RISK FACTORS

Gender

Gender disparity in injury are consistent and persistent. Gender patterns in injury do not

follow typical social justice analysis of health, in that men are at greater risk. Lifestyle and
behavioral risks as well as masculine socialization merit consideration. (Martin JA, Hamilton BE,
Sulton PD, et al., 2010).

The predisposition of male gender to injuries due to car accidents, fall, sports related
injury and others will likely to cause damage to the spinal cord due to fracture of the spinal
column and eventually it will cause compression or scaring to the said organ.

Age (65 years old and above)

With aging, degenerative changes will occur in all systems of the body, affecting now the
functions of the skeletal system. Bones become more fragile and less able to perform its
mechanical function, and the calcium stored in the bones are often depleted (Chan and Duque,
2012).

Loss of bone with aging is a universal phenomenon affecting both men and women and
is associated with reduced strength and increased fracture risk. In tubercular bone, bone loss
may occur as a result of increased remodeling rate and or a negative remodeling balance at the
level of individual bone remodeling unit of basic multicellular unit. And remodeling is defined as
bone metabolism or the process where mature bone tissue is removed from the skeleton,
followed by bone formation, where a new bone tissue is form.

The remodeling balance is determined by the amount of reabsorbed and that

subsequently formed, hence a negative balance may result to increased resorption, reduced
bone formation or combination of the two and possible trabecular thinning and preservation of
trabecular microarchitecture (P. Szalc, 2011).
Risky Behavior

Involving oneself to any form of risky activities predisposes oneself to injury and will
increase the possibility of spinal cord injury specially if the affected area is located at the posterior
part of a person.

Having a bone or joint disorder

There are several bone diseases that can weaken the bones due to destruction, this can
now cause deformity to the affected area. Thus, if affectation of the spinal area is suspected it
can cause injury or damage to the spinal cord.

PATHOPHYSIOLOGY

Injury to the spinal cord caused by (1) overstretching of the spinal column, (2) fracture
due to traumatic accident may lead to compression or damage. This is due now to the bone
fragments that have scattered along the site of injury. Also, another cause of SCI will be (3) non-
traumatic which involve diseases in the joint and bones that causes different neurologic deficits
depending on the severity and extent of damage and location of the injury in the spinal cord.

Injury to the spinal cord can rupture the blood vessels that supply the organ, this leads to
hemorrhage, thus, a decrease blood supply in the area. The decrease in blood supply to the area
is further aggravated by compression of blood vessels due to the accumulation of serous
component and vasoconstriction of the blood vessels in an attempt to prevent further bleeding.
This event, compromised blood flow, now causes hypoxia or hypoperfusion. When the
vasospastic blood vessels relax, reperfusion of the ischemic area will lead to the production of
free radicals NO (Nitric oxide) and ONOO- (Peroxynitrite), these are unstable isomers structure of
nitrate (Zouhal H.C, 2008). Creation of free radicals can cause oxidative degradation of lipid
membrane in the neural cell, that leads to depolarization and released of glutamate in the
synaptic area in the nerves. Excessive glutamate level stimulates the NMDA/AMPA/Kainite
receptors, thus there will be an influx of calcium ion into the cell, hence excitotoxicity and neural
damage that will lead to apoptosis or cell death.
 Rise in the cytoplasmic calcium levels can also triggers cascade of lytic enzymes such as
calpain, a protein belonging to the family of calcium-dependent, non-lysosomal cysteine
proteases (proteolytic enzymes) expressed ubiquitously in mammals and many other organisms,
phospholipase, an enzyme that release fatty acids from the second carbon group of glycerol and
lipoxygenase, an iron-containing enzyme. These lytic enzymes promote the disruption of
mitochondrial election transport chain function, a process that produces energy for the cell.
dysfunction to the mitochondrial function decrease the production of ATP and eventually cell
death will follow due to the decreased energy production that needed by the cell to function
effectively.

Phospholipase A2 also recognizes the sn-2 acyl bond of phospholipids and catalytically
hydrolyzes the bond releasing arachidonic acid arachidonic acid and further converted to
prostaglandin synthetase that is responsible for the production of PGF2 (prostacyclin alpha) a
potent vasoconstrictor, TXA2 ( thromboxane A2) which regulates the production of platelet, and
PGI2 ( prostacyclin). These prostaglandin lipid molecules induce ischemia of the gray matter, and
produces more free radicals that causes peroxidation of neural lipid membranes and the
production of lactic acid that can damage the cell in the affected area.

When there is a damage in the spinal cord tissue, there will be invasion of phagocytic cells
such as macrophages, neutrophils and also monocyte. These cells are responsible in the
production of cytokines and chemokine that will further exacerbate inflammation, therefore
edema will occur, and it can compress and eventually compromises the blood supply going to the
spinal cord.

The affectation of autonomic nervous system will most likely to happens when the
damage involves the thoracic nerve and the above nerve, because spinal nerves controlling the
sympathetic nervous system response are located at this region, hence there will be a loss of
sympathetic tone and vasodilation of blood and artery will be its later effect. Vasodilation affects
the distribution of blood into the different part of the body including the spinal cord arteries,
hence, there will be cellular decreased 02 supply leading to decreased tissue perfusion. This
cascade effect can contribute to the aggravation of the condition.
 Depending on the severity and extent of damage or injury to the spinal cord, spinal cord
injury can be classifying as complete wherein there will be a complete motor and sensory
function to the level below the injury. Incomplete SCI implies there is some residual motor or
sensory function below the level of injury. The prognosis for return of function is better in an
incomplete injury because of preservation of axonal function. Incomplete injuries may manifest
in a variety of patterns but can organized in to certain patterns or syndromes that occur more
frequently and reflect the predominant area of the cord involved.

Central cord syndrome is a condition called central cord syndrome occurs when injury is
predominantly in the central gray or white matter of the cord. Because the corticospinal tract
fiber are organized with those controlling the arms located more centrally and those controlling
the leg located more laterally, some external transmission may remain intact. Motor function of
the upper extremities is affected, but lower extremities may not be affected or may be affected
to a lesser degree with some sparing of sacral sensation. Bowel, bladder, and sexual function are
affected by various degree.

Anterior cord syndrome is usually caused by damage from infarction of the anterior spinal
artery, resulting in the damage to anterior two thirds of the spinal cord. The deficit result in loss
of motor function provided by the corticospinal tracts and loss of pain and temperature sensation
from damage to the lateral spinothalamic tracts. the effect is a loss of voluntary motor function,
proprioception loss from the ipsilateral side of the body, and contralateral loss of pain and
temperature sensation for all levels below the lesion.

Conus medullary syndrome involves damage to the conus medullaris or the sacral cord
and lumbar nerve roots in the neural canal. Functional deficits resulting from this type of injury
usually result in flaccid bowel and bladder function, as well as altered sexual function. Sacral
segment occasionally show preserved reflexes if only the conus is affected. Motor function in the
legs and feet may be impaired without significant sensory impairment. Damage to the
lumbosacral nerve roots in the spinal canal usually results in LMN and sensory neuron damage
know as cauda equine syndrome. Functional deficits present as various patterns of asymmetric
flaccid paralysis, sensory impairment and pain.