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NI2 > Spinal Cord Injury > Flashcards

Spinal Cord Injury Flashcards

1
Q

What is a SCI?

A

An insult to the spinal cord resulting in temporary or permanent change to its normal motor, sensory or autonomic function

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2
Q

What are the components of the spinal cord?

A
  • 31 spinal nerves (mixed nerves i.e. motor & sensory)
  • 2 enlargements (brachial & lumbosacral plexus)
  • Anterior/ventral segments: Motor
  • Posterior/dorsal segments: Sensory
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3
Q

What is the role of the spinal cord?

A

Transmits sensory & motor messages relating to
- pain
- movement
- temperature
- touch
- vibration
between the brain & skin, joints muscles & internal organs

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4
Q

What are the main spinal tracts?

A
  • Dorsal columns (movement awareness, light touch & proprioception)
  • Anterior & posterior spinocerebellar (movement awareness, proprioception)
  • Lateral spinothalamic (pain & temperature)
  • Anterior spinothalamic (deep touch)
  • Anterior & lateral corticospinal (motor)
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5
Q

What is the aetiology of SCI?

A
  • Traumatic or non-traumatic
  • Greatest incidence in 15-25 years, 85% male
  • Over 60 years: Male = female
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6
Q

What is primary SCI?

A

Initial mechanical trauma includes traction & compression of neural elements:

  • Fractured/displaced bone fragments, disc material, ligaments
  • Damaged blood vessels, axons, neural-cell membranes
  • Micro-haemorrhages
  • Spinal cord swelling
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7
Q

What is secondary SCI?

A

Hypoperfusion & excitotoxicity

  • Release of toxic chemicals (e.g. glutamate) from damaged cells, axons & vessels
  • Causes damage to surrounding areas (increases extent/height of SCI)
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8
Q

What are the causes of traumatic SCI?

A
  • MVA/MBA
  • Falls
  • Diving/water sports
  • Violence (rare in Aus)
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9
Q

What are the causes of non-traumatic SCI?

A
  • Congenital & developmental disorders (e.g. CP)
  • Degenerative CNS disorders
  • Genetic/metabolic disorders
  • Infections (e.g. HIV)
  • Inflammatory (e.g. MS)
  • Ischaemic (e.g. aortic dissection, embolism)
  • Degenerative musculoskeletal conditions (e.g. RA)
  • Toxic (e.g. radiation)
  • Tumours
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10
Q

What does SCI affect?

A
  • Motor nerves
  • Sensory nerves
  • Autonomic nerves (sympathetic & parasympathetic)
  • Often damages both upper & lower motor neurons
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11
Q

What is an upper motor neuron lesion?

A
  • Lesion above the anterior horn cell/conus (e.g. spinal cord, brain stem, motor cortex)
  • Spinal cord reflexes intact
  • Spastic paralysis
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12
Q

What is a lower motor neuron lesion?

A
  • Lesion either in the anterior horn cell or distal to the anterior horn cell (injuries involving the cauda equina)
  • Loss of spinal cord mediated reflexes
  • Flaccid paralysis (muscle wasting)
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13
Q

How does a combination of UMN & LMN lesions occur?

A
  • Ischaemic damage to anterior horn cells of LMN (widespread)
  • Trauma to LMN at level of injury (specific damage)
  • Injuries at the conus
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14
Q

How are SCIs classified?

A

According to the level of injury, using the ASIA scale

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15
Q

What does the ASIA impairment scale provide information on?

review for exam in lecture notes

A
  • Neurological level of injury (most caudal segment with intact sensation & antigravity muscle strength)
  • Incomplete vs complete injury
  • 2 motor scores (0-5)
  • 2 sensory scores (0-2)
  • 1 neurological level (A-E): Tells you if complete/incomplete
  • Tested in supine
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16
Q

What is a complete SCI?

A
  • Total loss of sensory & motor function below injury level
  • 50% of lesions
  • Loss of function due to contusion to spinal cord, rarely complete transection
  • Combination of complete paralysis, partial paralysis & non-paralysed muscles
17
Q

What is an incomplete SCI?

A
  • Some function below injury level

- More common with non-traumatic SCI, however may present with a wide variety of impairments

18
Q

What is the role of a physio in SCI?

A
  • Respiratory care
  • Rehab/training of activities
  • Wheelchair skills (posture, technique)
  • Equipment prescription & home visits
  • Exercise & fitness training
  • Pain management
  • Prevention of secondary impairments
19
Q

What should a SCI physio assessment include?

A

Impairments

  • Loss of strength, sensation, fitness, muscle length & joint range
  • Spasticity

Activity limitations

20
Q

What are the primary impairments in SCI?

A
  • Loss of strength
  • Loss of sensation
  • Spasticity (only in UMN lesions)
  • ANS impairments
21
Q

What are the secondary impairments in SCI?

A
  • Contracture
  • Disuse weakness
  • CV deconditioning
22
Q

How is loss of strength treated in complete lesions?

A
  • Target strengthening of non-paralysed muscles

- Also includes partially paralysed muscles

23
Q

How is loss of strength treated in incomplete lesions?

A

Strengthening according to general neurological principles (based on Oxford grading)

24
Q

What are the characteristics of loss of sensation in SCI?

A
  • Dermatomal
  • Variable depending on lesion
  • Sensation assessed on ASIA sensory assessment
  • Sensory level of injury may differ from motor level of injury
25
Q

What are the characteristics of spasticity in SCI?

A
  • Present in up to 80% SCI
  • More detrimental in incomplete lesions
  • Tends to gradually increase over first year, then plateaus
26
Q

What does the medical management of spasticity include?

A

Pharmacological agents acting primarily within the CNS (e.g. baclofen), muscle or NMJ (e.g. botox)

27
Q

What are the characteristics of contracture in SCI?

A
  • Due to paralysis or spasticity
  • Can impact significantly on function, pressure management, cosmesis (appearance) & hygiene
  • May be a goal of treatment
  • Assessed with Tardieu
28
Q

What are the CV implications in SCI?

A
  • Secondary impairment due to deconditioning
  • Impact of SCI on ANS (e.g. max HR for SCI above T1 can be 130bpm)
  • Decreased ability to train central factors
  • Increased CVS requirements of new motor skills
  • CVD is the leading cause of death in long term SCI
29
Q

What are the autonomic functions of the spinal cord?

A
  • Heart rate
  • Peristalsis
  • Smooth muscle contraction
  • Sweating
  • Sympathetic (T1-L2): Fight/flight, BP, HR, bronchodilation of lungs etc
  • Parasympathetic (Cranial nerves & sacral segments): Rest & digest functions
30
Q

What is the main aim of acute management of SCI?

A

Reducing secondary injury to minimise extent of damage to the spinal cord

31
Q

What is the anterior horn cell?

A

Point in the spinal cord where spinal nerves synapse with motor effector nerves

32
Q

Why is spasticity not an impairment in LMN lesions?

A

Because the LMN needs to be intact for the stretch reflex to occur for spasticity

33
Q

Why is spasticity not always detrimental in complete lesions?

A
  • Spasticity/contracture can allow them to achieve functional activities
  • E.g. encourage spasticity/contracture in long finger flexors to allow for modified tenodesis grip
  • Helps prevent venous pooling
  • Allows for passive weight bearing during transfers
34
Q

Why is spasticity more detrimental in incomplete lesions?

A
  • Outcome is variable
  • Patients may recover function up to 2 years post injury
  • Need to prevent contracture to ensure max return to function
  • Focus is on knee flexors (long sitting), wrist flexors, PFs etc

NI2 (12 decks)

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