Spinal cord and Brain Flashcards
Area classification of spinal fractures
Based on the position within the vertebrae
Ant - front vert body, ALL, ant disc
Middle - back vert body, PLL, key to stability, most likely for nerve damage
Post - All aoprts outside vert body (spinous process, lamina ect)
Types of spinal fractures
- Compression (vertebral body)
- Normally in people with osteoporosis
- Not as sever, unless worst case being burst fracture
- MOI of sudden downward force (fall)
- Dislocation
- Ligaments/disc stretched or torn
- Normally leads to instability therefore needing surgery or brace
- Fracture dislocation
- Higher velocity injury
- Unstable
Impairments based on levels
C5 - deltoid (abduction)
C6 - biceps and brachialis (elbow flexion)
C7 - triceps (elbow ext)
C8 - 3rd finger flexion
T1 - 5th abduction
L2-hip flexion
L3- Knee ext
L4 - Ankle dorsiflexion
L5 - 1st toe extension
S1- Ankle plantar flexion
Functions lost during spinal shock
- Somatic reflexes (stretch, withdrawal)
- Autonomic reflexes
- Autonomic regulation of BP
Can return in several weeks
Muscle tone in relation to SCI
Hypotonia = flaccidity
- Lower motor neuron lesions at the site of SCI
- Can occur transiently after upper motor lesions due to shock
Hypertonia = spasticity (resistance to passive stress)
- At level and at all of the levels below SCI due to the pathway
ASIA scale grades
A - Complete, no sens or mot in S4-5
B - Incomplete, Sen but no mot below neurological level (including S4-5)
C - Incomplete, Mot function preserved below neurological level and more than half have grade 3 or less
D - Incomplete, Mot function preserved below neurological level and more than half have grade 3 or more
E - Normal
Necrosis vs apoptosis
Necrosis
- Internal swelling of many cells from physical injury
- Burst cell membrane and immune cells clean debris
Apoptosis
- Specific cell shrinks and fragments into apoptotic bodies which can be reused
Primary vs secondary spinal cord injury
Primary:
- Everything that happens at the time of injury, caused by mechanical impact
- Immediate cell death and neural disruptions
- Immediate vascular disruptions
- Blood brain barrier and BSCB disruption
- Neurogenic shock
Secondary
- Everything after (seconds, mins, ect)
- Can be mediated as it is driven by biological processes , stop some secondary injury
- Oedema, ischemia, oxidative stress, inflammation
Secondary spinal cord injury
Ischemia - Restricted blood supply to tissues (from primary injury of vessel damage). Results in apoptosis
Excitotoxicity - Excessive glutamate presence, neurons expel when damaged. Leads to apoptosis
Inflammation - Immune cells to clean debris and prevent infection, heightened response can lead to worse outcomes
Inflammatory response and APR (secondary injury) of spinal cord injury
- Inflammatory response consists of multiple phases
- Microglia (already present in CNS)
- Neutrophils
- Monocytes and macrophages, these are not present in CNS so come from other areas of the body (via APR)
- Acute phase response (APR)
- Direct damage causes glial cells to release extracellular vesicle into circulation
- Signals to liver to initiate APR, releases other immune cells such as leukocytes and mobilises to site of injury
6 key aspects for management and repair
- Perseveration of neural tissues
- Preservation of white matter
- Replacement of lost cells
- Regrow damage pathway
- Appropriately rewire and retrain circuitry (functionally appropriate)
Most people with SCI have silent mot or sens pathway meaning they are going to brain but just not registering. Could be improved with rehab.
Why is maintaining the blood supply to the brain important
The brain is very active metabolically, it has a very high demand for O2 and glucose but not effective way of storing either, resulting in it needing a continuous blood supply
Three intracranial fluid networks
- Vasculature (blood)
- Interstitial fluid
- Cerebrospinal fluid (produces at choroid plexus)
Intestinal fluid can free flow and mix with CSF. If one part is disrupted then oedema may form from backup
Is brain tissue inhomogeneous
Brain tissue is inhomogeneous meaning it is made up of a variety of cells, ECM is %70 water
2 ways in which intercranial components can be effected by external load
- Direct contact
- When the skull is displaced or deformed resulting from high kinetic energy and low cranial momentum (fixed head)
- Differential motion
- Acceleration/deceleration forces impart large momentum, rotational, tensile and shear forces with low kinetic energy
- Content lagging behind motion of the skull
How does the direction of impact effect external loading
The outcome for different intracranial components vary depending on the direction of impact (linear vs oblique)
- Oblique (more common)
- Produces both linear and rotation kinematics
- Brain more sensitive to rotation as it will cause shear
- Linear
- Strain is lower in linear
Brain biomechanics
- Poris fluid saturated solid
- Low permeability
- Has a high bulk modulus meaning that it volume will not be decreased when pressure exerted all around
- Soft and compliant, low compression modulus but even lower shear modulus
- Viscoelastic material (faster strain rate, brain becomes stiffer)
Regional inhomogeneity
- White matter is stiffer than grey in compression, however this is dependent on the region as it is anisotropy meaning directionally dependent.
- Grey matter is isotropic meaning different directions of loading matter less.
- Grey matter is normally more stiff to shear than white (depending on position)
How does brain mass and size relate to loading
- Smaller brains (older) tolerate greater acceleration/deceleration forces due to decreased momentum
- Brain and spinal cord are at right angles which may increases rotational shearing forces
- Brain more susceptible to damage in AP direction (Dural folds limit lateral), it is longer longitudinally meaning more potential for movement (axonal injury)
Difference between acquired brain injury and traumatic brain injury
Acquired
These are all types of brain injuries that occur after birth:
- Traumatic brain injury, stoke, tumour ect
- Majority occur in young males in MVAs
Traumatic
A traumatically induced structural injury of physiologic disruption of brain function as a result of an external force (doesn’t include stroke, tumour ect)
Signs of traumatic brain injury
- Period of loss or decreased level of consciousness
- Loss of memory for events (immediately before or after injury)
- Alteration in mental start at time of injury (confusion, slow thinking)
- Neurologic effects (weakness, balance, speech, general sensory)
4 main pathological features of TBI (primary)
This is irreversible damage that occurs at time of injury.
Can be focal, multi focal or diffuse
- Axonal injury
- Vascular injury
- Contusion
- Laceration
Diffuse axonal injury info
This is leading causes of morbidity associated with TBI. Axons are a viscoelastic material meaning with rapid deformation then produce a brittle response.
- Rotations (unrestricted head movement after impact) that contained an axial component produce the greatest injury risk
Diffuse axonal injury secondary mechanisms
- Damage to the axonal cytoskeleton from tension
- plastic deformation → axonal undulation and misalignment.
- Mechanical damage to sodium channels → sodium influx
- Axonal swelling
- Triggers calcium influx
- Calcium activate proteolysis further damaging cytoskeleton
This shows that even if the axon does not immediately shear then these mechanics can cause it to be
deformed and subsequently shear
- Impaired axonal transport
- Accumulation of proteins in axonal swelling (when they cant get to end of axon)
- Secondary axotomy
- Accumulation of proteins in axonal swelling (when they cant get to end of axon)
Extradural/epidural
- Traumatic head injury with skull fracture
- Ruptures middle meningeal, separates dura from bone
- Contained by Dural structures leading to biconvex shape (limited expansion)
Subdural
- Shaking of head causes shearing of bridging veins (deceleration injury)
- Older patients due to cerebral atrophy these veins are already under increased tension
- Crescent shaped haematoma, not contained by sutures but cant cross Dural folds
- Mass effect causes midline shift
Can be difficult to diagnoses if slow developing due to potential space
Subarachnoid
- Cerebral vessels bleed into subarachnoid space (aneurysm), blood mixes with CSF
- Can cause focal ischemia
- Neck stiffness
Intracerebral (parenchymal)
- Small arterioles and capillaries within brain
- Parenchymal = bulk of substance
Brain contusion
These are focal surface bruises, cell death (initial necrosis then secondary apoptosis), bleeding and oedema.
Normally occurs at the crest of gyri (closest to skull), most common in temporal and frontal lobe (come in contact with front of skull)
They are wedged shaped, broad closest to the skull
Have coup and countercoup
What is mass effect
Centre of mass of brain has been moved due to presence of pathology (bleeding, tumour ect)
Glasgow Coma Scale
- Functional scoring
- Take lowest GCS score in first 48 hours
- Mild TBI = 13-15, Moderate = 9-12 and Severe <9 (score from 3-15)
- May change over time, normally drug or alcohol involved in MVA which will hinder score
Determining outcome and severity of brain injury
Mortality is determining with GSC score, time to return to consciousness and CT findings
Mild may progress
Worse outcomes for symptoms include SAH and SDH, displaced skull fracture
Secondary traumatic brain injury
Focal, multifocal or diffuse:
- Ischemic - hypoxic damage
- Brain swelling/oedema (increased BBB permeability from damage)
- Raised intracranial pressure (tissue swelling will increase this but cell swelling wont)
- Abnormal osmotic balance from:
- Increases BBB permeability
- Abnormal cell metabolism
- Cell membrane dysregulation (influx of water into cell)
- Neuroinflammation
- Infection
Secondary traumatic brain injury
Focal, multifocal or diffuse:
- Ischemic -> hypoxic damage
- Brain swelling/oedema (increased BBB permeability from damage)
- Raised intracranial pressure (tissue swelling will increase this but cell swelling wont)
- Abnormal osmotic balance from:
- Increases BBB permeability
- Abnormal cell metabolism
- Cell membrane dysregulation (influx of water into cell)
- Neuroinflammation (too much is bad)
- Infection
Stroke causes and types
This is a spontaneous event
The brain is very active metabolically (high requirement for O2 and glucose) but has no effective way to store this, requires continuous and adequate blood supply.
An abrupt vascular insufficiency is referred to as a stroke and is either:
- Ischaemic (block)
- Haemorrhagic (bleed)
Ischaemic stroke
- Most common
- Blockage of blood flow to CNS via:
- Thrombus (blood clot)
- Embolus (piece of plaque or thrombus travels from its original site and blocks an artery), arthrosclerosis risk factor for this
- Transient ischemic attach are short periods (vison occlusion or dizzy)
- Occlusion will result in infarction of predictable area (area supplied)
- Circle of Willis can compensate if gradual occlusion but the further the distance the less it can do so
Two types of haemorrhagic stroke
Intracerebral haemorrhage (ICH) Subarachnoid haemorrhage (SAH)
Intracerebral haemorrhage (ICH)
- Bleeding into brain tissue
- Main cause is hypertension
- Common are basal ganglia and thalamus
- Pontine haemorrhages have highest mortality (survival functions)
- Cell death from mechanical forces and chemical toxicity (BBB breakdown)
- Perihematomal oedema increases intracranial pressure causing herniation
Subarachnoid haemorrhage (SAH)
- Common cause is rupture of intracranial aneurysm
- Develop at branch points of arteries (circle of Willis is common)
- Will cause transient global ischemia, toxic effect of blood in subarachnoid space
- Can also cause delayed cerebral ischemia
- Systemic response = increased sympathetic NS activity, angiotensin system activation, inflammatory cytokines
Have worst headache of life, +/- nick stiffness
Clinical signs of SAH
- Most severe headache
- Sudden onset (reaching max pain in <1 min)
- Neck pain/stiffness
Stroke incidence vs mortality
Incidence = Ischaemic > ICH > SAH
Mortality = SAH > ICH > Ischemic
Stroke risk factors
Modifiable = smoking, alcohol, BP
Non modifiable = Age, gender, family history, previous incident
MNLs and their effects
Upper - hypertonia (below level of injury in SCI)
Spasticity, resistance to passive stretch
Lower - hypotonia (at level of injury)
Can occur acutely after UML (spinal shock)
Diffuse axonal injury
There can be damage to axons from shear forces associated with unrestricted head movement (containing an axial component ) at time of injury.
However, there can still be damage done to the axons after this event. Rapid tensile stretch -> damage to cytoskeleton -> plastic deformation and axonal undulation and misalignment -> mechanical damage to sodium channels (sodium influx) -> axonal swelling -> triggers calcium influx -> proteolysis will further damage cytoskeleton
Another way this can occurs is when their is impaired axonal transport mechanisms. This impairment will mean proteins cannot get the end of the axon and will accumulate causing a swelling resulting in secondary axotomy
Mild GCS score notes
A mild GCS score of 13-15 does not mean it cannot progress.
Loss of consciousness <30 mins
Most common TBI
Does sensitivity to strain rates differ over life span
Yes, infants insensitive to strain rates. Adults and toddlers are.
