Spinal cord injuries (SCI)

Dr.Anas Alashram
Spinal cord tracts
Somatosensory pathways

 The dorsal column medial laminscus

 Spinothalamic tract
 Spinocerebellar tract
 Spinoreticular tract
 The dorsal column medial laminscus

 Fine touch, vibration,

proprioception, two point
discrimination, and
stereognosis
 Spinothalamic tract
 Anterior spinothalamic
tract: crude touch

 Lateral spinothalamic
tract: pain and temperature
 Spinocerebellar tract

 Proprioception from muscle spindle and

golgi tendon
 Touch and pressure to cerebellum

 Dorsal spinocerebellar--- Ipsilateral

 Ventral spinocerebellar--- Ipsilateral and
contralateral
 Spinoreticular tract

 Deep and chronic pain to

reticular formation
Motor pathways

 Corticospinal tract
 Vestibulospinal tract
 Rubrospinal tract
 Reticulospinal tract
 Tectospinal tract
Corticospinal tract

 Primary motor cortex (10%

uncrossed) to ventral gray
matter.
 Voluntary motor control
 Vestibulospinal tract
 From vestibular neucleus
(uncrossed)
 Control muscle tone,
postural reflex, and
antigravity muscles.
Rubrospinal tract

 Originate from nerve cells in

red nucleus cross the mid
line and descend to ventral
gray matter
 Assist in motor function
 Reticulospinal tract

 From reticular formation in brainstem to

ventral and lateral column
 Terminates both dorsal gray matter
(modify transmission of sensations
especially pain) and ventral (influence
gamma motor neurons and spinal reflexes)
Tectospinal tract

 From superior colliculus

(midbrain) to ventral grey
matter.
 Assist in head turning
reponse to visual stimuli.
Spinal cord Vertebral column
C1-C3 C1-C3 (same)
C4-C8 C4-C7(add 1)
T1-T8 T1-T6(add 2)
T9-T12 T6-T9(add3)
L1-L2 T10
L3-L4 T11
L5 T12
S1-S5 & Co L1
Cauda equina L2-Co
Epidemiology

 250,000 to 500,000 new spinal cord injuries annually.

 Spinal Cord Injury can occur as a result of non-traumatic causes (16%) and
traumatic causes (84%).

 Non-traumatic spinal cord injuries occur as a result of disease, infection and

congenital defects

 Males account for 80% of new cases

 The average age at injury has gone up from 29 years old (1970) to 42 years
old currently.
• SCI typically affects: the cervical level of the spinal cord (50%) with the
single most common level affected being C5; thoracic level (35%); lumbar
region (11%).

Complete Incomplete
Tetraplegia 18.3% 34.1%
Paraplegia 23.0% 18.5%
Etiology

• Motor vehicle accidents (36 - 48%)

 Falls (17 - 21%)
 Violence (i.e., gunshot wounds)
 Sports injuries.

 Forces involved can be hyperflexion (forward movement of the

head); hyperextension (backward movement); lateral stress
(sideways movement); rotation (twisting of the head);
compression (force along the axis of the spine downward from
the head or upward from the pelvis); or distraction (pulling apart
of the vertebrae).
 Classification
 There are many classifications:
• Level of the lesion:
 Paraplegia
 Tetraplegia
• Completeness of the lesion:
 Complete: no motor or sensory functions below the lesion
 Incomplete lesion: some motor or/and sensory functions are
preserved (S4/S5)
Incomplete SCI syndromes
Anterior cord syndrome

 Due to flexion injury

 Motor & pain, temperature sensation are lost bilateral below level
of lesion
Central cord syndrome

 Due to hyperextension injury

 Impairment of function in UEs more than LEs
Brown sequard syndrome

 Due to penetrating objects or wound

 Ipsilateral loss of motor function & position sense below level of
lesion

 Contralateral loss of pain and temperature below level of lesion

Posterior cord syndrome

 Due to compression by tumor or infarction of posterior spinal

artery

 Proprioception, stereognosis, two point discrimination, vibration

are lost below level of lesion
Cauda equina syndrome

 Occur at or below L1
 Lead to LMNL
Conus meullaris syndrome

 Injury in sacral cord and lumber nerve root

 Loss of motor & sensation for LEs , diminished bladder reflex

 UMNL at level of injury

 LMNL below level of injury
 Conus medullaris syndrome
 Conus medullaris syndrome is an injury to the end of the spinal cord, located at
about the T12–L2 vertebrae in adults. This region contains the S4–S5 spinal
segments, responsible for bowel, bladder, and some sexual functions, so these
can be disrupted in this type of injury. In addition, sensation and the Achilles
reflex can be disrupted.[29] Causes include tumors, physical trauma, and
ischemia.
Diagnostic Procedures

 MRI Scans have become the golden standard for imaging

neurological tissues such as the spinal cord, ligaments, discs, and
other soft tissues. Only MRI sequences of sagittal T2 were found
to be useful for prognosticative purposes.

 Spinal fractures and bony lesions are better characterized by

computed tomography (CT) and vascular injuries can be detected
by using an MR angiography or by a CT scan.
 Surgical intervention
 May required for stability, alignment
or to prevent further damage. Bone
graft may also be used.
 The most commonly used device to
stabilize the spine: harrington rods.
 After surgery, patient is placed in cast
or body jecket for 3 months or more.
Primary complications
Spinal Shock

 It is characterized initially by an absence of all reflex activity,

impairment of autonomic regulation resulting in hypotension and
loss of control of sweating and piloerection.

• In addition to the loss of deep tendon reflexes, there is a loss of the

bulbocavernosus reflex, the cremasteric reflex, a Babinski response,
and a delayed plantar response.

• The initial period of total areflexia lasts approximately 24 hours.

This is followed by a gradual return of reflexes 1 to 3 days after
injury, a period of increasing hyperreflexia lasting 1 to 4 weeks, and
final hyperreflexia 1 to 6 months after injury
Motor and Sensory Impairments

• Following SCI there will be either complete (paralysis) or partial

(paresis) loss of muscle function below the level of the lesion.
Disruption of the ascending sensory fibers following SCI results
in impaired or absent sensation below the level of the lesion.

• The clinical presentation of motor and sensory impairments

depends on the specific features of the lesion. These include the
neurological level and the completeness of the lesion.
Autonomic dysreflexia

• Typically AD occurs in lesions above T6 (above sympathetic

splanchnic outflow).

• It is more common with complete injury, but it may also occur

with an incomplete SCI

• Although AD is more common in the chronic stage o recovery

(more than 3 to 6 months after injury), it may also occur in the
early stages after SCI.
Initiating Stimuli Signs and Symptoms
Bladder distention/irritation* Hypertension (rise in systolic BP 20–30
mm Hg)
Bowel distention/irritation* Bradycardia
Stimuli that would normally be painful Severe headache
below level of lesion
Gastrointestinal irritation Feeling of anxiety
Sexual activity Constricted pupils
Labor Blurred vision
Skeletal fracture below level of injury Flushing and piloerection above level of
lesion
Electrical stimulation below level of lesion Dry, pale skin below level of lesion (due
to vasoconstriction)
Nasal congestion
Increased spasticity
Intervention

 The onset of symptoms should be treated as a medical emergency.

 If lying flat, the patient should be brought to an upright position,

in as much as blood pressure will be lowered in this position, and
loosen any tight clothing or restrictive devices.

 Blood pressure and pulse should be monitored. The individual

should be questioned as to possible triggers, starting with urinary
system. The drainage system should be examined first. If the
patient is using an indwelling catheter it should be checked to
make sure it is not blocked. If any type of blockage is found it
should be removed immediately. If the patient catheterizes
intermittently, a catheter should be placed and the bladder
drained.
 The patient should then be questioned about when the last bowel
movement occurred and checked for an impaction.

 The patient’s body should be examined for triggering stimuli such

as tight clothing, restricting catheter straps, abdominal binders, or
anything that may be a noxious stimulus.

 If hypertension and other symptoms do not subside with the

identification and elimination of specific triggers, medical and/or
nursing assistance should be sought emergently. Pharmacological
intervention may be required to lower blood pressure.
Spastic hypertonia

 Spastic hypertonia typically emerges below the level of lesion

after spinal shock evolves.

 There is a gradual increase in spastic hypertonia during the first 6

months and a plateau is usually reached 1 year after injury.

 Various stimuli including positional changes, cutaneous stimuli,

environmental temperatures, tight clothing, bladder or kidney
stones, fecal impactions, catheter blockage, urinary tract
infections, decubitus ulcers, and emotional stress may trigger or
increase spasticity and muscle spasms.
Cardiovascular Impairment

 Parasympathetic signals to the heart arise from the vagus nerve,

decreasing heart rate and contractility.

 Sympathetic input comes from spinal segments T1 to L2 through

the sympathetic trunk, which runs parallel to the spinal cord
Sympathetic input increases heart rate and contractility and
peripheral vasoconstriction.

 A rostral SCI will result in a loss of sympathetic communication

between the brainstem and the heart, while parasympathetic input
remains intact. This causes bradycardia and dilation of the
peripheral vasculature below the level of the lesion. Because of
the disrupted balance between sympathetic and parasympathetic
input, as well as a lack of or decrease in active muscle contraction
and prolonged time in bed, orthostatic hypotension is often
 Symptoms of orthostatic hypotension include blurred vision, ringing in the ears,
light-headedness, and fainting.

 Orthostatic hypotension is usually only significant in people with SCI above

T6.

 To minimize these effects when mobilizing patients early after SCI, the
cardiovascular system should be allowed to adapt gradually by a slow
progression to the vertical position. This frequently begins with elevation of the
head of the bed and progresses to a reclining wheelchair with elevating leg rests
and use of a tilt table.

 Vital signs should be monitored carefully, and the patient should always be
moved very slowly.

 Use of compressive stockings and an abdominal binder may further minimize

these effects
Impaired temperature control

 After damage to the spinal cord the hypothalamus can no longer

control cutaneous blood flow or level of sweating.

 Individuals with cervical-level injuries and complete injuries

demonstrate more impairment.

 Initially after injury hypothermia may occur due to peripheral

vasodilation. Later, hyperthermia is more likely due to the lack of
sympathetic control of sweat glands.
Pulmonary impairment

 In people with high cervical injuries, pulmonary problems are the

leading cause of death both in the early and late stages of
recovery.

 Individuals with injuries below T10 are likely to have near-

normal ventilatory and respiratory function.

 10% of people with complete tetraplegia develop pneumonia or

atelectasis 1 year after injury.
 With high spinal cord lesions at C1 and C2, phrenic nerve
innervation and spontaneous respiration are lost.

 The only muscles of respiration that are intact are accessory

muscles: sternocleidomastoid, upper trapezius, and cervical
extensors.

 An artificial ventilator or phrenic nerve stimulator is required to

sustain life.
 C3- and C4-level injuries have partial diaphragm innervation, as
well as scalenes, levator scapulae, and trapezius.

 In the acute stage of recovery individuals with an injury at these

levels (C1-C4) will require mechanical ventilation.

 Injuries at C5–C8 have a fully innervated diaphragm, as well as

many accessory muscles. Some cough ability is preserved;
however, it is usually weak.
 The primary muscles of expiration are the abdominals and internal
intercostals.

 Normally, relaxed expiration is essentially a passive process that

occurs through elastic recoil of the lungs and thorax. However, the
abdominals and internal intercostals contribute several important
functions related to movement of air out of the lungs.

 Loss of these muscles significantly decreases expiratory efficiency.

Control of the abdominal muscles originates from T5–T12. When
fully innervated, they play an important role in maintaining
intrathoracic pressure for effective respiration.
 Paralysis or paresis of the scalenes and
intercostal muscles also results in the
development of an altered breathing pattern,
called paradoxical breathing pattern.

 This pattern is characterized by flattening of

the upper chest wall, decreased chest wall
expansion, and a dominant epigastric rise
during inspiration.
Bladder dysfunction

 The effects of bladder dysfunction following SCI pose a serious

medical complication requiring consistent and long-term
management.

 Urinary tract infections (UTIs) are a major cause of mortality and

morbidity in people with SCI.

 Patients with lesions that occur above the conus medullaris and sacral
segments develop a spastic or hyperreflexic bladder. This
 is also termed a UMN bladder. Following a lesion of the sacral
segments or conus medullaris, a flaccid or areflexic bladder
develops.5 This is also termed a LMN bladder.
 A spastic or hyperreflexic bladder (UMN lesion) contracts and
reflexively empties in response to a certain level of filling
pressure. The reflex arc is intact with this type of injury.

 A flaccid or areflexive bladder (LMN lesion) is essentially flaccid

because there is no reflex action of the detrusor muscle.
 There are generally two types of bladder dysfunction: failure to
store urine and failure to empty urine.

 Inability to store urine may be due to an areflexive sphincter or

spastic detrusor muscle.

 Inability to empty the bladder sufficiently may be due to an

areflexive bladder or a sphincter that is unable to relax.

 Dyssynergia between the detrusor and sphincter can also cause

incomplete drainage of the bladder.
 Bladder Management
 The primary goal of bladder management is to prevent or minimize urinary tract
complications. These include UTIs, hydronephrosis (swelling of kidney due to backup of
urine), renal calculi, bladder calculi, and vesicoureteral reflux (backward flow of urine up
the ureter).

 Because of impaired bladder function almost 50% people with SCI will develop UTIs.

 In the early stage of recovery, while the patient is still in spinal shock, the bladder is
flaccid and an indwelling catheter is inserted. After the patient is stable during
rehabilitation, the most frequently used method of bladder management is intermittent
catheterization.

 Briefly stated, the program involves establishing a fluid intake pattern of approximately
2000 mL/day. Intake is stopped late in the day to reduce the need for catheterization
during the night. Initially, the patient is catheterized every 4 hours. A record is maintained
of voided and residual urine. While in the hospital, sterile intermittent catheterization
should be done; after discharge, a clean technique can be used.
 Other methods of bladder management include suprapubic
tapping and the Valsalva maneuver. Suprapubic tapping involves
tapping directly over the bladder with fingertips, causing a
reflexive emptying of the bladder. This technique only works for
individuals with an UMN bladder without dyssynergia between
the detrusor and sphincter

 Individuals with an areflexive bladder can use the Valsalva

maneuver, which is done by straining.
Bowel dysfunction

 Over 98% of people with SCI report problems with bowel care and 34%
require some level of assistance with bowel care

 In spinal cord lesions above S2 there is a spastic or reflex bowel (UMN

lesion). Because the parasympathetic and internal sphincter connections
from S2–S4 are intact, reflex defecation can occur when the rectum fills
with stool.

 In S2–S4 or cauda equina (peripheral nerves) lesions a flaccid or

areflexive bowel (LMN lesion) develops. With an areflexive bowel the
parasympathetic connections from S2–S4 are not intact so the bowel will
not reflexively empty. This can cause feces to become impacted and,
because the external sphincter is flaccid, incontinence can occur.
 Bowel management
 Safety and an appropriate, well-timed bowel care routine are
common goals for bowel management. Safety includes
continence in order to maintain intact and healthy skin, prevent
damage to colorectal structures, and prevent AD due to bowel
dysfunction.

 A typical bowel program involves establishing a daily (or every

other day) pattern of eliciting a bowel movement. The exact time
of day is chosen by the patient based on lifestyle needs and
should be done consistently at the same time of day. This is
usually in the morning or late evening.
 People with a reflex bowel require the use of suppositories and digital
stimulation techniques to cause a reflex defecation.

 Digital stimulation involves manual stretch of the anal sphincter, either

with a lubricated gloved finger or an orthotic digital stimulator. This stretch
stimulates peristalsis of the colon and evacuation of the rectum (mediated
by S2, S3, and S4). Valsalva maneuver and abdominal massage may also
be performed.

 Nonreflex bowel management relies on manual evacuation techniques and

gentle Valsalva.

 Other factors that can play a role in maintaining a consistent, safe bowel
program include eating a diet with appropriate amount of fiber, fluid
intake, physical activity, stool softeners, laxatives, and bulking agents.
Sexual dysfunction

 Sexual capabilities are divided between UMN (damage to the

cord above S2–S4) and LMN lesions. Generally speaking,
erectile capacity is greater in UMN lesions than in LMN lesions
and greater in incomplete lesions than in complete lesions.
Secondary complications
Pressure sores

 Pressure sores are ulcerations of soft tissue (skin or subcutaneous

tissue) caused by unrelieved pressure and shearing forces.

 Up to 36% of people with SCI develop pressure sores during

inpatient rehabilitation

 Pressure sores are a serious medical complication, are a major

cause of delayed rehabilitation, and may even lead to death.
 Impaired sensory function and the inability to make appropriate
and timely positional changes are influential factors in the
development of pressure sores. Individuals with complete SCI are
more likely to develop a pressure ulcer than patients with
incomplete SCI (iSCI).

 Other important factors associated with the development of

pressure ulcers are (1) tetraplegia; (2) spasticity; (3) bladder or
bowel incontinence; (4) limited mobility and self-care; (5)
nutritional deficiencies; (6) prolonged immobilization during
recovery; (7) smoking; and (8) noncompliance with skin care.
Supine Prone Side-lying
Occiput Ears (head rotated) Ears
Scapulae Shoulders (anterior Shoulders (lateral
aspect) aspect)
Vertebrae Illiac crest Greater trochanter
Elbows Male genital region Head of fibula
Sacrum Patella Knees (medial aspect
from contact between
knees)
Coccyx Dorsum of feet Lateral malleolus
Heels Medial malleolus
(contact between
malleoli)
Deep vein thrombosis

 Deep venous thrombosis (DVT) results from development of a

thrombus within a vein.

 People with SCI are at risk of developing DVT due to lack of

mobility and active muscle contraction of the LEs, which leads to
stasis and hypercoagulability.

 Management of this secondary complication focuses on

prevention. Nonpharmacological interventions include early
mobilization, compression stockings and boots, and pneumatic
compression sleeves.
Pain

• Traumatic
• Nerve root
• Spinal cord dysthesia
• musculoskeletal
• Traumatic pain:
• Due to trauma

• Management:
• Immobilization
• Analgesics
• TENS
• Nerve root pain:
• Due to damage to nerve root
• Sharp, burning sensation
• Follows dermatomal pattern
• Most common in cauda equina injuries

• Management:
• Pharmacological
• TENS
• Surgical
• Spinal cord dysthesia:
• Painful sensation below level of lesion
• Diffuse (not dermatomal)
• Numbness, pins, needle
• Describe as phantom limb pain
• Management: pharmacological
• Musculoskeletal pain:
• As shoulder pain: due to faulty (poor) position, excessive function,
ROM

• Management:
• Proper alignment
• Stretching
• Strength
• Proper wheelchair propulsion
Contractures

 Contractures develop secondary to prolonged shortening of

structures across and around a joint, resulting in limitation in
motion.

 The most important management consideration related to the

potential development of contractures is prevention.

 Once contractures have developed it is extremely difficult to

reverse the process. A consistent and concurrent program of range
of motion (ROM) exercises, positioning, and splinting is
important to maintain joint motion and prevent contracture.
Heterotopic ossification

• Due to local pressure, hypoxia, abnormal Ca metabolism,

microtrauma

• Early symptoms of HO including swelling, joint and muscle pain,

decreased ROM, erythema, and local warmth near a joint.

• Differs from myositis ossifications which result from injury

• Most common sites: hip, knee, but can occur in elbows, shoulder,
spine
Osteoporosis

 There is a rapid bone mineral loss in the first 4 to 6 months after injury.
Bone mineral density (BMD) continues to decrease up to 3 years after
injury; however, this may continue longer

 It is most common in the LEs, although osteoporosis may also occur in

the UEs in people with cervical SCIs.

 Fracture incidence may be as high as 46%.

 Rehabilitation strategies used to prevent or reduce BMD loss are

functional electrical stimulation and weight-bearing activities either with
a standing frame or orthotics and assistive devices.
Prognosis

 An incomplete lesion (ASIA B, C, or D) is a good prognostic

indicator of greater likelihood of recovery of motor function.

 Preservation of pinprick sensation at 4 months after injury in the

LEs or sacral region is associated with a good prognosis for
motor recovery at 1 year after injury.

 Recovery of motor function generally plateaus around 12 to 18

months after injury.
 Functional Expectations for Patients With
Spinal Cord Injury
 C1, C2, C3

 Available movements (Talking, Mastication, Sipping, Blowing )

 Breathing requires a ventilator or nerve stimulator to the diaphragm.

 Dependent for bed mobility and transfers
 Independent in wheelchair after helped into it
 Can do pressure relief in power reclining wheelchair with head, chin, or
mouth controls
 Communication devices and environmental controls are often needed.
 Dependent for feeding, dressing, and bowel and bladder care
 C4
 Available movements (Scapular elevation)

 Dependent for bed mobility and transfers

 Independent in wheelchair and pressure relief in power reclining
wheelchair
 Communication devices and environmental controls are often
needed.
 Dependent for feeding, dressing, and bowel and bladder care
 C5
 Available movements (Elbow flexion and supination, Shoulder external
rotation, Shoulder abduction and flexion to ~90°)

 Moderate to maximum help needed for bed mobility

 Maximum help needed for sliding board transfers, except for rare cases of
independence. Able to do side-to-side pressure relief in wheelchair.
 Independent in electric wheelchair with hand drive
 Independent in manual wheelchair with quad pegs for indoor mobility
 Independent in self-feeding with setup and use of adaptive equipment
 Needs help with upper body dressing
 Dependent for bowel and bladder care
 C6
 Available movements (Shoulder flexion, extension, internal rotation, and adduction
Scapular abduction, protraction, and upward rotation, Forearm pronation, Wrist extension
(tenodesis grasp))

 Independent bed mobility and level transfers; may need minimal help for uneven
transfers.
 Independent side-to-side pressure relief.
 Independent with lightweight manual wheelchair on level ground, gentle slopes, and 2-
inch curbs
 Can take off armrests and footplates independently
 Drives adapted van independently
 Independent in self-feeding with use of adaptive equipment
 Independent with upper body dressing
 Needs help with lower body dressing
 Dependent for bowel and bladder care
 C7
 Available movements (Elbow extension, Wrist flexion, Finger extension)

 Independent in uneven transfers over greater distances

 Independent with wheelchair push-up
 May be able to transfer floor to wheelchair
 Independent in manual wheelchair on slightly uneven ground, low curbs,
and standard ramps
 Independent with all self-cares with some help needed for bowel care
 May stand in parallel bars with braces
 C8
 Available movements (Finger flexion)

 Mostly the same as C7, but with greater ease and better hand use
 Independent bladder function with intermittent catheterization
 Independent bowel function with digital stimulation
 Independent car transfers and may be able to get wheelchair
loaded
 T1 to T12
 Available movements (Improved trunk control with more caudal SCI, Increased
respiratory reserve, Pectoral girdle stabilized for lifting objects)

 Independent in all transfers and pressure relief

 Independent with manual wheelchair on curbs, ramps, wheelies, and uneven
ground
 Able to load wheelchair into car and drive with hand controls
 Able to walk short distances with leg braces locked straight and crutches or walker
 Walking with leg braces and walker possible
 Walking a long distance may be hard, and wheelchair use is still needed due to the
high energy needed.
 L1, L2
 Available movements (Hip flexion, Hip adduction)
 Independent transfers from bottom of tub.
 Walking with leg braces and crutches possible, but wheelchair
use still needed due to high energy needed.
 L3-S1
 Available movements (Knee extension, Strong hip flexion, Strong
knee extension, Knee flexion, Ankle dorsiflexion, Ankle
plantarflexion, Ankle eversion, Toe extension)
 Walking with leg braces and straight canes
 May use wheelchair for sports or long distances
 S2,S3

 Walking without leg braces possible, but may be needed due to

muscle imbalances