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SPINAL CORD INJURY

Definition

Spinal Cord Injury (SCI) is a traumatic or non-traumatic injury to the spinal cord, leading to
alterations in a person ‘s motor, sensory and autonomic functions, causing disabilities and hurdles to a
person physically and socially.

Etiology

Traumatic

 Motor vehicular accident (42%)

 Falls (27.1%)
 Violence (15.3%)
 Recreational activities (7.4%)
 Other etiologies (6.3%)

Nontraumatic

 Vascular malfunctions (AV malformation, thrombosis, embolus, hemorrhage)

 Vertebral subluxations secondary to RA or DJD
 Infections (syphilis, transverse myelitis)
 Spinal neoplasms
 Syringomyelia
 Abscesses of the spinal cord
 Neurological diseases (MS, amyotrophic lateral sclerosis) 


Epidemiology 


 ♂>♀ (4:1)
 Lowest incidence for people <15 y.o.
 Highest incidence for people 16-30 y.o.


Pathophysiology


Primary Injury 


 Flexion injury
o head-on collision or blow to the back of the head or trunk
o This is the most common mechanism of SCI causing wedge fracture of anterior
vertebral body, tearing of posterior ligaments, fracture of posterior elements,
disruption of disk, and anterior dislocation of vertebral body.

 Compression injury
o vertical or axial blow to the head resulting to concave fracture of
endplate,explosion or burst fracture, teardrop fracture, and rupture of disk.

 Hyperextension injury

o strong posterior force such as rear-end collision or falls hitting chin on a
stationary object producing fractures to posterior elements, avulsion fracture of
anterior aspect of vertebrae, rupture of anterior longitudinal ligament, and rupture
of disk.

 Flexion-rotation injury

o posterior to anterior force directed at rotated vertebral column inducing a fracture
to posterior peduncles, articular facets and laminae, rupture to posterior and
 interspinous ligaments, subluxation or dislocation of facet joints, and thoracic or
lumbar spine locking

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Secondary injury cascade – a series of biochemical processes that occur after an SCI that causes further
neuronal damage beyond the mechanical damage incurred at the impact.

Clinical Manifestations
1. Spinal shock
 Period of areflexia 

 (-) reflex activity, flaccidity, and loss of sensation and motor function below the level of the
lesion 

 (-) DTR 

 (-) bulbocavernosus reflex, cremasteric reflex, and delayed plantar response 

 (+) bulbocavernosus is one of the first indicators that spinal shock is resolving 

 lasts for several days to weeks 

2. Motor and sensory impairments

Complete or partial loss of muscle function below the level of the lesion 


Impaired or absent sensation below the level of the lesion due to disruption of ascending

 sensory fibers 

 Clinical presentation depends on the specific feature of the lesion (neurological level,

 completeness of the lesion, and the symmetry of the lesion [transverse or oblique]) 

3. Autonomic dysreflexia (hyperreflexia)
 Typical pathologic autonomic reflex occurring in lesions above T6 (above sympathetic

 splanchnic outflow) but has also been reported in patients with T7 and T8 injuries.

 Incidence varies. 

 Seen in both patients with complete and incomplete lesions. 

 Produces an acute onset of autonomic activity from noxious stimuli below the level of the

 lesion. 

 ↑ BP due to a mass reflex response initiated by an afferent input from a stimulus reaching

 the lower spinal cord. 

 Impulses stimulate the receptors in the carotid sinus and aorta, signaling the vasomotor

 center to readjust peripheral resistance but cannot pass following SCI to counteract

 hypertension. Hypertension will persist if not treated immediately. 

 Emergency situation 

 Death may result


Initiating stimuli 

 Most common cause is bladder distension 

 Others (rectal distension, pressure sores, urinary stones, bladder infections, noxious

 cutaneous stimuli, kidney malfunction, urethral or bladder irritation, environmental

 temperature changes) 

 Following passive hip stretching 


Symptoms 

 Hypertension, bradycardia, headache (sever or pounding), profuse sweating, ↑ spasticity,
restlessness, vasoconstriction below the level of the lesion, vasodilation (flushing) above the
level of the lesion, constricted pupils, nasal congestion, piloerection (goose bumps), and
blurred vision.

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 Intervention
 Onset of symptoms should be treated as a medical emergency
 Patient should be brought to sitting to lower the BP
 Drainage system should be checked immediately since bladder distension is a primarycause of
autonomic dysreflexia
 Clamped catheter should be released
 Check drainage for internal or external blockage or twisting
 Patient‘s body should be checked for irritating stimuli (tight clothing, restricting catheterstraps,
abdominal binders)

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 Seek medical and/or nursing assistance immediately if symptoms do not subside orsource of
irritation cannot be located
 Drug therapy (antihypertensives) may be indicated if more conservative approaches
areunsuccessful
 Notify team members of occurrences of autonomic dysreflexia allowing careful monitoringfor
several days
 Document patient‘s symptoms, precipitating stimuli, methods of relief

4. Postural hypotension (orthostatic hypotension)

 ↓ BP when assuming an erect or vertical position caused by a loss of sympathetic
vasoconstriction control
 Peripheral venous and splanchnic bed pooling due to lack of muscle tone
 ↓ cerebral blood flow and venous return causing dizziness, lightheadedness, fainting
 Occur more frequently with lesions of the cervical and upper thoracic regions
 Resulting to edema and is complicated by ↓ lymphatic return

5. Impaired temperature control

 Due to damage of the spinal cord, hypothalamus cannot control thermoregulatoryresponses
 (-) ability to shiver
 (-) vasodilation in response to heat; (-) vasoconstriction in response to cold
 (-) sweating results with excessive compensatory diaphoresis above the lesion level
 More frequent problem with cervical lesions

6. Respiratory impairment
 C1 and C3 lesion: requires artificial ventilator or phrenic nerve stimulator to sustain life
 Lumbar lesion: full innervation of both primary and secondary respiratory muscles thusnot
needing support
 Pulmonary complications (especially bronchopneumonia and pulmonary embolism)
areresponsible for a high mortality during the early stages of tetraplegia.

7. Spasticity
 Characterized by hypertonicity, hyperactive stretch reflex, and clonus, resulting fromrelease of
intact reflex arcs from CNS control
 It occurs below the lesion level after spinal shock subsides
 Gradual ↑ in spasticity in the 1st 6 months; plateau after 1 year from injury
 ↑ spasticity by multiple stimuli: positional changes, cutaneous stimuli,
environmentaltemperatures, tight clothing, bladder or kidney stones, fecal impactions, catheter
blockage, urinary tract infections, decubitus ulcer, andemotional stress

8. Bladder dysfunction
 UTI: most frequent medical complication during the initial medical rehabilitation period
 During the stage of spinal shock, the urinary bladder is flaccid
 Primary Reflex Control originates from S2,S3,S4 within the Conus Medullaris which is
thespinal integration center for micturition
 UMN lesion: Spastic bladder dysfunction, intact micturition reflexes
 LMN lesion: flaccid bladder dysfunction, loss of micturition reflexes

9. Bowel dysfunction

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  Two types:
o Spastic/Reflex bowel – lesions above the Conus Medullaris
o Flaccid/Non reflex bowel - Conus Medullaris or Cauda Equina lesions
10. Sexual Dysfunction
Male response: Directly related to level and completeness of injury.
UMN: damage to the Conus Medullaris
LMN: damage to Conus Medullaris or Cauda Equina

o Erectile Capacity
o UMN > LMN, incomplete lesion > complete lesion
Two types of erections:
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 Reflexogenic – response to external physical stimulation of thegenitals
or perineum. Intact reflex arc is required (S2,S3,S4).
 Physiogenic – cognitive activities such as erotic fantasy.
Mediatedfrom the cerebral cortex (Thoracolumbar or sacral cord
centers)
o Ejaculation
o LMN > UMN, lower level > higher level cord lesions, incomplete >
completelesion
o Low level of fertility was associated with impaired spermatogenesis and
aninability to ejaculate
Female Response
o Function of women remaining capable of sexual intercourse following SCI
o Sexual response follow a pattern related to location of lesion
o UMN lesions: (+) Reflexogenic components of sexual arousal
(Vaginallubrication, engorgement of labia and clitorial erection). Psychogenic
responsewill be lost.
o LMN lesions (-) reflex response, (+) psychogenic response
 Menstruation
o Menstrual cycle is interrupted for a period of one to three months following injury
 Fertility and pregnancy
o Potential for conception is unimpaired
o Pregnancy under close medical supervision: increase risk for impairedrespiratory
function, labor may not be perceived due to impaired sensation. Labor may also
precipitate the onset of autonomic dysreflexia

Classification of SCI
I. Based on limb involvement

Tetraplegia – complete paralysis of all four extremities and trunk, including respiratory muscles.
Results from lesions of the cervical cord.

Paraplegia – complete paralysis of all or part of the trunk and both lower extremities. Resulting
from lesions of the thoracic or lumbar spinal cord or cauda equine

II. Based on lesion level (ASIA scoring)

Neurological Level – most caudal level of the spinal cord with normal motor and sensory
functionon both the left and right side of the body.

Motor Level – most caudal segment of the spinal cord with normal motor function bilaterally.

o Determine by testing the strength of a key muscle on the right and left side of the
body at myotomes adjacent to the suspected level of impairment.
o Motor Index Score is – calculated by adding the muscle scores of each key muscle
group; a total score of 100 is possible.
Sensory Level – most caudal segment of the spinal cord with normal sensory function bilaterally.
o Typically determined by testing the patient‘s sensitivity to light touch and pin prick on
theleft and right side of the body at key dermatomes
o Sensory Index Score – Calculated by adding the scores of each dermatome; a total
scoreof 112 is possible for each pin prick and light touch.

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Skeletal Level – Level at which the greatest vertebral damage is found by means of
radiologicalexamination

Completeness of injury
o Complete injury – having no sensory or motor function in the lowest sacral segment (S4
and S5). o Incomplete injury – having motor and/or sensory function below the
neurological level includingsensory and/or motor function at S4 and S5.
o Zone of partial preservation – intact motor and/or sensory functions are present below
theneurological level; S4 and S5 have no motor and sensory function

ASIA Impairment Scale

A = complete: no motor or sensory function is preserved in the sacral segments S4 and S5.
B = incomplete: sensory but no motor sensory function is preserved below the neurological level,
and includes the sacral segments S4 and S5.
C = incomplete: motor function is preserved below the neurological level, and more than half of
key muscles below the neurological level have a muscle grade less than 3.

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 D = incomplete: motor function is preserved below the neurological level, and at least half of key
muscles below the neurological level have a muscle grade of 3 or more.
E = normal: motor and sensory function is normal.

Clinical Syndromes

Brown-Sequard Syndrome – hemisection of the spinal cord, typically caused by penetration wounds.
Clinical features:
o asymmetry
o Ipsilateral side:
 Loss in sensation in the dermatome segment on the same level of the lesion
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 Lateral column damage: Decreased reflex, lack of superficial reflexes, clonus,
and (+)Babinski sign.
 Dorsal column damage: loss of proprioception, kinesthesia, and vibratory senses
o Contralateral side:
 Spinothalamic tract damage: loss of sense of pain and temperature
beginningseveral dermatome segments below the level of the injury.

Anterior cord syndrome – damage to the anterior portion of the cord and/or the anterior spinal artery
resulting from cervical region flexion injuries (fracture, dislocation, or cervical disk protrusion).
Clinical features:
o Corticospinal tract damage: loss of motor function

o Spinothalamic tract damage: loss of sense of pain and temperature

Central cord syndrome – occurs from cervical region hyperextension injuries or congenital/degenerative
narrowing of the spinal canal. Compressive forces results to hemorrhage or edema.
Clinical features:

o More severe neurological involvement of the upper extremities than the lower extremities
(cervical tracts are more centrally located)

o Varying degrees of sensory impairment occur but less severe than motor deficits

o Normal sexual, bowel and bladder function
o Patient recover the ability to ambulate but with some remaining distal UE weakness

Posterior cord syndrome – extremely rare syndrome resulting to impairment of function served by the
posterior columns.
Clinical features:
o Preservation of motor function, sense of pain, and light touch
o Loss of proprioception and epicritic sensations below the level of the lesion o Typical
wide-based steppage gait pattern

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Sacral Sparing – incomplete lesion in which the most centrally located sacral tracts are spared.

Clinical features:
o Perianal sensation
o External anal sphincter contraction
Cauda equina injuries – spinal injury with damage to peripheral nerve roots below the L1 vertebral level
and is frequently incomplete. Classified as LMN injuries with a potential to regenerate but full
reinnervation is uncommon.
Conus medularis – refers to a tapering segment of the spinal cord at the L1 vertebral level.

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Filum terminale – refers to the threadlike propagation of the spinal cord below the origin of the lumbar
nerves.

Mechanism of injury
Areas most commonly injured: between C5 and C7; between T12 and L2
1. Shearing – occurs when a horizontal force is applied to the spine relative to the adjacent segments
2. Distraction – traction force and is the least common mechanism (whiplash injuries)

Diagnosis
Immediate:
o In an accident, spinal cord injury must be considered at the scene. Movement and
transportationof the patient, especially when in a coma, should be done with extreme caution.
Most spinal injuries occur in conscious patients who complain of pain, numbness or difficulty
with limb movements.
o On examination, tenderness over the spinous processes, paraspinal sweeling or a gap between the
spinous processes may be present, indicating rupture of an interspinous ligament.
o Neurogenic paradoxical ventilation (indrawing of the chest on inspiration due to absent
intercoastal function) may occur with cervical cord damage
o Indications of SCI: Absence of limb reflexes bilaterally in flaccid limbs, unresponsive to painful
stimuli (unless death is imminent from severe head injury).
o Occurrence of painless urinary retention or priaprism
Imaging studies:
o Straight x-ray – note swelling, malalignments, widening of the interspinous distance or disc
space, damage to vertebral body, apophyseal joints, or spinous process.
o CT scan – demonstrates more extensive fractures and aids identification of regions not clearly
shown on x-rays.
o Magnetic Resonance Imaging (MRI) – may provide additional information of soft disc prolapse
or hematoma within the spinal canal, but seldom influences management.
o Myelography

Differential Diagnosis
Infectious disorders:
o Tabes dorsalis
o Tropical spastic parapaersis

Demyelinating cord disorder

Structural disorders:
o Spinal cord compression o Herniated disc syndrome o Spinal cord infarction
o Spinal cord transection

Prognosis
The potential for recovery from SCI is directly related to the extent of damage to the spinal cord
and/or nerve roots.

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Three primary influences on potential for recovery:
1. Degree of pathological changes imposed by the trauma
2. Precautions taken to prevent further damage during the rescue
3. Prevention of additional compromise of neural tissue from hypoxia and hypotension during
acutemanagement

o Early appearance of reflex activity in cases of complete lesion is a poor prognostic indicator
with no motor improvement is expected other than that which may occur from nerve return.
o Incomplete lesions indicated by motor function below the neurological level of the lesion
with sensation and/or motor anal function intact is good prognostic indicators of likely
significant motor improvement.

Complications
 Respiratory Complications
o Most common of deaths for individuals with SCI; Pneumonia (71.2%)
o Weak and/or paralyzed muscles leads to reduced ventilation of the lungs

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o Difficulty in clearing secretions due to inadequate or absent strength of coughingmuscles
leading to fluid buildup in the lungs resulting to atelecatasis andpneumonia
 Pressure Sores (33.5%)
o Ulcerations of soft tissues caused by unrelieved pressure and shearing forces which subject to
infection which can migrate to bones
o Serious medical complications, major cause of delayed rehabilitation, and may cause death.
o Two most influential factors that lead to pressure ulcers:
 Impaired sensation
 Inability to change positions
o Intensity and pressure also directly relates to extent of pressure ulcers o
o Other factors:
 Loss of vasomotor control
 Spasticity
 Skin maceration from exposure to moisture
 Trauma, such as adhesive tape or sheet burns
 Nutritional-deficiencies
 Poor general skin condition
 Secondary infections
 Deep Vein Thrombosis (15%)
o Results from development of thrombus from formation of clot within the vessel and is a
dangerous complication because of its potential to break free andbecome an emboli which
can lodge into pulmonary vessels leading to death
o Loss of normal pumping mechanism of the LE musculature is the most important contributor
to developing DVT in SCI. Slowing the blood flow, allowing higherconcentrations of
procoagulants to develop in localized areas causing thrombusformation.
o Factors that contribute to DVT formation:
 Prolonged pressure
 Age
 Loss of vasomotor tone. Immobility, sepsis, venous stasis,
hypercoaguability and trauma are also factors that contribute to DVT formation.
 Contractures
o Secondary to prolonged shortening of structures resulting to LOM. All joints of
the body are at risk for contractures.
o Faulty positioning, heterotropic ossification, edema, and imbalance of muscle pullcontribute
to the direction and location of contracture development
o Hip joint is particularly prone to flexion deformities (IR and adduction)
o Shoulders may develop tightness in flexion or extension (depends on position,but with IR
and adduction)
o Factors that places SCI patients at high risk for contractures:
 Lack of active muscle function eliminates normal reciprocal stretching or opposing
muscles

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  Presence of spasticity results in prolonged unopposed muscle shortening in a static
position
 Flaccidity may result in gravitational forces maintaining a relatively consistent joint
position
 Heterotropic (Ectopic) Ossification
o Osteogenesis in soft tissues below the level of lesion with an unknown cause
o May develop in tendons, connective tissue between muscle, aponeurotic tissue, or peripheral
aspects of the muscle, and typically occurs adjacent to large joints (hips and knees most
commonly involved)
o Early symptoms (resemble those of thrombophlebitis):
 Swelling
 Decreased ROM
 Erythema
 Local warmth near joint
 Elevated serum alkaline phosphatase levels
 Negative radiographic findings – seen posive in leter stages
 Pain
o Traumatic pain - may arise from fractures, ligamentous or soft tissue damage,
muscle spasm or early surgical interventions, subsides with healing
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o Nerve Root Pain – a stabbing, burning, or shooting pain following a dermatomalpattern that
may arise from damage to nerve roots at or near the site of cord damage caused by acute
compression or tearing of nerve roots, or secondary to spinal instability, periradicular scar
tissue and adhesion formation, or improper reduction.
o Spinal Cord Dysesthesias – peculiar, most often painful sensations below the level of lesion;
diffuse and not follow a dermatome distribution described as burning, numbness, pins and
needles, tingling feeligs, and sometimes abnormal proprioceptive sensations. Dysesthesias
subside over time, but are more persistent in long-standing cauda equine lesions.
o Musculoskeletal pain – may occur above the level of the lesion and frequently involves the
shoulder joint. Often related to faulty posturing and/or inadequate ROM, resulting in
tightening of the joint capsule amd surrounding soft tissue structures.
o Osteoporosis and renal calculi – changes in calcium metabolism below the level of the lesion
leading to osteoporosis. Large concentration of calcium present in the urinary system
creating a predisposition to stone formation causing renal calculi.

Medical/Pharmacologic Management
Emergency Care
- Management of SCI begins at the location of the accident, wherein techniques used inmoving
and managing the patient immediately following the trauma can influence prognosissignificantly.
- With suspected SCI, efforts should be made to avoid both active and passive movements ofhe
spine, which can be done by strapping the patient to a spinal backboard or a full-body adjustable
backboard, using a cervical collar, and assistance from multiple personnel in moving the patient
to safety, all the while maintaining the spine in a neutral and anatomical position to prevent
further neurological damage
- Upon ER arrival, focus of care is o medically stabilizing the patient, with performance of a
complete neurological exam. X-rays and imaging studies should be done to determine extent of
damage and plans of management.
- Another important focus is preventing the progression of neurological impairment by restoring
vertebral alignment and early immobilization of the fracture site.
- Unstable spinal fractures are given priority for reduction and fixation, and secondary injuries
are then addressed, and a urinry catheter is inserted.
Fracture stabilization
- Reduction and immobilization of spinal injuries can be achieved via conservative or
operativemethods. There is clear evidence supporting the use of both closed and open reduction
as effective, wherein closed reduction uses traction forces and weights while operative treatment
includes arthrodesis with plate or rod fixation.
Immobilization
- Following reduction, the spine is immobilized using tongs, halo devices, turning frames, beds,
and orthoses to allow healing.
o Tongs – used primarily as a temporary mode of skeletal traction, with replacement using a
halo device. These are inserted laterally on the outer table of the skull, accomplishing traction

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 by attachment of a traction rope to the skull fixation. In supine, the rope is threaded through a
pulley with weights that hang freely.
o Halo devices – commonly used to immobilize cervical fractures, and consist of a halo ring
with four steel screws that attach directly to the outer skull. The halo is attached to a body
jacket or vest by four vertical steel posts. Because of this structural configuration, these are
contraindicated with severe respiratory compromise.
- Assist in reducing secondary complications of prolonged bed rest, permit earlier
progression to upright activities, allow earlier involvement in a rehabilitation program,
and reduce the length and cost of hospital stay.
o Turning frames and Beds – (Stryker frame) consists of an anterior and posterior frame
attached to a turning base. In turning from a supine position, the anterior frame is placed on
top of the patient. A circular ring clamps in place to secure the two frames during turning.
- Primary benefit is that these devices allow positional changes while maintaining
anatomical alignment of the spine
- Disadvantage: positioning is limited to prone and supine, cannot accommodate obese
patients, and are unsuitable for unconscious patients
o Thoracolumbosacral Orthoses – commonly used to immobilize the spine in patients with
thoracic or lumbar injuries, and allow earlier involvement in a rehabilitation program. These
are usually bivalve to allow for removal during bathing and skin inspection.

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PT Management
PT examination
Respiratory examination
o Function of respiratory muscles – strength and tone of the diaphragm, abs andintercostals, as
well as respiratory rate
o Chest expansion – circumferential measurements should be taken at the level of theaxilla and
xiphoid process using a cloth tape measure. Normal chest expansion isapproximately 2.5-
3inches at the xiphoid process
o Breathing pattern – accomplished by manual palpation over the chest and abdominalregion
and by observation
o Cough – allows patient to remove secretions. Assess using functional, weakfunctional, and
nonfunctional classification
o Vital Capacity – use hand-held spirometer
Integument
o Meticulous and regular skin inspection is needed
o Patient education regarding skin care is crucial and should be initiated early
o Combines both visual observation and palpation
Sensation
o Detailed examination of superficial and deep sensations should be completed withparticular
emphasis on pin prick and light touch responses Tone and DTR
o Muscle tone should be examined with reference to quality, muscle groups involved, and
factors that appears to increase or decrease tone.
o DTR most commonly examined and their levels of innervations are the biceps (C5), ECRL
(C6), triceps (C7), quadriceps (L3), and gastrocnemius (S1)
MMT and ROM
o Testing should be done with caution in order to avoid placing stress on the fracturesite

PT Interventions
I. Acute Phase
A. Respiratory management
1. Deep breathing exercises – T6 lesions have innervated intercostals deep breathing.
2. Glossopharyngeal breathing - appropriate for patients with high level cervical lesions (C4can
cough with glossopharyngeal breathing)
3. Airshift maneuver – provides patient with an independent method of chest expansion.
This maneuver involves closing the glottis after a maximum inhalation, relaxing the
diaphragm, and allowing air to shift from the lower to upper thorax
4. Strengthening exercises – diaphragm, abdominal muscles, accessory muscles forbreathing
5. Assisted coughing – C5 patient can cough with manual pressure to diaphragm
(C7independent manual cough)
6. Abdominal support – abdominal corset or binder

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 7. Stretching- pectoral and other chest wall muscles

B. ROM and positioning

 While the patient is immobilized in bed or on a turning frame, full ROM exercises shouldbe
completed daily except in areas that are contraindicated or require selective stretching
 If possible, ROM should be completed in both prone and supine positions (prone positionis
contraindicated for some patients owing to fracture or respiratory compromise)
 Prone: Attention should be directed towards these motions:
 Shoulder extension
 Hip extension
 Knee flexion
 In paraplegia:
 Motions of trunk and some hip motions are contraindicated
 SLR more than 60 ̊ and hip flexion 90 ̊ should be avoided to avert strain on
thelower thoracic and lumbar spine
 In tetraplegia:
 Motion of the head and neck is contraindicated pending orthopedic clearance
 Shoulder stretching should be avoided during acute period; however, the
patientshould be positioned out of usual position of comfort(internal rotation,
adductionand extension of shoulders, elbow flexion, forearm pronation, wrist
flexion)
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 Patients with SCI do not require full ROM in all joints, because some joints benefit fromallowing
tightness to develop in certain muscles to enhance function. Conversely, somemuscles require a
fully lengthened range.
 After acute phase, the hamstrings will require stretching to achieve SLR or approximately100 ̊ to
allow for many functional activities such as sitting, transfers, and LE dressing. Care should be
taken not to overstretch these muscles so the remaining tightness can be used for passive pelvic
stabilization in sitting.
 Positioning splints for the wrist, hands and fingers are an important early consideration.
Alignment of the fingers, thumb and wrist must be maintained for functional activities or future
dynamic splinting.
 High level lesion wrist position: neutral, with web space maintained, with flexed fingers. If wrist
extensors are functional(fair muscle grade), a C-bar or short opponens splint is usually sufficient.
 In preventing heel cord tightness and pressure sores, ankle boots or splints are used. They
suspend the heel in space and distribute pressure evenly along the lower leg.
 Once patient has orthopedic clearance, patient is placed on a schedule to increasetolerance to
prone position, with the ankles positioned at a 90 ̊ angle.

C. Selective Strengthening
During acute phase, certain muscles must be strengthened cautiously to avoid stress at
fracture site. There is contraindication to application of resistance to musculature of the scapula and
shoulders (for tetraplegia), and musculature of the pelvis and trunk (for paraplegia)
 In planning exercise programs, emphasize bilateral UE activities to avoid asymmetric
rotational stresses on the spin.
 Strengthening exercises appropriate for acute phase:
o Bilateral manually resisted motions in straight planes
o Bilateral UE PNF patterns
o Progressive resistive exercises using cuffing weights/dumbbells
 Tetraplegia: emphasis on strengthening anterior deltoid, shoulder extensors, biceps and lower
trapezius. If present, wrist extensors, triceps and pectorals should also be emphasized.
 Paraplegia: all UE muscles should be strengthened, with emphasis on shoulder depressors,
triceps, and latissimus dorsi, which are required for ambulation and transfers
 Stress early involvement in functional activities

D. Orientation to the Vertical Position

 Patient is cleared for upright activities once fracture site is stabilized, but due to possible
postural hypotension, gradual acclimation to upright postures is advised.
 Using abdominal binder and elastic stockings and wraps will retard venous pooling.
 Upright actvities can be initiated by slowly elevating the hed of the bed and progressing to a
reclining or tilt-in-space wheelchair with elevating leg rests.

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  Vital signs should be monitored carefully and documented during this period.

II. Subacute/ Active Rehabilitation phase

A. Continuing Activities
o Many of the treatment activities initiated during the acute period will be continued
o Respiratory management, ROM and positioning will continue
o Patient will be involved in a continuing and expanded program of resistive exercises for
all muscles that remain innervated (PNF, PRE)
o Development of motor control and muscle reeducation techniques directed at appropriate
muscles are indicated
o Regaining postural control and balance by substituting upper body control and vision is
emphasized
o Focus is on improved cardiovascular response to exercise using interval training using
UE aerobic activity (UE ergometer)

B. Skin Inspection
o Patient will be instructed to gradually assume responsibility for skin inspection using
mirrors with handles or wall mirrors to assist them. If unable to do it by himself, educate
patient on how to instruct others to do skin inspection.

C. Mat Programs
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Sequence:
o Achieving stability withihn a posture then progressing through controlled mobility to
functional skills
o From symmetrical bilateral activities to weight shifting and movement, then improving
timing and speed
o Often individual components of more complex functional skills
o Should be initiated as soon as patient is cleared for activity
Mat programs improves strength and functional ROM, awareness of the new center of
gravity, promotes postural stability, facilitates dynamic balance, and assists with
determining the most efficient and functional methods for accomplishing specific tasks.

D. Functional Outcomes and Appropriate Interventions

C1-C4
 Breathing: Dependent: Uses ventilator and suction equiptment (C1-C3)
 Cannot clear secretions
 Bowel: total assistance – insertion of suppository & digital stimulation
 Urinary: Total assistance – insert indwelling catheter or external penile catheter
 Total assist for transfers
 Wheelchair: Power - independent, Manual – total assist
 Eating, communication, transportation: total assist
C5
 Breathing: low endurance and VC due to paralyzed intercostals, requires assistance to
clear secretions
 Bowel and Urinary: Total assist
 Bed mobility: needs some assistance but independent in direction of care and controlling
bed
 Total assist for transfers
 Wheelchair: power – independent, Manual – independent to some assist
 Eating: independent with equipment with total assist for setup (cutting food)
 Dressing/Bathing: Total assist
 Communication: independent to some assist with equipment
 Transport: independent with specialized equipment
C6-C7
 Breathing: same as C5
 Bowel: some to total assist; independent suppository insertion and rectal stimulator using
suppository inserter and digital bowel stimulator
 Urinary: independent self-catheterization through a continent urinary diversion; total
assist for indwelling catheter
 Bed mobility: some assist

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  Transfers: some assist to independent
 Wheelchair: Manual – independent indoors, some assist outdoors
 Eating: Independent
 Dressing/Bathing: Independent upper body, some/total assist lower body
 Communication: Independent
 Driving: Independent from wheelchair
C8
 Breathing: same as C5
 Bowel: Independent digital stimulation, suppository insertion and perineal hygiene
 Urinary: Independent intermittent catheterization
 Bed mobility: Independent
 Transfers: Independent w/ or w/o transfer board
 Wheelchair: Manual: Independent on all surfaces
 Standing: Some assist to independent
 Eating and Communication: Independent
 Dressing/Bathing: Some assist to independent with adaptive equipment
 Driving: Independent car if independent with transfer and wheelchair loading/unloading.
Independent driving modified van
T1-T12
 Breathing: same as C5 for higher level thoracic lesions
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 Bowel, Urinary, Bed mobility, Transfers, Wheelchair: same as C8
 Standing: Independent, ambulation for exercise only
 Eating/Dressing/Communication: Independent
 Driving: Independent car with hand controls and modified van
L1-S5
 Normal respiration
 Bowel, Urinary. Bed mobility, Wheelchair: same as T1-T12
 Transfers: Independent
 Standing: Independent
 Ambulation: Functional if only 1 KAFO needed
 Eating/Dressing/Communication: Independent
 Driving: Independent car with controls depending on level of lesion
E. Prescriptive Wheelchair
 Most patients with SCI will use wheelchair as the primary means of mobility
General considerations:
1. Seat depth should be approximately 1-2in back from the popliteal space for even
weight distribution on thighs.
2. Floor-to-seat height is important. If chair is sling type, a seat cushion will be required.
3. Consider back height. If patient will not be pushing the wheelchair, a high back may
be desired for added stability and comfort. If the patient has tetraplegia and will be
pushing the wheelchair, the back height recommended would be one below the
inferior angle of the scapula so the axilla is free of the handles during functional
activities.
4. Seat width and depth is variable and should be fitted to the anthropometric
characteristics of the patient
5. Patients with LE spasticity may require heel loops and/or toe loops on the footrests to
keep the feet in place
6. Removable armrests and detachable swing-away leg rests are important components
of wheelchairs used by many patients with SCI.

 Wheelchair skills
 The patient should be taught how to operate all the specific parts of the
wheelchair.
 Wheelchair mobility activities should begin on level surfaces and progress to
outdoor, uneven surfaces.
 Patients with sufficient UE strength should be taught wheelies for independent
curb climbing
 Patient should be instructed in pressure relief techniques from a sitting position.

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 10-15 seconds of pressure relief for every 10 minutes of sitting should be part of
the daily routine. Techniques include: wheelchair push-ups, hooking an elbow or
wrist around the push handle and leaning toward the opposite wheel, and wrist
around the push handle and leaning toward the opposite wheel, and hooking one
elbow or wrist around the push handle and leaning forward.

F. Ambulation after SCI

o Regaining the ability to walk is a common goal for most individuals following an SCI.
Factors influencing the success or failure in attaining this goal are that the patient must
possess adequate muscle strength, postural alignment, ROM and sufficient cardiovascular
endurance to initiate gait training.
 Therapists should be realistic with patients and provide a clear picture of the costs and
potential benefits
 Patients who wish to learn to ambulate following SCI should be given the option even
though potential is small.
 Individuals with complete SCI must rely on orthotic devices, assistive devices,
adequate ROM, amd strengthening neurologically intact musculature for standing and
walking.
 Full ROM in hip extension is essential in attaining balance in upright position.
 The absence of knee flexion and plantarflexion contractures is also important in
attaining upright standing balance.

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 Other factors that may restrict ambulation: severe spasticity, loss of propriocecption,
pain, presence of secondary complications such as decubitus ulcers, heterotopic
ossification at the hips, or deformity.
 Degree of incomplete SCI is an important prognostic factor for determining
ambulation potential

 Gait training for individuals with Complete SCI

Orthotic prescription
 Patients with complete thoracic lesions will require KAFOs, wherein the ankle
joint are usually locked in 5-10’ of dorsiflexion to assist hip extension at heel
strike
 Scott-Craig orthosis is another type of KAFO prescribed for patients with
paraplegia, and consists of standard double uprights, an offset knee joint
providing improved biomechanical alignment, bail locks, a posterior thigh band,
an anterior tibial band, adjustable ankle joint, and a sole plate that extends beyond
the metatarsal heads.
Gait Training Strategies
A swing-through type of gait pattern should be the ultimate goal for
functional ambulators with KAFOs. In teaching this pattern, it is important to stress a
smooth, even cadence. Relevant training activities are:
 Putting on and removing orthoses
 Sit-to-stand activities
 Trunk balancing
 Push ups
 Turning around
 Jack-knifing
 Ambulation activities in parallel bars
 Assistive devices(forearm crutches most often for paraplegia)
 Standing from the wheelchair with crutches
 Crutch balancing
 Ambulation activities
 Travel Activities
 Elevation Activities
 Controlled falling
 Locomotor Training for individuals with Incomplete SCI
Train like you walk:
1. The LEs are extemely loaded for weightbearing, minimizing, or eliminating loading
of the arms
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 2. The posture, trunk, pelvis, and limb kinematics are coordinated and specific to the
task of walking
3. Compensatory strategies for movement are minimized or eliminated

G. Functional Electrical Stimulation

 Application of low level electrical current to improve function in paralyzed and/or weak
muscles
 Can be used for a variety of purposes which include: cardiovascular training, breathing,
UE function, ambulation, transfers and standing, and bowel and bladder functions
 Can be applied using surface electrodes, percutaneous electrodes or surgically implanted
electrodes.

III. Chronic Phase

Adjustment to Disability
o SCI is a catastrophic event with a profound effect on the injured person as well as on
family members
o Successful adjustments is thought to have occurred when the disability is no longer the
dominant concern on the person’s life.
o Despite an overwhelming sense of loss initially after SCI, most persons eventually learn
to cope emotionally and conform to their premorbid personality styles of interacting with
the environment.
o Depressions and anxiety are usually present early after SCI

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Quality of Life
o Determination of the individual’s satisfaction with life
o Some factors appear to affect quality of life positively, such as mobility and ADL
independence, emotional support, good overall health, self-esteem, absence of
depression, physical and social activities and integration, being married and employed,
having completed more years of education, and living at home.
o Dissatisfaction with life after SCI seems more related to social disadvantages than to
physical limitations.
Recovery-Enhancing Therapies
o Most patients with SCI experience some degree of spontaneous neurologic recovery
which occurs as a result or resolution of the acute pathology, with recovery of nerve roots
and spinal cord at the level of lesion.
Late Neurologic Decline
o New motor or sensory deficits are reported to develop in 20-30% of persons with chronic
SCI.
o Most common is entrapment of a peripheral nerve, especially the median nerve at the
carpal tunnel, or ulnar nerve at the elbow.
o Further damage may be caused by post- traumatic syringomyelia.

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