A) Complete transaction of the spinal cord:

Causes:

o Acute (sudden):

- Trauma e.g. fracture spines, gun shots or stab wound.

- Inflammation of the spinal cord.

- Thrombosis or hemorrhage in its blood supply.

o Chronic (gradual): Tumors or prolapsed disc.

Effects: depends upon the site of the lesion, if the lesion is in the cervical segment above the origin of the phrenic nerves, death occurs within few minutes due to failure of respiration (as in hanging). If the lesion is below the origin of the phrenic nerve the patient will live and pass in the following stages:

1) Stage of shock (spinal shock):

Duration of spinal shock: In human; 2-6 weeks, it is shorter in lower animals.

Effects of spinal shock:

A- Permanent effects: (do not recover at all).

1- Loss of all sensation (cutaneous, deep and visceral) below the level of the lesion due to lesion of ascending tracts.

2- Paralysis of all muscles below the level of the lesion due to lesion of the descending motor tracts (pyramidal and extra-pyramidal tracts).
B- Temporal effects: ( can recover in the next stage)

1) ABP ↓ : due to interruption of vaso-motor tract from the VCC in the medulla to the spinal vaso-motor centers in the spinal cord.

2) Loss of all reflexes:

· Loss of superficial reflexes: Abdominal, cremastric, planter and withdrawal reflexes.

· Loss of stretch reflex: loss of MT.

· Loss of deep reflexes: All tendon jerks are lost.

· Loss of visceral reflexes:

a) Micturition reflex is lost, so urine accumulates inside the bladder until its pressure exceeds the tone of the internal urethral sphincter where the urine begins to dribble drop by drop, without control and sensation. This condition is known as “ retention with overflow “.

b) Defecation reflex is lost, so feces accumulates in the rectum until its pressure exceeds the tone of the internal anal sphincter where the feces pass to outside, without control and sensation. This condition is known as ” retention with overflow “.

3) Body temperature ↓ due to loss of MT and ↓ ABP.

4) Appearance of bed sores (cutaneous ulcers) in the pressure areas e.g. in the back and gluteal region due to:

- Ischemia which results from: ↓ blood flow which results from ↓ ABP and loss of MT, also results from compression of B.V in the recumbent position.

- Loss of pain sensation.

- Bacterial contamination.

Causes of spinal shock: It is due to interruption of supra spinal facilitatory impulses coming from the higher centers to activate the lower spinal centers.

Treatment of spinal shock:

1- Good nursing to prevent bed sores by:

- Change the position of the patient every 2 hours maximally.

- Massage of the pressure areas with alcohol to harden the skin.

2- Antibiotics to prevent bed sores and urinary tract infection which are the common cause of death in this condition.

2) Stage of reflex activity:

During this stage the spinal centers recover their own activity and result in some recovery e.g.:

1- ABP gradually rises to normal due to recovery of spinal vaso-motor centers.

2- Recovery of reflexes:

a. Superficial reflexes: Withdrawal reflex is the first reflex to reappear. Planter reflex becomes Babiniski sign with dorsi-flexion of big toe and fanning of the outer 4 toes.

b. Stretch reflex: MT↑ in 2 phases:

- Early, MT ↑ in flexors more than extensors. So, the LL are flexed → paraplegia in flexion.

- Late, MT ↑ in extensors more than flexors. So, the LL are extended → paraplegia in extension.

c. Deep reflexes: The tendon jerks appear again, but it is weaker in the early phase and exaggerated (↑) in the late phase, when the MT ↑ in extensors.

d. Visceral reflexes: reappear in the form of:

a) Automatic micturition in which stretch of the bladder with urine send afferent impulses to micturition center, which send efferent impulses to evacuate the bladder without control and without sensation.

b) Automatic defecation in which stretch of the rectum with feces send afferent impulses to defecation center, which send efferent Impulses to evacuate rectum without control and without sensation.

e. Appearance of new reflexes e.g. ” mass reflex “ which occurs in late cases of the disease. In this condition scratching the skin leads to wide spread response e.g. flexion of both LL, contraction of anterior abdominal wall, profuse sweating, ↑ABP and may be micturition and defecation. It is due to irradiation which occur between the spinal centers below the level of the lesion due to ↓ resistance.

3- Body temperature ↑ to normal due to ↑ MT and ↑ ABP.

4- Bed sores slightly recovered due to ↑ ABP and ↑ MT which lead to ↑ blood flow to the affected area.

3) Stage of failure of reflex activity:

It is due to inhibition of spinal centers by toxemia which results from bed sores and urinary tract infection. It this stage all conditions return back again as in stage of shock:

o ABP ↓ again.

o All reflexes are lost; MT, tendon jerks are lost. Micturition and defecation becomes retention with overflow.

o Body temperature ↓.

o Bed sores ↑ which leads to toxemia and death.

B) Hemi-section of spinal cord: (Brown Sequard syndrome)

It results from damage of one or more segments at one side only of the spinal cord. Hemi-section causes the following effects:

1- Above the level of the lesion:

Cutaneous hyperesthesia (i.e. sensitivity to touch, pain and temperature) in a narrow area of skin in the same side. It is due to irritation of dorsal roots above the level of the lesion.

2- At the level of the lesion:

- Loss of all sensations (cutaneous, deep and visceral) due to lesion of all sensory nerves.

- LMNL due to lesion of AHCs and motor nerves.

- Loss of all reflexes (superficial, deep and visceral) due to interruption of reflex arc.

3- Below the level of the lesion:

a) At the same side:

1- Loss of all sensations carried by Gracil & Cuneate tracts which ascend in the same side.

- Loss of fine touch ( tactile localization, tactile discrimination, steriognosis and texture of material).

- Loss of deep or proprioceptive sensations (sense of position, sense of movement, sense of deep pressure, sense of muscle stretch and muscle tension).

- Loss of vibration sense.

2- UMNL due to lesion of pyramidal & extra-pyramidal tracts.

3- VD of B.V in the same side. Later on, recovery of spinal vaso-motor centers returns it to normal.

b) In the opposite side:

Loss of sensations carried by spin-thalamic tracts ( lateral and ventral) which cross and ascends in the opposite side. So, there is loss of:

- Crude touch sensation (carried by V. Sp. Th. tract).

- Pain and temperature sensations (carried by L. Sp. Th. tract).

C) Quadrant lesion of the spinal cord:

a) Posterior quadrant lesion: Leads to

1- Lesion of Gracil & Cuneate tracts which results in:

· Loss of fine touch sensations.

· Loss of proprioceptive sensations.

· Loss of vibration sense.

2- Lesion of pyramidal tract: UMNL.

3- Lesion of inhibitory extra-pyramidal tracts: ↑ MT (spastic paralysis)

b) Anterior quadrant lesion: leads to:

1- Lesion of spino-thalamic tracts (ventral & lateral), this results in loss of crude touch, pain and temperature sensations from the opposite side below the level of the lesion.

2- Lesion of AHCs: LMNL on the same side, at the level of the lesion.

3- Lesion of facilitatory extra-pyramidal tracts: ↓MT (flaccid paralysis).

D) Sryngo-myelia:

It means dilatation of the central canal of the spinal cord due to gradual erosion of the grey matter around it. It is more common in the cervical region, but it may extend downward into the thoracic segments or upwards into the brain stem. Sryngo-myelia produces the following:

Early: Damage of the spino-thalamic tracts ( lateral & ventral) which cross in front of the central canal, this leads to loss of pain, temperature and crude touch at the same level on both sides.

Late: progressive erosion leads to damage of the AHCs at the same level on both sides → LMNL.

More late: Erosion extend and may lead to damage of the ascending and descending tracts in the white matter:

o Lesion of ascending tracts → loss of sensations below the level of the lesion.

o Lesion of descending tracts → UMNL below the level of the lesion.

o Lesion of the descending vaso- motor tract → VD of BV below the level of the lesion.