Spinal Cord Injury: Treatments and Rehabilitation (cont.)
What Happens When the Spinal Cord Is Injured?
A spinal cord injury usually begins with a sudden, traumatic blow to the
spine that fractures or dislocates vertebrae. The damage begins at the moment of
injury when displaced bone fragments, disc material, or ligaments bruise or tear
into spinal cord tissue. Axons are cut off or damaged beyond repair, and neural
cell membranes are broken. Blood vessels may rupture and cause heavy bleeding in
the central grey matter, which can spread to other areas of the spinal cord over
the next few hours.
Within minutes, the spinal cord swells to fill the entire cavity of the
spinal canal at the injury level. This swelling cuts off blood flow, which also
cuts off oxygen to spinal cord tissue.
Blood pressure drops, sometimes
dramatically, as the body loses its ability to self-regulate. As blood pressure
lowers even further, it interferes with the electrical activity of neurons and
axons. All these changes can cause a condition known as spinal shock that can
last from several hours to several days.
Although there is some controversy among neurologists about the extent and
impact of spinal shock, and even its definition in terms of physiological
characteristics, it appears to occur in approximately half the cases of spinal
cord injury, and it is usually directly related to the size and severity of the
injury. During spinal shock, even undamaged portions of the spinal cord become
temporarily disabled and can't communicate normally with the brain. Complete
paralysis may develop, with loss of reflexes and sensation in the limbs.
The crushing and tearing of axons is just the beginning of the devastation
that occurs in the injured spinal cord and continues for days. The initial
physical trauma sets off a cascade of biochemical and cellular events that kills
neurons, strips axons of their myelin insulation, and triggers an inflammatory
immune system response. Days or sometimes even weeks later, after this second
wave of damage has passed, the area of destruction has increased - sometimes to
several segments above and below the original injury - and so has the extent of
disability.
Changes in blood flow cause ongoing damage
Changes in blood flow in and around the spinal cord begin at the injured
area, spread out to adjacent, uninjured areas, and then set off problems
throughout the body.
Immediately after the injury, there is a major reduction in blood flow to the
site, which can last for as long as 24 hours and becomes progressively worse if
untreated. Because of differences in tissue composition, the impact is greater
on the interior grey matter of the spinal cord than on the outlying
white
matter.
Blood vessels in the grey matter also begin to leak, sometimes as early as 5
minutes after injury. Cells that line the still-intact blood vessels in the
spinal cord begin to swell, for reasons that aren't yet clearly understood, and
this continues to reduce blood flow to the injured area. The combination of
leaking, swelling, and sluggish blood flow prevents the normal delivery of
oxygen and nutrients to neurons, causing many of them to die.
The body continues to regulate blood pressure and
heart rate during the first
hour to hour-and-a-half after the injury, but as the reduction in the rate of
blood flow becomes more widespread, self-regulation begins to turn off. Blood
pressure and heart rate drop.
Excessive release of neurotransmitters kills nerve cells
After the injury, an excessive release of neurotransmitters (chemicals that
allow neurons to signal each other) can cause additional damage by overexciting
nerve cells.
Glutamate is an excitatory neurotransmitter, commonly used by nerve cells in
the spinal cord to stimulate activity in neurons. But when spinal cells are
injured, neurons flood the area with glutamate for reasons that are not yet well
understood. Excessive glutamate triggers a destructive process called excitotoxicity, which disrupts normal processes and kills neurons and other
cells called oligodendrocytes that surround and protect axons.
An invasion of immune system cells creates inflammation
Under normal conditions, the blood-brain barrier (which tightly controls the
passage of cells and large molecules between the circulatory and central nervous
systems) keeps immune system cells from entering the brain or spinal cord. But
when the blood-brain barrier is broken by blood vessels bursting and leaking
into spinal cord tissue, immune system cells that normally circulate in the
blood - primarily white blood cells - can invade the surrounding tissue and
trigger an inflammatory response. This inflammation is characterized by fluid
accumulation and the influx of immune cells -
neutrophils,
T-cells,
macrophages,
and monocytes.
Neutrophils are the first to enter, within about 12 hours of injury, and they
remain for about a day. Three days after the injury, T-cells arrive. Their
function in the injured spinal cord is not clearly understood, but in the
healthy spinal cord they kill infected cells and regulate the immune response.
Macrophages and monocytes enter after the T-cells and scavenge cellular debris.
The up side of this immune system response is that it helps fight infection
and cleans up debris. But the down side is that it sets off the release of
cytokines - a group of immune system messenger molecules that exert a malign
influence on the activities of nerve cells.
For example, microglial cells, which normally function as a kind of on-site
immune cell in the spinal cord, begin to respond to signals from these
cytokines. They transform into macrophage-like cells, engulf cell debris, and
start to produce their own pro-inflammatory cytokines, which then stimulate and
recruit other microglia to respond.
Injury also stimulates resting astrocytes to express cytokines. These
"reactive" astrocytes may ultimately participate in the formation of scar tissue
within the spinal cord.
Whether or not the immune response is protective or destructive is
controversial among researchers. Some speculate that certain types of injury
might evoke a protective immune response that actually reduces the loss of
neurons.
Free radicals attack nerve cells
Another consequence of the immune system's entry into the CNS is that
inflammation accelerates the production of highly reactive forms of oxygen
molecules called free radicals.
Free radicals are produced as a by-product of normal cell metabolism. In the
healthy spinal cord their numbers are small enough that they cause no harm. But
injury to the spinal cord, and the subsequent wave of inflammation that sweeps
through spinal cord tissue, signals particular cells to overproduce free
radicals.
Free radicals then attack and disable molecules that are crucial for cell
function - for example, those found in cell membranes - by modifying their
chemical structure. Free radicals can also change how cells respond to natural
growth and survival factors, and turn these protective factors into agents of
destruction.
Nerve cells self-destruct
Researchers used to think that the only way in which cells died during spinal
cord injury was as a direct result of trauma. But recent findings have revealed
that cells in the injured spinal cord also die from a kind of programmed cell
death called apoptosis, often described as cellular
suicide, that happens days
or weeks after the injury.
Apoptosis is a normal cellular event that occurs in a variety of tissues and
cellular systems. It helps the body get rid of old and unhealthy cells by
causing them to shrink and implode. Nearby scavenger cells then gobble up the
debris. Apoptosis seems to be regulated by specific molecules that have the
ability to either start or stop the process.
For reasons that are still unclear, spinal cord injury sets off apoptosis,
which kills oligodendrocytes in damaged areas of the spinal cord days to weeks
after the injury. The death of oligodendrocytes is another blow to the damaged
spinal cord, since these are the cells that form the myelin that wraps around
axons and speeds the conduction of nerve impulses. Apoptosis strips myelin from
intact axons in adjacent ascending and descending pathways, which further
impairs the spinal cord's ability to communicate with the brain.
Secondary damage takes a cumulative toll
All of these mechanisms of secondary damage - restricted blood flow,
excitotoxicity, inflammation, free radical release, and apoptosis - increase the
area of damage in the injured spinal cord. Damaged axons become dysfunctional,
either because they are stripped of their myelin or because they are
disconnected from the brain. Glial cells cluster to form a scar, which creates a
barrier to any axons that could potentially regenerate and reconnect. A few
whole axons may remain, but not enough to convey any meaningful information to
the brain.
Researchers are especially interested in studying the mechanisms of this wave
of secondary damage because finding ways to stop it could save axons and reduce
disabilities. This could make a big difference in the potential for recovery.
Next: What Are the Immediate Treatments for Spinal Cord Injury? »
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