia

(loss of all sensations on same side). There is no motor or sensory loss on

opposite side.


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Below the level: Motor loss: On ipsilateral side UMN paralysis (due to damage to

pyramidal & extra-pyramidal tracts. On the opposite side no motor loss. Sensory loss: On ipsilateral side loss of fine touch, 2 pt tactile

discrimination, vibration & proprioception (damage todorsal column medial leminiscal system).

On opposite side pain & temperature, tickle, itch & crudetouch.

This sensory loss is 2-3 dermatomes below the level ofspinal cord, because of oblique crossing over of STT toopposite side.


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Sensations carried by dorsal columns lost

on same side.

Sensations carried by spino-thalamic tract

lost on opposite side.

In BSS, when we concentrate on motor losson

same side (ipsilaterally), on opposite side,

sensory lossis important, because of loss ofpain & temperature sensations, which matter

the patient.


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This syndrome was named by Brown

Sequard as:

* PREDOMINENT MOTOR LOSSIPSILATERALLY &

PREDOMINENT SENSORY LOSS

CONTRALATERALLY.


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If hemisection of spinal cord involves

thoracic segments, then sympathetic

fibers are involved & then Fall in B.P

V.D

Fall in TPR

Loss of sweating in effected part.


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INCOMPLETE TRANSECTIONOF SPINAL CORD: Damage to spinal cord tissue is between

COMPLETE TRANSECTION &HEMISECTION.

CAUSES:

Fracture / dislocation of vertebral columndue to stab or bullet wound.

Accident.

Tumor (expanding tumor).


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STAGES: Same stages as in complete transaction.

1) STAGE OF SPINAL SHOCK:

Same features as in completetransaction.

2) STAGE OF REFLEX ACTIVITY:

Some differences from the features in

complete transection.


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Differences:

1) Skeletal muscle tone appears 1st .

*PARAPLEGIA IN EXTENSION.

CAUSE:

In incomplete transection VST &

Ret.ST escape (these are excitatory for

extensors).


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2) Extensor thrust reflex:

Demonstration:

Pt is lying on back & leg is flexed on knee. Examiner with palm of hand, exerts upward

pressure on sole of flexed leg.

Leg becomes extended due to contraction of

extensors of leg & thigh.

That is why EXTENSOR THRUST.


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PHILIPSONS REFLEX:

One leg of patient is gently flexed, the

other leg becomes extended. After sometime, flexed leg becomes

extended, while extended leg becomesflexed.

Alternate stepping movements arepossible reflexly, but not voluntarily.


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3) RECOVERY:

During recovery stage, below the level of

transection UMN paralysis. Sensations dont recover.


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SYRINGOMYELIA: Disease in which excessive

overgrowth of neuro-glial tissue with

cavity formation in grey matter aroundcentral canal of spinal cord.

SYRINGO-BULBIA:

If disease effects the brain stem.


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features: 1) DISSOCIATED ANESTHESIA

2) LMN PARALYSIS

3) UMN PARALYSIS


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DISSOCIATED ANESTHESIA:

Loss of pain & temperature sensation.

Touch, vibration & proprioception intact.

Loss of pain & temp due to damage to lat STtract mainly in anterior commissure, wherefibers cross over.

Withdrawal reflex absent (loss of pain / temp)

severe tissue damage. If patient is SMOKER BURNT FINGERS!!!

(typical feature).


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LMN paralysis:

In muscles of hand or maximally, arm &

shoulder.


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UMN paralysis:

Of legs.


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TABES DORSALIS:(NEURO-SYPHILIS) CAUSITIVE ORGANISM:

SYPHILIS ORGANISM destruction of

sensory nerve fibers at entrance of dorsalnerve root into spinal cord.

TARGET: lower thoracic & lumbar

segments of spinal cord.


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Features: 1) SEVERE STABBING PAIN.

2) LOSS OF PAIN.

3) LOSS OF PROPRIOCEPTION. 4) HYPOTONIA.

5) TENDON JERKS ABSENT (ankle &

knee jerks affected 1st

). 6) ATONIC BLADDER.

7) ARGYL ROBERTSON PUPIL.


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SEVERE STABBING PAIN:

In legs.

Hypersensitivity to touch & temperature.

Parasthesias (numbness).

Severe pain due to stimulation of dorsal

nerve fiber by the organism.


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LOSS OF PAIN:

Later on due to complete destruction.


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LOSS OF PROPRIOCEPTION:

Ataxia (movements not coordinated

cant walk properly).


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ATONIC BLADDER:

Abnormality of micturition.

Sensory nerve fibers damaged.

Reflex arc for micturition not complete.

Urine accumulates in bladder distention

of bladder bladder becomes atonic overflow dribbling.


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ARGYL ROBERTSON PUPIL (ARP):

Pupil constricts during accomodation or

near response BUT Pupil fails to constrict in response to light

SO

(ACCOMODATION REFLEX +) but

(LIGHT REFLEX ) because the fibersinvolved in light reflex are damaged.

Lesions of Spinal Cord

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