LESIONS OF SPINAL CORD:

SECTION OF DORSAL NERVE ROOT: If only 1 dorsal nerve root is cut no appreciable sensory loss. Why?

 This is because of overlapping of adjacent dermatomes. To have sensory loss, at least 3 sensory roots should be damaged. When there is damage to 3 dorsal nerve roots loss of all sensations in the effected area. Fine touch, vibration, proprioception (D.C.T), Tickle & itch (A.S.T.T), Pain (L.S.T.T).

Features of section of dorsal 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 control movements.

Section of ventral nerve root:

Ventral root of spinal nerve contains somatic motor fibers & autonomic nerve fibers. So in section, both of these fibers are cut.

Features of section of ventral nerve root:

1) LOSS OF VOLUNTARY MOVEMENTS (FLACCID PARALYSIS) in affected part, loss of muscle tone. 2) LOSS OF SUPERFICIAL & DEEP REFLEXES (reflex arc is broken). These features are due to paralysis of SOMATIC MOTOR FIBERS. If lesion is in thoracic & lumbar segments of spinal cord, then SYMPATHETIC NERVE FIBERS are damaged.

Features of lesion of sympathetic 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 effected part, the skin becomes dry.

SECTIONS OF SPINAL CORD:

A) COMPLETE TRANSECTION. B) HEMISECTION OR BROWN SEQUAARD SYNDROME. C) INCOMPLETE TRANSECTION OF SPINAL CORD.

COMPLETE TRANSECTION OF SPINAL CORD:

CAUSES: 1) FRACTURE / DISLOCATION of vertebral column due to stab wound or bullet wound. 2) due to expanding TUMOR. 3) ACCIDENT.

 When there is complete transaction, features are divided in 3 stages: 1) STAGE OF FLACCIDITY (SPINAL SHOCK). 2) STAGE OF REFLEX ACTIVITY. 3) STAGE OF FAILURE OF REFLEX ACTIVITY.

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.

 IF TRANSECTION IS AT T1 OR ABOVE LOSS OF VASOMOTOR TONE FALL IN TPR & B.P LIMBS CLOD, BLUE & DRY. BED SORES MAY APPEAR.

CAUSE OF SPINAL SHOCK:

LOSS OF TONIC FACILITATORY EFFECT OF HIGHER CENTRES ON SPINAL CORD NEURONS, through Corticospinal, Reticulospinal & Vestibulospinal tracts. Lasts for 2-3 weeks. Spinal cord neurons are functionless.

2) STAGE OF REFLEX ACTIVITY:

* TONE RETURNS FIRST IN THE SMOOTH MUSCLE & SPHINCTERS. When tone appears in urinary & anal sphincters retention of urine & feces. Vasomotor tone may appear because SPINAL CORD SYMPATHETIC PRE-GANGLIONIC NEURONS learn to function without the excitatory effect of higher centers.

When vasomotor tone appears, then: B.P increases Blood flow to limbs improves. Skin changes in the limbs recover.

 TONE also begins to appear in SKELETAL MUSCLE. It first appears in the FLEXORS, but tone is not equal 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.

 Muscles start contraction during reflex action. There may be spontaneous involuntary contractions involving mainly FLEXORS. FLEXOR REFLEX / WITHDRAWAL REFLEX can be elicited. It is also accompanied by CROSSED EXTENSOR REFLEX, but response is less than normal. There is MASS REFLEX.

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 it contains small amount of urine. This is due to increased intra-vesical pressure resulting from contraction of anterior abdominal wall muscles. Sweating also returns.

 In males erection can occur on physical stimulation of genitalia. Muscle tone returns in EXTENSORS. After months of transaction there is UMN type of paralysis, below the level of lesion. Sensory loss not recovered. Muscles cant contract voluntarily.

 Automatic bladder & automatic defecation: because reflexes can be activated by higher centers. When urine accumulates bladder reflex initiated emptying of bladder but no voluntary control. If patients skin is scratched around anus & bladder defecation & urination occurs. Training is done. Reflexes do not recover stage of failure of reflex activity.

3) STAGE OF FAILURE OF REFLEX ACTIVITY:

Severe infection or toxemia condition worsens. Different reflexes difficult to elicit. (elicited at higher intensity of stimuli). Response during these reflexes is decreased. Muscle tone decreases. Bed sores appear. Patient worse & worse.

HEMISECTION OF SPINAL CORD OR BROWN SEQUARD SYNDROME:

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.

LEFT HEMISECTION OF SPINAL CORD

NO MOTOR LOSS NO SENSORY LOSS NO MOTOR LOSS NO SENSORY LOSS

NO MOTOR LOSS, HYPERESTHESIA

LMN PARALYSIS, ANESTHESIA

NO MOTOR LOSS LOSS OF STT Sensations (pain, temperature, crude touch, tickle, itch)

UMN PARALYSIS LOSS OF DCT Sensations (fine touch, vibration, proprioception, tactile discrimination.

Above the level:

No motor loss on same side & on opposite side. hyperesthesia: ipsilaterally, due to irritation of cut ends of sensory nerve fibers. No sensory loss on opposite side.

LEFT HEMISECTION OF SPINAL CORD

NO MOTOR LOSS NO SENSORY LOSS NO MOTOR LOSS NO SENSORY LOSS

NO MOTOR LOSS, HYPERESTHESIA

LMN PARALYSIS, ANESTHESIA

NO MOTOR LOSS LOSS OF STT Sensations (pain, temperature, crude touch, tickle, itch)

UMN PARALYSIS LOSS OF DCT Sensations (fine touch, vibration, proprioception, tactile discrimination.

At the level:
Ipsilaterally, there is LMN type of paralysis, due to damage to ventral horn motor neurons (they are lower motor neurons). Ipsilaterally, there is a band of anesthesia (loss of all sensations on same side). There is no motor or sensory loss on opposite side.

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 to dorsal column medial leminiscal system). On opposite side pain & temperature, tickle, itch & crude touch. This sensory loss is 2-3 dermatomes below the level of spinal cord, because of oblique crossing over of STT to opposite side.

 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 loss on same side (ipsilaterally), on opposite side, sensory loss is important, because of loss of pain & temperature sensations, which matter the patient.

 This syndrome was named by Brown Sequard as: * PREDOMINENT MOTOR LOSS IPSILATERALLY & PREDOMINENT SENSORY LOSS CONTRALATERALLY.

 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.

INCOMPLETE TRANSECTION OF SPINAL CORD:

Damage to spinal cord tissue is between COMPLETE TRANSECTION & HEMISECTION. CAUSES: Fracture / dislocation of vertebral column due to stab or bullet wound. Accident. Tumor (expanding tumor).

STAGES:
Same stages as in complete transaction. 1) STAGE OF SPINAL SHOCK: Same features as in complete transaction. 2) STAGE OF REFLEX ACTIVITY: Some differences from the features in complete transection.

Differences: 1) Skeletal muscle tone appears 1st . *PARAPLEGIA IN EXTENSION. CAUSE: In incomplete transection VST & Ret.ST escape (these are excitatory for extensors).

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.

 PHILIPSONS REFLEX: One leg of patient is gently flexed, the other leg becomes extended. After sometime, flexed leg becomes extended, while extended leg becomes flexed. Alternate stepping movements are possible reflexly, but not voluntarily.

 3) RECOVERY: During recovery stage, below the level of transection UMN paralysis. Sensations dont recover.

SYRINGOMYELIA:
Disease in which excessive overgrowth of neuro-glial tissue with cavity formation in grey matter around central canal of spinal cord. SYRINGO-BULBIA: If disease effects the brain stem.

features:
1) DISSOCIATED ANESTHESIA 2) LMN PARALYSIS 3) UMN PARALYSIS

DISSOCIATED ANESTHESIA: Loss of pain & temperature sensation. Touch, vibration & proprioception intact. Loss of pain & temp due to damage to lat ST tract mainly in anterior commissure, where fibers cross over. Withdrawal reflex absent (loss of pain / temp) severe tissue damage. If patient is SMOKER BURNT FINGERS!!! (typical feature).

 LMN paralysis: In muscles of hand or maximally, arm & shoulder.

 UMN paralysis: Of legs.

TABES DORSALIS: (NEURO-SYPHILIS)

CAUSITIVE ORGANISM: SYPHILIS ORGANISM destruction of sensory nerve fibers at entrance of dorsal nerve root into spinal cord. TARGET: lower thoracic & lumbar segments of spinal cord.

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.

SEVERE STABBING PAIN: In legs. Hypersensitivity to touch & temperature. Parasthesias (numbness). Severe pain due to stimulation of dorsal nerve fiber by the organism.

 LOSS OF PAIN: Later on due to complete destruction.

 LOSS OF PROPRIOCEPTION: Ataxia (movements not coordinated cant walk properly).

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.

 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 fibers involved in light reflex are damaged.