Spinal Cord Injury Flashcards
What is a SCI?
An insult to the spinal cord resulting in temporary or permanent change to its normal motor, sensory or autonomic function
What are the components of the spinal cord?
- 31 spinal nerves (mixed nerves i.e. motor & sensory)
- 2 enlargements (brachial & lumbosacral plexus)
- Anterior/ventral segments: Motor
- Posterior/dorsal segments: Sensory
What is the role of the spinal cord?
Transmits sensory & motor messages relating to
- pain
- movement
- temperature
- touch
- vibration
between the brain & skin, joints muscles & internal organs
What are the main spinal tracts?
- 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)
What is the aetiology of SCI?
- Traumatic or non-traumatic
- Greatest incidence in 15-25 years, 85% male
- Over 60 years: Male = female
What is primary SCI?
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
What is secondary SCI?
Hypoperfusion & excitotoxicity
- Release of toxic chemicals (e.g. glutamate) from damaged cells, axons & vessels
- Causes damage to surrounding areas (increases extent/height of SCI)
What are the causes of traumatic SCI?
- MVA/MBA
- Falls
- Diving/water sports
- Violence (rare in Aus)
What are the causes of non-traumatic SCI?
- 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
What does SCI affect?
- Motor nerves
- Sensory nerves
- Autonomic nerves (sympathetic & parasympathetic)
- Often damages both upper & lower motor neurons
What is an upper motor neuron lesion?
- Lesion above the anterior horn cell/conus (e.g. spinal cord, brain stem, motor cortex)
- Spinal cord reflexes intact
- Spastic paralysis
What is a lower motor neuron lesion?
- 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)
How does a combination of UMN & LMN lesions occur?
- Ischaemic damage to anterior horn cells of LMN (widespread)
- Trauma to LMN at level of injury (specific damage)
- Injuries at the conus
How are SCIs classified?
According to the level of injury, using the ASIA scale
What does the ASIA impairment scale provide information on?
review for exam in lecture notes
- 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
What is a complete SCI?
- 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
What is an incomplete SCI?
- Some function below injury level
- More common with non-traumatic SCI, however may present with a wide variety of impairments
What is the role of a physio in SCI?
- Respiratory care
- Rehab/training of activities
- Wheelchair skills (posture, technique)
- Equipment prescription & home visits
- Exercise & fitness training
- Pain management
- Prevention of secondary impairments
What should a SCI physio assessment include?
Impairments
- Loss of strength, sensation, fitness, muscle length & joint range
- Spasticity
Activity limitations
What are the primary impairments in SCI?
- Loss of strength
- Loss of sensation
- Spasticity (only in UMN lesions)
- ANS impairments
What are the secondary impairments in SCI?
- Contracture
- Disuse weakness
- CV deconditioning
How is loss of strength treated in complete lesions?
- Target strengthening of non-paralysed muscles
- Also includes partially paralysed muscles
How is loss of strength treated in incomplete lesions?
Strengthening according to general neurological principles (based on Oxford grading)
What are the characteristics of loss of sensation in SCI?
- Dermatomal
- Variable depending on lesion
- Sensation assessed on ASIA sensory assessment
- Sensory level of injury may differ from motor level of injury
What are the characteristics of spasticity in SCI?
- Present in up to 80% SCI
- More detrimental in incomplete lesions
- Tends to gradually increase over first year, then plateaus
What does the medical management of spasticity include?
Pharmacological agents acting primarily within the CNS (e.g. baclofen), muscle or NMJ (e.g. botox)
What are the characteristics of contracture in SCI?
- Due to paralysis or spasticity
- Can impact significantly on function, pressure management, cosmesis (appearance) & hygiene
- May be a goal of treatment
- Assessed with Tardieu
What are the CV implications in SCI?
- 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
What are the autonomic functions of the spinal cord?
- 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
What is the main aim of acute management of SCI?
Reducing secondary injury to minimise extent of damage to the spinal cord
What is the anterior horn cell?
Point in the spinal cord where spinal nerves synapse with motor effector nerves
Why is spasticity not an impairment in LMN lesions?
Because the LMN needs to be intact for the stretch reflex to occur for spasticity
Why is spasticity not always detrimental in complete lesions?
- 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
Why is spasticity more detrimental in incomplete lesions?
- 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
