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What are the 3 phases of recovery?
acute
subacute
persistent
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
Describe the subacute phase
after 72 hours
people have different understandings of persistent symptoms
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
What are examples of co-morbidities?
neck injury
msk injury
sleep issues
anxiety
pressure in head
What are examples of pre-morbidities?
personality
previous concussion
How does the DSM define persistent symptoms?
cognitive deficits in attention and memory
at least 3 or more symptoms including HA, dizziness, fatigue, irritability, apathy, personality change, or sleep or affective disturbances
present for 3 months of greater
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
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
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
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
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
How does CISG define persistent symptoms?
persistent symptoms > 2 weeks of symptoms in adults
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
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,
What are the symptom clusters?
somatic/physical
cognitive
cervicogenic
vestibuloocular
headache
mood/affect
sleep-related
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
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
What is the pathophysiology of physiological concussion disorder?
persistent alterations in cellular metabolism, cerebrovascular physiology “metabolic mismatch”
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
what are the treadmill results for someone with a physiological concussion?
early symptom limited threshold (5-15 mins)
what is the physical exam for a physiological concussion?
normal physical exam
may have elevates resting HR
what is the treatment for a physiological concussion?
submaximal aerobic exercise prescription
treatment of co-existing dysfunctions
what is the pathophysiology of a vestibulo-ocular concussion?
isolated dysfunction of central and peripheral components of vestibulo-ocular neurological subsystem
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
what are the treadmill results for a vestibulo-ocular concussion?
able ot exercise for 15-25 mins
what is the physical exam of a vestibulo-ocular concussion?
impaired convergence, accommodation, saccades, and VOR
positive Dix-Hallpike Maneuver
what is the treatment for vestibulo-ocular concussion?
submaximal aerobic exercise prescription
targeted vestibular and vision therapy
what is the pathophysiology of a cervicogenic concussion disorder?
isolated mechanoreceptive or proprioceptive dysfunction within cervical spine neurological sub-system
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
what are the treadmill results for cervicogenic concussion?
able to exercise for 15-25 mins
what is the physical exam for cervicogenic concussion?
decreased ROM
sub-occipital and paraspinal neck tenderness
impaired cervical spine proprioception
what is the treatment for cervicogenic concussion?
cervical spine manual therapy
gaze and postural stabalization
submaximal aerobic exercise prescription
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
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
What are mechanisms behind why exercise helps concussion recovery?
neutrophins → BDNF
improvements to ANS/normalization of cerebral blood flow
neuroendocrine
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
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
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
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)
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
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
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
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
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
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)
What are the 2 pathways visual info is conveyed by?
magnocellular stream
parvocellular stream
involved in different components
Explain the parvocellular process (Central/focal vision)
seeing fine details, identification of what we are seeing
conscious vision
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)
What are rehabilitation exercises for vision related interventions?
visual perception
convergence/divergence/accommodation
saccades and smooth pursuits
gaze stability
visual acuity
spatial awareness
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
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
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
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
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
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
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
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
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
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”
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)
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
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
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
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
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
When was the first use of CTE?
1940 bowman and blau
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
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
When did correlation between concussion history, MCI and depression happen?
2005 and 2007
Guskieweicz et al
what did mckee establish?
2009
further characterize CTE pathologic findings in ewview of 48 autopsy confirmed cases
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
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%)
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
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
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
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
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
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
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
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
CTE and football
very common in football
only in american findings though - not canada
CTE and other neurodegenerative diseases (comorbidites)
nearly all those with CTE had AD, frontotemporal dementia, lewy body disease, or ALS
Prevalence of CTE in general population
98.3% history of traumatic brain injury
participation in sports - 34%
military veterans - 19%
women - 40.6%
Other causes of abnormal tau protein other than head injury?
ageing
natural consequence
drug use
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
what are cons of using CT, fMRI, CSF as biomarker for concussion?
costly
radiation
CSF: infection, leakage, back pain, nausea
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
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
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
examples of biomarkers of brain injury?
neuroinjury
s100b
NSE
GFAP
UCH-L1
tau
inflammation
IL6
TNFa
neuroendocrine
GH
cortisol
prolactin
TSH
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)
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
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)
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
what are the 4 modalities of case studies in concussion MRI?
effects at early injury
ASL: blood flow
highly variable blood flow response at early injury
symptom severity
BOLD: brain function
shows functional networks related to symptom severity
brain recovery at medical clearance
DTI: white matter microstructure
lingering white matter abnormalities at medical clearance
long-term brain changes
T1: grey matter morphology
shows long term declines in frontal grey matter
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
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
what are 3 ways to identify a suspected concussion?
self reported signs and symptoms
observed signs & symptoms from coaches, teachers, and/or parents
peer-reported signs & symptoms from child/youth
youth report more than just self report
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
Note
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