Spinal Cord Injury

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SPINAL CORD INJURY Definition Spinal cord injury is an insult to the spinal cord resulting from traumatic or non-traumatic damage,that may lead to significant alterations of a person’s motor, sensory and autonomic functions. Relevant Anatomy Etiology Traumatic (70%) Vehicular accidents (42.1%) Falls Violence Sports (7.6%) Nontraumatic (30%) Disease (AV malformation, Thrombosis, Embolus, Hemorrhage) Vertebral subluxations secondary to arthritis or DJD Infections (syphilis or transverse myelitis, spinal neoplasms, syringomyelia) Neurological diseases (MS/ALS) Epidemiology > (4:1) 5 2 % 1 1 % 3 7 % Age group 16-30 y.o Elderly Others Pathophysiology Secondary injury cascade – the series of biochemical processes that occur following an SCI, and that cause further damage beyond the mechanical damage sustained by impact. Vasoconstriction of blood vessels supplying the cord leads to ischemia of the gray matter. It is mediated by rapid release of vasoactive substances (serotonin, thromboxanes, platelet- activating factor, peptidoleukotrienes, opioid peptides) after SCI. Increased intraneuronal calcium concentrations because of elevated excitatory amino acids (glutamate, aspartate) leads to development of edema at the site of injury. This begins within minutes of injury, peaks at 8 hours and remains for at least a week. Activation of phospholipases A2 and C by the increased intracellular calcium concentrations, leading to the production of free radicals and free fatty acids and matabolites, which cause damage to local cell membranes Rise in potassium in the extracellular space causes cell membrane damage, which causes depolarization of other neuronal cells and conduction block Iron from microhemorrhages in the central gray matter leads to further tissue damage as well as catalyzes further production of oxygen free radicals Neutrophil migration to the site of injury causes cellular injury by lysosome enzyme action. Macrophages then phagocytose cell debris. Clinical Manifestations 1. Spinal shock - period of areflexia

Transcript of Spinal Cord Injury

Page 1: Spinal Cord Injury

SPINAL CORD INJURYDefinition

Spinal cord injury is an insult to the spinal cord resulting from traumatic or non-traumatic damage,that may lead to significant alterations of a person’s motor, sensory and autonomic functions.

Relevant Anatomy

EtiologyTraumatic (70%)

Vehicular accidents (42.1%)FallsViolenceSports (7.6%)

Nontraumatic (30%)

Disease (AV malformation, Thrombosis, Embolus, Hemorrhage)Vertebral subluxations secondary to arthritis or DJDInfections (syphilis or transverse myelitis, spinal neoplasms, syringomyelia)Neurological diseases (MS/ALS)

Epidemiology

♂ > ♀ (4:1)

52%

11%

37%

Age group

16-30 y.oElderlyOthers

Pathophysiology Secondary injury cascade – the series of biochemical processes that occur following an SCI, and that cause further damage beyond the mechanical damage sustained by impact. Vasoconstriction of blood vessels supplying the cord leads to ischemia of the gray matter. It is

mediated by rapid release of vasoactive substances (serotonin, thromboxanes, platelet-activating factor, peptidoleukotrienes, opioid peptides) after SCI.

Increased intraneuronal calcium concentrations because of elevated excitatory amino acids (glutamate, aspartate) leads to development of edema at the site of injury. This begins within minutes of injury, peaks at 8 hours and remains for at least a week.

Activation of phospholipases A2 and C by the increased intracellular calcium concentrations, leading to the production of free radicals and free fatty acids and matabolites, which cause damage to local cell membranes

Rise in potassium in the extracellular space causes cell membrane damage, which causes depolarization of other neuronal cells and conduction block

Iron from microhemorrhages in the central gray matter leads to further tissue damage as well as catalyzes further production of oxygen free radicals

Neutrophil migration to the site of injury causes cellular injury by lysosome enzyme action. Macrophages then phagocytose cell debris.

Clinical Manifestations1. Spinal shock

- period of areflexia- (-) all reflex activity, flaccidity, loss of sensation and motor function below the level of lesion- (-) DTR- (-) bulbocavernosus and cremasteric reflex- Delayed plantar response - A positive bulbocavernosus reflex is one of the 1st indicators that spinal shock is resolving- May last for several days to weeks

2. Motor and Sensory impairments- Impaired/absent sensation due to disruption of ascending sensory fibers- Complete/partial loss of muscle function below lesion level- Clinical presentation depends on the features of the lesion (neurologic level, completeness

and symmetry)3. Postural Hypotension

- ↓ BP when assuming an erect position caused by a loss of sympathetic vasoconstriction control

- ↓ cerebral blood flow and venous return the heart = dizziness/ fainting- More common in cervical and upper thoracic lesions

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4. Impaired Temperature Control- Loss of control of hypothalamus = loss of internal thermoregulatory responses.- (-) sweating and ability to shiver - (-) vasodilation in response to heat, and (-) vasoconstriction in response to cold.- Compensation: excessive diaphoresis above lesion

5. Respiratory Impairment- C1-C3 lesions: artificial ventilator or phrenic nerve stimulator- Lumbar lesions: full innervation of respiratory muscles not needing support.- Pulmonary complications (bronchopneumonia, pulmonary embolism) are responsible for a

high mortality during early stages of tetraplegia.6. Spasticity

- Results from release of intact reflex arcs from CNS control and is characterized by hypertonicity, hyperactive stretch reflexes, and clonus.

- Occurs below the level of lesion after spinal shock subsides. - Gradual ↑ in 1st 6 months; plateau reached 1 year post-injury- ↑ by multiple stimuli: positional changes, cutaneous stimuli, environmental temperatures,

tight clothing, bladder or kidney stones, fecal impactions, catheter blockage, UTI, decubitus ulcers, emotional stress

7. Bladder Dysfunction- UTIs: among the most frequent medical complication during the initial medical rehabilitation

period.- During spinal shock, bladder is flaccid without any tone and bladder reflexes- Primary reflex control originates from the sacral segments of S2, S3, and S4 within the conus

medullaris.- Px with lesion above conus medullaris – spastic or reflex bladder: reflexively empties in

response to a certain level of filling pressure- Px with lesion of the conus medullaris/cauda equina – flaccid or nonreflex (autonomous)

bladder8. Bowel Dysfunction

- 2 types: spastic or reflex bowel- lesion above the conus medullaris; flaccid or nonreflex bowel- lesion in cauda equina/ conus medullaris.

9. Sexual DysfunctionMale Response: directly related to level and completeness of injury. UMN: above conus/cauda; LMN: below conus medullaris or cauda equina

Erectile Capacity - UMN > LMN lesions, incomplete lesions > complete lesions.- Two types of erections:

Reflexogenic – occur in response to external physical stimulation of the genitals or perineum. An intact reflex arc is required (S2, S3, S4).

Psychogenic – occur through cognitive activity such as erotic fantasy. These are mediated from the cortex either through the thoracolumbar or sacral cord centers.

Ejaculation- LMN >UMN lesions, lower-level > higher-level lesions, and incomplete > complete

lesions- Low level of fertility, impaired spermatogenesis.

Female response: follow a pattern related to location of lesion.- UMN lesions: + reflexogenic components of sexual arousal (vaginal lubrication,

engorgement of labia, clitoral erection) - LMN lesions: + psychogenic responses but (-) reflex responsesMenstruation- Cycle interrupted for a period of 1-3 months following injury. After this, normal

menses returnFertility and Pregnancy

- Potential for conception unimpaired- Needs close supervision: ↑ risk for impaired respiratory function, initiation of

labor not felt due to impaired sensation, labor may precipitate autonomic dysreflexia.

Classification of SCITetraplegia – refers to complete paralysis of all four extremities and trunk, including the respiratory muscles, and results from lesions of the cervical cord.Paraplegia – refers to 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 equina.

Lesion levelNeurological level – is the most caudal level of the spinal cord with normal motor and sensory function on both the left and right sides of the body.

If there is a wide range of differences between motor and sensory levels on the right and left side of the body, it is not appropriate to assign a single neurological level, instead, each of the sensory and motor levels on the right and left should be documented separately.

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

Motor level is assessed 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.

Motor index score is calculated by adding the muscle scores of each key muscle group; a total score of 100 is possible

Sensory level – is the most caudal segment of the spinal cord with normal sensory function bilaterally.

Sensory level is determined by testing the patient’s sensitivity to light touch and pin prick on both sides of the body at key dermatomes, and scoring is based on a 3-point scale where 0= absent, 1= impaired, and 2 = normal.

Sensory index score is calculated by adding the scores for each dermatome; a total score of 112 is possible for each PP (pin prick) and LT (light touch)

Skeletal level – the level at which, by radiological examination, the greatest vertebral damage is found

Myotomes:C5 - Deltoid (shoulder abduction)C5,C6 - Biceps (elbow flexion)C7 - Triceps (elbow extension)C8 - Flexor carpi ulnaris (ulnar deviation)

Extensor carpi ulnarisT1 - Interossei (digit abduction/adduction)L2, L3 - Iliopsoas (hip flexion)L3,L4 - Quadriceps (knee extension)L5 - Tibialis Anterior (ankle DF) Extensor hallucis longus (big toe extension)S1 - Gastrocnemius (ankle PF)

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Key Dermatomes:C2 - occipital protuberanceC3 - supraclavicular fossaC4 - top of the acromioclavicular jointC5 - lateral side of the antecubital fossaC6 - thumbC7 - middle fingerC8 - little fingerT1 - medial or ulnar side of antecubital fossaT2 - apex of the axillaT3 - third intercostal spaceT4 - fourth intercostal space (nipple line)T5 - fifth intercostal spaceT6 - sixth intercostal space (xiphisternum)T7 - continuation of 7th intercostal spaceT8 - continuation of 8th intercostal spaceT9 - continuation of 9th intercostal spaceT10 - continuation of 10th intercostal spaceT11 - continuation of 11th intercostal spaceT12 - inguinal regionL1 - 1/3 distance between T12 and L3L2 - midanterior thighL3 - medial femoral condyleL4 - medial malleolusL5 - dorsum of the foot at the 3rd MTP jointS1 - lateral heelS2 - popliteal fossa in the midlineS3 - ischial tuberosityS4/5 - perianal area

Completeness of injuryComplete injury – is an SCI having no sensory or motor function in the lowest sacral segments (S4 & S5)Incomplete injury – is an SCI having motor and/or sensory function below the neurological level including sensory and/or motor function at S4 & S5Zones of partial preservation – areas of intact motor and/or sensory function are present below the neurological level even though S4 & S5 have no motor and sensory function.

ASIA Impairment ScaleA = Complete: No motor or sensory function is preserved in the sacral segments S4 to S5.B = Incomplete: Sensory but not motor function is preserved below the neurological level and

includes the sacral segments S4 to 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.

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.

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Clinical Syndromes

<Brown Sequard syndrome

Brown Sequard Syndrome - Usually due to penetration wounds (gunshot/stab)Features: Assymetrical

Ipsilateral side: Loss of sensation in the dermatome at same level of lesion Depressed reflexes, lack of superficial reflexes, clonus, + Babinski (lateral column

damage) Loss of proprioception, kinesthesia, vibratory sense (dorsal column damage)

Contralateral side: Loss of sense of pain and temperature several dermatome segments below the

level of injury (spinothalamic tract damage)

< Anterior cord syndrome

Anterior Cord Syndrome – flexion injuries of the cervical region (compression, fracture, dislocation, cervical disc protrusion)

Structures damaged: anterior cord/ vascular supply (anterior spinal artery)Features: Corticospinal tract damage = loss of motor function Spinothalamic tract damage = loss of sense of pain and temperature below level of

lesion

< Central cord syndromeCentral Cord Syndrome – hyperextension injuries to cervical region or congenital

/degenerative narrowing of spinal canal Compressive forces leads to hemorrhage and edemaFeatures: More severe neurological involvement of UE than LE (because cervical tracts are

more centrally located) Varying degrees of sensory deficits but less severe than motor impairments Normal sexual, bowel and bladder function Px typically able to ambulate with some remaining distal UE weakness

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< Posterior cord syndromePosterior Cord Syndrome – extremely rare, seen with tabes dorsalis (found in late stage

syphilis)Features: Preservation of motor function, pain sensation and light touch Loss of proprioception and combined cortical sensations below lesion level Wide based steppage gait pattern

Sacral Sparing – incomplete lesion in which most centrally located sacral tracts are spared and is one of the first signs that a cervical lesion is incomplete

Features: Perianal sensation External anal sphincter contraction

Cauda Equina Injuries – lesion at L1 vertebral level and is frequently incomplete. It is classified as LMN injury with the potential to regenerate, though full reinnervation is not common.

Mechanisms of injury- Areas most susceptible to injury: between C5 and C7 ; between T12 and L2

1. Main mechanisms of injury includes flexion, compression, hyperextension and flexion with rotation

2. Contributing mechanisms includes shearing and distraction of SC

Diagnosis Immediate:

The possibility of spinal cord injury must be considered at the scenet of the accident and all movements and transportation of the patient undertaken with extreme caution especially when comatose. Most spinal injuries occur in conscious patients who complain of pain, numbness or difficulty with limb movements.Examination may reveal tenderness over the spinous processes, paraspinal swelling or a gap between the spinous processes, indicating rupture of an interspinous ligament.Neurogenic paradoxical ventilation (indrawing of the chest on inspiration due to absent intercostals function) may occur with cervical cord damageBilateral absence of limb reflexes in flaccid limbs, unresponsive to painful stimuli, indicates SCIPainless urinary retention or priapism may occur

Imaging studies:Straight X-rays – note malalignments, swelling, widening of interspinous distance or disc space, damage to vertebral bodyCT Scan – may demonstrate more extensive fractures than X raysMagnetic Resonance Imaging (MRI)Myelography

Differential DiagnosisInfectious disorders:

Tabes dorsalis Tropical spastic parapaersis

Demyelinating cord disorderStructural disorders:

Spinal cord compression Herniated disk syndromeSpinal cord infarctionSpinal cord transection

PrognosisPotential for recovery from SCI is directly related to the extent of damage to the spinal

cord and/or nerve roots. The primary influences on recovery potential are:1. Degree of pathological changes imposed by trauma2. Precautions taken to prevent further damage during rescue3. Prevention of additional compromise of neural tissue from hypoxia and hypotension during

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

Complications1. Respiratory Complications

Weak/paralyzed muscles of inspiration leads to reduced ventilation of the lungs, and inadequate strength of coughing muscles makes it difficult to clear secretions, leading to fluid buildup in the lungs resulting in atelectasis and pneumonia.

2. Pressure SoresThese are among the more frequent medical complications following SCI and are caused by unrelieved pressure and shearing forces, which subject areas to infection which can migrate to bone. Pressure sores are a serious medical complication and major cause of delayed rehabilitation, and may even cause death.The two most influential factors that lead to development of pressure sores are impaired sensory function and the inability to make appropriate positional changes. Intensity and pressure also directly relates to the extent of the pressure sore. Other important factors are:Loss of vasomotor controlSpasticitySkin maceration from exposure to moistureTrauma, such as adhesive tape or sheet burnsNutritional-deficienciesPoor general skin conditionSecondary infections

3. Deep Vein ThrombosisDVT results from development of a thrombus within a vessel, and is a dangerous complication because it has the potential to break free of the attachment and become an emboli, which can lodge in pulmonary vessels, leading to death.The most important contributor to developing DVT in SCI is the loss of normal pumping mechanism of the LE musculature, slowing the flow of blood, allowing higher

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concentrations of procoagulants to develop in localized areas, causing thrombus formation.Prolonged pressure, age, loss of vasomotor tone, immobility, sepsis, venous stasis, hypercoagulability and trauma are also factors that contribute to DVT formation.

4. ContracturesPatients with SCI develop irreversible contractures secondary to prolonged shortening of structures across and around a joint, resulting in limitation of motion. All joints of the body are at risk for contractures.Faulty positioning, heterotrophic ossification, edema, and imbalance of muscle pull contribute to the direction and location of contracture developmentThe hip joint is particularly prone to flexion deformities (IR and adduction)The shoulder may develop tightness in flexion or extension (depending on positioning, but with IR and adduction)Factors that places SCI patients at high risk for developing contractures include:

o Lack of active muscle function eliminates normal reciprocal stretching of opposing muscles.

o Presence of spasticity results in prolonged unopposed muscle shortening in a static position

o Flaccidity may result in gravitational forces maintaining a relatively consistent joint position.

5. Heterotrophic OssificationExtra-articular and extracapsular osteogenesis in soft tissues below the level of the lesion with an unknown cause.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).

Early symptoms (resemble those of thrombophlebitis)o Swellingo Decreased ROMo Erythemao Local warmth near jointo Elevated serum alkaline phosphatase levelso Negative radiographic findings (early stage) – positive in later stages

6. PainIs a common occurrence following SCI

Traumatic Pain – is related to extent and type of trauma sustained as well as the structures involved; may arise from fractures, ligamentous or soft tissue damage, muscle spasm, or early surgical interventions, and subsides with healing.

Nerve Root Pain – a sharp, stabbing, burning, or shooting pain following a dermatomal pattern that may arise from damage to nerve roots at or near the site of cord damage, and can be caused by acute compression or tearing of nerve roots, or secondary to spinal instability, periradicular scar tissue and adhesion formation, or improper reduction.

Spinal Cord Dysesthesias – peculiar, often painful sensations below the level of lesion. These are diffuse and do not follow a dermatomal distribution, described as burning, numbness, pins and needles, tingling feelings, and sometimes abnormal proprioceptive sensations. Dysesthesias subside over time, but are more persistent in long-standing cauda equina lesions.

Musculoskeletal Pain – occur above the lesion and frequently involves the shoulder joint; often related to faulty positioning and/or inadequate ROM, resulting in tightening of the joint capsule and surrounding soft tissue structures.

Osteoporosis and Renal Calculi – caused by changes in calcium metabolism following SCI and occurs below lesion level. After SCI, bone resorption exceeds formation, resulting in a net loss of bone mass, increasing susceptibility to fracture. The resorbed calcium is present in the urinary system, predisposing patient to stone formation.

Medical/Pharmacological Management Emergency Care

- Management of SCI begins at the location of the accident, wherein techniques used in moving and managing the patient immediately following the trauma can influence prognosis significantly.

- With suspected SCI, efforts should be made t avoid both active and passive movements of the 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 on medically stabilizing 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 urinary catheter is inserted.

Fracture stabilization- Reduction and immobilization of spinal injuries can be achieved via conservative or

operative methods. 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.Tongs – are 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 by attachment of a traction rope to the skull fixation. In supine, the rope is threaded through a pulley with weights that hang freely.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.

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

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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 bivavled to allow for removal during bathing and skin inspection.

PT Management PT examination Respiratory examination

- Function of respiratory muscles – strength and tone of the diaphragm, abs and intercostals, as well as respiratory rate

- Chest expansion – circumferential measurements should be taken at the level of the axilla and xiphoid process using a cloth tape measure. Normal chest expansion is approximately 2.5-3in. at the xiphoid process

- Breathing pattern – accomplished by manual palpation over the chest and abdominal region and by observation

- Cough – allows patient to remove secretions. Assess using functional, weak functional, and nonfunctional classification

- Vital Capacity – use hand-held spirometer Integument

- Meticulous and regular skin inspection is needed. - Patient education regarding skin care is crucial and should be initiated early- Combines both visual observation and palpation.

Sensation- Detailed examination of superficial and deep sensations should be completed with particular

emphasis on pin prick and light touch responses. Tone and DTR

- Muscle tone should be examined with reference to quality, muscle groups involved, and factors that appear to increase or decrease tone.

- 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- Testing should be done with caution in order to avoid placing stress on the fracture site.

Functional statusPT Interventions I. Acute phase A. Respiratory management

1. Deep breathing exercises – T6 lesions have innervated intercostals for deep breathing.

2. Glossopharyngeal breathing – appropriate for patients with high-level cervical lesions (C4 can 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 for breathing

5. Assisted coughing – C5 patient can cough with manual pressure to diaphragm (C7 independent manual cough)

6. Abdominal support – abdominal corset or binder7. Stretching – pectoral and other chest wall muscles

B. ROM and positioningWhile the patient is immobilized in bed or on a turning frame, full ROM exercises should be 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 position is contraindicated for some patients owing to fracture or respiratory compromise)Prone: Attention should be directed towards these motions:o Shoulder extensiono Hip extensiono Knee flexion

In paraplegia:o Motions of trunk and some hip motions are contraindicatedo SLR more than 60° and hip flexion beyond 90° should be avoided to avert strain on

the lower thoracic and lumbar spineIn tetraplegia:o Motion of the head and neck is contraindicated pending orthopedic clearanceo Shoulder stretching should be avoided during acute period; however, the patient

should be positioned out of the usual position of comfort (internal rotation, adduction and extension of shoulders, elbow flexion, forearm pronation, wrist flexion)

Patients with SCI do not require full ROM in all joints, because some joints benefit from allowing tightness to develop in certain muscles to enhance function. Conversely, some muscles require a fully lengthened range. After acute phase, the hamstrings will require stretching to achieve SLR or approximately 100° 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 increase tolerance to prone position, with the ankles positioned at a 90° angle.

C. Selective StrengtheningDuring 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 spine.Strengthening exercises appropriate for acute phase:- Bilateral manually resisted motions in straight planes- Bilateral UE PNF patterns- Progressive resistive exercises using cuff weights/dumbbellsTetraplegia: 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

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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 activities can be initiated by slowly elevating the head of the bed and progressing to a reclining or tilt-in-space wheelchair with elevating leg rests.Vital signs should be monitored carefully and documented during this period.

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

Sequence: - Achieving stability within a posture then progressing through controlled mobility

to functional skills- From symmetrical bilateral activities to weight shifting and movement, then

improving timing and speed- Often individual components of more complex functional skills- Should be initiated as soon as patient is cleared for activityMat 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 InterventionsC1-C4

Breathing: Dependent: Uses ventilator and suction equipment(C1-C3)Cannot clear secretionsBowel: total assistance – insertion of suppository & digital stimulationUrinary: Total assistance -insert indwelling catheter or external penile catheterTotal assist for transfersWheelchair: Power – independent, Manual – total assistEating, communication, transportation: total assist

C5Breathing: low endurance and VC due to paralyzed intercostals, requires assistance to clear secretionsBowel and Urinary: total assistBed mobility: needs some assistance but independent in direction of care and controlling bedTotal assist for transfersWheelchair: Power – independent, Manual – independent to some assistEating: independent with equipment w/ total assist for setup (cutting food)Dressing/Bathing: Total assistCommunication: Independent to some assist with equipment

Transport: Independent with specialized equipmentC6-C7

Breathing: same as C5Bowel: some to total assist; independent suppository insertion and rectal stimulator using suppository inserter and digital bowel stimulatorUrinary: independent self-catheterization through a continent urinary diversion; total assist for indwelling catheterBed mobility: some assistTransfers: some assist to independentWheelchair: Manual – independent indoors, some assist outdoorsEating: IndependentDressing/Bathing: Independent upper body, some/total assist lower bodyCommunication: IndependentDriving: Independent from wheelchair

C8Breathing: same as C5Bowel: Independent digital stimulation, suppository insertion and perineal hygieneUrinary: Independent intermittent catheterizationBed mobility: IndependentIndependent transfers w/ or w/o transfer boardWheelchair: Manual: Independent on all surfacesStanding: Some assist to independentEating and Communication: IndependentDressing/Bathing: Some assist to independent with adaptive equipmentDriving: Independent car if independent with transfer and wheelchair loading/unloading. Independent driving modified van

T1-T12Breathing: Same as C5 for higher level thoracic lesionsBowel, Urinary, Bed mobility, Transfers, Wheelchair: same as C8Standing: Independent, ambulation for exercise onlyEating/Dressing/Communication: IndependentDriving: Independent car with hand controls and modified van

L1-S5Normal respirationBowel, Urinary, Bed mobility, Wheelchair: same as T1-T12Transfers: IndependentStanding: IndependentAmbulation: Functional if only 1 KAFO neededEating/Dressing/Communication: IndependentDriving: Independent car with controls depending on level of lesion

E. Prescriptive Wheelchair- Most patients with SCI will use a wheelchair as the primary means of mobilityGeneral considerations:1. Seat depth should be approximately 1-2 in back from the popliteal space for even weight distribution on thighs2. 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. It patient has tetraplegia and will be pushing the wheelchair, the back height recommended would be one below the

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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 patient5. Patients with LE spasticity may require heel loops and/or toe loops on the footrests to keep the feet in place6. 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. 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 hooking one elbow or wrist around the push handle and leaning forward.

F. Ambulation after SCI- 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, and strengthening neurologically intact musculature for standing and walking.

- Full ROM in hip extension is essential in attaining balance in the upright position.- The absence of knee flexion and plantarflexion contractures is also important in

attaining upright standing balance.- Other factors that may restrict ambulation: severe spasticity, loss of

proprioception, pain, presence of secondary complications such as decubitus ulcers, heterotrophic 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 SCIOrthotic prescription

- Patients with complete thoracic lesions will require KAFOs, wherein the ankle joints 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 consist 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 device (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 SCITrain like you walk: 1. The LEs are maximally loaded for weightbearing, minimizing, or eliminating loading of the arms2. The posture, trunk, pelvis, and limb kinematics are coordinated and specific to the task of walking3. Compensatory strategies for movement are minimized of eliminated

G. Functional Electrical StimulationApplication of low-level electrical current to improve function in paralyzed and/or weak musclesCan 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

- SCI is a catastrophic event with a profound effect on the injured person as well as on family members

- Successful adjustment is thought to have occurred when the disability is no longer the dominant concern in the person’s life.

- 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.

- Depression and anxiety are usually present early after SCI Quality of Life

- Determination of the individual’s satisfaction with life- 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.

- Dissatisfaction with life after SCI seems more related to social disadvantages than to physical limitations

Recovery-Enhancing Therapies- 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

Page 10: Spinal Cord Injury

- New motor or sensory deficits are reported to develop in 20-30% of persons with chronic SCI

- Most common is entrapment of a peripheral nerve, especially the median nerve at the carpal tunnel, or ulnar nerve at the elbow.

- Further damage may be caused by post-traumatic syringomyelia

References O’Sullivan, Susan, Physical Rehabilitation, 5th ed., pp 185; 937 – 990.Braddom, Randall, Physical Medicine & Rehabilitation, 4th ed., pp 1293 – 1337.DeLisa, Joel, Physical Medicine & Rehabilitation Principles and Practice, 5th ed., p 672Pablo-Santos, Ramona Luisa, Physical Examination, p 165Lindsay, Kenneth, Neurology and Neurosurgery Illustrated, 5th ed., p 415-417