C H A N G I N G P E R S P E C T I V E S I N C O N C U S S I O N M A N A G E M E N T

S T E V E N J . K A R A G E A N E S , D O , FA O A S M M E D I C A L D I R E C T O R , M E R C Y E L I T E S P O R T S M E D I C I N E

PA S T- P R E S I D E N T, A O A S M

N O S I N G L E T E S T C A N D I A G N O S E C O N C U S S I O N

N O S I N G L E T E S T C A N R E L I A B LY D E T E R M I N E R E C O V E R Y

W E S T I L L D O N O T K N O W A L O T A B O U T C O N C U S S I O N S

B U T W E A R E G E T T I N G C L O S E R

D E F I N I T I O N

• Neurosurgery journal study reviewed 5000+ studies

• 26 met criteria

• 1st evidence-based criteria for concussion diagnosis

P R E VA L E N T I N D I C AT O R S

• Observed and documented disorientation or

confusion immediately after the event

• Impaired balance within 1 day after injury

• Slower reaction time within 2 days after injury

• Impaired verbal learning and memory within 2

days after injury

C A U S E

• BIOMECHANICAL FORCES

• Functional impairments without overt structural

damage

• Rapid acceleration/deceleration

• Rotational forces considered a “prerequisite” for

widespread injury to cause a concussion Patterson ZR, Holahan MR. Understanding the neuroinflammatory response following concussion to develop treatment strategies. Front. Cell. Neurosci., 12 December 2012

Ibrahim, N. G., Ralston, J., Smith, C., and Margulies, S. S. (2010). Physiological and pathological responses to head rotations in toddler piglets. J. Neurotrauma 27, 1021–1035

R O TAT I O N A L F O R C E S

• Stretching and shearing of axonal and cell membranes

(i.e., diffuse damage) —>

• Unchecked flux of ions through formerly regulated

channels and membranes —>

• Indiscriminate release of excitatory neurotransmitters —>

• Instigates a widespread, and potentially excitotoxic,

neuronal depolarization —> Patterson ZR, Holahan MR. Understanding the neuroinflammatory response following concussion to develop treatment strategies. Front. Cell. Neurosci., 12 December 2012

R O TAT I O N A L F O R C E S

• Adenosine triphosphate (ATP)-dependent Na+/K+

pumps work in overdrive —>

• Increases glucose metabolism = Hyperglycolysis —>

• Overproduction of lactate =disrupts neural function Patterson ZR, Holahan MR. Understanding the neuroinflammatory response following concussion to develop

treatment strategies. Front. Cell. Neurosci., 12 December 2012

R O TAT I O N A L F O R C E S

• Acute hyperglycolysis state lasts minutes to hours—>

• Prolonged hypoglycolysis —mismatch in glucose

supply vs. demand

• May produce immediate PCS symptoms, leave brain

vulnerable to secondary injuries Patterson ZR, Holahan MR. Understanding the neuroinflammatory response following concussion to develop treatment strategies. Front. Cell. Neurosci., 12 December 2012

I N C I D E N C E

HIGHEST

• Rugby 4.18 (per 1000 AE)

• Hockey 1.20

• American football 0.53

Pfister T, Pfizer K, Hagel B, et al. The Incidence of Concussion in Youth Sports. A Systematic Review and Meta-Analysis Br J Sports Med. 2016;50(5):292-297. 

I N C I D E N C E

LOWEST

• Volleyball 0.03

• Baseball 0.06

• Cheerleading 0.07

Pfister T, Pfizer K, Hagel B, et al. The Incidence of Concussion in Youth Sports. A Systematic Review and Meta-Analysis Br J Sports Med. 2016;50(5):292-297. 

S Y M P T O M S

• Headache (93%)

• Dizziness (75%)

• Difficulty concentrating (57%)

• Confusion (46%)

• Visual disturbance or photosensitivity (38%)

Meehan WP III, d’Hemecourt P, Comstock RD: High school concussions in the 2008–2009 academic year:

mechanism, symptoms, and management. Am J Sports Med 38:2405–2409, 2010

C O N C U S S I O N R AT I N G

• SIMPLE: resolves within 7-10 days (95%)

• COMPLEX: longer than 10 days

• COMPLEX concussion not the same as POST-CONCUSSIVE SYNDROME (PCS)

• PCS: > 3 months symptoms

C O N C U S S I O N R AT I N G

• Recurrent concussion increases odds

• Symptoms most likely to lead to PCS

• Sensitivity to light

• Retrograde amnesia

• Difficulty concentrating

• Insomnia

• Zuckerman SL et al. Predictors of postconcussion syndrome in collegiate student-athletes. Neurosurg Focus. 2016 Apr; 40(4): E13

P O S T- C O N C U S S I V E S Y N D R O M E ( P C S )

S C AT 5 S I D E L I N E T E S T• Sideline assessment tool

• Baseline testing

• Updated in 2017

• More specific step-wise process

• Still have full-contact practice

as a stage to “clear”

C H A N G I N G P E R S P E C T I V E S

Mechanism

Diagnosis

Treatment

N E U R O I N F L A M M AT I O N

Brain, Behavior, and Immunity Volume 46, May 2015, Pages 1-16

A review of the neuro- and systemic inflammatory responses in post concussion symptoms: Introduction of the “post-inflammatory brain syndrome” (PIBS).

Lead author: Michel Rathbone, McMaster University

I N F L A M M AT I O N

• Post-concussive syndrome—>post-inflammatory brain syndrome

• Explains numerous types of symptoms in PCS

• Explains concussion-like symptoms in patients with no history of head trauma: systemic inflammatory responses

N E U R O I N F L A M M AT I O N

• Occurs independently of changes in BBB permeability

• Seen in response to almost all neurological disorders, including concussions

A C U T E R E S P O N S E

• Interleukin-1 (pro-inflammatory)

• Rise in IL-1β precedes secretion of ciliary neurotrophic factor (CNTF) and nerve growth factor (NGF)

• Promote growth and survival of neurons

• Aids in defense against injury

• Prolonged exposure could be neurotoxic

A C U T E R E S P O N S E

• Tumor necrosis factor-α

• Early mediator of CNS damage

• Also neuroprotective and neurotoxic

A C U T E R E S P O N S E

• Interleukin-6 (IL-6)

• Key regulator during acute phase of inflammatory response

• Also neuroprotective and neurotoxic

N S A I D S ?

• Shown to be not effective

• Targeting this inflammatory cascade has not worked

• Timing:

• Too soon: interfere with neuroprotective effects of inflammation

• Too late: damage too great to overcome

O M E G A - 3 F FA

• Supplementation with O3FA before a

concussion

• Protects against reduced plasticity of neurons

and impaired learning

• Normalizing levels of proteins associated with

neuronal circuit function, cognitive processing,

synaptic facilitation, neuronal excitability, and

locomotor control

Wu A, Ying Z, Gomez-Pinilla F. Dietary omega-3 fatty acids normalize BDNF levels, reduce oxidative

damage, and counteract learning disability after traumatic brain injury in rats. J. Neurotrauma. 2004; 21:

1457–67

O M E G A - 3 F FA

• Case study of a young boy with sTBI from a motor vehicle accident

• In a persistent vegetative state

• After starting O3FFA supplementation, improved

• Able to walk for HS graduation 3 months later

O M E G A - 3 F FA

• Mills JD, Bailes JE, Sedney CL, et al. Omega-3 fatty acid supplementation and reduction of traumatic axonal injury in a rodent head injury model. J. Neurosurg. 2011; 114: 77–84

• Wu A, Ying Z, Gomez-Pinilla F. Omega-3 fatty acids supplementation restores mechanisms that maintain brain homeostasis in traumatic brain injury. J. Neurotrauma. 2007; 24: 1587–95

• Wu A, Ying Z, Gomez-Pinilla F. The salutary effects of DHA dietary supplementation on cognition, neuroplasticity, and membrane homeostasis after brain trauma. J. Neurotrauma. 2011; 28: 2113–22.

• Bailes JE, Mills JD. Docosahexaenoic acid reduces traumatic axonal injury in a rodent head injury model. J. Neurotrauma. 2010; 27: 1617–24.

O M E G A - 3 F FA

• No human studies with high evidence

• Two human studies currently ongoing

• NCAA division 1 athletes with 2200 mg

of DHA for 30 days after onset of a

concussion

• 14 to 18 y/o with 2 g of DHA daily for 3

months

Ashbaugh A, McGrew C. The Role of Nutritional Supplements in Sports Concussion Treatment.

Curr Sports Med Rep. 2016 Jan-Feb;15(1):16-9

• Found in turmeric

• Animal supplementation with curcumin before a concussion

• Improved balance

• Transduction and monitoring of cellular energy compared with controls

• Promising but no human trials

Ashbaugh A, McGrew C. The Role of Nutritional Supplements in Sports Concussion Treatment. Curr Sports Med Rep. 2016 Jan-Feb;15(1):16-9

C U R C U M I N

• Neuroprotective and neuroregenerative abilities and reduces inflammation

• Effects improved with Vitamin D

• Cochrane Review did not find it helps but not enough data, studies inconsistently done

P R O G E S T E R O N E

O T H E R S U P P L E M E N T S

• Resveratrol

• Melatonin

• Creatine

• Vitamin C, D, and E

• Scutellaria baicalensis (Chinese herb)

N E U R O I N F L A M M AT I O N

• Not quite the same as general inflammation

• Manipulating neuroinflammation key to treating long-term symptoms of concussion

W H E N I S A C O N C U S S I O N G O N E ?

C U R R E N T M E T H O D

• Symptoms must resolve

• No symptoms return during exercise protocol

C O M P U T E R I Z E D N E U R O P S Y C H T E S T I N G

• Insufficient validity and test–retest reliability

• Can have metabolic changes from concussion even

when ImPACT returns to baseline

• 17% of concussions had normal ImPACT

• 20-40% of nonconcussed athletes showed

cognitive impairment

P E T S C A N

• Uses radio-labeled metabolic analogs to measure

brain glucose metabolism

• Lower glucose metabolism in concussed patients

correlate with cognitive disturbances

• Very promising but more research needed to

determine potential clinical utility and validate

F U N C T I O N A L M R I

• Blood-oxygen-level-dependent (BOLD) fMRI • Detects changes in oxygenation state of hemoglobin • Changes in concussed brain activation detected acutely and

months after injury • Hard to interpret, expensive, not always covered

M A G N E T I C R E S O N A N C E S P E C T R O S C O P Y

• Measures the concentrations of molecules

associated with brain metabolism

• Concussion significantly lowers gray matter

glutamine and N -acetylaspartate (NAA) levels

• Increases white matter creatine and choline levels

• May help determine metabolic recovery from

concussion and determine return to play

M A G N E T I C R E S O N A N C E S P E C T R O S C O P Y

• Study: One cohort of patients with concussion

• Symptoms resolved in about 3 days

• Took 30 days for the NAA level and NAA/Cr ratio

to return to baseline

Vagnozzi R, Signoretti S, Cristofori L, et al. Assessment of metabolic brain damage and recovery following mild

traumatic brain injury: a multicentre, proton magnetic resonance spectroscopic study in concussed patients.

Brain. 2010;133:3232–3242.

T R E AT M E N T

A P P R O A C H T O T R E AT M E N T

• Comprehensive

• Active

• Proactive

• Engagement

F O U R D O M A I N S O F S Y M P T O M S

• Physical

• Cognitive

• Emotional

• Sleep

T R E AT M E N T

• Acute

• School

• Cognitive

• Visual

• Auditory

• Psych

• Endocrine

• Vestibular

• Rehabilitation

• Exercise

• Sleep

A C U T E : C O G N I T I V E R E S T

• Concussion: Neuroinflammatory concept

• Similar approach to an acute ankle sprain

• 72-hour inflammatory phase

• Treatment goal—calm down inflammation

C O G N I T I V E R E S T

• No reading, video games, computer screens longer than 30 minutes (or when symptoms are provoked)

• Minimal texting

• Avoid loud music

• Avoid activities requiring focus

C O G N I T I V E R E S T

• May do light physical activity that does not cause symptoms or risk further injury

• Frequent naps allowed (no longer than 30 minutes)

C O G N I T I V E R E S T — S C H O O L

• No school first post-concussive day

• Strongly consider no school for 1st 3 days

• Communication with school officials is key

• Understand athlete’s stress

R E T U R N T O L E A R N

• Can tolerate 30-45 minutes of concentrated activity

without symptoms

• Gradual return: half days, then full day

• Give athlete detailed accommodations

Santiago S. Adolescent Concussion and Return-to-Learn. Pediatr Ann. 2016 Mar 1;45(3):e73-5.

S C H O O L A C C O M M O D AT I O N S

• Rest during school day

• Reduction in workload

• Shorter assignments

• More time to complete work

• Wear hat to block fluorescent lights

S C H O O L A C C O M M O D AT I O N S

• Shortened school days (alternate half-days)

• Shortened classes

• Fewer activities requiring exertion

• Breaks during school day (quiet location)

• Line guide (bookmark or index card) when reading to reduce the work involved for the eyes to scan

S C H O O L A C C O M M O D AT I O N S

• Quiet room to complete assignments or tests

• Avoid noisy events or areas (cafeteria, pep rally, sporting events)

• Tutoring or peer helper

• Tests reduced or postponed

C O G N I T I V E A S S E S S M E N T

B R A I N A C T I V I T Y

• Changes in alpha, beta, theta, delta brain wave activity

• Gray and white matter can suffer injury

• As gray matter recovers, may not be reintegrated into neural network function—>”not working”

• White matter: high speed relay system connecting to cortex

• Gray matter highly plastic, white matter is not

B R A I N M A P P I N G — Q E E G

• qEEG: Quantitative Electroencephalography

• Multiple EEG electrodes measuring activity (32 leads) and digitally processed

• Assess changes in brain wave frequency bands

• “Map” areas of brain with slower brain wave activity

• Assess coherence

C O H E R E N C E

• Correlation between regions: high connectivity

• Connectivity reflects amount of processing brain devotes to a certain activity

• Changes in coherence can reflect difficulties in processing

N E U R O F E E D B A C K

• Guided by qEEG

• Helps to improve brain wave activities

• Computer games

• NF can treat ADHD, depression, anxiety, addictions

• Improve connectivity and coherence

Courtesy Derek Jones, Anatomical Concepts UK

U S E I N C O N C U S S I O N / P C S

• Active treatment for various cognitive PCS symptoms

• Concentration

• Memory

• Headaches

• Proactive method of treating acute symptoms

E N D O C R I N E

E N D O C R I N E

• Pituitary protected by sella turcica but stalk vulnerable to TBI forces

• Stalk connected to anterior pituitary and hypothalamus

• TBI can lead to stalk rupture, hypothalamic abnormalities and hyoppituitarism

E N D O C R I N E

• 4% of patients with TBI sustained an associated neuroendocrine disorder of the hypothalamic-pituitary axis

• 40-63% of fatal cases of TBI reveal postmortem pathologic findings of the hypothalamus/anterior pituitary

P I T U I TA R Y G L A N D

• Anterior lobe: growth hormone [GH], [3] thyrotropin, corticotropin, gonadotropins

• Released by neuropeptide-releasing hormones from the hypothalamus

• Posterior lobe: vasopressin, oxytocin

• Produced by hypothalamus, stored in lobe for release

• Not affected by pituitary stalk trauma

P I T U I TA R Y G L A N D

• 5-90% incidence (Endocrine Feb 2014)

• 27.5% hypopituitarism in some form out of 1000+ TBI cases

P I T U I TA R Y G L A N D

• Most common endocrine complications after TBI:

• Decreased ADH (SIADH/dilutional hyponatremia)

• Decreased Growth Hormone

Bazarian JJ, Cernak I, Noble-Haeusslein L, Potolicchio S, Temkin N. Long-Term Neurologic Outcomes After Traumatic Brain Injury. Journal of Head Trauma Rehabilitation. 2009; 24(6):439-451.e

G R O W T H H O R M O N E

• Fatigue

• Growth problems

• Weight gain

• Low blood pressure

• Low libido

• Loss of muscle mass

• Amenorrhea

O T H E R E N D O C R I N E E F F E C T S

• Hypothyroidism: fatigue, constipation, weight gain, irregular menstrual periods, cold intolerance

• Hyperprolactinemia: irregular menstrual periods, nipple discharge, and erectile dysfunction

Bazarian JJ, Cernak I, Noble-Haeusslein L, Potolicchio S, Temkin N. Long-Term Neurologic Outcomes After Traumatic Brain Injury. Journal of Head Trauma Rehabilitation. 2009; 24(6):439-451.e

E N D O C R I N E

• Screen for hormonal disorders (lab tests)

• Refer for appropriate treatment

H E A R I N G

H E A R I N G

• Loud or numerous noises provoke symptoms

• Temporary threshold shift

• Symptoms can last long time

H E A R I N G P R O T E C T I O N

T R E AT M E N T

• Lower constant decibel exposure

• Avoid situations with loud or numerous noises

• Educate patient

V I S U A L

V I S U A L

• Visual testing newer trend in sideline eval

• 50% of brain “circuits” linked through vision

• Many susceptible to disruption from head injury

V I S U A L

• Visual testing newer trend in sideline eval

• 50% of brain “circuits” linked through vision

• Many susceptible to disruption from head injury

K I N G - D E V I C K T E S T

• Assesses visual function and attention integrity

• 1-2 minutes to perform

• Track saccadic eye movements

• Athlete rapidly reads numbers on 3 test cards

• Score = total time required (seconds)

S A C C A D I C E Y E M O V E M E N T

Rapid, ballistic movements of the eyes that abruptly change the point of fixation

K I N G - D E V I C K T E S T

• KD 75% sensitive in detecting concussion

Galetta KM, Morganroth J, Moehringer N, et al: Adding vision to concussion testing: a prospective study of

sideline testing in youth and collegiate athletes. J Neuroophthalmol 35:235–241, 2015

• SAC + BESS: miss 10% of concussions (n=20)

• SAC + BESS + KD: all concussions detected

Ventura RE, Jancuska JM, Balcer LJ, et al. Diagnostic Tests for Concussion: Is Vision Part of the Puzzle? J Neuro-

Ophthalmol 2015; 35: 73-81.

V I S U A L D I S R U P T I O N

• Headache

• Loss of balance

• Blurred vision

• Inattention

• Poor memory

• Vertigo

• Dizziness

• Anxiety

• TMJ

• Neck pain

B I N O C U L A R V I S I O N D Y S F U N C T I O N

• Eyes not aligned after TBI

• Muscles in and around eyes overwork when focusing

• Increased tension

• Treatment goals: progressive relaxation

T R E AT M E N T

• Prism glasses

• Vision therapy

• Decrease work on eyes

P S Y C H O L O G I C A L

P S Y C H O L O G I C A L A S S E S S M E N T

• Assess emotional symptoms and track

• Risk factors

• Isolation from team activities

• History of mental health disorders (anxiety)

• Poor social support

• Poor/no communication with team/training staff

S Y M P T O M S

• Personality changes

• Sad, withdrawn

• Irritable/emotional

• Mood swings

• Nervous

• Paranoia

T R E AT M E N T

• Keep tracking athlete

• Keep athlete engaged —>goal-oriented

• Education

V E S T I B U L A R D Y S F U N C T I O N

V E S T I B U L A R D Y S F U N C T I O N

• Connected with visual

• Positional, heart rate, head movement, body movement

S Y M P T O M S

• Dizziness/Vertigo

• Motion Sensitivity/ Height Phobia

• Tinnitus

• Lightheadedness

• Blurred vision/Double vision/Trouble Focusing

• Photophobia

• Imbalance (especially in dark)

V E S T I B U L A R A S S E S S M E N T

• Dynamic Visual Acuity Testing (DVA)

• Dynamic Gait Index (DGI)

• Functional Gait Assessment (FGA)

• BESS Test

• VOMs

V E S T I B U L A R R E H A B F O C U S

• Fine motor

• Reaction time

• Eye head coordination

• Fatigue

• Vision

• Balance

• Dual task performance

• Body mechanics/posture

R E H A B I L I TAT I O N

P H Y S I C A L T H E R A P Y

• Cervical injury often missed

• Weaker cervical stabilizers increase risk of concussion

• Whiplash mechanism —> no MRI findings

• Goal-oriented activity for patient

P H Y S I C A L T H E R A P Y G O A L S

• Treat MSK pain

• Improve functional movement

• Improve cervical stability and control —> prevent concussion

• Integrate with vestibular and visual treatment

• Exercise protocol

E X E R C I S E

P H Y S I C A L A C T I V I T Y

• Old thinking: no exercising until symptoms resolve

• New thinking: exercise once athlete can tolerate

• Keep intensity very low then progress as tolerated

• Default to no exercise in 1st 72 hours if unsure

Leddy J, Hinds A, Sirica D et al. The Role of Controlled Exercise in Concussion Management. PM R. 2016 Mar;8 (3 Suppl):S91-S100.

Leddy JJ, Willer B. Use of graded exercise testing in concussion and return-to-activity management. Curr Sports Med Rep 2013;12: 370-376.

E X E R C I S E W I T H S Y M P T O M S

• Research supports avoiding complete rest after acute phase of injury

• Exercise enhances recovery*

* Baker JG, Freitas MS, Leddy JJ, et al. Return to full functioning after graded exercise assessment and progressive exercise treatment of post concussion syndrome. Rehabil. Res. Pract. 2012;2012:705309

P H Y S I C A L A C T I V I T Y

• Buffalo Concussion Treadmill Test

• Only functional test shown to safely and reliably reveal physiological dysfunction in concussion

• Can differentiate concussion from other diagnoses (eg, cervical injury, depression, and migraines)

• Quantify clinical severity and exercise capacity of concussed patients

Leddy J, Hinds A, Sirica D et al. The Role of Controlled Exercise in Concussion Management. PM R. 2016 Mar;8 (3 Suppl):S91-S100.

Leddy JJ, Willer B. Use of graded exercise testing in concussion and return-to-activity management. Curr Sports Med Rep 2013;12: 370-376.

B U F FA L O C O N C U S S I O N T R E A D M I L L T E S T

• Based on the Balke cardiac protocol

• Starting speed is 3.2-3.6 mph at 0% incline

• Incline 1% at minute 2, then 1% per minute after

• Maintain same speed until athlete cannot continue

• Stop when 3 pts on 1-10 VAS compared to pre-test

Leddy J, Hinds A, Sirica D et al. The Role of Controlled Exercise in Concussion Management. PM R. 2016 Mar;8 (3 Suppl):S91-S100.

Leddy JJ, Willer B. Use of graded exercise testing in concussion and return-to-activity management. Curr Sports Med Rep 2013;12: 370-376.

B U F FA L O C O N C U S S I O N T R E A D M I L L T E S T

• Record heart rate at threshold of symptom exacerbation

• Safe for PCS athletes to exercise to 74% max HR

• Can be used in light aerobic exercise stage

• Compare HR when symptoms exacerbated to athlete’s

theoretical maximum HR

• Closer the two numbers are shows how close athlete is to

recovery

E X E R C I S E P R O T O C O L

• Should be started when athlete appears to be recovered from concussion

• Athlete “feels” normal, ready to play again

• No symptoms or back to baseline level

• SCAT 5 back to baseline

• EP NOT something athlete tries to see if s/he can do in order to RTP faster

E X E R C I S E P R O T O C O L

• Conflicts with when doctor needs to clear athlete

• Protocol NOT intended to see if athlete can take a hit

• Testing whether brain can handle increased blood pressure and heart rate

• FLAW: Not sport/activity specific

• LAST STAGE: Full contact practice

S L E E P

S L E E P

• Seen in up to 84% of TBI

• 20% have sleep cycle disruptions > 3 yrs

• Unable to initiate or maintain sleep

• Cannot cycle through REM sleep stages

• Can last months or years after concussion

Zeitzer JM, et al. Insomnia in the context of traumatic brain injury. nJRRD, 46 (6), 2009

S L E E P T R E AT M E N T

• Melatonin: 5mg at dinner

• Sleep hygiene

• No devices or reading in bed

• White noise

• Avoid blue light sources

S L E E P T R E AT M E N T

• Take naps no longer than 30 minutes

• Caffeine naps also helpful

• Evaluate for sleep apnea, neck pain

Sandsmark DK, Elliot JE, Lim MM. Sleep-wake disturbances after traumatic brain injury: synthesis of human and animal studies. Sleep. 2017;20(10). doi:10.1093/sleep/zsx044

END