2. - Neil Armstrong
DEFINITION
Spinal cord injury is defined as traumatic damage
to the spinal cord or nerves at the end of the spinal
canal.
This affects the conduction of sensory and motor
signals across the site of the lesion.
3. CLINICALLY RELEVANT ANATOMY
• It begins as a downward extension of medulla oblongata at the
level of C1 vertebra and extend down to the level of lower
border of L1 vertebra.
• The lowest part of spinal cord is conical and is called as conus
medularis.
• Conus continuous below with a fibrous cord called filum
terminale.
4. You have 31 pairs of nerves and nerve roots in your spinal
cord. These include:
▪ Eight cervical nerve pairs (nerves starting in your neck
and running mostly to your face and head).
▪ Twelve thoracic nerve pairs (nerves in your upper body
that extend to your chest, upper back and abdomen).
▪ Five lumbar nerve pairs (nerves in the low back that
run to your legs and feet).
▪ Five sacral nerve pairs (nerves in the low back
extending into the pelvis).
5. The spinal cord contains longitudinally oriented spinal tracts (white matter) surrounding
central areas (gray matter) where most spinal neuronal cell bodies are located.
The grey matter is organized into segments comprising sensory and motor neurons.
Axons from spinal sensory neurons enter and
axons from motor neurons leave the spinal
cord via segmental nerves or roots.
Each root receives sensory information from
skin areas called dermatomes. Similarly, each
root innervates a group of muscles called a
myotome.
8. • Varying degrees of paralysis,
including
tetraplegia/quadriplegia, and
paraplegia
• Difficulty breathing
• Problems with bladder and
bowel function
• Frequent infections
• Bedsores
• Chronic pain
• Headaches
• Changes in mood or personality
• Loss of libido or sexual function
• Loss of fertility
• Nerve pain
• Chronic muscle pain
SYMPTOMS
9. PATHOPHYSIOLOGY
• Compression or shearing of spinal cord results in destruction of both grey &
white matter.
• Damage is greatest at the level of damage & may extend few segments above or
below.
• Central part of the cord suffers more damage when compared to peripheral
parts.
• Neurologic damage that results from trauma is only partly due to initial damage
to cord neurons.
10. Following trauma, within hours process of progressive tissue destruction begins
within cord → significantly extend region of neuronal damage.
Secondary reaction include: ischemia, edema, demyelination & necrosis of spinal
cord.
Secondary effects: hemorrhage, ischemia, local electrolyte derangements,
inflammatory reactions & local accumulation of various bio-reactive substances.
Later, necrotic region of spinal cord undergoes resorption & replaced by scar tissue
or formation of cysts or cavities.
11. CLASSIFICATION
There are two types of spinal cord injuries,
1. Complete spinal cord injuries
2. incomplete spinal cord injuries.
Complete SCIs are the most serious and occur when the spinal cord is injured,
eliminating the brain’s ability to send signals below the injury site.
For an injury impacting the lumbar spinal cord, for example, it can lead to paralysis
below the waist while preserving your motor functions in your upper body and arms
(paraplegia).
For complete injuries in the cervical spine, however, this often leads to a loss of motor
function in the lower and upper body (tetraplegia, which is also known as quadriplegia).
12. • All tracts ascending below the level of the lesion & all tracts descending
from above the level of lesion are interrupted.
• Both motor & sensory functions below the level of lesion are affected.
• Radicular pain, segmental paresthesias & localised vertebral pain at the
level.
• Initial spinal shock followed by hypertonia, hyperreflexia, spasticity
below the level of lesion.
• Bladder & bowel disturbances because of disruption of ANS
disruption.
• Spastic bladder, constipated bowel.
• Anhydrosis, trophic changes, impaired temperature control &
vasomotor instability below level of lesion
13. Incomplete SCIs commonly result from compression or damage being inflicted to
the spinal cord that reduces the brain’s ability to send signals below the injury site.
Because of the partially-compromised condition of the spinal cord, incomplete injuries
vary drastically from person to person. Some sensory and motor functions may be
slightly compromised in some or nearly eliminated in others. Additionally, some
incomplete injuries result in triplegia, or the loss of sensation and movement in one arm
and both legs.
Some of the most common types of incomplete or partial spinal cord injuries include:
Anterior cord syndrome:
This type of injury, to the front of the spinal cord, damages the motor and sensory
pathways in the spinal cord. You may retain some sensation, but struggle with
movement.
14. • Reflects destruction of anterior 2/3rds
of the spinal cord.
• Damage to anterior gray matter containing alpha motor neurons, as well as
corticospinal & spinothalamic tracts of anterior & lateral white matter.
• Pain & temperature & motor control below the level of lesion are lost.
• Common causes ischemia (anterior spinal artery) & trauma.
• Flexion type of injury or actue IVDP
Posterior cord syndrome:
• Damage restricted to dorsal columns.
• Impaired fine touch, vibratory sense & joint position sense.
• Usually cause of tabes dorsalis, CNS form of syphilis characterised by
marked sensory ataxia caused by loss of dorsal proprioceptive pathways.
• Rarely cause of trauma – hyperextension type.
15. Central cord syndrome:
This injury is an injury to the center of the cord, and damages nerves that carry signals
from the brain to the spinal cord. Loss of fine motor skills, paralysis of the arms, and
partial impairment in the legs are common. Some survivors also suffer a loss of bowel
or bladder control, or lose the ability to sexually function.
Spinothalamic tracts which decussate through central cord are the first ones to get
damaged – pain & temperature loss.
Normal tactile sense.
Associated with severe hyperextension injury to the neck.
Brown-Sequard syndrome:
This variety of injury is the product of damage to one side of the spinal cord. The
injury may be more pronounced on one side of the body; for instance, movement
may be impossible on the right side, but may be fully retained on the left. The degree
to which Brown-Sequard patients are injured greatly varies from patient to patient.
16. • Lateral cord syndrome.
• Ipsilateral loss of fine touch, vibratory
sense & position sense along with
ipsilateral upper motor neuron deficits.
• Pain & temperature loss on
contralateral side.
• Penetrating injuries(stab)
17. Pain:
• Three main types of pain are seen in patients with spinal cord injury.
• Local pain- damage to local bony & ligamentous structures surrounding the
cord.
• Radicular pain- damage to sensory nerve roots. Excruciating, dermatome wise
distribution.
• Diffuse aching or burning pain- attributed to dysfunctional spinal cord pain
pathways.
CLINICAL FEATURES
18. Sensory abnormalities:
• Paresthesias due to abnormal activity in dorsal root & dorsal column
pathways that convey touch.
• Sensory loss at the level & below the lesion.
Muscle weakness:
• LMN type of weakness at the level of lesion.
• Atrophy, hypotonia, hyporeflexia or areflexia & fasciculations in involved
muscle.
• UMN type of weakness below the level of lesion.
• Hyperreflexia, spasticity & abnormal reflex pattern e.g. babinski’s sign.
• Weakness in neurally intact muscles can be seen due to disuse atrophy.
19. Abnormal reflexes & muscle tone:
Due to Corticospinal involvement.
Urinary incontinence & other forms of visceral dysfunction:
• Neurogenic bladder
• Loss of thermoregulatory function
• Respiratory muscle weakness during phrenic nerve damage
Pathways for volitional control of micturition and automatic control of
breathing, sweating & blood pressure are located in ventral half of lateral
column, ventral to corticospinal tracts.
20. Spinal shock:
• It is a state of areflexia characterized by loss of tone, loss of reflexes and total
inactivity.
• Sudden loss of connection between the higher centers and the spinal cord
could be the cause of shock.
• The period of spinal shock last for 24 hours to weeks but usually resolved
within 24-48hr.
21. Neurogenic bladder:
1. Atonic bladder
Loss of tone in detrusor muscle.
It also called flaccid neurogenic bladder or hypoactive neurogenic
bladder.
Caused by destruction of sensory nerve fiber (pelvic)of bladder.
Absence of stretch signals , detrusor muscle loses the tone and
become flaccid
Now urine overflows in drops as and when it enters the bladder
It is called overflow incontinence or overflow dribbling.
22. 2. Automatic bladder
• It is characterized by hyperactive micturition reflex, loss of voluntary
control .
• Complete transection of spinal cord above sacral segments , the
urinary bladder loses the tone and results in overflow incontinence.
• Damage to the spinal cord above micturition center which is S2,S3,
S4
3. Uninhibited neurogenic bladder
• Bladder with frequent uncontrolled micturition caused by lesion in
midbrain.
• It also called spastic neurogenic bladder or hyperactive neurogenic
bladder.
23. Neurogenic bowel:
Neurogenic bowel is the loss of normal bowel function. It's caused by a
nerve problem. A spinal cord injury or a nerve disease may damage the
nerves that help control the lower part of your colon. This is the part of
the body that sends solid waste out of the body.