Spinal Cord
Injury (SCI)
Dr. Katie Dabrowski, PT, DPT
Let’s review some anatomy first
Spinal Cord Structure
• The SC extends to the level of
L1/L2 vertebrae
• There are 31 pairs of spinal
nerves
• 8 cervical nerves (C1-C8)
• 12 thoracic nerves (T1-T12)
• 5 lumbar nerves (L1-L5)
• 5 sacral nerves (S1-S5)
• 1 coccygeal nerve
Spinal Cord
Structure
• The first 7 cervical nerves (C1-C7)
exit above their respective
vertebra
• C8 exits between C7 and T1
vertebrae
• All other spinal nerves exit below
their respective vertebra
Spinal Cord
Structure
• Conus medullaris = the tapered
lower end of the spinal cord at
L1/L2
• Cauda equina = the remaining
spinal nerves that are not
considered the spinal cord
(remember, the spinal cord
formally ends at L1/L2)
Conus medullaris
Cauda equina (Latin for “horse’s tail)
Spinal cord and its relation to the spinal column
Spinal Cord
Structure
*Has meninges continuous
with the brain
Dura Mater
Arachnoid Mater
Pia Mater
Internal
Configuration
Internal
configuration
• Each level of the spinal
cord has a slightly different
configuration
• But the organization is the
same:
• The grey matter is organized
internally, as the “butterfly”
pattern
• White matter is in the
surrounding areas
Spinal Cord Cross Section
I. Grey Matter
a. Anterior (ventral) horn
-Motor innervation to skeletal
muscle
-Specific motor distribution in the
anterior horn (proximal muscles
represented medially; distal
muscles represented more
laterally)
*This example is in the lumbar region
*This exists similarly in the cervical region, but of course,
muscles for the upper extremity
Spinal Cord Cross Section
II. White Matter
Ascending and descending tracts
-Ascending tracts are sensory
tracts carrying information from
the outside world into the spinal
cord and into the brain
-Descending tracts are motor
tracts carrying information from
the brain, to the spinal cord, and
to the muscles of the body for
motor function
Now we can
learn more
about SCI
Spinal Cord
Injuries
Traumatic:
• Motor vehicle/motorcycle collisions
(39.2%)
• Falls (28.3%)
• Violence/GSW (14.6%)
• Sports (8.2%)
• Diving into shallow water (9.7%)
Non-traumatic:
• Cancer
• Multiple sclerosis
• Inflammation of spinal cord
• Arthritis
Complete vs. Incomplete Injuries
• A complete spinal cord injury causes permanent damage to the area
of the spinal cord that is damage, and the areas below it
• Paraplegia or quadriplegia are results of complete spinal cord injuries
• Essentially there is no ability for the brain to send signals to the area below
the site of the injury, therefore no motor or sensory function
• An incomplete spinal cord injury refers to partial damage to the
spinal cord – a person will retain some feeling and/or motor function
below the injury site
American
Spinal Injury
Association
(ASIA) Scoring
System
How SCIs are scored – we won’t get in-
depth on this, but feel free to ask
questions if you have any.
Types of Incomplete SCIs: A few
examples
Central Cord Syndrome:
-Affects center of the spinal cord
-Results mostly in loss of sensation and motor movement in the
arms
-Legs are usually less affected
Anterior Cord Syndrome:
-Affects the anterior portion of the spinal cord
-Interferes with motor and sensory pathways of touch, pain,
and temperature
Brown-Sequard Syndrome:
-Rare, but is a lesion of one half of the spinal cord that results in
loss of motor and sensory functions below the injury site
Cervical Spinal Cord Injuries
• Cervical portion of the spine = 7 cervical
vertebrae (C1-C7) and nerves C1-C8
• Because the cervical spine is the closest to the
brain and affects the largest portion of the
body, cervical spinal cord injuries are the most
severe.
• An injury in the cervical region results in
quadriplegia, meaning there is limited or
absent feeling or movement below the
shoulders/neck.
Cervical Spinal
Cord Injuries:
C1-C4
• Most severe spinal cord injury
• Paralysis in arms, hands, trunk, and legs
• Potential inability to breathe independently, cough, or
control bowel/bladder
• Impaired/reduced ability to speak
• Quadriplegia (all 4 limbs affected)
• Potential need for complete assistance with activities of
daily living (eating, dressing, bathing, getting in/out of bed)
• May be able to use a power chair with special controls
• Likely needs 24-hour care
• Watch this video here on a C3 level of injury
Cervical Spinal
Cord Injuries:
C5
• Can raise arms and bend elbows
• Likelihood of some or total paralysis of wrists, hands, trunk,
and legs
• Can speak and use diaphragm, but beathing is weakened
• Little or no voluntary control of bowel or bladder
• Can use power wheelchair to be independent
• An example of a C5 injury
Cervical Spinal
Cord Injuries:
C6
• Can raise arms and bend elbows and move wrists
• Likelihood of some or total paralysis of hands, trunk, and
legs
• Can speak and use diaphragm, but beathing is weakened
• Little or no voluntary control of bowel or bladder, but may
be able to manage independently with catheters due to
hand function
• Can move in and out of wheelchair and bed with assistive
equipment
• Watch a person with a C6 injury transfer from bed to
wheelchair
Cervical Spinal
Cord Injuries:
C6, C7, C8
C6:
• Can raise arms and bend elbows and move wrists
• Likelihood of some or total paralysis of hands, trunk, and legs
• Can speak and use diaphragm, but beathing is weakened
• Little or no voluntary control of bowel or bladder, but may be able to
manage independently with catheters due to some hand function
• Can move in and out of wheelchair and bed with assistive equipment
• Watch a person with a C6 injury transfer from bed to wheelchair
C7:
• Can straighten arm and have normal movement of shoulders
• More independent
• Can drive an adaptive vehicle
• Little or no voluntary control of bowel or bladder, but may be able to
manage independently with catheters due to some more hand function
C8:
• Can grasp and release objects with hand
• Same as above, otherwise
Thoracic Spinal Cord Injuries
• Thoracic portion of the spine = 12 thoracic
vertebrae (T1-T12) and nerves T1-C12
• Nerves T1-T5 affect muscles of upper chest,
mid back, and abdominals; these nerves also
help control the rib cage, lungs, and
diaphragm for breathing function
• Nerves T6-T12 affect muscles of abdominals
and back. These nerves are important for
balance and posture, as well as coughing.
Thoracic
Spinal Cord
Injuries
T1-T5:
• Typically affect abdominal and lower back muscles, as well
as the legs, and result in paraplegia
• Arm and hand function is usually normal
T6-T12:
• Paraplegia
• Little or no voluntary control of bowel/bladder, but can
manage on their own with special equipment
In general:
• Have normal arm, hand, and upper-body movement
• Use a manual wheelchair
• Learn to drive a modified car
• Stand in standing frame or walk with braces
Lumbar Spinal Cord Injuries
• Lumbar portion of the spine = 5 lumbar
vertebrae (L1-L5) and nerves L1-L5
• In general, loss of function in hips and legs but
upper extremities and trunk are fine
• Little or no voluntary control of
bowel/bladder, but can manage on heir own
with special equipment
• Depending on leg strength, may require
wheelchair or walking with braces
Sacral Spinal Cord Injuries
• Sacral portion of the spine = sacrum = 5 bones
fused together.
• S1 nerves affect hips and groin
• S2 nerves affect backs of thighs
• S3 nerves affect buttocks
• S4 nerves affect perineal area
• Some loss of function hips and legs
• Little or no voluntary control of bladder/bowel
but can manage with special equipment
• Affects sex organs
• Usually can walk
Pathophysiology of SCI
Pathophysiology
of SCI
Primary injury to the spinal cord typically
occurs via one of these mechanisms – and
can be traumatic (gun shot wound, fall,
knife) or atraumatic (medical condition,
inflammation, cancer):
• Transection
• Contusion
• Compression
But what really causes lasting damage are
the secondary injuries of spinal cord injury.
Secondary Injury of SCI
• Secondary injury begins
within minutes following the
initial primary injury
• It continues for weeks or
months, causing progressive
damage of spina cord tissue
surrounding the legion site
• It is suggested that these
biochemical processes are
more damaging to the
spinal cord than the primary
injury itself
Secondary
Injury of SCI:
Acute Phase
• Begins immediately following SCI
• Includes:
• Vascular damage
• Ionic imbalance
• Neurotransmitter accumulation (excitotoxicity)
• Free radical formation
• Calcium influx
• Lipid peroxidation
• Inflammation
• Edema
• Necrotic cell death
Secondary
Injury of SCI:
Sub-Acute
Phase
• Includes:
• Apoptosis
• Demyelination of surviving axons
• Wallerian degeneration
• Axonal dieback/retraction
• Matrix remodeling
• Formation of a glial scar around the injury site
Secondary
Injury of SCI:
Chronic
Phase
• Includes:
• Formation of a cystic cavity
• Progressive axonal dieback/retraction
• Maturation of the glial scar
Let’s dive deeper
into pathophysiology
of SCI secondary
injury
I. Vascular
injury,
ischemia,
and hypoxia
• Disruption of SC vascular supply and
decreased perfusion of blood to the area is
one of the earliest consequences of injury
• Shock in SCI patients due to excessive
bleeding and neurogenic shock results in
even less SC perfusion, and therefore
ischemia
• Small spinal arteries often rupture
II. Ionic
imbalance,
excitotoxicity,
and oxidative
damage
• Within a few minutes after primary SCI, the
combination of direct cellular damage and
ischemia/hypoxia triggers a significant rise
of extracellular glutamate (the main
excitatory neurotransmitter in the CNS)
• This results in calcium influx inside of cells,
and this calcium overload results in
oxidative damage and mitochondrial failure
• Increased calcium also damages white
matter, astrocytes, oligodendrocytes, and
myeline sheaths
• Within the first few hours after injury,
myelin density decreases and calcium-
mediated apoptosis occurs
II. Ionic
imbalance,
excitotoxicity,
and oxidative
damage
• Mitochondrial calcium overload also results
in ATP depletion, therefore disabling the
ATP-dependent Na+/K+ pump that is so
crucial for maintaining ion balance in
neurons
• This causes an increase in intracellular Na+,
and also further increases intracellular Ca2+
• The more the cell depolarizes because of
the Na+ and Ca2+ infiltration, more Cl- and
water enters the cell, causing swelling and
edema and furthering the ionic imbalance
• Axons are more susceptible to damage
when ionic imbalance is in the picture
II. Ionic
imbalance,
excitotoxicity,
and oxidative
damage
• SCI also results in the production of free
radicals and nitric oxide (NO)
• This leads to glycolysis failure, ATP
depletion, and cell death
• Oxidation of lipids and proteins marks one
of the key mechanisms of secondary injury
following SCI
III. Cell
Death
• Following SCI, neurons and glial cells die via
necrosis as a result of the mechanical
damage at the time of primary injury
• This continues along through the acute and
subacute stages of injury
• Necrosis occurs due to: Toxic blood
component accumulation, glutamate
excitotoxicity and ionic imbalance, ATP
depletion, inflammatory molecule increases,
and free radicle formations
• Apoptosis occurs within hours after primary
injury – it occurs primarily in the cells that
survive the primary injury
IV. Neuroinflammation
• Inflammation can be both beneficial and
detrimental for the outcome of SCI
• 0-2 days post injury: Recruitment of microglia,
astrocytes, and neutrophils to injury site
• 3 days post injury: Recruitment of
macrophages, B- and T-lymphocytes to injury
site to produce antibodies
• In SCI, the production of antibodies
against injured spinal cord tissue
exacerbates neuroinflammation and
causes further tissue destruction
• Inflammation is of course present in the
beginning stages of injury, but can persist for
the remainder of a patient’s life
IV.
Neuroinflammation:
Astrocytes
• Astrocytes aren’t an immune cell per se, but
they play vital roles in the neuroinflammatory
process in CNS injury and disease
• In the normal CNS, astrocytes play a major role
in maintaining CNS homeostasis via:
• Maintaining structure and function of
blood-brain barrier
• Provide nutrients and growth factors to
neurons
• Remove excess fluids, ions, and
neurotransmitters
• Astrocytes react to CNS injury via:
• Increasing cytokine and chemokine
production to increase inflammatory
molecules
V. Glial Scar
• Traumatic SCI triggers the formation of a glial
scar tissue around the injury epicenter
• The glial scar begins to form within the first
hours after SCI, and remains chronically in the
spinal cord tissue
• It serves as a protected barrier that prevents
the spread of infiltrating immune cells into
adjacent spinal segments
• Despite this protective role of the glial scar, its
evolution and persistence in the subacute and
chronic stages of injury is considered an
inhibitor for spinal cord repair and regeneration
What do we
see
clinically?
What do we
see
clinically?
What do we
see
clinically?
What do we
see
clinically?
A success story!
• One of my favorite patients of all times!
• He came into the SCI unit with a central cord injury at the C6 level,
meaning his major deficits were in his upper extremities but he also had
extreme spasticity and ataxia of his lower extremities, so he could not
walk.
• For the majority of our time working together, he was in a power
wheelchair and we worked on him learning to move around his bed, sit
at the edge of the bed, transfer to/from the bed and wheelchair, and
eventually stand with a LOT of support in front of a mirror.
• By the end of our time together, he was able to stand in the parallel bars
(again, with a LOT of support)
• On his last day of inpatient rehab with me, he told me his final goal was
to stand and hug me.
• A year later, I visited him and his family and was greeted by him walking
to open the door of a restaurant, completely unassisted. Yeah, I may
have cried a little…
Permission was given for using these photos.
Optional Discussion Board Post: Q&A
• I’ve included an optional discussion board post for any further
questions on SCI
• I’ve worked extensively in SCI rehab and it is by far one of my favorite
populations to treat – please don’t hesitate if you have any questions
at all or curiosities you want to explore!
