Spinal Cord Injuries
OBJECTIVES:
At the end of this lecture , the student will be able to :
1. Identify the major etiologic factors involved in traumatic and nontraumatic spinal cord injuries (SCI) .
2. Describe the clinical features following damage to the spinal cord.
3. Describe the potential secondary complications associated with SCI .
4. Identify the anticipated functional expectations for spinal cord patients
at various lesion levels .
5. Identify and describe appropriate assessment and treatment procedures
of both acute and chronic phases of management .
Introduction:
Spinal cord injury (SCI) has been identified as a low-incidence,
high-cost disability requiring tremendous changes in the patient's
lifestyle.
Etiology:
Spinal cord injuries can be divided into two main etiological
categories; traumatic and non-traumatic injuries. Traumatic SCI are the
most common, which may result from motor vehicle accident, fall or
gunshot wound. Non-traumatic injuries may be due to tumors, transverse
myelitis and vascular causes.
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Functional classification of spinal cord injuries:
Spinal cord injuries are divided typically into two broad functional
categories; quadriplegia and paraplegia. "Quadriplegia" refers to partial
or complete paralysis of all four extremities and trunk, including
respiratory muscles. It results from lesion of the cervical cord.
"Paraplegia" refers to partial or complete paralysis of both lower
extremities with or without trunk involvement. It results from lesion of
the thoracic or lumber cord or sacral roots.
Designation of lesion level:
The most commonly used method to determine the level of SCI is
to indicate the most distal uninvolved or partially involved nerve root i.e.
the power of muscles supplied by that root is at least grade 3+ according
to manual muscle testing.
Classification of SCI according to the severity of the lesion:
* Complete lesion:
It is characterized by loss of sensory and motor functions below the
level of lesion. It is caused by complete transaction, severe compression
or extensive vascular impairment of the cord.
* Incomplete lesion:
It is characterized by preservation of some sensory or motor
functions below the level of injury. Preservation of function indicates that
some viable neural tissue is crossing the area of the injury to more distal
segments. Incomplete lesions often result from contusions produced by
pressure on the cord from displaced bone and/or soft tissues or from
swelling within the spinal canal.
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Clinical picture:
- Spinal shock:
Immediately following SCI, there is a period of areflexia. It results
from abrupt withdrawal of connections between higher centers and the
spinal cord. It is characterized by absence of all reflex activity, flaccidity
and loss of sensation below the level of lesion.
- Motor deficits and sensory loss:
Following spinal cord injury, there will be either complete or
partial 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 lesion level. The clinical presentation of motor and
sensory deficits is dependent on the specific features of the lesion. These
include the neurologic level, the completeness of the lesion, the symmetry
of the lesion (transverse or oblique) and the presence or absence of sacral
sparing.
- Impaired temperature control:
After damage to the spinal cord, the hypothalamus can no longer
control cutaneous blood flow or level of sweating. This autonomic
(sympathetic) dysfunction results in loss of internal thermoregulatory
responses. The ability to shiver is lost; vasodilatation does not occur in
response to heat nor vasoconstriction in response to cold.
- Respiratory impairment:
Respiratory dysfunction varies depending on the level of the lesion.
In lesions between Cl and C3, phrenic nerve innervation and spontaneous
respiration are significantly impaired or lost. An artificial ventilator or
phrenic nerve stimulation is required to sustain life. In contrast, lumber
lesions present with full innervation of both primary (diaphragm) and
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secondary (neck, intercostals and abdominal) respiratory muscles. All
patients with quadriplegia and those with high level paraplegia
demonstrate some compromise in respiratory function. The level of
respiratory impairment is directly related to the lesion level and the
residual respiratory muscle function.
Patients with a complete lesion at C4 will have loss of vasomotor
control. As a result of paralysis of the vasoconstrictors, there is a marked
vasodilatation initially. This causes blockage of the nasal air passages,
which adds to the difficulties of respiration. This phenomenon is known
as "Guttmann's sign".
Spasticity:
Spasticity results from release of intact reflex arcs from the central
nervous system control and is characterized by hypertonicity, hyperactive
stretch reflexes and clonus. It typically occurs below the level of lesion
after spinal shock subsides. There is a gradual increase in spasticity
during the first six months and usually reaches a plateau one year after
injury. It is increased by multiple internal and external stimuli, including
positional changes, cutaneous stimuli, environmental temperatures, tight
clothing, bladder or kidney stones, catheter blockage, urinary tract
infections and emotional stress. Spasticity varies in degree of severity.
- Bladder dysfunction:
The effect of bladder dysfunction following SCI is a serious
medical complication, requiring consistent and long-term management.
Urinary tract infection (UTI) is the most frequent medical complication
during the initial medical / rehabilitation period. During the stage of
spinal shock, the bladder is flaccid. All muscle tone and bladder reflexes
are absent. Medical considerations during this period are focused on
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establishing an effective system of drainage and prevention of urinary
retention and infection.
The spinal integration center for micturation is the conus
medullaris. Primary reflex control originates from the sacral segments of
S3,4,5. Following spinal shock, one of two types of bladder conditions will
develop, depending on location of the lesion. Patients with lesions that
occur within the spinal cord above conus medullaris typically develop a
reflex neurogenic bladder. Following a lesion of the conus medullaris or
cauda equina, an autonomous, or non-reflex neurogenic bladder develops.
Reflex (upper motor neuron) bladders reflexly empty in response to a
certain level filling pressure. The reflex arc is intact. Autonomous or nonreflex (lower motor neuron) bladders are essentially flaccid because there
is no reflex action of the detrusor muscle.
Secondary complications:
1. Pressure sores:
Pressure sores are ulcerations of skin or subcutaneous tissue,
caused by unrelieved shearing forces. They are subject to infection which
may migrate to bone. It is a major cause of delayed rehabilitation and
may lead to death. Impaired sensory function and the inability to make
appropriate positional changes are the most important factors in the
development of pressure sores. Other factors include:
a) Loss of vasomotor control, which lowers tissue resistance to pressure.
b) Spasticity, with resultant shearing forces between bony surfaces.
c) Skin maceration from exposure to moisture (e.g. urine).
d) Nutritional deficiencies as low serum protein and anemia.
e) Secondary infections.
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2. Autonomic dysreflexia:
Autonomic dysreflexia (hyper-reflexia) is a pathologic autonomic
reflex that occurs in lesions above T6 (above sympathetic outflow), which
lead to hypertension. This clinical syndrome produces an acute onset of
autonomic activity from noxious stimuli below the level of the lesion.
Following SCI, impulses from the vasomotor center can not pass the site
of the lesion to counteract the hypertension. Owing to lack of inhibition
from higher centers, hypertension will persist if not treated promptly. The
most common stimuli for this pathologic reflex are bladder or rectal
distention, pressure sores, urinary stones, bladder infections and noxious
cutaneous stimuli.
3. Postural hypotension:
Postural hypotension is a decrease in blood pressure, which occurs
when a patient is moved from a horizontal to a vertical position. It is
caused by a loss of sympathetic vasoconstriction control. The problem is
enhanced by lack of muscle tone, causing peripheral venous blood
pooling. Reduced cerebral flow and decreased venous return to the heart
also may occur. In many patients who are immobilized for up to 6 to 8
weeks, episodes of postural hypotension are a fairly common occurrence
during early progression to a vertical position. They tend to occur more
frequently with lesions of the cervical and upper thoracic regions.
Patients will often describe the onset as feelings of dizziness, faintness or
impending "blackout". Although the exact mechanism is not clearly
understood, the cardiovascular system, over time, gradually reestablishes
sufficient vasomotor tone to allow assumption of the vertical position.
4. Heterotopic (Ectopic) bone formation:
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Heterotopic bone formation is osteogenesis in soft tissues below
the level of the lesion, which is of an unknown etiology. However,
multiple theories have been proposed, including tissue hypoxia secondary
to circulatory stasis, abnormal calcium metabolism, local pressure and
micro trauma related to aggressive range of motion exercises. Heterotopic
bone formation is always extra-articular and extra-capsular. It may
develop in tendons, in connective tissue between muscles or in the
peripheral aspects of muscle. It must be differentiated from myositis
ossificans, which results from injury to a muscle and is characterized by
bony deposits within muscle tissue. No relationships have been found
between the development of heterotopic bone formation and level of
injury, amount of exercise or degree of spasticity or flaccidity.
Heterotopic bone formation typically occurs adjacent to large joints, with
the hips and knees most commonly involved. Other joints include the
elbows, shoulders and spine. Early symptoms of heterotopic ossification
resemble those of thrombophlebitis, including swelling, decreased range
of motion, erythema and local warmth near a joint.
5. Contractures:
Contractures develop with prolonged shortening of structures
across and around a joint, resulting in limitation in motion. Contractures
initially produce alterations in muscle tissue but rapidly progress to
involve capsular and pericapsular changes. Factors place the patient with
SCI at risk for developing joint contractures are lack of muscle function,
flaccidity, spasticity, faulty positioning, ectopic bone formation and
imbalances in muscle pull. The hip joint is particularly prone to flexion,
internal rotation and adduction. The shoulder may develop flexion or
extension, depending on early positioning. Both patterns at the shoulder
are associated with internal rotation and adduction.
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6. Deep venous thrombosis (DVT):
Deep venous thrombosis (DVT) results from development of a thrombus
(abnormal blood clot) within a vessel. It has the potential to break free of
its attachment and float freely within the venous blood stream. Such
mobile clots are known as emboli. They may block pulmonary vessels
and result in death. In SCI, DVT is due to loss of the normal pumping
mechanism provided by active contraction of lower extremity
musculature. This slows the flow of
blood, allowing higher
concentrations of pro-coagulants (thrombin) to develop in localized areas.
Prognosis:
The potential for recovery from SCI is directly related to the extent of
damage to the spinal cord and / or nerve roots. There are three main
factors that affect potential for recovery : (1) the degree of pathologic
changes imposed by the trauma . (2) the precautions taken to prevent
further damage during rescue .(3) prevention of additional compromise of
neural tissue from hypoxia and hypotension during acute management.
Formulation of a prognosis is initiated after spinal shock has subsided
and is guided by whether or not the lesion is complete. Following spinal
shock , a lesion is generally considered complete in the absence of any
sensory or motor function below the level of damage . With incomplete
lesions some evidence of sensory and/or motor function is noted below
the level of the lesion after spinal shock subsides . The rate of recovery
will decrease, and a plateau will be reached . When the plateau is
reached; and no new muscle activity is observed for several months, no
additional recovery can be expected in the future.
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MANAGEMENT
Acute Phase
It starts from the onset of injury until the fracture site is stable and upright
activities can be initiated .
I- Emergency Care
Management of SCI begins at the location of the accident . Techniques
used in moving and managing the patient immediately following the
trauma can influence prognosis significantly. When
a spinal injury
suspected , efforts should be made to avoid both active and passive
movements of the spine by strapping the patient to a spinal back board ,
use of a supporting cervical collar, and assistance from multiple
personnel in moving the patient safely . On arrival at the emergency
room , initial attention is focused on stabilizing the patient medically .
Attention is directed toward preventing progression of neurologic
impairment by restoration
of vertebral alignment and early
immobilization of the fracture site.
II – Fracture stabilization
Cervical Injuries
Immobilization of unstable cervical fractures is achieved via skeletal
traction. Traction can be applied by use of tongs attached to the outer
skull from supine lying position ( Fig. 1).
Fig.(1):Cervical
Tongs.
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Thoracic and Lumber Injuries
Fractures of these sites are immobilized through bedrest or by application
of a body cast or jacket .The expanded use of spinal orthotics also has
allowed for earlier mobility activities . Plaster or plastic body jackets
function to immobilize the spine while allowing earlier involvement in a
rehabilitation program .
III - Surgical Intervention
Surgery may be indicated to restore bony anatomic alignment , to prevent
further damage to the cord and to stabilize the fracture site. Compared
with spontaneous healing
times, surgical stabilization allows earlier
initiation of rehabilitation activities .
Surgical interventions for cervical fractures include decompression and
fusion by bone grafting . Frequently, surgery for thoracic and lumbar
injuries requires use of an internal fixation device, which may be used in
combination with bone grafts. The patient is immobilized by spinal
orthosis after surgery for at least 3 months .
IV – Physical therapy assessment
 Respiratory
assessment
(muscle
strength
of
intercostals;
diaphragm; and abdominals , chest expansion , breathing pattern ,
and cough) .
 Skin assessment : Skin inspection combines both visual
observation and palpation . Particular attention should be paid to
areas most susceptible to pressure . Patient education related to
skin care is crucial and should be initiated early .
 Sensory assessment : Superficial and deep sensations are fully
assessed .
 Tone and deep reflexes .
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 Manual muscle testing and ROM test : Caution should be taken
when resisting shoulder muscles in cervical injuries i.e.
quadriplegia and around lower trunk and hip in paraplegia .
 Functional assessment .
V – Physical Treatment
1. Respiratory management and Skin care .
2. ROM and positioning :Full ROM should be completed daily except for
those areas that are contraindicated . With paraplegia , SLR greater than
60 degrees or hip and knee flexion more than 90 degrees are avoided .
With quadriplegia movement of the head and neck or stretching of
shoulder should be avoided .
3. Selective strengthening : All remaining muscles should be maximally
strengthened . Stress at fracture sites is avoided e.g. musculature around
shoulder and scapula in quadriplegia and those of the hip and trunk in
paraplegia . Bilateral exercises are carried out for upper extremities to
avoid rotational stresses on the spine .
4. Orientation to the vertical position after radiographic stability of the
fracture site . Gradual acclimation to upright posture is effective with the
use of abdominal binder to prevent venous pooling .
5. Bladder training programs: The primary goal of bladder training is to
allow the patient to be free from a catheter and to control bladder
function.
Automatic bladder , intermittent catheterization is the most frequently
used program . Its aim is to establish reflex bladder emptying at regular
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and predictable intervals in response to a certain limits of filling. It
involves restricted fluid intake to 2000 ml/day . It is taken about 150 –
180 ml / hour from morning to early evening . Initially the patient is
catheterized every 4 hours before which the patient should try to void
bladder by one of the manual techniques (such as stroking , kneading , or
tapping the surapubic region or thigh and lower abdominals) . Calculation
of the residual and voided urine volumes should be recorded . As bladder
emptying becomes more effective , the residual volume decreases and
time interval between catheterization is expanded .
Autonomous bladder , one of the previously mentioned techniques can
be used to help voiding . In addition , giving strengthening exercises to
lower abdominals , pelvic floor and gluteal muscles . Interfrential and
faradic stimulation are of great benefit in such cases . Finally , in sensory
atonic bladder , pulling of pubic hair or allowing the patient to listen to
the sound of water will increase the sensory awareness of bladder
fullness.
Subacute Stage
All the assessment procedures performed during the acute stage will be
continued with completion of all avoided muscle testing and ROM .
Physical therapy management
(a) Emphasis will remain on respiratory management , ROM
exercises and positioning .
(b) Resisted exercises for all innervated muscles especially shoulder
depressors that will help in independent transfer .Different
methods can be used such as PNF , progressive resisted exercises ,
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weights , dumbles , pulley system and suspension therapy . Also
before encountering patient into ADL training , balance and
endurance exercises are stressed .
(c) ADL training include bed and mat activities , transfer , wheel chair
activities , exercises inbetween parallel bars .
(d) Gait training with or without walking aids such as walkers ,
crutches either elbow or axillary or cane . Ptients who become
functional ambulators are those whose trunk muscles (abdominals
and erector spinae) are at least grade fair . Full hip extension ROM
is essential in attaining balance in upright position .
Gait expectations of complete paraplegics :
Above T10 ----------- Swing to gait .
T10 – L1 -------------- Four point gait .
Below L1 ------------- Swing through gait .
(e) Elevation activities :The easiest pattern of ascent is with stairs
backward to the patient and descent with stairs forward .
(f) Training for controlled falling .
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