Lecture 2: Brain Injury Flashcards
Brain damage caused by events AFTER birth (not congenital or genetic)
Aquired brain injury
An anoxic brain injury is what?
* Is it genetic or aquired?
Anoxic brain injury - happens when the brain is deperived of oxygen
* Think something like cardiac arrest, stroke, tumor, infection all causing some kind of brain injury
Its Aquired
Alteration in brain function caused by an external force
Traumatic Brain Injury
* Evidence of brain pathology caused by an external force (think blunt force)
Multiple systems involved, leads to secondary impairment. Think getting a lascerantion the impacts the integumentary system as well as the brain
Example of a Mild Traumatic Brain injury
Concusion
* Common: atheletes - incidence highest in female atheletes
Motor vehicle releated accidents often lead to what kind of TBI?
Moderate/Severe
What scale is commonly utilized w/ traumatic brain injury?
Glasgow coma scale
What are the 2 leading causes of brain injury associated hospitilizations?
1) Falls (ederly) - most at risk greater than 75 years old
2) Motor vehicle releated incidents
NOTE: Individuals who survive TBI often experience persistent morbidity, with reduced participation and productivity driving the need for ongoing supports for them and their familys
Penetrating break in the skull is open or closed TBI?
* What are breached?
* What is exposed
* Is it focal or diffuse?
Open
Meninges are breached
Brain exposed
Focal injury (we can pinpoint it)
* Focal = releating to center or point of interest
NOTE: This can lead to vascular injury
Non-penetrating, no skull fracture or laceration on brain
* Open or closed
* What often causes this?
* Is it focal or diffuse?
Closed
Coup/Countercoup
* This is that sloshing of brain back and forth
* Often happens in MVA
Can be both focal and diffuse
KNOW: Subarachnoid and subdural hemorrhage can occur w/ diffuse injury
Coup/Contercoup
Primary TBI (this is the first thing that happens)
1) Brain tissue contacts an object - typically open injury
* Penetrating injury
* Leads to: contusions, lacerations, hematomas
2) Rapid acceleration/deceleration - typically closed injury
* Shear, tensile and compression forces
* Diffuse axonal injury (DAI), tissue tearing, hemorrhages
This can all trigger a metabolic cascade
NOTE: Primary traumatic brain injury occurs at the movent of impact and is the direct result of an external force aplpied to the head.
Secondary = Physiological and biochemical changes that occur after the inital injury. This can include swelling, increased intracranial pressure, and inflammation, which may lead to further damage to cels over time.
Diffuse axonal injury, tissue tearing, hemorrhages typically happen w/ open or closed TBIs?
Closed
* do to that coup/counter coup
Cell death due to secondary effects of hypoxia and hypotension, ischemia, edema and elevated intracrainial pressure changes
Secondary injury
Happens after some primary TBI
Blast injury is made up of a primary, secondary, and tertiary response. Explain what each is for this varient of brain injury
1) Primary: Direct effect of overpressure from blast
2) Secondary: Shrpnel contracting person
3) Tertiary: person thrown backwards
Moving of that intracrainal pressure is going to create a herniation somewhere (the brain needs to go somewhere when pressures change)
* often downwards herniation through foramen magnum
* can also affect arteries supplying cerebrum
Which of the following causes a primary injury releated to TBI
* Cell death due to hypoxia
* Brain tissue contacting an object
* Formation of a gematoma
* Diffuse axonal injury
Brain tissue contacting an object
NOTE: If its a closed injury that axonal injury happens after that coup countercoup (brain is sheared back and forth)
What space is between the skull and the dura matter?
Epidural space
What space is between the skull and the brain?
Subdural
Space within the skull
Intracerebral space
What is a contusion?
Bruise in the brain
What is a Hematoma?
* What are the three kinds?
Pooled blood outside a blood vessel
1) Intracerebral
2) Epidural
3) Subdural
What is a hemorrhage
* Our 3 kinds
active bleeding / burst vessel
* can be intracerebral
* Subdural
* Subarachnoid
KNOW: Vascular injury can lead to ischemia/infraction/stroke
Vascular injury can lead to changes in intracrainal pressure
* Brain can be displaced
* Intracrainial pressure increased (because the brain is pushed more over to one side)
Hypotension is #
* What can this often cause?
Systolic BP less than 90 mmHg occuring between injury aand resuscitation can occur
Can often cause hypoxia
What can occur because of blockages resulting in decreased blood in the brain, by decreased oxygen in the blood due to concomitant pulmonary insult, or by internal bleeding or extremity injures that cause excessive blood loss?
Hypoxia
KNOW: Hypoxia often comes secondary to something else
* Think, an external injury causes you to lose blood = hypotension = hypoxia (not getting enough BF = not enough O2)
Injuries that result in hypoxia do what to mortality rate?
* What does it do to morbidity?
* Is early hypotension good or bed?
doubles mortality rate
Significant increase in morbidity (having a desease or symptom of a disease)
KNOW: early hypotension is also a strong predictor of poor outcomes
Intracranial hypertension increases or decreases intracranial pressure
Increases (duh)
KNOW: Intracranial pressures elevates after injury
What monitors intracranial pressure?
* How does it work
Intracranial pressure monitored via ventricular catheter
* Allows some CSF to drain to reduce ICP
* NOTE: ICP is typically incraesed following an injury (makes sense, more BF to the area = more pressure in skull)
Ventriculostomy
Normal intracranial Pressure?
5-20
What is our goal for intracranial pressure in an acute care setting?
20 mmHg
* NOTE: normal is 5-20mmHG
Paranchymal changes: refer to alterations in the functional tissue of an organ, particulary in the brain. In the context of brain injury, this can include various types of damage or abnomraltities in the brains cellular structure
Shear and tensile forces that disrupt the axolemma (cell body around axon)
Axonal injury
* This is a parenchymal change or diffusse axonal injury
* Diffuse becuse often happens in the cou countercou motion
Distal axon will detach an trigger
* What do the myelin sheaths do?
Wallerian degernation (happens when severed/detached)
* Wallerian degeneration: Process that occurs when a nerve fiber is injuried. It involves the. degreernation of the axon and its myelin sheath distal to the site of injury. This happens because the nerve fiber loses its connection to the body, leading to the breakdown of the aon.
* When conditions right the axon may regerenate over time
This triggers reactional axonal swelling, forming retraction clumps that are full of axon material - detecte in the injured brain within 12 hours of injury
Myelin sheaths pull away from the axon
NOTE: Wallerian degernation happens btoh in CNS and PNS but more sucessful in PNS
These axonal changes may be distrubted throughout the brain regardles of site of impact (so happening everywhere)
In axonal injury (shear and tensile forces that disrupt axolemma) will they present similar to a stroke or tumor?
No
In a stroke or tumor you won’t have that shearing force that breaks those axons
* Stroke / tumor is going to be cutting off area / pressing on an area
NOTE: in diffuse axonal injury (often caused by that coup / countercoup) the intact axons are interspersed among damaged axons (its a mess)
Metabolic cascade revisited - excitotoxcivity and freee radial formation
* Secondary cell death by necrosis of the cellular membrane results from edema (so changes happening right away and then days and months later)
* Apoptosis or programmed cell death from within the cell through changes in the DNA can result in cell loss that occurs days, weeks, or months after injury
* There is evidence of the potential for recovery of function based on the possible sprouting of undamage axons to reoccupy the areas left vacant by degenerating axons - just doesnt work as well in the CNS
* Excess clutamate releated (its released in times of inflamamtion) - further becomes more excito toxic
I like this picture
KNOW:
Neurons deprived of oxygen for a prolonged period die and do not regerenate such as in stroke or truamtic injury; excitotoxicity may add more damage
EXcitoxicity is cell death caused by the over excitation of neurons due to large quantites of glutamate –> excessive glutamate kills postsynaptic neurons
Oxygen deprived neurons release large quantities of glutamate, an excitatory neurotransmitter, from their axon terminals
Rehab research: Neurorestoration (neurogensis and angiogensis): No known drug provides signficant neuroprotection for individuals with strok TBI or neurodegenerative disease
Shifting in normal brain symmetry =
Herniation
What is the most common herniation?
Transtentorial and downward, at the lateral tentorial membrane seperating the cerebral hemisheres from the posterior fossa
really just know it shifts downward
* Due to gravity and space (foramen magnum)
Which of the following values is normal intracranial pressure?
* 37
* 23
* 11
* 4
11
5-20mmHg is normal
What imaging is mostly utilized for TBI?
CT
Seconary = MRI
Imaging for SCI is typically done at the same time because this area could also be damaged
What goes the glasgow coma scale rate?
* What are the scores for severe, moderate, and mild (quiz)
* It ratess these scores based on 3 repsonses. What are these 3 variables?
Rates the severity of brain injury
Mild = 13-15
Moderate = 9-12
Severe = 8 or less
3 responses:
1) Eye opening
2) Motor response
3) Verbal response
This is how its scored
Mild TBI Loss of consciousness =
Moderate TBI =
Severe TBI =
0-30min
30-24hrs
>24hrs
I think I really need to know that the longer the LOS is the more severe
KNOW: In moderate to severe TBI there is normally that loss of consciouness that lasts a while
* typically consciouness is recovered
* Lucid period
* Neurologic deterirtation (HA, decline in mental status, focal neurological findings)
KNOW: Cognitive impairment does not mean theyll have physical impairement (they don’t go hand in hand)
Following TBI: Motor:
Cerebral shock: period of time where they are flacid and non responsive (think w/ LOC)
Slowly replaced gradually by increased tone, spasticity and rigidity
* Remember, this is an upper motor neuron syndrome
* So tone, spasticity etc. will all come up after that inital period of shock - so upper motor neuron signs
Abnormal movements depending on which areas of the brain has been injuired
Paroxysmal sympathetic hyperactivity is also known as
* What is it?
* What happens to HR, BP, RR, temp
What are triggers?
How long does it take to resolve?
Storming
Physical reaction from pt where their body starts to shake and works its way up and gets very intense. Its building
Increased:
* HR
* BP
* RR
* Temp
* sweating
* Motor posturing (becoming tense all over)
Triggers: Some kind of noxious stimuli (think pain, suctioning, passive movement, sonstipation)
* These intitate cycles of sympathetic overactivity, but reponses may also be exaggerated to stimuli that are typically not considered painful
Typically resolves several months after injury, but overactivity to external stimuli could persist in more subtle ways beyond the acute period
Long term risk of developing alzheimers disease, parkinson’s disease, frontotemporal dementia and chronic traumatic encephalopathy increase w/ TBI
Link between TBI and depression and anxiety disorders
What happens to the HR in storming?
* increase or decrease
Increase
Lowest level of consciousness
COMA
Its a complete state of unresponsiveness
Advanced brain failure
Unconscious/Unarousable
Eyes closed
No sleep wake cycles
No response to painful stemuli
May be ventilator dependet
May not demonstrate reflex reactions
Wakeful unresponsiveness is also called
* What do they have?
* Are their sleep wake cycles
* Are they aware of surroundings?
* Do they have reflexes
* Permanent/Persistant vegeative times for TBI
* Permanent/Persistant vegetative times for anoxic brain injury?
Vegetative state
* Normalization of vegeative functions - respiration, digestion and BP (so we have those vegetaive functions still, but the higher level brain is not working)
* NOTE: They can be weaned off the ventilator if on it prior
Slee wake cycles present
**No awareness of surroundings - meaninful cognitive and communcation are absent
Reflexes in response to externial stimuli - movement will not be reproduciblec
* So they will have reflexes?
Permanet/persistent vegeative state: lacks meaningful motor or cognitive function and complete absence of awareness or self or the environment for a period greater than 1 year after TBI and 3 months after anoxic brain injury
Minimally conscious state
* What are sleep wake cycles like?
* Can they be aroused?
* What will they do when stimuli is present
* What can they do visually?
Irregular sleep wake cycles
Normalization of vegetative functions - respiration, digestion and BP
May be aroused, minimal evidence of self or environmental awareness
Cognitively mediated behaviors occur inconsistently
Instead of withdrawing of withdrawing or posturing to stimuli patients will localize to stimuli and may inconsistently reach for objects
Patients may localize to sound location and demonstrate sustained visual fixation and visual pursuit
* So they can follow you across the room
* may look at you if you slam the door