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Neuromotor II COPY > SCI > Flashcards

SCI Flashcards

1
Q

What are the causes of SCI?

A
  1. Trauma - main cause, 90% of cases
  2. Spinal arteriovenous malformation (AVM) - abnormal tangle of vessels that are on or near the SC that cause compression or hemorrhage
  3. Vertebral subluxations secondary to RA/DJD
  4. Transverse myelitis
  5. Abscess
  6. Cancer
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2
Q

What are the mechanisms of traumatic injury?

A
  1. Fractured vertebrae - burst fracture most common
  2. Dislocation of vertebrae
  3. Shearing
  4. Distraction
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3
Q

What are the most most common sites of traumatic SCI?

A

C5-C7
T12-L2
- transitional vertebrae where there is less stability and generally where a lot of force energy will go

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4
Q

What are the classifications of SCI?

A
  1. Tetraplegia (Quadriplegia, same thing) - all 4 limbs plus trunk
  2. Paraplegia - LEs and maybe some trunk
  3. Neurological level of injury (NLI)
  4. Complete vs. Incomplete injury
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5
Q

How do you find the sensory level for NLI? motor level?

A
  • Sensory level = Last normal intact dermatome to pinprick and light touch
  • Motor level = Last normal myotome with a MMT of 3/5 AND the above segment is intact with a MMT of 5/5
  • Document for each side of the body
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6
Q

What levels cannot be tested via myotomes? how would you define these?

A
  • C1-C4, T2-L1, S2-S5

- Motor level is defined as same as sensory level

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7
Q

How would you define the NLI to a single level?

A

Lowest segment of spinal cord that motor and sensory function is normal on both sides

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8
Q

What are the muscle groups and levels for C5-T1?

A 
C5 = elbow flexors
C6 = Wrist extensors
C7 = Elbow extensors
C8 = Finger Flexors
T1 = Finger abductors
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9
Q

What are the muscle groups and levels for L2-S1?

A 
L2 = Hip flexors
L3 = Knee extensors
L4 = Ankle DFs
L5 = Long toe extensors
S1 = Ankle PFs
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10
Q

No sensory or motor function in the lowest sacral segments (S4-S5); Demonstrated by absence of anal sensation “saddle area” and absence of voluntary anal sphincter contraction

A

Complete injury

- absence of anal sensation and absence of anal contraction

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11
Q

Motor and/or sensory function are present below the level of the lesion including the sacral segments (S4-S5); Have anal sensation “saddle area” and voluntary anal sphincter contraction

A

incomplete injury

  • Sacral sparing
  • good for function
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12
Q

According to the ASIA impairment scale, what does ABCDE grading mean?

A 
A = Complete
B = Sensory incomplete (anal sensation)
C = Motor incomplete
D = Motor incomplete
E = Normal
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13
Q

Motor and/or sensory function is present below the neurological level, but patient has no function at S4 and S5; Applies only to ASIA A complete lesion

A

Zones of partial preservation

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14
Q

Hemisection of the spinal cord (damage to one side); Ipsilateral loss of proprioception, light touch, and vibration below the level of lesion due to dorsal column damage; Ipsilateral loss of motor function below the level of lesion, clonus and decreased reflexes from lateral corticospinal damage; Contralateral loss of pain and temperature sensation several dermatome segments below injury due to damage of spinothalamic tracts

A

Brown- Sequard Syndrome

- generally caused by GSW or stab

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15
Q

Related to flexion injuries of cervical region; Damage to anterior cord and vascular supply from anterior spinal artery; Loss of motor function, pain, and temperature below level of lesion on both sides; Proprioception, light touch, and vibration are preserved because of the separate vascular supply

A

Anterior cord syndrome

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16
Q

Most common SCI syndrome; Hyperextension injuries of the cervical region or narrowing of the spinal canal (severe stenosis); Compressive forces result in hemorrhage and edema; More severe involvement of UE than LE (Cervical motor tracts are more centrally located); Sensory deficits less severe than motor

A

Central cord syndrome

- loss of distal UEs, specifically fine motor control

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17
Q

Starts at lower border of approx. L1 vertebra; Incomplete (large number of nerve roots involved); LMN injury; Bowel and bladder changes, saddle anesthesia, and LE paresis/paralysis; Can regenerate but not common

A

Cauda equina injury

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18
Q

Period of areflexia; Loss of motor and sensory function below level of lesion; Several hours to several weeks - typically subsides in 1-3 days

A

spinal shock
- Bulbocavernous reflex first sign of spinal shock subsiding (pressure to the penis or clitoris with a response of contraction of the anus)

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19
Q

Occurs in SCI in lesions above T6 (but can be as low as T8); Increase in blood pressure (No vasodilation below the level of the lesion so above the level of lesion BP gets very high); More common after 3-6 months post injury; Episodes gradually subside over first 3 years post SCI

A

Autonomic Dysreflexia

- Medical Emergency (stroke)

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20
Q

What are causes of autonomic dysreflexia?

A
  1. Bladder distension (urinary retention) and bladder infections***
  2. Rectal distension
  3. Pressure sores
  4. Kidney stones
  5. Environmental temp changes
  6. Tight fitted clothing
  7. Any noxious stimulus
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21
Q

What are the symptoms of autonomic dysreflexia?

A
  1. Hypertension
  2. Bradycardia - brain attempts to bring down BP
  3. Severe, pounding headache
  4. Profuse sweating
  5. Increased spasticity
  6. Restlessness
  7. Flushing above the level of lesion
  8. Constricted pupils
  9. Goosebumps
  10. Blurred vision
  11. Nasal congestion
22
Q

What are interventions for autonomic dysreflexia?

A
  1. Sit up if lying down to decrease BP (put feet down if able)
  2. Check catheter
  3. Check for other irritations
  4. If symptoms do not subside then get help - Notify medical staff and document episode; Check for bowel impaction; Bladder irrigation; Anti-hypertensives may be indicated
23
Q

Caused by loss of sympathetic vasoconstriction control; Enhanced by loss of muscle tone

A

Orthostatic hypotension

24
Q

How do you treat orthostatic hypotension?

A
  1. Slow progression to the vertical position (tilt table, working on tolerance)
  2. Move patient very slowly during transfers if possible
  3. Continual monitoring of vital signs
  4. Compression garments and abdominal binder
  5. Medications
  6. Tolerance to vertical position gradually improves
25
Q

Temp control is an autonomic dysfunction; Body temp is significantly influenced by external environment; Loss of internal thermoregulation below level of lesion
What symptoms do you see?

A
  1. No shivering
  2. No vasodilation (heat) and vasoconstriction (cold)
  3. No sweating below lesion; diaphoresis above lesion
26
Q

What are respiratory impairments seen in levels C1-C3? C4-T10?

A

C1-C3 injuries are ventilator dependent

C4-T10 will have some degree of compromised respiratory function

27
Q

What accessory muscles are paralyzed under C3? What level SCI will not effect respiration at all?

A
  1. Ext intercostals results in decreased chest expansion and inspiratory volume
  2. Abdominals and int intercostals results in decreased expiratory efficiency and volume and low position of diaphragm
  3. Ext obliques results in less efficient cough
  • T11
28
Q

What are complications of respiratory impairment?

A
  1. Retention of secretions
  2. Atelectasis
  3. Pulmonary infections
29
Q

What altered breathing patterns leading to postural changes are seen in respiratory impairment?

A
  1. Flattening of upper chest wall
  2. Decreased chest wall expansion
  3. Dominant epigastric rise during inspiration
30
Q

How long does spasticity take to plateau?

A

Gradual increase during first 6 months; plateau at 1 year

- usually interferes with rehab

31
Q

What treatments are used for spasticity of respiratory m’s

A

Treated with Baclofen, Botox, etc.

In severe cases: surgical treatment options - Tenotomy or myotomy, Rhizotomy

32
Q

What are bladder complications of SCI?

A
  1. UTI’s. - very common
  2. Spastic/ hyperreflexic pladder (UMN injury)
  3. Flaccid/ areflexic bladder (LMN injury)
33
Q

Bladder dysfunction:
Contracts and reflexively empties in response to a level of filling pressure; Injury above the conus medullaris; Typically T11-L1 vertebral injury or higher

A

Spastic or hyperreflexic bladder

34
Q

Bladder dysfunction:

Can be emptied using manual techniques; Injury of the conus medullaris; Typically T11-L1 vertebral injury or below

A

Flaccid or areflexic bladder

35
Q

What is the primary goal of bladder training programs?

A

to be free of catheter and to control bladder function

36
Q

What are the types of bladder training programs?

A
  1. Intermittent catheterization - Used for both types
  2. Suprapubic tapping (spastic bladder) - tapping directly over bladder with fingertips; works for some, not all
  3. Valsalva or Crede technique (flaccid bladder) - pushing on the bladder to empty
37
Q

What are the bowel programs for flaccid and spastic bowel?

A
  1. Spastic bowel (UMN injury) - Suppositories and digital stimulation
  2. Flaccid bowel (LMN injury) - Straining or manual evacuation techniques
    - Establish a regular pattern of evacuation
    - Bladder and bowel management is an extremely high priority for most patients
38
Q

What is the stereotype of sexual dysfunction for SCI?

A

physical disability can be thought to depress or eliminate sex drive

  • often neglected
  • important component of rehab
39
Q

What is the female response for sexual dysfunction in SCI?

A
  1. Women still have the ability to have sex and bear children
  2. Menstruation can be interrupted following injury but returns to normal
  3. Pregnancy needs close medical supervision; considered high risk - Impaired respiratory function; Autonomic dysreflexia; Failure to perceive onset of labor; Inability to push
40
Q

What is the male response for sexual dysfunction in SCI in terms of erection?

A
  • Higher chance of erection with UMN lesions or Incomplete lesions
  • UMN lesion - Erection via reflexogenic or psychogenic
  • LMN lesion - Erection just through psychogenic (difficult to achieve)
41
Q

What is the male response for sexual dysfunction in SCI in terms of ejaculation?

A

Higher incidence of ejaculation with LMN lesions (lower level of spinal cord) and Incomplete

42
Q

What causes pressure ulcers?

A
  1. Lack of sensation
  2. Inability to change positions
  3. Loss of vasomotor control - lowers tissue resistance to pressure
  4. Shearing forces (due to spasticity or during transfers)
  5. Moisture
  6. Trauma
  7. Nutritional deficiencies
43
Q

How do you prevent pressure ulcers?

A
  1. Frequent turning
  2. Specialized beds and W/C cushions
  3. Education on pressure relief techniques – seated push ups
  4. Regular skin inspection
44
Q

When are DVTs most frequent?

A

first 2 months following injury

45
Q

How do you prevent DVTs in SCI?

A
  1. Anticoagulants
  2. Turning program
  3. PROM
  4. Elastic support stockings
  5. Elevate LE’s to facilitate venous return
46
Q

Osteogenesis of soft tissues below level of lesion; Etiology is unknown ; Extra-articular and extracapsular; Develops in tendons, connective tissue between muscles, aponeuroses; Most common in hip and knee

A

Heterotopic ossification

  • does not develop within mm (differentiate from myositis ossificans)
  • treated with medication and PT should maintain ROM
47
Q

What does pain result from in SCI?

A
  1. Initial trauma that caused the SCI
  2. Nerve roots
  3. Spinal cord dysesthesias (like phantom limb pain, not seen often, over surgical sites where fusion has occurred)
  4. Musculoskeletal system - Shoulder pain is common
48
Q

What causes osteoporosis and kidney stones in SCI? where is osteoporosis seen?

A

Caused by changes in calcium metabolism
Rate of resorption is greater than new bone formation
Osteoporosis below level of lesion
Results in large concentrations of calcium in urinary system

49
Q

How do you treat osteoporosis and kidney stones?

A

Restrict calcium in diet (?) - makes osteoporosis worse
Encourage high protein foods
Early weightbearing activities

50
Q

What is supported by evidence for treatment of painful shoulders in chronic SCI?

A

strengthening and optimal movements

  • 12 week HEP paired with instruction to optimize movement techniques
  • Resulted in significant and persistent reduction in shoulder pain and significant improvements in strength and quality of life

Neuromotor II COPY (7 decks)

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