Spinal Cord Injury Flashcards
Complete Spinal Cord Injury
Absence of sensory and motor function below lesion level
Incomplete Spinal Cord Injury
Involves partial preservation of sensory and motor functions below the lesion level
Better prognosis than complete SCI due to preserved axon function: occur more frequently than complete SCI
Methylprednisone
corticosteroid used for SCI to... Stabilizes cell membranes, Decreases inflammation, Increases nerve impulse generation, Improves blood flow to the damaged area; Must be administered in first 3-8 hours after injury
Common causes of SCI
Transection
Compression
Infection
Degenerative Disorders
Transection
Complete severance of the cord;
All sensory & motor information is interrupted at or below lesion level
Causes of Transection
Traumatic injury including: Auto accidents Knife wounds Gun shot wounds Diving accidents
Compression
Impingement of the cord;
Symptoms depend on the severity of the injury
Causes of Compression
Trauma
Tumor
Vertebral degenerative joint disease
Infection
May compromise the integrity of the cord;
Polio is an example
Degenerative Disorders
Can damage the SC tracts;
Example: Amyotrophic lateral sclerosis (ALS) results in bilateral degeneration of the ventral horn & pyramidal tracts;
Involves both LMN and UMN damage
SCI Non-Traumatic
10%- Most likely to occur with narrowing spinal canals;
Possible Causes: disc prolapse, vascular insult, neoplasm, RA, radiation, spinal stenosis, cardiac arrest, aortic aneurysm, infection
SCI Traumatic
Most involve a single level or limited number of contiguous vertebrae;
Result from forces that create violent motions of head or trunk:
MVA, jumps, falls, athletic injury, diving accidents or GSW’s
Traumatic Cervical Injury
C5 and C7 most often areas of injury;
Flexion, vertical loading, and extension accompanied by rotation or lateral flexion
Traumatic Thoracic Injuries
Less likely to be injured due to rib cage; T12-L1 junction is most common site of injury;
Flexion motion or vertical compression can cause wedge compression or burst fractures of the vertebral bodies damaging the spinal cord
Traumatic Lumbar Injuries
Usually incomplete due to large vertebral canal and good vascular supply; Most injuries occur at L1 or L2 levels, below these levels the cauda equina is less likely to sustain a complete injury
Neuropathology
Most damage is caused by secondary sequelae of initial trauma beginning progressive tissue destruction within the cord; travels up or down 1-3 segments
Mechanism of Secondary Tissue Destruction
Ischemia, Edema, Demyelination and destruction
Ischemia
decreased blood flow to traumatized area may be due to chemicals in the body that cause vasoconstriction or thomboses, metabolic disturbances or elevated pressure due to edema
Edema
abnormal concentrations of sodium and potassium in the extracellular tissue. causes an increase in osmotic pressure in the damaged area of the cord and creates excessive edema in this area.
Demyelination and destruction
calcium ions accumulate in the injured cells. This disrupts functioning and causes demyelination and destruction of the cell membrane and axonal cytoskeleton. The necrosis of axons then progresses to scar tissue formation
Spinal Shock
Temporary phenomenon that occurs after trauma to the spinal cord in which the cord ceases to function below the lesion
How long does it take spinal shock to resolve?
Within 24 hours of injury
What does sparing of sensation or voluntary motor function indicate?
lesion is incomplete
Paraplegia
only lower extremities are involved, resulting in weakness (paraparesis) or paralysis
Tetraplegia
all 4 extremities are involved, also known as quadriplegia or quadriparesis ( weakness)
What muscle Grade of strength is needed to have intact innervation?
3+/5
UMN
Carries motor info from the cortex or subcortical regions to CN; all SC injuries & diseases that affect the cord between the levels of C1-T12
LMN
Carries info from the motor cell bodies in the ventral horn to the skeletal muscles and includes: CN, L1-L2 vertebrae, Cauda Equina, and Peripheral nerves
UMN Lesion Sign
Spasticity, hyperactive reflexes, clonus, flaccidity
LMN Lesion Sign
Flaccidity, Hyporeflexia, muscle atrophy, fibrillations, and fasciculations
Brown-Sequard Syndrome
Pathology: SC hemisection (half of it);
Ipsilateral loss of motor control and spasticity below the lesion level, Ipsilateral loss of discriminative touch, pressure, vibration, and proprioception, Pain & Temp lost Contralaterally below lesion level, Pain & Temp lost bilaterally at lesion level
Anterior Cord Syndrome
Discriminative touch, vibration, pressure, and proprioception are spared;
Bilateral voluntary motor control lost below the level of the lesion, flaccidity at and below the lesion level,Bilateral loss of pain and temperature
Central Cord Syndrome
Cavitation of the central cord in the cervical segments causing loss of UE sensation loss and motor functioning with normal lower extremity functioning
Central Cord Syndrome symptoms
Bilateral loss of pain and temperature of UE’s (spinothalamic tracts)
Flaccidity of UE’s (ventral horn)
Posterior Cord Syndrome
Affects posterior and posterolateral white funiculi of the SC
Causes of Posterior Cord Syndrome
Degeneration of the SC from severe vitamin B12 deficiency
Pernicious anemia, AIDS
Posterior Cord Syndrome Symptoms
Bilateral loss of discriminative touch, pressure, vibration and proprioception (dorsal column) Bilateral spastic paralysis (lateral corticospinal tract) Bilateral ataxia (spinocerebellar tract)
Anterior Horn Cell Syndrome
LMN damage caused by disease processes that destroys motor neurons in the ventral horn
Anterior Horn Cell Syndrome Symptoms
bilateral flaccidity in muscles innervated by the affected SC level
Example: Poliomyelitis- acute viral disease affecting the ventral horn motor cell bodies
Cauda Equina
Injury below L1 that results in damage to lumbar and sacral nerve roots, regeneration may be possible since damage is to peripheral nerve roots
Cauda Equina Symptoms
sensory loss, weakness in both legs, areflexia, neuropathic pain, paralysis and loss of bladder/bowel may occur
Sacral Sparing
incomplete lesion in which the most centrally located sacral tracts are spared
Autonomic Dysreflexia in SCI
Acute episode of exaggerated sympathetic reflex responses in SCI tract that occurs because higher center reflex regulation is lost, usually in SCI’s at T6 and above
Autonomic Dysreflexia symptoms
Severe hypertension Bradycardia Severe headache Vasodilation Flushed skin Profuse sweating above the lesion level
Causes of Autonomic Dysfelexia
Full bladder or rectum Stimulation of pain receptors Ingrown toenails Dressing changes Visceral contractions
Complications for SCI
Pressure Ulcers Autonomic Dysreflexia Postural Hypotension Pain Contractures Heterotopic Ossification (HO) Thermoregulation Edema Deep Vein Thrombosis (DVT) Osteoporosis & Renal Calculi Respiratory Compromise Bladder & Bowel Dysfunction Sexual Dysfunction Spasticity
Common Areas For Pressure Ulcers
Scapula, Elbow, Sacrum, Ischium, Heel, Ball of Foot
Postural or Orthostatic Hypotension
Low BP when moving from horizontal to vertical position
Lack of an efficient muscle tone AND loss of sympathetic
vasoconstriction response in the LE’s causes Venous Pooling in LE’s.
Decreased cardiac output and blood volume following
immobilization of 6-8 weeks.
Symptoms of Postural or Orthostatic Hypotension
Sudden drop in BP
Dizziness
Fainting
Blackout
Antiepileptic drugs (anitsezure drugs)
Gabapentin (Neurontin)
Carbamazepine (Tegretol)
Tricyclic antidepressants and anticonvulsants
Heterotopic Ossification (HO)
Abnormal bone formation including spurring in the intra-articular joint space or the soft tissues around the joint (below the level of the injury).
Potential Causes of Heterotopic Ossification
Tissue hypoxia
Abnormal calcium metabolism
Local trauma
Clinical signs of Heterotropic Ossification
ROM limitations
Swelling, warmth, pain
Fever may or may not be present
PT management of HO
Gentle ROM
Deep Vein Thrombosis (DVT)
Risk is greatest in the first 2 - 3 months after injury
Loss of muscle pumping contributes to thrombus formation.
Presentation: swelling, heat, pain in involved area, usually calf.
May not have positive Homan’s sign due to sensory impairment.
Prevention of DVT
Regular turning programs & early mobilization
Elastic supports & sequential compression devices for LEs
assist with venous return.
Prophylactic anticoagulants - oral warfarin (Coumadin) or IV
heparin
Cause of Osteoporosis & Renal Calculi
Changes in Calcium metabolism
Decreased weight bearing may lead to demineralization of bones
Can lead to vertebral compression fractures and other fractures.
Calcium from bones is absorbed into the blood → deposited in Kidneys → Kidney stones
Ways to minimize OP and Renal Calculi
Early mobilization
Therapeutic standing
Administration of calcium supplements
Good dietary management
Respiratory Compromise
Decreased respiratory capabilities can be serious & life threatening.*
Develop as a result of decreased innervation to muscles of respiration & immobility.
Decreased Tidal volume and Vital capacity.
Respiratory Muscles
Diaphragm (C3-5) – Phrenic n.
-Primary muscle of inspiration
-If injury at or above this level may require ventilator or phrenic nerve stimulator.
External intercostals –
-Assist with inspiration & are innervated segmentally starting at T1
Paraplegia below T12 –
-Innervation to the intercostals is intact & should be able to use the diaphragm and intercostals equally.
Abdominals:
-Upper abs (T7-9); Lower abs (T9-11)
Bladder and Bowel Function are innervated by:
The lower sacral segments (S2-4).
T/F During SPinal shock the bladder is flaccid.
TRUE
T/F Males after SCI will never function sexually again.
FALSE
Males with UMN Lesions have potential for reflex erections if sacral arch is intact via reflex.
Ability for normal sexual response is limited for patients with both UMN & LMN injuries
Males have problems with fertility
T/F Women with SCI can get pregnant and have children
TRUE
Pregnant women with SCIs are usually hospitalized due to not feeling the contractions indicating labor.
PT Management of Spasticity
Positioning, static stretching, weight bearing, cryotherapy, aquatics, FES
Pharmacological Management of Spasticity
Intrathecal Baclofen pumps
-More effective in ↓ LE tone because of catheter placement (Katz, 1988)
“Botox”- Botulism injections
-Botulism Toxin A injected directly into spastic muscle
-Inhibits release of Acetylcholine at the neuromuscular junction
-Temporary paralysis of muscle
Surgical Interventions for Spasticity
Neurectomies: surgical excision of nerve segment
Rhizotomies: surgical procedure resecting the dorsal or sensory root of a spinal nerve
Myelotomies: tracts within the spinal cord are severed
Tenotomies: surgical release of a tendon
Nerve & motor point blocks: injectable phenol temporarily reduces spasticity (3-6 months)
C1-3 lesion key muscles and capabilities
Face and neck
Capable of talking, mastication, sipping and blowing. Dependent self care
C4 lesion key muscles and capabilities
Diaphragm and trapezius
Capable of respiration and scapular elevation, ventilator usually not needed
C5 lesion key muscles
biceps, brachialis, brachioradialis, deltoid, infraspinatus, rhomboids, and supinator
C5 lesion movement capabilities
Capable of elbow flexion and supination, shoulder external rotation, abduction to 90 and limited shoulder flexion.
C5 lesion functional abilities
Mod to min assistance required for LE dressing and rolling, dependent for slide board transfers, driving possible with a van lift
C6 lesion key muscles
Extensor carpi radialis, infraspinatus, lats, pec major, serratus anterior and teres minor
C6 lesion movement capabilities
capable of shoulder flexion/extension, internal rotation and adduction,
Scapular abduction and upward rotation
Forearm pronation
Wrist extension (tenodesis grip)
C6 lesion functional abilities
Can become independent in self care with equipment
Can be independent in rolling and unsupported sitting
Use of manual WC for house mobility
Manual coughing technique
Can drive with hand controls and live without assistance if well motivated
C7 lesion key muscles
Extensor pollicis lingus and brevis, extrinsic finger estensors, flexor carpi radialis and triceps
C7 lesion movement capabilities
elbow extension, wrist flexion, finger extension
C7 lesion functional capabilities
Independent in LE self ROM exercises,
Can us manual WC with friction hand rims for community integration
May need button hook for independent dressing
Able to get WC in/out of car
C8 lesion key muscles
extrinsic finger flexors, flexor carpi ulnaris and flexor pollicis longus and brevis
C8 lesion movement capabilities
capable of full use of all UE muscles except intrinsics of hand
C8 lesion functional capabilities
Independent in home except heavy work,
May need tub seat, grab bars etc
Able to work in building without architectural barriers
T1-T5 lesion key muscles
top half of intercostals, long muscles of back, intrinsic finger flexors
T1-T5 lesion movement capabilities
Capable of full use of UE’s, improved trunk control, increased respiratory reserve
T1-T5 functional capabilities
Independent in all areas including care transfers, able to negotiate curbs
Standing table for physiologic standing
Participates in WC sports
T6-T8 lesion key muscles
Long muscles of back including sacrospinalis and semispinalis
T6-T8 lesion movement capabilities
Improved trunk control and respiratory reserve
T6-T8 lesion function capabilities
Independent in swing to gait in parallel bars with bilat KAFOs for short distances,
Will use WC for community locomotion
T9-T12 lesion key muscles
Lower abdominals, all intercostals
T9-T12 capabilities
Increased endurance and improved trunk control
Ind swing to or through gait on level surfaces with KAFOs and walker or forearm crutches
Ind floor to WC and tub transfer
May me ind house ambulators, will use WC for outdoor locomotion and energy conservation
T12-L3 lesion key muscles
gracilis, iliopsoas, quadratus lumborum, rectus femoris and sartorius
T12-L3 lesion movement capabilities
hip flexion and adduction, knee extension
T12-L3 lesion functional abilities
Ind swing to or through or 4 pt gait with bilateral KAFO’s and forearm crutches
Ind home ambulators, can be community ambulators
L4-L5 lesion key muscles
low back muscles, medial hamstring, posterior tib, quads, tibialis anterior
L4-L5 lesion capabilities
Strong hip flexion and knee extension, weak knee flexion
Ind home ambulators, can be community ambulators
Causes of Anterior Cord Syndrome
Infarct (spinal cord stroke)
Ischemia
Trauma (flexion injury to Cervical Spine)
Cases of Brown-Sequard Syndrome
MS
Stab wounds/ GSW
Tumor
Causes of Central Cord Syndrome
Hyperextension injuries with minor trauma to cervical region
narrowing or stenotic changes in SC due to arthritis
congenital stenosis
Autonomic dysreflexia occurs when
after spinal shock has resolved and normal autonomic reflexes return, can initially occur or recur at any time during patient’s lifespan
PT Management for Pressure Ulcers
Instruct in patient relief
Teach family and/or care-giver weight shifting (3-4) times an hour regardless of surface
1 minute of pressure relief for every 15-30 minutes of sitting
Skin Inspections with mirror
Seating Cushions
Autonomic Disreflexia
Occurs in patients with SCI above T6
Caused by SNS instability
Descending +/- input to sympathetic neurons lost
Autonomic responses are discharged as a result of a noxious sensory stimulus (UTI, full bladder, blocked catheter, blocked bowel, Pressure Sores)
These symptoms lead to: autonomic stimulation, Vasoconstriction, Rapid and Massive rise in BP
Receptors in carotid sinus and aorta adjust to peripheral vascular changes
Due to the injury impulses are unable to travel below the level of the injury to lower BP
Symptoms of Autonomic Dysreflexia
Flushed Face Pounding Headache Anxiety Profuse Sweating above level of lesion Very High BP Bradycardia
PT Management of Autonomic Dysreflexia
Check bladder/catheter
Monitor BP
Notify Nurse/Physician
Initiate emergency responses if not resolved withing 10 minutes!!!!
PT management of Orthostatic Hypotension
Monitor BP: Don’t let it drop below 70/40 mmHg (Cardiac Arrest)
Recline patient and elevate LE’s
Use of Abdominal Binder and/or Pressure Stockings
Causes of Pain
Irritation & damage to neural elements, mechanical
trauma, surgical interventions, poor handling & positioning
Common types/terms of pain
Dysesthetic Pain = Phantom pain= Deafferentation Pain
Common Complaints of Pain
Numbness, Tingling, Burning, Shooting and aching pain, and vissceral discomfort below the level of injury
Can be exaggerated by noxious stimuli, UTI, spasticity, Bowel Impaction, and cigarette smoking
Medications for pain
Ibuprofen (Motrin)
Naproxen (Naprosyn)
Indomethacin (Indocin)
Contractures
Develop as a result of flexor reflex activity and from prolonged shortening of muscles around a joint
Prolonged Positioning
Instruct in a good stretching program
Regular Prone Positioning
At least 20 minutes/day
Prone positioning also relieves pressure on ischial tuberosities and aeration to the buttocks
Pharmacological Management of HO
Etidronate (Didronel)
Thermoregulation
Body temperature regulated by the sympathetic nervous system
Hypothalamus: Location of mechanisms for body temperature
After SCI, communication between hypothalamic temperature regulators and sympathetic function below the lesion level become disrupted.
Body’s ability to control blood vessel responses that conserve or dissipate heat is lost
-Ability to sweat & shiver are lost
-At risk of hypothermia due to peripheral vasodilation.
-Later at risk of hyperthermia due to lack of sweat gland control.
Higher level injuries → greater disturbances in temperature control
Edema
Presence of an abnormal accumulation of fluid in interstitial tissue
Frequently occurs in SCI as a result of immobility →
Increased venous pressure →
Abnormal pooling of blood in abdomen, lower limbs, and
extremities
T/F If you suspect DVT don’t worry about it, there is no need to call a nurse or doctor.
FALSE
*If suspected call physician immediately = medical
emergency!
*If suspected or confirmed = rest and no LE exercises.
Interventions for Respiratory Compromise
Early mobilization, corsets, diaphragmatic strengthening and incentive spirometry
2 Possibilities after spinal shock
Reflex or Spastic bladder (lesion above S2, UMN)
-Sacral reflex is intact.
-Bladder will automatically empty in response to inner, filling pressure at certain level.
Nonreflexive or Flaccid Bladder (cauda equina or conus medullaris, LMN)
-Sacral reflex is not absent.
-Bladder can be emptied by applying lower abdominal pressure.
Symptoms of Bladder and Bowel Dysfuction
Fever, chills, nausea, HA, increased spasticity, autonomic dysreflexia, dark or bloody urine.
Managment of Bladder and Bowel Function
Bladder training programs -Intermittent catheterization -Timed voiding -Manual stimulation Establish regular bowel program -Regular schedule of bowel evacuation -High-fiber diets, adequate fluids, stool softeners -Manual stimulation or evacuation
Spasticity
Prevalence is higher in patients with cervical & incomplete injuries
After spinal shock resolves, reflexes return and can increase tone/spasticity.
Noxious stimuli and quick stretching results in increased reflexia and hypertonicity.
Potential Advantages to Increase in Tone
Maintains muscle bulk Prevent atrophy Maintenance of circulation Assist with transfers & bed mobility Increased tone to anal sphincter may aid in a bowel program
