Traumatic Brain Injury (TBI) and Chronic Traumatic Encephalopathy (CTE) Flashcards
traumatic brain injury (TBI)
- occurs when a force to the head causes neuropathological damage and impairement of brain function
- mild vs. moderate/severe
- mild TBI (mTBI) is often used interchangeably with concussion
chronic traumatic encephalopathy (CTE)
progressive neurodegenerative disorder usually caused by repetitive head trauma
TBI - primary injury
stage of closed head injury
occurs at the time of impact
focal
- contusions/brusing
diffuse
- diffuse axonal injury
TBI - secondary injury
stage of closed head injury
occurs after impact
several pathologies, mostly leading to increased intracranial pressure, bleeds, and cell death
can lead to:
- edema
- ischema
- hemorrage
- seizures
open head injury
aka penetrating head injury
- penetration from outside resulting in focal damage (e.g. gunshot wound, stabbing)
closed head injury
no open wound with damage resulting in diffuse damage (e.g. fall or car accident)
edema
swelling resulting in increased intracranial pressure
ischema
disruption of cerebral blood flow
leads to hypoxia/anoxia
hemorrhage
bleeding or development of blood clots
moderate/severe TBI & memory (Rigon et al., 2020)
spatial reconstruction/relational memory task
WORSE IN:
- accuracy
- misplacement
-compared to healthy comparison participants, individuals with a history of moderate-severe TBI performed significantly worse on a relational memory task
-more individuals were identified as memory impaired on the spatial reconstruction task than the standard neuropsychological measure of episodic memory (CVLT)
mild TBI and memory (Monti et al., 2013)
- compared to matched controls, individuals who had an mTBI decades ago were less accurate on a face-scene relational memory task (middle aged groups)
-c ompared to matched controls, individuals who had an mTBI decades ago had smaller hippocampi bilaterally
- compared to matched controls, there was no impairment evident in memory or neuroimaging in individuals with recent mTBI (young groups)
- these findings implicate the combination of aging and a history of mTBI as the source of the deficit observed in the MI group, rather than mTBI alone
TBI and aging
- moderate to severe TBI raises risk of developing AD later in life
* whether these cases are actually CTE masquerading as AD remains to be seen - CTE seems to be due to repeated mTBIs/concussions and sub-concussive blows to the head
- not just the big hits
CTE and aging
- symptoms typically appear in middle-age
- approx in 40’s but can be earlier or later
- usually symptoms onset after retirement
- symptoms can occur while still playing (generally more mild)
- diseases gets worse with progressing age
emergence of CTE?
many NFL players commit suicide in a way to preserve brain
brain changes after one season of football (Hivard et al., 2019)
- 38 football players wore accelometers on helmet all season and had MRIs pre and post season
FINDINGS:
- decrease in integrity of corticospinal tract in right midbrain
- the biggest changes that were happening in brain were individuals who had highest # of rotational hits
CTE time course
- symptoms typically appear in middle-age
- approx in 40s, but can appear earlier or later
** usually symptoms onset after retirement
** symptoms can occur while still playing (generally more mild)
- approx in 40s, but can appear earlier or later
CTE cognitive changes
- main complaints seem to be of memory loss and later, executive dysfunction
- memory loss seems to be greatest for recent events
*difficulty forming new memories - also have difficulty with planning, judgement
CTE psychological changes
- major affective/emotional component present in all stages of disease
* depression
* rage/anger
* lack of inhibition leading to outbursts - motor dysfunction also common
* gait disturbances (e.g. some difficulty walking smoothly)
tau depositions
earliest accumulation of deposition occurs in:
* depths of cortical sulci
* near blood vessels (perivascular regions)
in moderate stages tau is found in hippocampus and MTL
axon damage
in addition to NFT formation, axon damage is seen in all four stages of CTE
** possible that this damage is accounting for any clinical symptoms observed in the early stages, as NFT formation is not that dense
differentiating CTE and AD – patient history
former football player with multiple TBIs more likely to have CTE than a librarian
differentiating CTE and AD – age of onset of symptoms
CTE affects people younger than AD
- CTE onset approx 40s w more variability
- AD onset typically above age 65, with risk increasing greatly into 70s and 80s
differentiating CTE and AD – memory deficit
in the early stages of CTE research, it seems memory probs may be somewhat similar to those of AD
- initial symptoms of difficulty for recent, declarative memories
differentiating CTE and AD – emotional/affective symptoms
- both can have depression, but seems more common in CTE
- explosive anger, rage, and impulsivity more common in CTE
differentiating CTE and AD – more symptoms
gait disturbances and movement problems more common in CTE, though not unheard of in AD
differentiating CTE and AD – pattern of tau deposition
AD-earliest deposition in hippocampus and entorhinal cortex, then spreading to cortical areas
CTE-earliest deposition in depths of cortical sulci and around blood vessels, then spreading to hippocampal region and other cortical areas
differentiating CTE and AD – amyloid deposition
much more common in AD
CTE patients seems to have little amyloid in brain
