KPE368 Final Exam

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What are the 3 phases of recovery?

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What are the 3 phases of recovery?

  • acute

  • subacute

  • persistent

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Describe the acute phase

  • 24-48 hours

  • decrease in but overtime resolves

  • principles within acute phase: rest, avoid high risk sport, avoid stimuli/stressors and provide education

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Describe the subacute phase

  • after 72 hours

  • people have different understandings of persistent symptoms

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How is concussion multifactorial?

  • centre of it is neurometabolic cascade disruption

  • co-morbidities: things that contribute to it (neck injury)

  • pre-morbidities: what the patient brings in (previous concussion, sleep disorders, etc.) and can increase recovery time

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What are examples of co-morbidities?

  • neck injury

  • msk injury

  • sleep issues

  • anxiety

  • pressure in head

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What are examples of pre-morbidities?

  • personality

  • previous concussion

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How does the DSM define persistent symptoms?

  1. cognitive deficits in attention and memory

  2. at least 3 or more symptoms including HA, dizziness, fatigue, irritability, apathy, personality change, or sleep or affective disturbances

    1. present for 3 months of greater

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How does WHO define persistent symptoms?

presence of 3 or more symptoms that must be present in the first month of injury: HA, dizziness, fatigue, irritability, insomnia, and concentration or memory difficulties

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What are the differences between how WHO and DSM define persistent symtoms?

  • DSM symptoms have to be present for 3 months or greater

  • WHO 3 or more symptoms have to be present in the first month of injury

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What are the problems with how persistent symptoms are defined by WHO and DSM?

  • doesnt tell you timeline

  • one is more short term the other is long term

  • cant have new symptoms

    • e.g. have dizziness in 2nd month

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Why has the diagnosis of PCS disorder been controversial?

  • symptoms have been associated with other conditions (e.g. depression, migraines, etc.)

  • athletes can begin to experience aerobic deconditioning 1-2 weeks of inactivity

    • what cant be debated it persistent symptoms result in substantial functional disability

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What was the previous name ‘persistent symptoms’ was referred to? How did it help?

  • change from Post-Concussion Syndrome (PCS) to persistent symptoms

  • change in name added no value

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How does CISG define persistent symptoms?

persistent symptoms > 2 weeks of symptoms in adults

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How was risk reduced in patients with PCS?

Moser et al. showed that 61.5% of adolescents with persistent symptoms after concussion improved after receiving education and reassurance and engaging in 1 week of prescribed exercise

  • dark room, avoid stimulus

  • considered gold standard

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Why is the efficacy of rest being challenged?

  • taking away benefits of PA

  • dysregulation of day to day

  • changing up stimulus is important

  • psychological component (used to moving, helps with getting energy out, helps with sleep, lifestyle)

  • social (social interaction, self esteem, lack of togetherness,

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What are the symptom clusters?

  • somatic/physical

  • cognitive

  • cervicogenic

  • vestibuloocular

  • headache

  • mood/affect

  • sleep-related

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What is the BCTT used for? Who developed it?

  • Buffalo Concussion Treadmill Test (BCTT)

  • used as rehab intervention for those with persistent symptoms

  • university of buffalo

  • barry willer & john leddy

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Describe how the BCTT works

  • patients walk on a treadmill at a speed of 3.0 - 3.3 mph at 0% grade

  • the grade is increased by 1% after 1 minute

  • the grade is continuously increased by 1%/min during first 15 mins

  • after 15 mins, speed increased by 0.2 - 0.4 mph/min

  • test terminated after symptoms at >3 change in symptoms or 25 mins

  • stop and take their HR, take 80% of that and prescribe it as exercise level

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What is the pathophysiology of physiological concussion disorder?

persistent alterations in cellular metabolism, cerebrovascular physiology “metabolic mismatch”

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what are the symptoms of a physiological concussion?

  • mild mod HA “pounding” at rest

  • dizziness, nausea, fatigue, and sensitivities

    • sx made worse by PA and CE

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what are the treadmill results for someone with a physiological concussion?

early symptom limited threshold (5-15 mins)

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what is the physical exam for a physiological concussion?

normal physical exam

may have elevates resting HR

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what is the treatment for a physiological concussion?

  • submaximal aerobic exercise prescription

  • treatment of co-existing dysfunctions

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what is the pathophysiology of a vestibulo-ocular concussion?

isolated dysfunction of central and peripheral components of vestibulo-ocular neurological subsystem

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what are the symptoms of a vestibulo-ocular concussion?

  • mild mod HA

  • eye strain typically absent at rest but CE exacerbates

  • intermittent blurred vision, dizziness, or focusing

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what are the treadmill results for a vestibulo-ocular concussion?

able ot exercise for 15-25 mins

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what is the physical exam of a vestibulo-ocular concussion?

  • impaired convergence, accommodation, saccades, and VOR

  • positive Dix-Hallpike Maneuver

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what is the treatment for vestibulo-ocular concussion?

  • submaximal aerobic exercise prescription

  • targeted vestibular and vision therapy

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what is the pathophysiology of a cervicogenic concussion disorder?

isolated mechanoreceptive or proprioceptive dysfunction within cervical spine neurological sub-system

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what are the symptoms of a cervicogenic concussion?

  • mild mod HA “dull”, occipital HA elicited by PA

  • neck pain or stiffness, decreased ROM, postural imbalance

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what are the treadmill results for cervicogenic concussion?

able to exercise for 15-25 mins

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what is the physical exam for cervicogenic concussion?

  • decreased ROM

  • sub-occipital and paraspinal neck tenderness

  • impaired cervical spine proprioception

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what is the treatment for cervicogenic concussion?

  • cervical spine manual therapy

  • gaze and postural stabalization

  • submaximal aerobic exercise prescription

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what is the submaximal exercise prescription?

  • advised exercise protocol

    • 80-90% of the HR achieved during treadmill testing

    • 20 mins of exercise, 5-6 days/week

    • follow up advised 1-3 weeks, and repeat treadmill testing

  • superivised initially or intermittent

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What were the results of the study to see if aerobic exercise resolved symptoms?

  • stationary bike 3 days after injury

  • 60% of max HR

  • 2 days on, 1 day off

  • resolution of symptoms faster in people that were given exercise protocol

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What are mechanisms behind why exercise helps concussion recovery?

  • neutrophins → BDNF

  • improvements to ANS/normalization of cerebral blood flow

  • neuroendocrine

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What is BDNF? How does it help improve concussion?

  • Brain Derived Neurotrophic Factor (BDNF) increases

  • involved in neuroplasticity, neuroprotection, growth and differentiation, during developing and in adult brain

  • direct administration increases cell proliferation in hippocampus and blocking BDNF reduces cell proliferation

  • important for memory

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What were the effects of studies testing BDNF?

  • greatest effect of exercise occurs on regions not directly related to motor system (hippocampus)

  • BDNF levels higher post aerobic exercise intervention

  • resistance training doesnt increase resting BDNF levels post intervention

  • no signficant differences observed between males and females, nor in serum vs plasma

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Describe the ANS mechanism for exercise and concussion symptoms

  • primary ANS control - hypothalamus damaged in concussion

    • proposed mechanism is uncoupling of connections between central ANS, arterial baroreceptors and the heart

      • affects CBF and cardiac rhythm

  • Affects cardiac function at and in exercise

    • elevated HR and altered HRV - interpreted to reflect altered balance of sympathetic and parasympathic input

  • physical deconditioning of cardiovascular system as a result of rest

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How does exercise training help concussion with the ANS mechanism?

  • improves CBF control and cerebral vasoreactivity (ability to maintain a steady supply of oxygenated blood)

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Describe the neuroendocrine mechanism for exercise improving concussion symptoms

  • central components of stress system located in hypothalamus and brainstem

  • paraventricular nuclei (PVN) of hypothalamus → corticotropin-releasing hormone (CRH)

  • locus coeruleus (LC) → catecholamines: norepinephrine; and epinephrine

  • physical exercise reduces urine epinephrine as a result of attenuation of sympathetic nervous tension

  • similar findings with cortisol

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how does serotonin act as a mechanism for exercise improving concussion symptoms?

  • serotonin may have structural effects on brain during development and adulthood

  • effects mood

  • a small molecule that functions as both neurotransmitter in the CNS and a hormone in the periphery

  • exercise interventions increase serotonin

    • chronic stress → decrease in serotonin

    • acute stress → increase serotonin

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Describe the mood/affect cluster and what are treatment options?

  • anxiety and depression levels 2x higher

  • non pharmagological: CBT

  • pharmacological: selective serotonin reuptake inhibitor (SSRI) e.g. celexa, prozac, zoloft

  • target different clusters

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Describe the headache cluster and what are treatment options?

  • various types

  • migraine vs tension-type

  • location: unilateral or bilateral, front or back

  • type: stabbing vs dull; frequent vs infrequent

  • treatment options:

    • non pharmacological

      • lifestyle strategies (stimulus, control use of caffeine/tobacco/alcohol, manual therapy)

      • manual therapy (for cervicogenic)

    • pharmacological

      • OTC pain meds/analgesics (acetaminophen, ibuprofen)

      • migraine specific medications

      • peri-neural injection

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Describe the sleep-wake cluster and what are treatment options?

  • 50% of patients report sleep disturbances following mTBI

    • insomnia

    • poor sleep maintenance

    • early awakening/delayed sleep onset

    • alterations in circadian cycle

  • treatment:

    • non pharmacological

      • no phone in bed, caffine, etc.

      • melatonin

      • magnesium and zinc supplementation

      • acupunture and mindfulness-based stress reduction therapy

    • pharmacological

      • modafinil and armodafinil

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Why are balance issues complicated?

  • multiple things contributing to balance

    • eyes (visual system)

    • ears (vestibular system)

    • body’s sense of where it is in space (proprioception)

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What are the 2 pathways visual info is conveyed by?

  • magnocellular stream

  • parvocellular stream

  • involved in different components

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Explain the parvocellular process (Central/focal vision)

  • seeing fine details, identification of what we are seeing

  • conscious vision

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Explain the magnocellular process (peripheral/ambient/spatial)

  • info about our surroundings, where we are in space, where objects are relative to us, and how we would like to move through space

  • motion processing system

  • peripheral range versus peripheral awareness

  • established by an interplay between vision, proprioception, posture and vestibular systems. this is pre conscious and anticipatory)

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What are rehabilitation exercises for vision related interventions?

  • visual perception

  • convergence/divergence/accommodation

  • saccades and smooth pursuits

  • gaze stability

  • visual acuity

  • spatial awareness

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What are optical interventions for vision related interventions?

  • lenses

  • prism

    • able to deviate the direction in which light rays are travelling

    • can walk more normal

    • can be kind of expensive

  • tints

    • filters the most problematic wavelengths

    • blue lights tints (on computer)

  • selective occlusion

    • can help with visual motion sensitivity, balance, and scrolling on a screen

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How is musculature in cervical spine effected in concussion?

  • activation of deep musculature in neck is important for stability and strength of cervical musculature

  • “load sharing” is optimized with appropriate contribution of deep musculature - dynamically and statically

  • it is frequently noted in literature, those who suffer from chronic or mechanical neck pain have weaker neck muscles

  • deep cervical flexors - hard to train, risk factors for concussion when those muscles are weak you have poor postural issues

    • when damaged → exacerbate issues

    • want to train in rehab

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What are the differences between males and females in neck muscles?

  • study with uni students

  • attached weight to their head, counter load balancing, released it to see how they would react

  • females weaker neck muscles

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What are the 3 stages in building deep cervical flexors?

  • pre rehab

    • isometric and dynamic stabilization

  • immediate

    • isometric neutral posture stabilization

    • avoid (excessive) movements/manipulations

  • later

    • movements, manual therapies, stabilization

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how is vestibular system effected in concussion?

  • ear has different canals contributing to how your body is aware in space

    • fluid movement in canals

  • when this is blocked, positional vertigo

    • little manual movement tilting, recalibrating the canals and making sure there is proper movement into those

      • easily corrected potential solution

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what is rehab for vestibular system?

  • multi modal programs adresses all aspects (sensory inputs, controller, motor outputs) of the balance control system

    • visual tracking/convergence exercises

    • gradual progression of head movements

    • standing balance exercises (eyes open, closed)

    • includes lots of components and hoping one sticks

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what are characteristics of “punch drunk”

  • in 1928, dr martland noticed clinical condition in boxers

  • they developed:

    • unsteady gate

    • mental confusion

    • slowed muscular response

    • hesitant speech

    • tremors

    • dragging of leg or foot when ambulating

    • facial characteristics similar to parkinsos

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what did they believe “punch drunk” was caused by

  • single or repeated blows to head or jaw, which caused hemorrhages in deeper portions of brain

  • condition more common in second rate fighters

  • association between exposure to boxing and likelihood of developing these features

  • irreversible

  • progressive even after retirement

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Parker in 1934

  • reporting 3 cases of TE

  • high prevalence of exposure

  • clinical picture complex

  • suggestion of diffuse and scattered lesions of brain affecting different systems at one and the same time

  • assume difficulties resulted from repeated injuries to brain during pugilistic careers

  • exact pathological mechanism not known

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Roberts study in 1969

  • clinical + pathological features

  • clinical

    • 3 stages:

      • affective disturbances and psychotic symptoms

      • social instability, psychiatric symptoms, memory loss, development of parkinsons

      • general cognitive dysfunction

  • pathology

    • in 37 (17%) lesions of nervous system detected by:

      • neuropsychological assessment

      • radiological techniques of that era, such as pneumoencephalography “air study”

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Corsellis et al. 1973

  • 15 retired boxers studied post mortem

  • neuropathological findings of dementia pugilistica

  • specifically:

    • cerebral atrophy

    • atrophy of the mammillary bodies

    • thinning of hypothalamic floor

    • enlargement of lateral and third ventricles, cavum septum pellucidum (cavum septi pellicidi)

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Corsellis et al. 1973 additional key features

  • increase in astrocytes

    • type of glial cell → metabolic support, regulation of ion concentration in extracellular space, nervous system repair

  • presence of neuro-fibrillary tangles

    • tau - hyperphosphorylated - insoluble

    • unlike with AD, tangles were seen in absence of senile plaques

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What is tau?

  • tubulin associated unit

  • ties that hold microtubule rails together - come undone, the neurons’ internal transportation networks fail, often resulting in death of neuron as well

  • tau phosphorylation plays both physiological and pathological roles in cell

  • in pathological conditions in which there is an imbalance in phosphorylation/dephosphorylation of tau, aberrant tau phosphorylation

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what is amyloid?

  • general term for protein fragments that the body porduces normally

  • beta amyloid is protein fragment snipped from an amyloid precursor protein

  • not clear of actual role, but in healthy brain protein fragments are broken down and eliminated (esp. in sleep)

  • become problematic when they lose their structure and normal physiological function → deposits as plaques → disrupt healthy surrounding tissues

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what are the differences between senile (amyloid) plaques and nfts?

  • senile (amyloid) plaques

    • protein fragments and accumulate to form hard, insoluble plaques

    • found between neurons

  • neurofibrillary tangles

    • tangles consist primarily of tau, forms part of a structure called a microtubule

    • tau protein is abnormal (hyperphosphorylation) the microtubule structures collapse

    • found within neurons

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Late 1980’s/early 90’s Roberts et al.

  • reexamined brain

  • more sensitive and modern immunochemistry techniques

  • discovered large numbers of diffuse b-amyloid plaques (comparable to those seen in AD)

  • this is important because prior to 90s it was assumed “senile plaques” were not present in dementia pugilistica

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When was the first use of CTE?

  • 1940 bowman and blau

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Omalu’s 2005 neurosurgery case study

  • first documented case of long-term neurodegenerative changes in a retired professional NFL player consistent with CTE

  • complete autopsy

  • key finding: coricol amyloid plaques and NFTs were unacommpanied by tangles in medical temporal and hippocampus

    • typical changes of AD

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what was the backlash to omalu et al 2005?

  • by NFL

  • misinterpretation of their neuropathological findings in relation to characteristics of chronic CTE

  • failure to provide adequate clinical history

  • no proof of significant injury so cant state it is “traumatic”

  • offensive linemen have low incidence of MTBI compared with other position players

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When did correlation between concussion history, MCI and depression happen?

2005 and 2007

Guskieweicz et al

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what did mckee establish?

  • 2009

  • further characterize CTE pathologic findings in ewview of 48 autopsy confirmed cases

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McKee et al. 2009

  • review of 48 cases of CTE recorded in literature and document detailed findings of cte in athletes

  • behaviour:

    • memory and behaviour disturbances

    • parkinsonism, speech difficulties, gait abnormalities

  • neuropathologically:

    • atrophy of cerebral hemispheres, medial temporal lobe, thalamus & mamillary bodies

    • dilation of lateral ventricles / septi pellucidi

    • tau-positive neurofibrillary tangles & astrocytic tangles

    • b-amyloid inconsistent feature

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McKee et al. 2013

  • post mortem brains of 85 histories with repetitive MTBIS

  • 68 subjects CTE

  • stage correlated with increased duration of football play

  • CTE sole diagnosis in 43 cases (63%), 8 motor neuron disease (12%), 7 alzheimers disease (11%)

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Differences between AD and CTE

  • more brown/rust then AD

  • NFTS more concentrated at depths of sulci

  • NFT cluster and around vasculature (perivascular)

  • NFTS distributed preferentially to superficial layers

  • astrocytic tanlges or NFTS in mamillary body

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what are clinical features of CTE?

  • can only be diagnosed post mortem

  • progressive cognitive, motor, and mood decline

    • early symptoms:

      • memory problems, confusion, headaches

      • depressive symptoms and suicide ideation

      • poor impulse control and short temper

  • some patients develop signs of parkinsons

  • not considered linear progression from concussion

  • history of repetitive brain trauma

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CTE hypothesis #1

  • 1928 article, Martland proposed

  • brain injury due to single or repeated blows on head or jaw which cause multiple concussion hemorrhaes in deeper part of cerebrum. these hemorhages are then replaced by a gliosis or degenerative progressive lesion in areas involved

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CTE hypothesis #2

shear trauma to axons resulting = increased membrane permeability and ion shifts

leads to calcium influx and subsequent release… triggering tau and phosphorylation and aggregation

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CTE hypothesis #3

immune excitotoxicity

  • proinflammatory and anti-inflammatory cytokines and chemokines

  • additional head trauma occurs / frequent trauma microglia remain in a proinflammatory, exitotoxic mode

  • leads to progressive neurodegeneration and the deposition of hyperphosphorylated tau protein, resulting in neurofibrillary tangle formation

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CTE hypothesis #4

  • McKee et al propose that concussive impacts result in fluid waves within lateral ventricles that place a shear stress on the septum pellucidum

    • resulting in an enlarged cavum septum and septal fenestrations

  • ischemia also plays note

    • noting that tau pathology occurs at depths of sulci

  • they proporse damage to blood brain barrier and release of neurotoxins contributes to perivascular nests of tau-immunoreactive neurofibrillary tangles

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Other variables associated with disease burden of CTE

  • genetics

  • style of play

  • manner in which previous concussions managed

  • psychiatric and other mental disorders

  • alcohol and drug use

  • obesity

  • age related changes to brain, coexisting dementing illnesses

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agreed on consensus criteria for neuropathology of CTE

  • accumulation of hyperphosphorylated (p-tau) in neurons, astrocytes, and cell processes around small vessels in an irregular pattern at depths of cortical sulci

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CTE and football

  • very common in football

    • only in american findings though - not canada

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CTE and other neurodegenerative diseases (comorbidites)

  • nearly all those with CTE had AD, frontotemporal dementia, lewy body disease, or ALS

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Prevalence of CTE in general population

  • 98.3% history of traumatic brain injury

  • participation in sports - 34%

  • military veterans - 19%

  • women - 40.6%

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Other causes of abnormal tau protein other than head injury?

  • ageing

    • natural consequence

  • drug use

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what is a biomarker?

  • characteristic that is objectively measured and evaluated as an indicator of normal biological processes, pathogenic processes, or pharmalogic responses to a therapeutic intervention

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what are cons of using CT, fMRI, CSF as biomarker for concussion?

  • costly

  • radiation

  • CSF: infection, leakage, back pain, nausea

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what are neuroinjury markers?

  • concussion causes markers to be released from neuronal cell into surrounding environment

  • once released - called Damage Associated Molecular Patterns (DAMPs)

  • cross BBB which is more permeable now

  • body recognizes them - activates immune system

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how is concussion and immune response tied?

  • DAMPS released - microglial cells recognize and initiate

  • cytokines released

  • inflammatory response can cause injury to BBB, increasing permeability

  • DAMPS and cytokines make their way to blood activating peripheral immune system

  • immune cells in periphery enter brain to help

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how do peripheral tissues react to concussion?

  • neural circuitry disrupted in autonomic centres of brain due to concussion

  • activate peripheral tissues (e.g. adrenal, endothelium, liver)

  • molecules released from these tissues (hormones, cytokines)

  • biomarkers but not from brain

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examples of biomarkers of brain injury?

  • neuroinjury

    • s100b

    • NSE

    • GFAP

    • UCH-L1

    • tau

  • inflammation

    • IL6

    • TNFa

  • neuroendocrine

    • GH

    • cortisol

    • prolactin

    • TSH

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which 2 biomarkers are approved for clinical use? are they useful?

  • GFAP

  • UCH-L1

  • reduce unnecesary CTs

  • save money and exposure to radiation

  • not improving existing clinical measures (CT head rules)

  • concussion is symptom+mechanism (dont have straightforward mechanism - doctor has to make call)

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what have we learned by using biomarkers to study concussion pathophysiology?

  • males and females have different inflammatory responses to concussion

  • inflammation looks different in concussion

  • PRDX-6 and tau elevate after injury

    • PRDX-6: protect membrane and mitochondria

    • tau: axonal injury

  • neuroendocrine hormones uniqely correlated with specific symptoms

  • concussion history mediates inflammatory response

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confounds of biomarkers?

  • participation in collision sports strongly correlated with tau

  • molecules typically have more than 1 function in body

  • other things beyond concussion effect biomarker levels (stress, exercise) (UCH-L1 increase after exercise)

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what do we know about concussion cell level changes? (neuroimaging)

  • microstructural damage

    • impaired cell function

    • impaired communication

  • ionic + glutamate release

    • impaired cell function

    • metabolic dysfunction (mismatch)

  • autoregulatory changes

    • ischemia/oxidative stress

    • altered blood flow

  • sterile info

    • cellular swelling

    • altered blood flow

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what are the 4 modalities of case studies in concussion MRI?

  1. effects at early injury

    1. ASL: blood flow

    2. highly variable blood flow response at early injury

  2. symptom severity

    1. BOLD: brain function

    2. shows functional networks related to symptom severity

  3. brain recovery at medical clearance

    1. DTI: white matter microstructure

    2. lingering white matter abnormalities at medical clearance

  4. long-term brain changes

    1. T1: grey matter morphology

    2. shows long term declines in frontal grey matter

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Incidence Rates for Youth

  • excess of 600 per 100,000 children

  • around the world - 33 million concussions each year

  • youth sport - 12% of youth

  • females increasing a lot

  • most in fall and winter

  • not just from sports - motor vehicle

  • highest for children under 5

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why are we seeing increases in concussion? do you think kids are being less safe?

  • more education around concussion

  • people getting care after

  • more trainers/athletic therapists

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what are 3 ways to identify a suspected concussion?

  1. self reported signs and symptoms

  2. observed signs & symptoms from coaches, teachers, and/or parents

  3. peer-reported signs & symptoms from child/youth

  • youth report more than just self report

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whats important to remember when youth are experiencing concussion symptoms?

  • effects other parts of their life (social, school)

  • function - needs and what they love to do

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