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711 Adult Neurological Rehab > Spinal Cord Injury > Flashcards

Spinal Cord Injury Flashcards

1
Q

Complete Spinal Cord Injury

A

Absence of sensory and motor function below lesion level

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2
Q

Incomplete Spinal Cord Injury

A

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

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3
Q

Methylprednisone

A 
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
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4
Q

Common causes of SCI

A

Transection
Compression
Infection
Degenerative Disorders

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5
Q

Transection

A

Complete severance of the cord;

All sensory & motor information is interrupted at or below lesion level

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6
Q

Causes of Transection

A 
Traumatic injury including: 
Auto accidents
Knife wounds
Gun shot wounds
Diving accidents
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7
Q

Compression

A

Impingement of the cord;

Symptoms depend on the severity of the injury

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8
Q

Causes of Compression

A

Trauma
Tumor
Vertebral degenerative joint disease

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9
Q

Infection

A

May compromise the integrity of the cord;

Polio is an example

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10
Q

Degenerative Disorders

A

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

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11
Q

SCI Non-Traumatic

A

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

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12
Q

SCI Traumatic

A

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

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13
Q

Traumatic Cervical Injury

A

C5 and C7 most often areas of injury;

Flexion, vertical loading, and extension accompanied by rotation or lateral flexion

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14
Q

Traumatic Thoracic Injuries

A

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

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15
Q

Traumatic Lumbar Injuries

A

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

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16
Q

Neuropathology

A

Most damage is caused by secondary sequelae of initial trauma beginning progressive tissue destruction within the cord; travels up or down 1-3 segments

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17
Q

Mechanism of Secondary Tissue Destruction

A

Ischemia, Edema, Demyelination and destruction

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18
Q

Ischemia

A

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

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19
Q

Edema

A

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.

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20
Q

Demyelination and destruction

A

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

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21
Q

Spinal Shock

A

Temporary phenomenon that occurs after trauma to the spinal cord in which the cord ceases to function below the lesion

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22
Q

How long does it take spinal shock to resolve?

A

Within 24 hours of injury

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23
Q

What does sparing of sensation or voluntary motor function indicate?

A

lesion is incomplete

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24
Q

Paraplegia

A

only lower extremities are involved, resulting in weakness (paraparesis) or paralysis

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25
Q

Tetraplegia

A

all 4 extremities are involved, also known as quadriplegia or quadriparesis ( weakness)

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26
Q

What muscle Grade of strength is needed to have intact innervation?

A

3+/5

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27
Q

UMN

A

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

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28
Q

LMN

A

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

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29
Q

UMN Lesion Sign

A

Spasticity, hyperactive reflexes, clonus, flaccidity

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30
Q

LMN Lesion Sign

A

Flaccidity, Hyporeflexia, muscle atrophy, fibrillations, and fasciculations

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31
Q

Brown-Sequard Syndrome

A

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

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32
Q

Anterior Cord Syndrome

A

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

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33
Q

Central Cord Syndrome

A

Cavitation of the central cord in the cervical segments causing loss of UE sensation loss and motor functioning with normal lower extremity functioning

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34
Q

Central Cord Syndrome symptoms

A

Bilateral loss of pain and temperature of UE’s (spinothalamic tracts)
Flaccidity of UE’s (ventral horn)

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35
Q

Posterior Cord Syndrome

A

Affects posterior and posterolateral white funiculi of the SC

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36
Q

Causes of Posterior Cord Syndrome

A

Degeneration of the SC from severe vitamin B12 deficiency

Pernicious anemia, AIDS

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37
Q

Posterior Cord Syndrome Symptoms

A 
Bilateral loss of discriminative touch, pressure, vibration and proprioception (dorsal column)
Bilateral spastic paralysis (lateral corticospinal tract)
Bilateral ataxia (spinocerebellar tract)
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38
Q

Anterior Horn Cell Syndrome

A

LMN damage caused by disease processes that destroys motor neurons in the ventral horn

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39
Q

Anterior Horn Cell Syndrome Symptoms

A

bilateral flaccidity in muscles innervated by the affected SC level
Example: Poliomyelitis- acute viral disease affecting the ventral horn motor cell bodies

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40
Q

Cauda Equina

A

Injury below L1 that results in damage to lumbar and sacral nerve roots, regeneration may be possible since damage is to peripheral nerve roots

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41
Q

Cauda Equina Symptoms

A

sensory loss, weakness in both legs, areflexia, neuropathic pain, paralysis and loss of bladder/bowel may occur

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42
Q

Sacral Sparing

A

incomplete lesion in which the most centrally located sacral tracts are spared

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43
Q

Autonomic Dysreflexia in SCI

A

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

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44
Q

Autonomic Dysreflexia symptoms

A 
Severe hypertension
Bradycardia
Severe headache
Vasodilation
Flushed skin
Profuse sweating above the lesion level
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45
Q

Causes of Autonomic Dysfelexia

A 
Full bladder or rectum
Stimulation of pain receptors
Ingrown toenails
Dressing changes
Visceral contractions
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46
Q

Complications for SCI

A 
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
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47
Q

Common Areas For Pressure Ulcers

A

Scapula, Elbow, Sacrum, Ischium, Heel, Ball of Foot

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48
Q

Postural or Orthostatic Hypotension

A

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.

49
Q

Symptoms of Postural or Orthostatic Hypotension

A

Sudden drop in BP
Dizziness
Fainting
Blackout

50
Q

Antiepileptic drugs (anitsezure drugs)

A

Gabapentin (Neurontin)
Carbamazepine (Tegretol)
Tricyclic antidepressants and anticonvulsants

51
Q

Heterotopic Ossification (HO)

A

Abnormal bone formation including spurring in the intra-articular joint space or the soft tissues around the joint (below the level of the injury).

52
Q

Potential Causes of Heterotopic Ossification

A

Tissue hypoxia
Abnormal calcium metabolism
Local trauma

53
Q

Clinical signs of Heterotropic Ossification

A

ROM limitations
Swelling, warmth, pain
Fever may or may not be present

54
Q

PT management of HO

A

Gentle ROM

55
Q

Deep Vein Thrombosis (DVT)

A

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.

56
Q

Prevention of DVT

A

Regular turning programs & early mobilization
Elastic supports & sequential compression devices for LEs
assist with venous return.
Prophylactic anticoagulants - oral warfarin (Coumadin) or IV
heparin

57
Q

Cause of Osteoporosis & Renal Calculi

A

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

58
Q

Ways to minimize OP and Renal Calculi

A

Early mobilization
Therapeutic standing
Administration of calcium supplements
Good dietary management

59
Q

Respiratory Compromise

A

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.

60
Q

Respiratory Muscles

A

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)

61
Q

Bladder and Bowel Function are innervated by:

A

The lower sacral segments (S2-4).

62
Q

T/F During SPinal shock the bladder is flaccid.

A

TRUE

63
Q

T/F Males after SCI will never function sexually again.

A

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

64
Q

T/F Women with SCI can get pregnant and have children

A

TRUE

Pregnant women with SCIs are usually hospitalized due to not feeling the contractions indicating labor.

65
Q

PT Management of Spasticity

A

Positioning, static stretching, weight bearing, cryotherapy, aquatics, FES

66
Q

Pharmacological Management of Spasticity

A

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

67
Q

Surgical Interventions for Spasticity

A

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)

68
Q

C1-3 lesion key muscles and capabilities

A

Face and neck

Capable of talking, mastication, sipping and blowing. Dependent self care

69
Q

C4 lesion key muscles and capabilities

A

Diaphragm and trapezius

Capable of respiration and scapular elevation, ventilator usually not needed

70
Q

C5 lesion key muscles

A

biceps, brachialis, brachioradialis, deltoid, infraspinatus, rhomboids, and supinator

71
Q

C5 lesion movement capabilities

A

Capable of elbow flexion and supination, shoulder external rotation, abduction to 90 and limited shoulder flexion.

72
Q

C5 lesion functional abilities

A

Mod to min assistance required for LE dressing and rolling, dependent for slide board transfers, driving possible with a van lift

73
Q

C6 lesion key muscles

A

Extensor carpi radialis, infraspinatus, lats, pec major, serratus anterior and teres minor

74
Q

C6 lesion movement capabilities

A

capable of shoulder flexion/extension, internal rotation and adduction,
Scapular abduction and upward rotation
Forearm pronation
Wrist extension (tenodesis grip)

75
Q

C6 lesion functional abilities

A

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

76
Q

C7 lesion key muscles

A

Extensor pollicis lingus and brevis, extrinsic finger estensors, flexor carpi radialis and triceps

77
Q

C7 lesion movement capabilities

A

elbow extension, wrist flexion, finger extension

78
Q

C7 lesion functional capabilities

A

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

79
Q

C8 lesion key muscles

A

extrinsic finger flexors, flexor carpi ulnaris and flexor pollicis longus and brevis

80
Q

C8 lesion movement capabilities

A

capable of full use of all UE muscles except intrinsics of hand

81
Q

C8 lesion functional capabilities

A

Independent in home except heavy work,
May need tub seat, grab bars etc
Able to work in building without architectural barriers

82
Q

T1-T5 lesion key muscles

A

top half of intercostals, long muscles of back, intrinsic finger flexors

83
Q

T1-T5 lesion movement capabilities

A

Capable of full use of UE’s, improved trunk control, increased respiratory reserve

84
Q

T1-T5 functional capabilities

A

Independent in all areas including care transfers, able to negotiate curbs
Standing table for physiologic standing
Participates in WC sports

85
Q

T6-T8 lesion key muscles

A

Long muscles of back including sacrospinalis and semispinalis

86
Q

T6-T8 lesion movement capabilities

A

Improved trunk control and respiratory reserve

87
Q

T6-T8 lesion function capabilities

A

Independent in swing to gait in parallel bars with bilat KAFOs for short distances,
Will use WC for community locomotion

88
Q

T9-T12 lesion key muscles

A

Lower abdominals, all intercostals

89
Q

T9-T12 capabilities

A

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

90
Q

T12-L3 lesion key muscles

A

gracilis, iliopsoas, quadratus lumborum, rectus femoris and sartorius

91
Q

T12-L3 lesion movement capabilities

A

hip flexion and adduction, knee extension

92
Q

T12-L3 lesion functional abilities

A

Ind swing to or through or 4 pt gait with bilateral KAFO’s and forearm crutches
Ind home ambulators, can be community ambulators

93
Q

L4-L5 lesion key muscles

A

low back muscles, medial hamstring, posterior tib, quads, tibialis anterior

94
Q

L4-L5 lesion capabilities

A

Strong hip flexion and knee extension, weak knee flexion

Ind home ambulators, can be community ambulators

95
Q

Causes of Anterior Cord Syndrome

A

Infarct (spinal cord stroke)
Ischemia
Trauma (flexion injury to Cervical Spine)

96
Q

Cases of Brown-Sequard Syndrome

A

MS
Stab wounds/ GSW
Tumor

97
Q

Causes of Central Cord Syndrome

A

Hyperextension injuries with minor trauma to cervical region
narrowing or stenotic changes in SC due to arthritis
congenital stenosis

98
Q

Autonomic dysreflexia occurs when

A

after spinal shock has resolved and normal autonomic reflexes return, can initially occur or recur at any time during patient’s lifespan

99
Q

PT Management for Pressure Ulcers

A

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

100
Q

Autonomic Disreflexia

A

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

101
Q

Symptoms of Autonomic Dysreflexia

A 
Flushed Face
Pounding Headache
Anxiety
Profuse Sweating above level of lesion
Very High BP
Bradycardia
102
Q

PT Management of Autonomic Dysreflexia

A

Check bladder/catheter
Monitor BP
Notify Nurse/Physician
Initiate emergency responses if not resolved withing 10 minutes!!!!

103
Q

PT management of Orthostatic Hypotension

A

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

104
Q

Causes of Pain

A

Irritation & damage to neural elements, mechanical

trauma, surgical interventions, poor handling & positioning

105
Q

Common types/terms of pain

A

Dysesthetic Pain = Phantom pain= Deafferentation Pain

106
Q

Common Complaints of Pain

A

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

107
Q

Medications for pain

A

Ibuprofen (Motrin)
Naproxen (Naprosyn)
Indomethacin (Indocin)

108
Q

Contractures

A

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

109
Q

Regular Prone Positioning

A

At least 20 minutes/day

Prone positioning also relieves pressure on ischial tuberosities and aeration to the buttocks

110
Q

Pharmacological Management of HO

A

Etidronate (Didronel)

111
Q

Thermoregulation

A

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

112
Q

Edema

A

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

113
Q

T/F If you suspect DVT don’t worry about it, there is no need to call a nurse or doctor.

A

FALSE
*If suspected call physician immediately = medical
emergency!
*If suspected or confirmed = rest and no LE exercises.

114
Q

Interventions for Respiratory Compromise

A

Early mobilization, corsets, diaphragmatic strengthening and incentive spirometry

115
Q

2 Possibilities after spinal shock

A

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.

116
Q

Symptoms of Bladder and Bowel Dysfuction

A

Fever, chills, nausea, HA, increased spasticity, autonomic dysreflexia, dark or bloody urine.

117
Q

Managment of Bladder and Bowel Function

A 
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
118
Q

Spasticity

A

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.

119
Q

Potential Advantages to Increase in Tone

A 
Maintains muscle bulk
Prevent atrophy
Maintenance of circulation
Assist with transfers & bed mobility
Increased tone to anal sphincter may aid in a bowel program

711 Adult Neurological Rehab (12 decks)

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