Spinal cord injury (SCI) Flashcards
LO
- Compare and contrast the causes, outcome, cost, and impact of TBI and SCI
- Describe the biological processes that determine the outcome of TBI and SCI
- Analyse the similarities and differences between TBI and SCI
Acute spinal cord stats (2016)
12,500/year (US); 1,000-2,000/year (UK) – new cases in US and UK
42 – average age at injury (up from 29 in 1970’s)- age has increased over the past few decades because of factors like DIY for e.g., at older ages
~282,000 – number of people in the US living with an SCI
Males – 80% of new SCI cases
What are the common causes of death in patients with SCI?
What are these?
Pneumonia:infection that inflames the air sacs in one or both lungs
Septicaemia: when bacteria enters the blood stream and causing blood poisoning which triggers sepsis
What are the common causes of SCI?
Motor vehicle accidents
Sports injuries
Violence i.e., domestic violence, gunshot wound
Falls
Other
Tell me the anatomy of the spinal cord
Spinal levels (31 spinal nerves)
- Cervical 1- Cervical 8 (C1-C8)
- Thoracic 1 – Thoracic 12 (T1-T12)
- Lumbar 1 – Lumbar 5 (L1–L5)
- Sacral 1 – Sacral 5 (S1-S5)
- Coccygeal 1 (Co1)
Heterogenous depending on what levels of the spinal cord is damaged
Tell me about the information carried within the tracts of the spinal cord
Paraplegia and quadriplegia results in what?
Loss of motor control
Loss of sensation
Increased risk for other conditions/ diseases
Damage to what regions of the spinal cord results in Quadriplegia?
Tell me about the different severities
Anything in the Cervical region
If around C3-C4 means you quadriplegic which means you won’t be able to move limbs. Probably need a ventilator
C1-C2 means it won’t be favourable to survival
If you go down a few levels to say C6, you have kept ability to breath on own but sensation and motor function for voluntary movement is in shoulders but not a lot left in arms to move too much
Damage to what regions of the spinal cord results in Paraplegia?
Tell me about the different severities
Thoracic and lumbar injuries are below levels controlling arms, so looking at different levels of paraplegia. T6 is paralysis is below chest and in lumbar regions in L1 the abdomen and arms are fine, but legs are paralysed
Person is generally paralysed from their injury down
In 2004, a study was done on those who has quadriplegia and paraplegia, what was determined as their main priority for recovery?
It was hypothesised that walking would be the primary priority however…
Quadriplegics wanted arm and hand functions back
Paraplegics wanted sexual function back
This study was followed up in 2012, with a quality-of-life study
What are the two syndromes that are SCI-partial lesions.
Tell me about each one
Brown-Sequard syndrome: lose sensation like vibration and fine touch and motor movements on same side, response to pain and temperature lost on other side to injury
Central Cord syndrome: more common, in centre of spinal cord is central canal which is a tiny pathway involved in development of spinal cord, has CSF, narrows upon maturation. If have problems with central canal it can open and effect tissues, so all functions driven by tissues around that region would be damage. Interrupts central pathways.
How is SCI diagnosed?
Tell me about this
ASIS (American Spinal Injuries Association)- SCI diagnosis
ASIA scale is an indicator of severity of SCI used clinically (A-E).
- Determines sensory levels for right and left sides.
- Determines motor levels for right and left sides.
- Determines single neurological level – lowest spinal level that is normal on both sides.
- Determines whether is injury is complete or incomplete.
Is ASIS complete or incomplete?
What is spinal shock?
What is lost/ impaired?
A state of temporary loss of function in the spinal cord- often lasts 1 day, but can persist up to 1-month post-injury
Flaccid paralysis below the lesion (due to removal of descending/motor input) (replaced by spastic paralysis following spinal shock)
Loss of tendon reflexes
Impaired sympathetic outflow to vascular smooth muscle can cause decreased blood pressure (high cervical injury)
Absent sphincter reflexes and tone
What are some SCI related comparisons?
Vertebral fracture? Laceration of tissue
Compression
What are some lesion related comparisons?
- Contusion
- Necrosis, apoptosis
- Haemorrhage, oedema, breakdown of the BBB
- Swelling
- Excitotoxicity
- Diffuse axonal injury (DAI)
- Hyperthermia- dysregulation of sympathetic outflow, increased temperature
- Inflammation
With loss of function, what can this be?
- Local versus global
- Acute versus chronic (Primary versus secondary injury)
What types of influx can contribute to swelling?
Glutamate influx –> Na+ and Ca+ influx into cells –> Swelling
Tell me about the impact of injury as studied experimentally for acute –> chronic injury
* is where damage occurs and this is spreading as glial cells are responding, fluid becoming unbalanced
After 7 days: at epicentre, which has grown, damage tissue is seen floating, white region is fluid (cystic cavity)
After 14-30 days: it wants to fill the fluid cavity, so uses astrocytes which have become hypertrophic, to wall off region and make boundary between good bad tissue. These release a molecule to the border between the tissues (chondroitin sulphate proteoglycans (CSPGs)
Tell me about the glial scar and why this forms?
- After traumatic injury, the astrocytes become ‘reactive’
- Result = formation of a glial scar.
- Glial scar + myelin debris = area which growing axons cannot pass through (debris cannot be removed very easily)
- Axons do not grow on CSPGs or myelin
- Not a scar just has characteristics to it and is the new tissue
Tell me about reactive astrocytes
Become hypertrophic
Increase expression & secretion of inhibitory molecules including chondroitin sulphate proteoglycans (CSPGs).
Increase expression of normal molecules (Ex: Glial fibrillary acidic protein or GFAP)
Tell me about the different structures that make up the glial scar and how they arrange themselves
What do the glial scar and myelin debris make which creates an area which growing axons cannot pass through?
Glial scar (CSPGs) + myelin debris (NOGO-A, MAG) = create an area which growing axons cannot pass through
What affects the neuron viability in the SCI and give examples of some of these
Inflammatory cells (such as microglia, lymphocytes, macrophages) flood the lesion and release pro-inflammatory cytokines = affect neuronal viability
What affects the neuronal excitability in SCI?
Diffusible inflammatory mediators (nitrous oxide- free radical) = affect neuronal excitability
With SCI, the glial scar, myelin debris and degenerating axons all lead to what?
Axons/ neurons dying or degenerating
With Wallerian degeneration in PNS (what happens in a system that regenerates after injury)?
- Regrowth does occur in PNS
- Myelinated Schwann cells rather than oligodendrocytes in PNS
- Schwann cells respond to injury and become reactive, hypertrophic, and surround the region
- Systemic response in PNS
- Schwann cells and macrophages clear the debris, not glial scar as they don’t secrete CSPGs
- Schwann cells lay down ECM in organised fashion so axons can regrow
Tell me about the stages that occur in wallerian degeneration in the adult CNS
Tell me about Chromatolysis and what happens to the following structures…
- Nissl substances
- Neurons
Nissl substance stains rough endoplasmic reticulum and polyribosomes, important in protein synthesis. Note the lack of Nissl substance in the axon (as little protein synthesis occurring here)
Neurons undergoing chromatolysis have a displacement of the nucleus, loss of Nissl substance except around periphery of cell body. Neurons will usually undergo apoptosis.
Chromatolysis and axon re- and de-generation
Spinal cord injury and Traumatic Brain Injury- issues for repair and recovery
- Major biomedical problem and increasing in frequency
- Prevention is better than cure
- Prevent secondary damage, anti-inflammatory response, increase neuroprotection, increase axon protection
- Repair damage?
