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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.
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