3/27/2017...3/27/2017 1 Concussion and TBI: Dizziness and Balance Issues Susan L. Whitney, DPT, PhD, NCS, ATC, FAPTA School of Health & Rehabilitation Sciences Department of Physical

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Concussion and TBI: Dizziness and Balance Issues

Susan L. Whitney, DPT, PhD, NCS, ATC, FAPTA

School of Health & Rehabilitation Sciences

Department of Physical Therapy

Physical Therapy at the

University of PittsburghRanked #1- U.S. News & World Report

School of Health & Rehabilitation Sciences


UPMC Sports Concussion Program- Balance and Vestibular Team

Mickey W. Collins, PhD

Joseph M. Furman, MD, PhD

Luke Henry, PhD

Anthony Kontos, PhD

Anne Mucha, DPT, NCS

Cara Camiolo Reddy, MD

Patrick J. Sparto, PT, PhD

Susan L. Whitney, DPT, PhD

Summary of Legislation • State Educational Agencies are required to issue

concussions management regulations by Fiscal Year 2013 (October 1, 2013), in order to be eligible to receive funds under the Elementary and Secondary Education Act (ESEA).

• School districts required to develop and implement a standard plan for concussion safety and management that includes: ▫ education for students, parents, and school personnel ▫ best practices for safety standards, treatment, and

management ▫ standards for return to athletic and academic activities

• Students suspected of having sustained a concussion:▫ must be removed from the activity ▫ prohibited from resuming participation until the school receives

a written release from a health care professional.

Physical therapists are explicitly listed in the definition of “health care professional” involved in concussion care management and removal-from-play/return-to-play decisions, along with physicians, nurses, certified athletic trainers, and neuropsychologists.

APTA Efforts on Concussion Legislation

• APTA continues to stay actively engaged in the concussion management policy issues at multiple levels. In March 2010, APTA Board of Directors adopted a position that states the following:

• The American Physical Therapy Association (APTA) recognizes that concussions should be evaluated and managed by a multidisciplinary team of licensed health care providers. Physical therapists are an integral part of the multidisciplinary team. An individual suspected of having a head injury should be removed from participation in organized activity for assessment of concussion. If signs, symptoms, and behaviors of concussion are present, the individual should be prohibited from further participation until he or she is evaluated by and receives written clearance for return to participation from a licensed health care provider trained in the evaluation and management of concussion.

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APTA Position • Concussions are complex injuries that can

have diverse effects on the individual. • Management of concussions does not

completely fall within the expertise of any single health care discipline,

• Physical therapists make a unique contribution to the concussion care management team, particularly in the areas of balance and vestibular evaluation and rehabilitation.

APTA Position

• Policy should not restrict treatment of concussions to a narrow, exclusionary “list” of providers.

• APTA’s preferred language is “licensed health care provider trained in the evaluation and management of concussions”

Newest Guidelines

McCrory P et al

Phys Ther Sport 2013 May

Consensus statement on Concussion in Sport - The 4th International Conference on Concussion in Sport held in Zurich, November 2012.

Concussion:

“Getting your bell rung”

“Seeing stars”

“Dazed”

“Bump on the head”

“Dinged”

Definition of Concussion

Results in neuropathological changes, largely reflect a functional disturbance rather than a structural oneMay or may not involve loss of consciousnessResolution of symptoms follows a sequential courseTypically associated with grossly normal structural neuroimaging studies

Post concussive disorder is not just for athletes

Seen in persons post:Accident (fall, auto)

Blast injuries (wounded warriors)

Abuse

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Concussion: Negative Outcomes

Second Impact Syndrome (SIS)

Chronic Traumatic Encephalopathy (CTE)

Chronic Post Concussion Syndrome (PCS)

• Only in young (≤ 23 yo)

• Occurs when a second concussion sustained when still symptomatic from an earlier concussion

• Pathophysiology: Loss of autoregulation of cerebral blood flow; vascular engorgement; increased ICP; brainstem herniation

• Incidence: Rare

• between 1980 –2009

• 17 high school athletes fatalities due to second-impact syndrome

• Mortality 50%; Morbidity 100%

• Found in former athletes; potentially linked to repeated concussion

• Mechanism – abnormal deposits of protein tau, distinct from other tauopathies (AD, etc)

• Incidence: Unknown – Case Studies only

• Dx - post-mortem exam of brain

• Findings: cognitive impairment and neuropsychological symptoms (can be severe), parkinsonism, speech and gait abnormalities

• Challenge: Comorbidities such as ETOH dependence, drug abuse, genotype, etc

CTESecond Impact

Second Impact Syndrome

• Rare but catastrophic

• Seen only in the young (patients ≤ 23 yo)

• Occurs when an athlete sustains a second concussion (often minor) when still symptomatic from an earlier concussion

• Player might appear dazed, but often can leave the field under his own power

• Swelling can start within 15 seconds to a couple of minutes

• Brainstem failure within 2 to 5 minutes

Fig. 2. Images obtained after second impact. A: Head CT obtained after second impact. Arrows point to thin bilateral subdural hematomas.B: Sagittal T1-weighted brain MR image. Arrows point todownward descent of the midline structures. C: Axial T2-weighted MR image. Arrows point to thalamic injury. D: Axial diffusion-weighted MR image. Arrow points to left thalamic injury. Restricted diffusion was proven by calculation of apparent diffusion coefficient (not shown).

Weinstein et al. J Neurosurg: Pediatrics / Volume 11 / March 2013

Second Impact Syndrome• Mortality 50%; Morbidity 100%

• Dramatic and immediate brain swelling

• Pathophysiology: Loss of autoregulation of cerebral blood flow; vascular engorgement; increased ICP; brain herniation (inferomedial temporal lobe herniation, herniation of cerebellar tonsils through foramen magnum, brainstem compression

• Sometimes associated with a SDH seen on imaging

• Speculate that acceleration/deceleration forces set off this cascade (Byard 2009, Cantu 1998, Cantu 2010, Weinstein 2013)


CTE:From Boston University: Center for the Study of Traumatic

Encephalopathy

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Post Concussion Syndrome

• “Miserable minority”

• Up to 10-20% of patients

• No clear cut definition

• When recovery from concussive deficits persists beyond the normal window of recovery and become chronic

• Complex array of symptoms

Symptoms of PCS(Alexander 1995; Savola 2003)

• Impaired attention, memory, and/or executive functions

• Depression

• Poor sleep

• Dizziness

• Chronic pain (headache)

• Feeling frustrated or impatient, panic attacks

• Irritability, easily angered

• Sensitivity to noise and light

• Decreased alcohol tolerance

• Blurred vision

Epidemiology of Concussion/mTBI: Difficult to accurately report incidence, as concussion is grossly underreported

General Population • Approx 1.4 million incidents of TBI reported each year; w/ 75-90% classified as mild (CDC 2004)• Affects 123 persons per 100,000 in US yearly (Bazarian, 2005)

Sports • 2 million sports and recreation concussive injuries occur annually in US • CDC Toolkit for Physicians (2008), estimates up to 3.8 million• 20-30 % of high school football players have experienced at least 1 concussion (Powell 1999; McCrea 2004)

Military

•194,561 mTBI cases between 2000-2012 • OIF, OEF, OND

The Youth Concussion “Epidemic” Estimated 1.6-3.8 million sports and recreation

concussive injuries occur annually in US (CDC Toolkit for Physicians, 2008)

Between 1997-2007 the number of ED visits for 14-19 year olds for concussion TRIPLED!

> 40% of Concussions dx’d in ED occur in children/adolescents between 5-19 yo.

30-58% of ED-dx’d concussions due to Sports

Approx 9% of all high school sports injuries are concussions

(Bakhos 2010) (Meehan 2010)

Contact Sports:Participation Rates

1. Football (3X)

2. Boys’ Basketball

3. Girls’ Basketball

4. Baseball

5. Softball

6. Boys’ Soccer

7. Boys’ Wrestling

8. Girls’ Volleyball

9. Girls’ Soccer

10.Girls’ Field Hockey(Daneshvar 2011)

Baseball (.05 - .06)

Volleyball (.05)

Cheerleading (.06)

Boys’ Basketball (.07)

Softball (.07)

Lower: Football (.47-.6)

Girls’ Soccer (.32.-.35)

Boys’ Lacrosse (.3)

Boys’ Soccer (.22)

Girls’ Lacrosse (.2)

Which sports have highest risk?

Highest:

Incidence Rates for High School Sports (based on 1000 athletic exposures)

Trends: Concussion rate has steadily increased over time Girls – nearly 2x risk in similar sports

(Lincoln 2011; Gessel 2007)

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Taken from: Silver JM et al, Am J Psychiatry, 2009

2 million sports and recreation concussive injuries

annually in US

• Likely a HUGE underestimation

Goodman et al

Incident Rate

Head injuries occur at about 2 million per year 2003 CDC reported 5000,000 emergency visits and 200,000 hospitalizations

Currently more than 5 million individuals living with the effects of a traumatic brain injury

Men are two times more likely to sustain a head injury than women

Incidence rates of TBI in the ED in <19 year olds from Sports

and Recreation injuries is increasing

2001 153,375

2009 248,418

Concussion

Evidence exists that neurocognitive

deficits remain for as many as 14 days after a concussion even if the adolescent is not reporting any symptoms (McClincy MP et al, 2006; Valovich McLeod TC et al, 2006; Barlow, M, 2011)

Mechanism of Injury:

• Blow to head or body, direct impact notnecessary

• May be due to Blast

• Acceleration/Deceleration forces cause temporary deformation of axon (axonal stretching)

• Neurometabolic changes result, without visible abnormalities (normal CT/MRI)

• Physiologic changes at cellular level

• Neurons are “dysfunctional”, not destroyed(Giza 2001)

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Pathophysiology – Blunt Force:Axonal stretching causes:

Influx of Ca++/Efflux of K+

NA-K pump works overtime to restore normal membrane potential, requiring ’d ATP

Increase in energy requirements met by an increase in glycolysis

Elevated lactate levels

Occurs in setting of post-traumatic decrease in cerebral blood flow

Disrupted neuro-metabolism in brain results in “Energy Crisis” - Glucose demand ↑’s but Glucose supply ↓’s

Likely mechanism for post concussive vulnerability

brain is less able to respond adequately to a second injury

(Giza 2001)

What about Concussions due to BLAST??

With BLAST: (Hoffer 2010)

• Injury results in more global neurochemical changes

• Increased rates of hearing loss & cognitive deficits

• Increased rate of HA & disequilibrium in persons experiencing dizziness

• Symptoms tend to be more constant than intermittent

• Increased incidence of post blast vertigo (as opposed to dizziness)

• Rates of PTSD are high; Overlap of PTSD plays a significant role in the prognosis of patients post military-related mTBI

Blast Wave Pressure

Hurricane0.25 psi

200 km/hour

Blast100 psi

2,414 km/hour

Taken from: Barlow M, et al, 2011 with a sample of 106 children between 11-19 years of age.(PCS: post concussion syndrome)

Recovery From Sports Concussion:How Long Does it Take?

0

10

20

30

40

50

60

70

80

90

100

1 3 5 7 9 11 13 15 17 19 21 23 25 27 29 31 33 35 37 38 40+

All Athletes No Previous Concussions 1 or More Previous Concussions

N=134 High School Male Football Athletes

WEEK 1 WEEK 2 WEEK 3 WEEK 4 WEEK 5

Collins et al., 2006, Neurosurgery

40%ARE BETTER

60%ARE BETTER

80%ARE BETTER 90%

ARE BETTER

Collins et al., 2006, Neurosurgery

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Why don’t kids report concussions?

Athletes understood dangers of concussions (n=50; females and males)

Did focus groups: scenarios involving concussive symptoms and 6/9 groups would continue to play or would take a brief break and then return to play (3/9 groups)

Wanted to keep playing and knew that reporting symptoms might result in being removed from the game.

Why don’t kids report concussions?

athletes were hesitant to report symptoms to coaches if they did not result in significant pain or disability.

Knowledge of concussion does not seem to be a barrier, but coach approachability may be a problem

Crisman SP et al, J of Adol Health, 2013

Most Commonly Reported SymptomsHigh School & College Athletes n = 1,438; 1-7 days post

Kontos et al, 2012.

SYMPTOM PERCENT

# 1 Headache 75%

# 2 Difficulty Concentrating 57 %

# 3 Fatigue 52 %

# 4 Drowsiness 51 %

# 5 Dizziness 49 %

# 6 Foggy 47 %

# 7 Feeling Slowed Down 46 %

# 8 Light Sensitivity 45 %

# 9 Balance Problems 39 %

# 10 Difficulty with Memory 38 %

Post Concussion Migraine

Must meet the International Headache Criteria for Migraine (Headache classification committee of the IHS.

Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia 1988 8: 1-96.)

There are specific criteria for migraine dizziness (Newhauser et al, 2005; Marcus et al, 2004)

Can have headache associated with or unassociated with dizziness (Newhasuer et al, 2005)

Mild Concussion and Dizziness

Symptoms post mild TBIHeadache (may develop migraines)

Fogginess

Dizziness

Difficulty reading

Balance problems

Difficulty sleeping

Risk factors > 1 week

N=1,412 retrospectively (football and non-football concussions)

Those who presented with ≥4 sx in all athletes doubled the risk that they would be symptomatic for ≥1 weeks

History of prior concussion doubled the risk of concussion for those who played football

Drowsiness, nausea, concentration difficulties, and light sensitivity affected length of recovery

Chrisman SP et al, Brain Inj, 2013

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Risk factors > 1 week

Dizziness was the 2nd most common complaint (~78% of the participants) with headache the #1 complaint (95%)

Sensitivity to light/sound were associated with non-football players recovery

LOC was not signficant

Chrisman SP et al, Brain Inj, 2013

Symptom Checklists

Post-Concussion Symptom Scale (Lovell 2006)

Post-Concussion Symptom Inventory (Gioia 2008)

Graded Symptom Checklist (Guskiewicz 2004)

Rivermead Post-Concussion Symptoms Questionnaire (King 1995)

The problem with Symptom Checklists: Under-reporting & magnification are common!!

(McCrea 2004, Williamson 2006)

Findings after Concussion: Symptoms

Common Concerns and Interventions

Insomnia- medical (trazadone)

Headache- medical (amatadine)

Dizziness/vertigo-physical therapy

Management of the Post Concussive Patient: Multidisciplinary Team

Core Team: Additional Members:

•Neuropsychology •MD (w/ training in mTBI)•Physical Therapy (Vestibular, Orthopedic and/or Exertional)

•Neuro-Otology•Neuro-Opthalmology •Neuro-Optometry•Psychology/Psychiatry•Cognitive Therapy

In cases of young athletes:•Athletic Trainer/Coach•School

How is PT involved in Concussion Management?• Acute on-field evaluation (Sports & Military

PT’s)• Sub-acute assessment▫ Balance/Vestibular/Neurologic screen

• Rehabilitation/Return to Play/Activity▫ Balance/Vestibular Therapy▫ Management of co-existing Cervicogenic issues

related to HA/dizziness▫ Return to exertion

• APTA Position Statement

Which On-Field Symptom Predicts Protracted Recovery from Sports Concussion?

DIZZINESS

Lau et. al 2011

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“Fogginess”

• May be associated with a more severe course and protracted recovery

• “Foggy” athletes vs non-foggy athletes: ▫ Slower reaction time▫ Attenuated memory performance▫ Slower processing speed▫ Significantly higher number of other post-

concussion symptomsIverson et al., 2004 (high school athletes, N = 110)

Does the Hit Matter?

• What makes some hits more likely to produce injury?

▫ http://www.youtube.com/watch?v=16Z7-XRPcrw&feature=player_detailpage

▫ Rotational Acceleration▫ Braced for injury? (neck strength)(Meaney 2011)

Neck pain pre season in ice hockey players in Canada

• N=3,823 (age range 11-14)• Recorded baseline preseason sx of dizziness,

neck pain, and headaches on the Sport Concussion Assessment Tool

• Preseason reports of neck pain and headache were risk factors for concussion

(Schneider KJ et al, 2013)

Variables Related to Outcome

Exertion:

• Student athletes who engaged in high levels of activity in the weeks following concussion had increased symptoms and worsened neurocognitive data

• They also had significantly longer recovery time

Majerske et al., 2008


The King-Devick Test is an objective, physical method of evaluating visual tracking and saccadic eye movements.

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Cogsport

Headminders (CRI)

ANAM

ImPACT

MACE

Computer-Based Neurocognitive Testing

Military Acute Evaluation of Concussion (MACE)

Military Acute Evaluation of Concussion is being used in Iraq and Afghanistan

Designed to be used within the fist 48-72 hours

Can be administered by a corpsman

Consists of history and symptoms, cognitive screen, and neurologic eval

MACE

Cognitive componentsImmediate recall

Orientation

Delayed recall

Concentration

Subjective Assessment

Dizziness Handicap Inventory (DHI) (Jacobson 1990)

Activities-Specific Balance Confidence Scale (ABC) (Powell and Meyers 1995)

Post-concussive symptom scale by Lovell, Collins (1998)

Rivermead scale (King et al, 1995)

Screening for Referral

Aural symptoms

DizzinessIf yes, complete the Dizziness Handicap Inventory (Jacobson and Newman, 1990)

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Do they have dizziness with:

Looking up?

Walking in supermarket aisle

Getting out of bed?

Reading?

Quick head motions?

Turning over in bed?

Bending over?

Lying down?

Suggests possible

vestibular dysfunction

Space and motion phobia

Do you get dizzy in wide open spaces? (commonly seen after a vestibular disorder)

Space and Motion Discomfort▫ Jacob et al, 1993▫ Uneasiness created

by situational stimuli eg:

▫ Moving crowds, supermarkets, busy patterns, spiral staircases, heights, etc

▫ Heightened awareness of normal motion

Space and Motion Discomfort• Coexists frequently with MIGRAINE and/or

ANXIETY▫ Migraine-Related Dizziness (MRD)▫ Migraine-Anxiety Related Dizziness (MARD)

• Appears to be responsive to combined approach using medication, Vestibular Physical Therapy, & behavioral therapy (Whitney et al, 2005; Jacob et al, 2001)

• Patients with Space and Motion Discomfort will often require medication, vestibular rehab, and take longer to recover

Suggestive of a vestibular disorder

Are there times when dizziness occurs without headache post concussion?

Consider convergence spasm, convergence insufficiency, postural hypotension, BPPV, vestibular hypofunction

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Eye Abnormalities Commonly Seen

Convergence spasm (Chan and Trobe, 2002)

Convergence insufficiency (Kowal, 1992)With either of the above, the person post TBI may c/o difficulty reading, focusing, bending over, or moving from supine to sit

Convergence Insufficiency

Definition: Inability to maintain binocular eye alignment while looking at close objects

Sx: headache, blurred vision, eye strain, double vision

Often have an associated exotrophia (Arch Ophthalmol, 2008)

Incidence of convergence insufficiency is between 2 and 8% (Letourneau JE and Ducic S, 1988; Rouse MW et al, 1999)

Convergence Insufficiency

Use of a computer based eye exercise program helped to normalize near point convergence and to normalize their near exo deviations (Serna A et al, AAPOS, 2011)

Latent Strabismus (phoria/trophia)

With a concussion, this can slow a persons ability to compensate for a dizziness disorder

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Postural control

Falls

Staggering

Near falls

Veering during gait

Difficulty in the shower or in the dark

Balance Deficits Noted in Persons with TBI

Abnormalities on computerized dynamic posturography (CDP)

Increased AP sway

Increased ML sway

Abnormalities in subjective visual vertical

Slowing of postural adjustments

Bucket Test (Zwergal et al, 2009)

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Bucket test• Patients sit upright looking into a translucent plastic bucket so that the bucket rims prevent any gravitational orientation clues

• There is a dark, straight line

• The examiner rotates the bucket clockwise or counterclockwise to an end position and then slowly rotates it back towards the zero degree position

• Patients indicate ‘stop’ at the position where they estimate the inside bottom line to be truly vertical

• The examiner reads off the degrees on the outside scale

• Ten repetitions have to be performedZwergal (2009)

Bucket Test SVV MonocularLeft

SVV MonocularRight

SVV Binocular

Normal n=30 1.2 ± .7 1 ± .8 .9 ± .7

Acute peripheral or CVD n=30

8.9 ± 5.2 8.4 ± 4.8 8.3 ± 5

Zwergal (2009)

SVV Application Pathologic SVV

Acute peripheral vestibular neuritis

> 90%

Wallenberg syndrome > 90%

INO > 90%

Midbrain > 90%

Vestibular pseudoneuritis > 90%

• Healthy subjects align the bar within 1 – 2.5 deg of vertical

•Subjects with central (and peripheral) pathology align the bar greater than 2.5 deg from true vertical

Balance Testing

Use computerized dynamic postuography

The functional gait assessment

The BESS test

Healthy, 25yr, Male

NIH Toolbox Device

Fixed Support Surface

EO, Small Voluntary Sway

0 10 20 30 40 50 60 70 80 90 100-0.05

0

0.05

Acc

ele

ratio

n [V

]

Time [s]

Dan: A/P COP & A/P Accelerations -EO -SVS

0 10 20 30 40 50 60 70 80 90 100-1

0

1

CO

P [

cm]

Acc1y-LPfiltered

COPy

Design: Retrospective case series

Subjects: 114 subjects referred to vestibular rehab clinic by clinicians at UPMC Sports Concussion Program between 2006 and 2008

67 children/ 47 adults

70 F/44M

Age range: Median 17 (range 8- 73) years

Mean number of concussions: 1.4 ± .8

Time between the concussion and referral: Median

61 days (range: 6 - 2566)

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Intervention

Intervention: a customized program that was tailored to each subject’s impairments, and consisted of:

Gaze stabilization exercises

Standing balance exercises

Ambulation exercises

Outcome measures

Self report measures

Dizziness Rating

The Activities-Balance Confidence scale (ABC)

The Dizziness Handicap Inventory (DHI)

Performance measures

The Dynamic Gait Index (DGI)

The Functional Gait Assessment (FGA)

The Timed “Up & Go” (TUG)

The Five Times Sit To Stand (FTSST)

Dynamic Computerized Posturography

Baseline Description of Dizziness

Off balance 68%

Lightheadedness 54%

Spinning 46%

Nausea 38%

Sensation of motion 23%

Descriptive Data114 Subjects

30 did not return:Physical therapy was not indicated (n = 6)

The patient lived far away (n = 8)

The patient did not show (n = 16)

Eighty-four (84) patients returned for at least 1 additional visit

Median treatment duration: 33 (range 7-181) days/ Median numbers of visits: 4 (range 2-13)

Returned vs. Did Not Return

Subjects who did not return had significantly better scores on:

Dizziness severity (p = .008) ABC (p =.028) DHI (p = .014)

Returned vs. Did Not Return

Subjects who did not continue after initial evaluation had significantly better scores on:

DGI (p = .027)

FGA (p = .013)

Gait Speed (p = .033)

FTSTS (p < .001)

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Treatment effect(self report measures)

Outcome Measure

Pre-treatment Post-treatment p-value

Dizziness Severity

21(22) 12 (18) p < .001

ABC 64 (27) 84 (17) p < .001

DHI 49 (21) 30 (22) p < .001

Age effect (DHI)

Interaction effect (dizziness severity) Treatment effect(Performance measures)

Outcome Measure

Pre-treatment

Post-treatment

p-value

DGI 20 (3) 23 ( 1) p < .001

FGA 22 (5) 28 (3) p < .001

Gait Speed 1.02 (.28) 1.28 (.23) p < .001

TUG 9.7 (2.5) 7.8 (1.8) p < .001

FTSTS 13.1 (6) 9.7 (5) p < .001

SOT

0

20

40

60

80

100

Condition1

Condition2

Condition3

Condition4

Condition5

Condition6

Composite

Initial Eval

Discharge

Age effect [Functional Gait Assessment,(Wrisley et al, 2004)]

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Age effect (Five Times Sit to Stand Test (Whitney et al, Phys Ther, 2005)

Interaction effect (SOT- Condition 1)

Interaction effect (SOT Condition 2) Summary of Results

Treatment effect: All self report and performance measures improved

Age effect: DHI, FGA, FTSTS

Interaction effect: Dizziness rating, condition 1 & 2 of the SOT

Summary

Vestibular rehabilitation reduced dizziness and improved balance function after concussion

Vestibular rehabilitation was equally beneficial with children and adults

Exertional Training

When the person has no symptoms at rest (headache or dizziness), we can begin an aerobic training program

During the training we ask the person about:

Dizziness, fogginess, nausea, and headache

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What happens if you don’t get them to move?

Problems in school or may not be able to return to school

Might develop psychological problems

Inability to play games and text

Lose their social network

Inability to work

Deconditioned

Criteria for Return

IMPACT scores have improved

Can exercise or work without symptoms

Typically start back to school/work part-time and gradually resume normal function

Critical Rules

If headache or dizziness increase with a greater functional role, they need to back off regardless of age

Noise, light, movement, stress, and exertion (physical or mental) can all be triggers for symptoms

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Blow by blow: PT Concussion

Management

Susan L. Whitney, DPT, PhD, NCS, ATC, FAPTA

Professor in the Departments of Physical Therapy and Otolaryngology


Post Concussion Syndrome (mild TBI)

• Estimated 10-20% of patients post concussion

• No clear cut definition

• When recovery from concussive deficits persists beyond the normal window of recovery and become chronic

• 225,000 new persons each year show long term deficits as result of mTBI (Meaney 2011)

• Using Centers for Disease estimates, this may be 320,000 -760,000


DEFINITION - CONCUSSION

• A complex pathophysiologic process affecting the brain, induced by traumatic biomechanical forces secondary to direct or indirect forces to the head.

• Caused by a jolt to the head or body that disrupts the function of the brain.

• Typically associated with normal structural neuroimaging findings (ie CT scan, MRI).

Centers for Disease Control, 2007


DEFINITION - CONCUSSION

• Results in a constellation of physical, cognitive, emotional or sleep-related symptoms that may or may not involve a loss of consciousness (LOC).

• Duration of symptoms is highly variable and may last from several minutes to days, weeks, months, or longer in some cases.

Centers for Disease Control, 2007

Epidemiology of Concussion/mTBI: Difficult to accurately report incidence, as concussion is grossly underreportedGeneral Population

• Approx 1.4 million incidents of TBI reported each year; w/ 75-90% classified as mild (CDC 2004)• Affects 123 persons per 100,000 in US yearly (Bazarian 2005)

Sports • 2 million sports and recreation concussive injuries occur annually in US • CDC Toolkit for Physicians (2008), estimates up to 3.8 million• 20-30 % of high school football players have experienced at least 1 concussion (Powell 1999; McCrea 2004)

Military

•194,561 mTBI cases between 2000-2012 • OIF, OEF, OND


Epidemiology• Concussion is the most common acquired neurologic

disorder in children and young adults

(NIH, 2002)

• It is estimated that 1.6 - 3.8 million sports relatedconcussions occur annually in the United States

(Langlois et al., 2006)

• Concussion is estimated to cost $17 billion annually inthe United States

(NCIPC, 2003)

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Concussion complications• Concussion results in constellation of physical,

cognitive, emotional, and/or sleep-related symptoms

(Harmon et al., 2013; McCrory et al., 2013)

• The most frequent symptoms include headache (94%),dizziness (75%), impaired concentration (54%), andbalance problems (79%)

(Marar et al., 2012; Peterson et al., 2003)

• The prevalence of dizziness and balance problems afterconcussion suggest that the assessment of vestibularsystem is needed after concussion


Prevalence of vestibular disorder after concussion

• 74% of 72 individuals with concussion with post-traumatic dizziness were found to have positivevestibular abnormality findings

(Davies and Luxon, 1995)• 61% of 119 and 44% of 101 patients with closed

traumatic head injury had positive vestibularabnormality on caloric test and rotatory testrespectively

(Toglia et al., 1970)

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• The 74% prevalence of vestibularabnormalities in concussed individuals withpost-traumatic dizziness reported by Daviesand Luxon along with the 75% prevalence ofdizziness in individuals with concussionreported by Marar et al., suggest a 55%prevalence of vestibular disorders inindividuals with concussion

(Davies and Luxon, 1995; Marar et al., 2012)

• Unknown prevalence after sports-relatedconcussion 9

Prevalence of vestibular disorder after concussion

Blast Wave Pressure

• Hurricane

– 0.25 psi

– 200 km/hour

• Blast

– 100 psi

– 2,414 km/hour


TBI in MilitaryBlast vs Blunt Force Injury

With BLAST: (Hoffer 2010)

• Injury results in more global neurochemical changes

• Increased rates of hearing loss & cognitive deficits

• Increased rate of HA & disequilibrium in pts experiencing dizziness

• Symptoms tend to be more constant than intermittent

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Diagnosing Concussion


Concussion – Objective Measures Needed!

• Athletes & soldiers are often highly motivated to return to activity and will minimize deficit to return

• Conversely, other populations (such as mva/work injuries) may misrepresent disability due to secondary gain


Brain Metabolism is Related to RecoveryOver 200 High School Athletes Studied using fMRI

Tested w/in 7 days of concussion and at point of clinical recoveryHyperactivation predicts CLINICAL recovery time

Resolution of hyperactivation correlates with recovery on ImPACT

Lovell, Collins et al., Neurosurgery, 2007

vHIT

Normal vHIT FindingDepartment of Physical Therapy Acute Concussion Assessment Tools

SAC - Standard Assessment of Concussion

SCAT-3: Sports Concussion Assessment Tool-3

MACE - Military Acute Concussion Evaluation

•Sports sideline test Includes neurological screen•Abnormalities suggest further neuropsychtesting•(Putukian 2006)

•More complete: includes SAC and Maddocks question•Provides coordination and balance screen•(McCrory 2008)

•Derived from the SAC•Includes history of injury w/ assessment of helmet use, etc & components of SAC/SCAT•DVBIC (2006)

Poor ability of Acute tools to detect impairment beyond sideline

after day of injury, other measures needed

(Coldren 2010; Grubenhoff 2010)

4


The Pediatric Vestibular Symptom Questionnaire: A Validation Study

• 200 children without vestibular complaints

• 56 children(32 with concussion)

• The test discriminated with a sensitivity of 95% and specificity of 84%

Pavlou et al, 2015

20

15

10

5

0

-5

-10

-15

-20

T-score

Degrees360

315

270

225

180

90

45

0

135

Amplitude of Activated Brain Regions

Phase of Brain Activity relative to chair (clockwise) rotation

NystagmusBrain Signal

Functional Near-infrared Spectroscopy (fNIRS) has been developed to allow brain imaging during vestibular testing. We are the first group to ever show brain imaging of the human cortex during rotational vestibular tests.

Left

In-phase withclockwise rotation

In-phase withcounter-clockwise rotation


Diagnosing Concussion:

CT/MR are insensitive to concussion

• CT: only 3-10% are + in mTBI (Jagoda 2002)

• Only able to detect hemorrhage & edema

• MR: abnormal in 10-57% of cases (Hughes 2004)

• May detect white mater changes, small contusions, hemorrhages


Diagnosing Concussion: Advanced Techniques

• Functional MRI

• MR Spectroscopy

• Diffusion Tensor Imaging (DTI)

• Single Photon Emission CT (SPECT)

• Positron Emission Tomography (PET)

• EEG• NO current technology is able to individually dx or

establish safe return to activity



Symptom Report:

• Examples of existing scales:

• Post Concussion Symptom Scale (Aubrey 2002)

• Post-Concussion Scale (Lovell 2006)

• Graded Symptom Checklist (Guskiewicz 2004)

• Limitations: Self reports; subject to both under-report or magnification (McCrea 2004, Williamson 2006)



Neurocognitive Assessment

• Endorsed in management of post concussive patient (Aubry 2002, McCrory 2005, McCrory 2009)

• Value is greatest when baseline measure exists

• Not recommended as “stand alone” measure (Randolph 2005)

Types of Tests:

• Paper and pencil tests

• Computerized tests - eg: ImPACT, CogState Sport, Headminders CRI, Automated Neuropsychological Assessment Metrics (ANAM)

5


Early symptoms following concussion (Sports-Related)

1. Headache (71%)2. Feeling slowed down (58%)3. Difficulty concentrating (57%)4. Dizziness (55%)5. Fogginess (53%)6. Fatigue (50%)7. Visual blurring/double vision (49%)8. Light sensitivity (47%)9. Memory dysfunction (43%)10.Balance problems (43%)

(Lovell 2004)


Post Concussive Dizziness:

Present in 23% to 81% of cases in the first

days after injury (Griffiths 1979; Kisilevski 2001; Maskell 2006;

Maskell 2007, Terrio 2009; Kontos 2012)

In blast-related mTBI, most common post-injury symptom (Hoffer 2010)

Dizziness was the sole ON FIELD factor predictive of protracted (> 21 days) time to recovery (Lau 2011)


Common Vestibular Causes of Dizziness p mTBI

Peripheral:

• Benign Paroxysmal Positional Vertigo (BPPV)

• Labyrinthine Concussion

• Perilymphatic Fistula

Central:

• Post traumatic migraine

• Brainstem concussion

Adapted from Furman 2010

• Ocular Motor Problems• Autonomic/orthostatic • Cervicogenic Dizziness

Common Non-Vestibular Causes of Dizziness:

__ Department of Physical Therapy

BPPV• In sport-related concussion, incidence of

BPPV low (<5%) (Alsalaheen 2010)

• Is more prevalent in mild/moderate TBI


Motion Sensitivity:


Visual Motion Sensitivity

• Presents as difficulty tolerating school hallways, grocery stores, malls, etc

• VMS prevalent post concussion – 49% in first week

6



Clinical Assessments:• VOR Cancellation



Postural Control following Concussion:


Very common acutely and sub-acutely following concussion (Geurts 1996; Guskiewicz 1997; Guskiewicz 2000; Kontos 2012)

Often related to abnormalities in Sensory Organization

It appears that, in particular, the ability to utilize and process vestibular information needed for postural control may be affected in concussed athletes (Peterson 2003; Guskiewicz 2001)

Impaired Postural Control


Measuring Sensory Organization:

Computerized Dynamic

Posturography(Nashner, 1982)

Clinical Test for Sensory

Interaction in Balance (CTSIB)

Shumway-Cook A., HorakF. 1986

Balance Error Scoring System

(BESS)Guskiewicz, K. University of North

Carolina Sports Medicine Research Laboratory


Recent BESS Findings

• Balance tested in adolescents w/ and w/o concussion

• Total BESS score ≥ 21 identified acutely concussed vs healthy @ 60% sensitivity and 82% specificity

• After 2 weeks, total BESS score unable to differentiate between concussed & non-concussed

• However specific BESS conditions:

– Tandem/Firm & Tandem/Foam - discriminated between healthy & concussed > 2 weeks

– Feet Together/Foam – discriminated between newly concussed those >2 weeks post injury

Furman et al; AJSM 2013

7


Balance Dysfunction & Concussion

Balance Recovery from Concussion:

• Appears to resolve more quickly than other symptoms following concussion (Catena 2011, Guskiewicz 2003)

Clinical Subtypes Following Concussion

A Conceptual Framework for Evaluating and Managing Concussion

We are learning that sport-related concussion involves different clinical subtypes…

Collins et al, KSSTA; 2014.

Concussion

Ocular

Vestibular

Post-TraumaticMigrai

ne

Anxiety/

Mood

Cervical

Cognitive/Fatigu

e

UPMC Concussion Program

Using Concussion Subtyping for Clinical Management

Previous Concussions

Sex

Treatment and Rehab Pathways

Identify Concussion Subtype(s)

Risk Factors

Migraine

LD/ADHD

Concussion

Age

Mood Disorders, Vision Impairment, Other

Vestibular

Ocular

Cognitive

Migraine

Anxiety/Mood

Cervical


Collins et al, KSSTA; 2014.

Arriving at Subtype via Multidisciplinary Assessment:


Cognitive/Fatigue Subtype:

Collins et al, KSST, 2014

Cognitive/Fatigue • Common Subtype EARLY following

concussion • Symptoms:

• Fatigue• Feels best in am; headache w/

cognitive & physical activity• “End of day” symptoms• May have sleep deficits

8

Cognitive/Fatigue Subtype:

Vestibular/Ocular Screening (VOMS): • Normal

Computerized Neurocognitive Test Results• Global mild deficits across all composites• Deficits with retrieval rather than encoding

Some Questions to Ask• “Do you have a generalized headache that

increases as day progresses?”• “Do you feel more fatigued than normal at

the end of the day?”• “Do you feel more distractible in school/work

than normal?”

Cognitive/Fatigue


Treatment: Cognitive/Fatigue Subtype

Collins MW, Kontos A, et al, KSST, 2014

Cognitive/Fatigue

• Physical/Cognitive Breaks throughout day (no naps)

• Pharmacological (if persistent):• Neurostimulants (amantadine,

methylphenidate, etc)• Sleep aid if indicated

• Cognitive Therapy if protracted• Monitored exertion progression – potentially if

protracted

Return to School following Concussion

Homebound instruction

Partial attendance

Late starts/Early dismissals

Rest periods during day

Extra time for assignment completion

Excuse from non-essential assignments

Postpone or stagger testing

Excuse from standardized testing

Extra time and/or open book testing

Exams in small/quiet rooms

Tutor

Excuse from gym & attending sport practices

Excuse from assemblies, band/orchestra, woodshop

Lunch in quiet area

Preferential classroom seating

Accommodations for light/noise sensitivity (earplugs, ball cap, sunglasses, dimmer lights)

Books on tape

Audiotaped lectures

Provide note-taker or scribe

Provide classroom notes/powerpoint prior to class(McGrath 2010)


Ocular

Risk Factors: Personal/Family hx of ocular dysfunction

• “Lazy eye”; strabismus; eye patching; eye muscle surgery; prescribed reading glasses

Symptoms:

• Frontal headache w/ visual work

• Difficulties with visually based classes & activity

• Pressure behind the eyes

• Visual “focus” issues

• Blurry vision

• Double vision

Ocular/Visual Subtype

Computerized neurocognitive test results:• Deficits with Visual Memory, Reaction Time• Deficits with encoding rather than retrieval

Vestibular Ocular Motor Screening (VOMS): • Pursuits/Saccades• Near Point of Convergence (>5cm)

Some Questions to Ask• “Do you feel a frontal pressure in your head /behind eyes

when doing visual work?”• “Are you having trouble taking notes in class?”• “Do you have blurred or fuzzy vision while reading or

difficulty reading?”• “Are you having more significant difficulty in Math and/or

Science?”


Ocular



•Common Problems seen after Concussion:•Convergence Insufficiency•Convergence Spasm/Excess•Accommodative Insufficiency•Binocular vision deficits•Decompensated phorias/tropias•Saccade and pursuit eye movement impairment

•When photo-sensitivity is driving symptom•Suspect migraine

Ocular

9

Treatment: Ocular/Visual Subtype


Ocular

• Ocular Motor Training:

• Can be performed by vestibular therapy if deficits mild to moderate

• Behavioral optometry and formal vision therapy if moderate to severe, complicated, or not responding to vestibular rx

• Physical exertion – typically well-tolerated if isolated convergence insufficiency

Vestibular Subtype

Symptoms: • Dizziness • Nausea• Overwhelmed in visually-stimulating environments• Off balance• “One-step behind”

Risk factors: • Car sickness/motion sensitivity• Migraine• Anxiety

Vestibular


Vestibular Subtype

Vestibular-Ocular Screening symptom provocation

• VOR (vertical and/or horizontal)

• Visual motion sensitivity

Computerized Neurocognitive Test Results

• Deficits predominantly with Visual Motor Speed, Reaction Time

Some Questions to Ask

• “Do quick movements make you dizzy, foggy, anxious?”

• “Do busy environments cause you to have a headache or feel foggy, dizzy, anxious, tired?”

• “Do you become dizzy when looking up/down, turning head, walking down busy hallways?

VestibularVestibular Findings after Concussion:

BPPV

VOR Impairment

Balance Impairment

Visual Motion

Sensitivity

Vestibular Subtype Comorbidity:

• Coexists frequently with Migraine and/or Anxiety▫Vestibular Migraine▫Migraine-Anxiety Related Dizziness (MARD)

Vestibular

Post-Traumatic

Migraine

Anxiety/

Mood

Treatment: Vestibular Subtype

• Vestibular therapy

• Dynamic physical exertion protocol- @ end stages of vestibular therapy

• Pharmacological (if there is mood, migraine, sleep overlay)

• Tricyclic antidepressants -if migraine and/or sleep overlay

• Melatonin, trazodone, zolpidem - if sleep overlay

• SSRIs- if mood overlay

• Clonazepam - low dose; if anxiety is present

Vestibular

10

Anxiety/Mood Subtype:


Anxiety/MoodRisk Factors:

• Personal/Family hx of Anxiety• Migraine• Vestibular Disorders

Symptoms: • Ruminative thoughts• Hypervigilant• Fastidious• Feelings of being overwhelmed• Difficulties initiating/maintaining sleep

Vestibular/Ocular Motor Screening(VOMS):• Normal or only mildly provocative (more provocative if vestibular overlay)

Computerized Neurocognitive Test Results:• NORMAL- if not vestibular component• If vestibular component-deficits with Visual Motor Speed, Reaction Time (treat

vestibular component first!!)

Some Questions to Ask• “How often do you take inventory on your symptoms?”• “Do you have a difficult time turning off your thoughts?”• “Do you become symptomatic when thinking about your symptoms?”• “Have social activities been restricted?”• “How often do your parents ask about your symptoms?”• “Do others consider you to be a “worry-wart”?”

Anxiety/Mood Subtype: Anxiety/Mood


Treatment: Anxiety/Mood Subtype

Anxiety/

Mood


• Treat Vestibular comorbidity (Vestibular Therapy) – if present

• Treat Migraine comorbidity – if present

• Supervised Exertion Therapy (if vestibular component resolved)

• Once vestibular component resolved, push them hard!!

• Regulated schedule

• sleep, exercise, diet, hydration, stress

• Psychotherapy

• Pharmacological

• Antidepressants

• SSRIs, SNRIs, Tricyclic

• Benzodiazepines

• Clonazepam (low dose)

Post-traumatic Migraine Subtype:

Collins MW, Kontos A, et al, KSST, 2014

MigraineKey subjective complaints:• Variable headache and intermittently severe• Often wakes with headache• Nausea, Photo and/or phonophobia• Stress, anxiety, lack of exercise• Sleep dysregulation• May also present with Vestibular Migraine

Risk Factors: • Personal or family hx of migraine• Hx motion sensitivity • Hx “ice-cream headache”• Vestibular disorder• Anxiety

Vestibular/Ocular Motor Screening (VOMS):• Normal (unless Vestibular component present)

Computerized NeuroCognitive Testing:• Verbal and Visual Memory deficits • If vestibular component present-speed deficits as well

Some Questions to Ask• “Did you get migraines before injury?”• “Do headaches occur in morning after poor sleep?”• “Is your sleep dysregulated?”• “Do you get visual changes before or during a headache”• “Do you become highly sensitive to normal room noise or light

when you have a headache?”

Post-traumatic Migraine Subtype:

Migraine

Migraine

• Neuro-Vascular Event

• Pathophysiology:• Abnormal activation of

trigeminovascular system• Trigeminovascular system: sensory

afferents of cranial vasculature and dura matter

• Afferent information modulated centrally at brainstem and diencephalon

• Proposed “failure of central modulation” in migraine (Holland PR, Afridi S, ACNR 2014;V13(7):19-21)

• Genetic predisposition

• Following concussion, migraine susceptibility is increased

Migraine

11

A Migraine is NOT only a Headache:

MigrainePossible symptoms of Migraine:

• Headache

• Nausea, vomiting

• Photophobia, phonophobia

• Dizziness

• Sinus pressure/fullness

• Eye pain

• Neck pain• Trigeminal nuclei to upper cervical spine

• Frequent urination

• Pallor, Sweating

• Comorbid conditions w/ migraine: sleep disorders (Guidetti 2014), rosacea, motion sickness

• “Sinus” headaches are frequently mis-diagnosed migraine (Schreiber 2004)

Migraine Aura:• Aura occurs in up to 1/3 of migraines

• (Tfelt-Hansen PC; Cephalalgia 2010)

• Transient neurological symptoms – duration < 60min. Typically precedes HA

• Visual – most common (>90%) • Positive: lightening bolts, jagged lines, gold/silver sparkles, “scintillating

scotomas”• Negative: central scotomas (opaque holes in vision)

• Sensory (30-54%)• Unilateral slowly-progressing paresthesia and/or numbness

• Language (9-31%)• Expressive or Receptive disturbances

• Motor – may be associated w/ Familial Hemiplegic Migraine

• Cortical spreading depression (CSD) - proposed cause of aura

• Can have a migraine aura without headache

• If Aura occurs, + Migraine Dx

Cervical Subtype:Cervical

Symptoms:• Neck pain, stiffness, soreness

• Headaches, radiating from upper cervical spine forward

• Precipitated/aggravated by specific neck movements or sustained postures

Risk Factors:• Prior cervical spine injury

• High velocity trauma (eg: MVA)

• Unprepared for hit

• Strong rotational component to injury

Vestibular/Ocular Motor Screen (VOMS):• Normal

Computerized NeuroCognitive Testing:• Normal

Management - Cervical Subtype:

• Obtain imaging if suspected fracture/instability• Physical Therapy Evaluation/Treatment

Other Potential Management• Medication (muscle relaxants, analgesics)• Injection/Nerve Blocks• Massage• Acupuncture (Michels 2007, Heikkilä 2000)

• Surgery

Cervical


Eye findings following mTBI

Ocular Motor Examination (Adapted from Leigh 2006, Kattah 2009, Schubert 2010)

Observation Head Tilt, Ocular Tilt Reaction, Ptosis, etc

Visual Fields Confrontation testing to determine field cuts

Pupillary light reflex Optic N. or Cr N III

Extraocular Movements ROM of eyes ‐monocular and binocular

Ocular Alignment Cover Tests; Alternate Cover Tests; Maddox Rod

Gaze Fixation/HoldingAbility to maintain stable gaze without generation of other eye movements in 9 cardinal planes

Smooth Pursuits Ability to maintain slowly moving target on fovea of retina

SaccadesAbility to make single rapid eye movement to refocus image on fovea of retina

Optokinetic Nystagmus Reflexive jerk nystagmus occurring w/ visual flow

Vestibular/VOR Ability to stabilize gaze while head moves; BPPV

VOR Cancellation Ability to suppress VOR response centrally

VergenceAbility to move eyes simultaneously in opposite directions to fixate on an object (convergence/divergence)

12

Observation:

• Head turns/tilts

• Head tremors

• Eylid

– Ptosis

• Obvious eye misalignment

Courtesy: Suzanne Wickum, O.D.

https://www.google.com/search?q=cranial+nerve+3+palsy&espv=2&source=lnms&tbm=isch&sa=X&ei=_5wAVLjbEcq8ggTo9oJQ&sqi=2&ved=0CAYQ_AUoAQ&biw=729&bih=622#q=oculomotor+nerve+palsy&tbm=isch&facrc=_&imgdii=_&imgrc=VhkyQn5xX-ZEzM%253A%3BSH4km-ZepfYuTM%3Bhttp%253A%252F%252Fwww.wrighteyecare.com%252Fwp-content%252Fuploads%252F2013%252F07%252FNerve_Palsy_and_Paresis1.jpg%3Bhttp%253A%252F%252Fwww.wrighteyecare.com%252Fpatient-education%252Fnerve-palsy-and-paresis%252F%3B239%3B114

• Tropia:

• Deviation of visual axes during binocularviewing of a single target (ie, with visual fusion)

• Manifest deviation: readily observable; present in all circumstances. Focusing on target does not change

• Phoria:• Deviation of visual axes during monocular viewing of a single target

• Latent deviation: deviation is not always apparent. Need to break fusion and allow eyes to view target individually to test (eg: Alternate Cover Tests)

Types of Ocular Misalignments:

• Exo – outward (laterally)

• Eso – inward (medially)

• Hyper – upward

• (Hypo – downward – not used)

• Combine with tropia or phoria to fully describe the strabismus type

http://www.uofmhealth.org/sites/default/files/healthwise/media/medical/hw/h9991401_

001.jpg

Ocular Misalignment

• Ocular misalignment is common

• Compensation for ocular misalignments can become altered after concussion

• Decompensated ocular alignment can result in diplopia, blurred vision, headaches, eye strain, dizziness, difficulty reading, etc. and can greatly affect recovery from concussion

Why do we care about Ocular Alignment after Concussion?

Ocular Alignment Testing:

Cover Test: • Identifies tropia

Uncover Test: • Identifies tropia and

phoria

Alternate (Cross) Cover Test• Identifies tropia and phoria

General Instructions:• Must occlude vision in one

eye– Occluder– Hand– Business card

• Patient focus on a discreet target in midline

• Target distance: test both– Near target (18‐24 in) and– Distant target

• Environment free of distraction

Cover Test• While focusing on target, one eye is covered• Look for “movement of redress” of uncovered eye and

direction of movement• Identifies tropia of uncovered eye (eso/exo/hyper/hypo)

Uncover Test• Observe for movement of occluded eye when cover is

removed• In practice, cover and uncover tests may be done

together (“Cover/Uncover” Test)• Identifies phoria, if Cover part of test negative

Ocular Alignment Testing:

13

COVER TEST – watch what happens in the non‐occluded (LEFT) eye as the right eye is covered:

Uncover Tests: Watch what happens when the cover is removed:

• When covered, the eye moves to its preferred “resting” position. When the cover is removed, it returns to position where it can regain fixation. “Movement of redress” is the saccade that is observed.

• In the absence of a positive Cover Test, a positive Uncover Test reveals a phoria

Exophoria Esophoria

• Occluder quickly transferred from eye to eye

• Wait long enough (approx. 5 sec) before switching occluder – for eye to regain fixation

• Prevents binocular viewing

• Do multiple times – deviations grow over time

• In absence of positive Cover Test, identifies phoria

Alternate (Cross) Cover Test: Watch what happens in each eye as occluder is removed:

Exophoria

http://bestpractice.bmj.com/best‐practice/images/bp/en‐gb/689‐3_default.jpg

Vertical Misalignment

• Horizontal ocular misalignment is common in the general population

• Vertical is not

Vertical Misalignment Etiology• Skew Deviation

• Acquired, asymmetric disruption of supranuclear input from the otolithic organs that causes vertical misalignment with cover testing

• Etiology: Stroke and other brainstem pathology; peripheral vestibular lesion

• Ocular tilt reaction is a combination of a head tilt, skew deviation, and cyclotorsion of both eyes

• Trochlear N. Palsy

• Superior Oblique: Depression and intorsion

• Congenital

• Acquired (trauma, cerebrovascular, diabetes)

• Take home message: any new onset of vertical diplopia or ocular misalignment requires immediate workup

• Poorly compensated ocular misalignments can be a problem after mTBI

• MAY need referral to vision specialist –– ALWAYS refer any VERTICAL Misalignment

• MAY need additional visual exercises prescribed as part of rehab

• MAY need additional time for recovery

• DEMONSTRATE– COVER – UNCOVER – ALTERNATE COVER TESTS

SO WHAT IF THERE IS A MISALIGNMENT?

14

Smooth Pursuits

• Ability to track a slowly moving target

• Active up to 60°/sec

• Sensitive to CNS pathology, but not

specific to location

• Sensitive to Age!!

Test:

• Velocity: 20‐40°/sec

• Range: 30° in all directions

• Distance: Target @ 18 – 24 in.Abnormal: • Corrective saccades indicate abnormal pursuit gain; “Saccadic Pursuits”; “Saccadic Intrusions”• Impairment due to CNS pathology

SaccadesTesting:• Range: 30° in all directions (NOT greater)

• Discreet targets held @ 18 – 24 in. from patient

• Accuracy: Should be able to reach target without multiple saccades

Abnormalities:• Hypermetric saccades: “overshooting”

– Cerebellar disease

• Hypometric saccades: “undershooting”• Multiple etiology including normal aging if mild

• Common following mTBI

• Slowed

• Delayed

• Impaired saccades = CNS etiology

VergenceAbility to move eyes simultaneously in opposite directions to fixate on an object

• Convergence

• Divergence

• Convergence Testing:Patient fixates on target brought in SLOWLY along the mid‐sagittal plane toward the nose

• Normal diplopia no > than 5 cm from tip of nose (Scheiman 2003)

• Test at least 3X – to assess fatigue of system

Common Vergence Dysfunction following Concussion:

A. Convergence Insufficiency = reduced vergence response (≥ 6 cm from tip of nose)

B. Convergence Spasm = Increased vergenceresponse

Demonstrate:

• Smooth Pursuits

• Saccades

• Convergence

Holding Image on Retina

Tests: Tested with: If abnormal, dysfunction in:

Visual Fixation/ Gaze Holding

Able to maintain visual gaze on a single location

Observation, Recording

Brainstem, Cerebellum

Vestibular Ocular Reflex

Stabilizes images on fovea of retina during head movement

Head Thrust, DVA , Head Shaking Nystagmus Tests

Peripheral vestibular disorder, Brainstem

OptokineticReflex

Able to hold images stable on the retina during sustained or slow head rotation

Visual flow pattern such as optokineticdrum

Brainstem

15

Gaze Holding

• Abnormalities seen with peripheral vestibular & CNS pathology

• Test:– Light and Dark– Gaze in straight ahead & 8 eccentric positions– 30° in all directions– Assess nystagmus/inability to hold position

– Also look for reboundnystagmus w/ return

Gaze Holding Nystagmus

• Direction Fixed• May be due to peripheral

vestibular lesion • Direction Changing

• Central

Optokinetic Nystagmus

• Occurs normally when 80% or > of visual field occupied by repeating pattern

• Horizontal & Visual flows

• Best quantified with lab testing

• Abnormalities: absence, dysconjugate eye mvmts, asymmetry

• Watch for symptom provocation


Why is it important?

• Ocular Motor & Vestibular issues are common in mild TBI –should be part of the exam in these populations

• Pre-existing ocular motor issues can decompensate after mTBI

• Presence of ocular issues (even pre-existing) – have impact on recovery

• Intervention can be helpful if issues persist!

Vestibular & Ocular Motor Examination

• Baseline Symptoms – Record: Headache, Dizziness, Nausea & Fogginess on 0-10 scale prior to beginning screening

UPMC Vestibular/Ocular Motor Screening (VOMS)

Vestibular/Ocular Motor Test:Not

Tested

Headache

0‐10

Dizziness

0‐10

Nausea

0‐10

Fogginess

0‐10

Comments

BASELINE SYMPTOMS: N/A

Smooth Pursuits

Saccades – Horizontal

Saccades – Vertical

Convergence (Near Point) (Near Point in cm):

Measure 1: ______

Measure 2:______

Measure 3:______

VOR – Horizontal

VOR – Vertical

Visual Motion Sensitivity Test

UPMC Vestibular/Ocular-Motor Screening (VOMS) for Concussion

Mucha, A et al 2014


Smooth Pursuits - Test the ability to follow a slowly moving target.

• Examiner holds a fingertip at a distance of 3 ft. from the patient who tracks the smoothly moving target in the horizontal direction 1.5 ft. to the right and 1.5 ft. to the left of midline, 2 repetitions back and forth. Target moved slowly (2 seconds to go from left to right and 2 seconds to go right to left).

• Repeat moving the target smoothly and slowly in the vertical direction 1.5 ft. above and 1.5 ft. below midline for 2 complete repetitions.

• Record: Headache, Dizziness, Nausea & Fogginess ratings after the test.

VOMS – Smooth Pursuits

16


VOMS – Vertical & Horizontal Saccades

Test the ability of the eyes to move quickly between targets. • Horizontal Saccades: Examiner

holds two single points (fingertips) horizontally at a distance of 3 ft. from the patient, and 1.5 ft. to the right and 1.5 ft. to the left of midline (patient gazes 30º left and right) – 10 repetitions. Instruct the patient to move their eyes as quickly as possible from point to point. Record: Headache, Dizziness, Nausea & Fogginess ratings after the test.

• Vertical Saccades: Repeat the test with 2 points held vertically

Mucha, Collins, Elbin, Furman, Troutman-Enseki, DeWolf, Marchetti, Kontos. (in press)


• Measure the ability to view a near target without double vision.

• The patient focuses on a small target (approximately 14 point font size) at arm’s length and slowly brings it toward the tip of their nose. The patient stops moving the target when two distinct images seen or when outward deviation of one eye is

VOMS - convergence

Assess the ability to stabilize vision as the head moves. Examiner holds a target (approximately 14 point font size) @ midline at a distance of 3 ft.

• Horizontal VOR Test: The patient rotates their head horizontally while maintaining focus on the target of 20 degrees to each side, 10 cycles, at a speed of 180 beats/minute (one beat in each direction).

• Vertical VOR Test: The test is repeated with the patient moving their head vertically - 20 degrees up and 20 degrees down, 10 cycles @ 180 beats/minute

• Record: Headache, Dizziness, Nausea and Fogginess ratings 10 sec after each test is completed.

VOMS – Vestibular/Ocular Reflex (VOR) Department of Physical Therapy

VOMS – Visual Motion Sensitivity

Test visual motion sensitivity and the ability to inhibit vestibular-induced eye movements using vision. Patient stands with feet shoulder width apart,

facing a busy area of the clinic and the examiner guards patient.

The patient holds arm outstretched and focuses on their thumb. Maintaining focus on thumb, the patient rotates, together as a unit, their head, eyes and trunk at an amplitude of 80 degrees to the right and 80 degrees to the left at a speed of 50 beats/min (one beat in each direction) for 5 cycles back and forth.

Record: Headache, Dizziness, Nausea & Fogginess ratings after the test

UPMC VOMS Summary:

Horizontal and Vertical Smooth Pursuits

Horizontal and Vertical VOR

Convergence


Horizontal and Vertical Saccades

In conjunction with other measures, helps to identify presence of concussion

May indicate a vestibular and/or ocular motor issue. Refer when issues persist (> 2 wks)

When VOR and VMS items are positive, refer to a qualified Vestibular Physical Therapist for further assessment and management

For Convergence Insufficiency, Pursuit and Saccade abnormalities, refer to either a Vestibular PT or Vision specialist to evaluate and treat

What if VOMS is abnormal?

17


VOMS and Healthy Athletes

• 263 healthy NCAA athletes

• Internal consistency of the VOMS was high (Cronbach α = .97)

• 89% of athletes scored below cutoff levels (ie, 11% false-positive rate)

• Women (OR, 2.99 [95% CI, 1.34-6.70] and a history of motion sickness (OR, 7.73 [95% CI, 1.94-30.75]; P = .009) were more likely to have ≥1 VOMS scores above cutoff levels


VOMS and Healthy Athletes

• The VOMS has good internal consistency and an acceptable false-positive rate among healthy Division I collegiate student-athletes

Kontos A et al, Am J of Sports Med, 2016


Vestibular symptoms and recovery• Children and adults post concussion with

vestibular symptoms took longer for symptom resolution

Ellis MJ et al, J Neurosurg Peds, 2015

Eye Dysfunction following mTBI*

% mTBIn = 20

% Controlsn = 20

Ocular Misalignments (Vertical Phoria)

55% 5% 0.0012*

Ocular Misalignment(Horizontal Phoria)

45% 5% 0.0084*

Accommodative Dysfunction

65% 15% 0.0031*

Convergence Insufficiency 55% 5% 0.0012*

Saccadic impairment 30% 0% 0.0202*

Pursuit impairment 60% 0% <0.0001*

Capo´-Aponte et. al. Military Medicine 2012* Blast-related mTBI


Ocular Motor Findings: VergenceSystem Issues


Convergence Spasm

Marked by:• Spontaneous convergence• Pupillary constriction (miosis)• Inability to abduct eye(s) with gaze testingClinically:• Pt may describe dizziness associated with

spasm• Can be positionally induced (with Dix Hallpike,

etc)(Furman 2010, Knapp 2002, Chan 2002)

18


• Testing Convergence: Patient fixates on target brought in along the mid-sagittal plane toward the nose

– Near Point of Convergence: when target becomes double

– Normal NPC ≤ 6 cm from tip of nose (Scheiman 2003)

Abnormalities:

A. Convergence Insufficiency = reduced vergenceresponse (≥ 6 cm from tip of nose)

B. Convergence Spasm = Increased vergence response

Convergence: Ability of eyes to turn inward to focus on a near target • Hypometric saccades

• Slowed saccades

• Symptomatic w/ saccadic eye movements

Pursuits: Saccades:• “Saccadic” pursuits or

“Saccadic Intrusions”

• Symptomatic w/ pursuit movements

Ocular Motor findings after Concussion:

ATYPICAL w/ Concussion:

• Hypermetric saccades:

• “overshooting”/cerebellar sign

Ocular Misalignments:A . Tropia: Deviation of visual axes during binocular viewing of a

single target Manifest Deviation: i.e, present in all circumstances

B. Phoria:

Deviation of visual axes during monocular viewing of a single target

Latent deviation: deviation is not always apparent

• Named for where eye wants to be!

• Exo – outward (laterally)

• Eso – inward (medially)

• Hyper – upward

• Hypo - downward

Treating Ocular Motor Problems:

• The BEST evidence for treating visual disturbances w/ vision exercise is for Convergence Insufficiency: (Scheiman et al, 2011 - RCT & Cochrane review)

• Some evidence for treating other ocular motor problems w/ exercise (Ciuffreda 2008)

• Other management: Lens management (prism, tinted, etc); medication; surgery (rare)


Home Based Exercises

• Home based exercises (n=41) improved near point convergence from a mean of 24.2 cm to 5.6 cm over a 12 week training period

• 64% reported a resolution of sx post treatment (diplopia, headaches, and eye strain)

• http://www.computerorthoptics.comSerna A et al, J of AAPOS, 2011

ABNORMAL FINDINGS: When to Refer?

Refer to ER

• New, acute onset of vertical diplopia and/or skew deviations with cover/uncover testing

• New, acute onset of visual field cut

Refer to neurology/neuro-ophthalmology with new (not acute):

• Visual field cuts

• Vertical deviations with Cover/Uncover test

• Hypermetric saccades

• Downbeating nystagmus

19


ABNORMAL FINDINGS: When to Refer?Refer to Neuro-optometry or Neuro-

ophthalmology:

• Large convergence insufficiency

• Convergence spasm

• Vertical phoria

• Tropia

• Large phoria

• When smaller issues do not resolve with PT intervention


ABNORMAL FINDINGS: When to Refer?Refer to Otologist/Neuro-otologist

• Positive Head Thrust Test (if no workup)

• Positive Head Shake Nystagmus Test (if no workup)

Refer to Vestibular PT:

• BPPV suspected

• Abnormal VOR tests/symptom provocation

• Mild to moderate convergence insufficiency

• Mild to moderate ocular motor dysfunction


Recovery After Concussion

Recovery From Sport-related Concussion:How Long Does it Take?

0

10

20

30

40

50

60

70

80

90

100

1 3 5 7 9 11 13 15 17 19 21 23 25 27 29 31 33 35 37 38 40+

All Athletes No Previous Concussions 1 or More Previous Concussions

N=134 High School Male Football Athletes

WEEK 1 WEEK 2 WEEK 3 WEEK 4 WEEK 5

40%RECOVERED

60%RECOVERED

80%RECOVERED

(Collins et al., 2006, Neurosurgery)

What about the 20% that take

more than 21 days?!

FACTORS RELATED TO OUTCOME:

Constitutional Factors

30 days5 days

7 days

10 days 14 days

81 days

Predicting Protracted Recovery

Recovery for Concussed Dogs

Constitutional risk factors:Female

Youth

Migraine

Learning disabilityRepetitive Injury (≥3?)

20


Variables related to outcome:

Migraine history/symptoms:

• Athletes with post traumatic migraines had significantly lower cognitive performance compared with those with no HA or even those with non-migrainous HA

(Mihalik 2005, Collins 2003)

• Athletes with post traumatic migraine more likely to fall into protracted recovery group

(Kontos et al, 2013)

The influence of Post Traumatic Migraine on Protracted (>21 days) Recovery from Sports

Concussion? (N= 97)

Variable Wald pOdds Ratio 95% CI

PTM v. No Headache 7.60 .006 7.29 1.80-29.91

Headache v. No Headache

2.20 .14 2.83 0.72-11.20

PTM v. Headache 3.93 .04 2.57 1.10-6.54

Kontos et al, AJSM 2013.

HITs:

• Characteristics of the hit itself do not appear to be reliable predictor of concussion or concussion severity

• Used instrumented telemetry (HIT) in helmets of collegiate football hockey athletes

• 486,594 recorded head impacts; 48 concussions

• 17/48 (35%) - no specific impact event

(Duhaime 2012)

(Broglio 2012)

Which on-field symptoms predict protracted recovery from concussion?

87 Male HS Football Players (Mean Age = 16.2 years)

13 on-field signs/symptoms:

Groups divided into (based on clinical criteria):

RAPID= < 7 days until recovery (N =56) (Mean = 4.9 days)

PROTRACTED= > 21 days until recovery (N = 31) (Mean = 33.2 days)

Lau et al, 2011.

Determining Which On-Field Signs/Symptoms Were Most Predictive of Protracted Recovery

Variables Wald χ2

OR p 95% CI for OR

Dizziness 5.44 6.34 0.02 1.34 -29.91

LOC 2.53 0.27 0.11 0.54 – 1.35

Vomiting 1.45 0.42 0.23 0.10 – 1.72

Direct LR with 3 predictors: χ2 (3, 94)= 11.77, p= .008Predictors reliably distinguish between rapid and protracted recovery groups

Lau et al 2011

Fogginess:• May be associated with a

more severe course and protracted recovery

• “Foggy” athletes vs non-foggy athletes: • Slower reaction time

• Attenuated memory performance

• Slower processing speed

• Significantly higher number of other post-concussion symptoms

(Iverson 2004)

21


Management of Concussion

Cognitive Symptoms• “Fogginess”• Difficulty concentrating• Memory deficits• Cognitive Fatigue

Somatic Symptoms• Headaches• Dizziness• Nausea• Light/Sound

Sensitivity

Mood Disruption

• Irritability• Feeling sad• Anxiety

Sleep Alterations• Difficulty

falling asleep

• Fragmented sleep

• Too much/too little sleep

Postconcussion Disorder

Sleep Alterations• Difficulty falling asleep• Fragmented sleep• Too much/too little

sleep

Sleep Alterations: Adverse Effects

– Decreased quality of life

– Difficulty concentrating

– Higher risk of accidents

– Increased prevalence of GAD, MDD

– Higher rates of chronic pain

– Independent risk factor for poor physical and mental health

Morin, et al. Therapeutic options for sleep maintenance and sleep-onset insomnia. Pharmacotherapy. 2007; 27(1):89-110.


sleep

Sleep Alterations: Adverse Effects

1. Precede the onset of depression

2. Increase the risk of future depressive episodes

1. Increase the risk of suboptimal responses to antidepressants

Gillin JC. Are sleep disturbances risk factors for anxiety, depressive, and addictive disorders? Acta Psychiatr Scand Suppl 1998;393:39-43.

Ford D, Cooper-Patrick L. Sleep disturbances and mood disorders: an epidemiologic perspective. Depress Anxiety 2001;14:3-6.


sleep

Sleep Alterations: Etiology

• Neurophysiologic injury itself

• Preexisting sleep disorders

• Pain• Environmental stimuli• Pharmacologic effects• Drug withdrawal


sleep

Sleep Alterations: Treatment

• Behavioral Strategies– Sleep hygiene education– Relaxation therapies– Sleep restriction

• Pharmacology– Trazodone– Melatonin agonists– Nonbenzodiazepine

hypnotics

Morin, et al. 2007.

22

Mood Disruption• Irritability• Feeling sad• Anxiety

Mood Disruption: Treatment

• Psychotherapy

• Antidepressants– SSRIs– TCAs

• Anxiolytics– SSRIs– benzodiazepines

Somatic Symptoms• Headaches• Dizziness• Nausea• Light/Sound Sensitivity

Somatic Symptoms: Treatment

• Dizziness /Balance Disorders– Vestibular Therapy

• Headaches – Musculoskeletal– Vascular– Biochemical

– “Cognitive Fatigue”

Somatic Symptoms:Headaches

Medication overuse– Rebound headache

– Dose tolerance

– Dependency

18 to 45% incidence in patients with chronic PTH

Baandrup L, Jensen R: Chronic post-traumatic headache—a clinical analysis in relation to the International Headache Classification 2nd Edition. Cephalalgia 2005;25:132–8.

Haas DC: Chronic post-traumatic headaches classified and compared with natural headaches.

Cephalalgia 1996;16:486–93.


Musculoskeletal/Myofascial/Tension– Physical Therapy: ROM, modalities, massage

– Analgesics/Anti-inflammatories/Muscle relaxants

– Trigger Point Injections

– Nerve block (GON)

– Relaxation techniques

– Biofeedback and behavior modification


– Ca-channel blockers – verapamil*

– Anticonvulsants – topiramate – gabapentin*– valproic acid

– Beta-blockers– propranolol

– Antidepressants– fluoxetine*– duloxetine*– amitriptyline*– venlafaxine*

*Non-FDA approved indication

Magnesium:2 RCTs showed

decrease migraine frequency with

chronic supplementation

Migraine Abortives?TriptansErgotsMidrin

Inhibition of cortical

excitation

Restoring nociceptive

dysregulation

Migraine Headache – Prevention/Treatment

Cognitive Fatigue Headaches


Somatic Symptoms• Headaches• Dizziness• Nausea• Light/Sound Sensitivity

23


Cognitive Symptoms:Treatment

• Neurostimulants*– amantadine– methylphenidate– dextroamphetamine– atomoxetine– modafinil– CDP-choline?

*Non-FDA approved


Somatic Symptoms• Headaches• Dizziness• Nausea• Light/Sound

Sensitivity

Mood Disruption

• Irritability• Feeling sad• Anxiety

Sleep Alterations• Difficulty falling

asleep• Fragmented

sleep• Too much/too

little sleep

Lovell, 2006

Alternative Interventions in Concussion Management: Is there a

role?

Objective

• Be exposed to the latest findings related to alternative therapies including hyperbaric oxygen, supplements, and other interventions

Brain Directed Nutrients (Amen DG et al, 2013)

• Randomized, double blind, placebo‐controlled, crossover trial that did not include lifestyle interventions

• 30 healthy adults (15 men/15 women)

• The brain directed nutrients intervention consisted of 3 supplements: fish oil; a high‐potency, multiple vitamin/mineral supplement; and a brain enhancement supplement

Brain Directed Nutrients (Amen DG et al, 2013)

• Improvement in cerebral blood flow was seen for the BDNs as compared to the placebo in the prefrontal cortex, anterior and posterior cingulate gyrus, hippocampus, and cerebellum.

• There were also improvements in executive functioning, mood, and reduced hostility.

24

Ginko and brain function (Mix and Crews, 2002)

• Double blind randomized trial

• Neuropsychological tests and follow‐up self‐report questionnaires provided evidence of the potential efficacy of Ginkgo biloba EGb761 in enhancing certain neuropsychological/memory processes of cognitively intact older adults, 60 years of age and over

Dietary supplementation with the omega‐3 fatty acid (Mills JD et al, 2011)

• Previous work has shown positive effects using the omega‐3 fatty acid docosahexaenoicacid (DHA) in post‐injury treatment following traumatic and ischemic insults in rats

• Investigated the use of omega‐3 fatty acid PRIOR to injury (1 month)

• The supplement appeared to protect from excitotoxicity and inflammation plus assisted with membrane building

Vitamin D3 and D2

• Controls bone and calcium metabolism but is also involved in immunoregulation

• Can serve as an anti‐inflammatory agent

Magnesium and TBI in rats

• Mg2+ therapy was effective in promoting cognitive recovery following brain injury

• The authors suggest that the Mg2+ may be task and dose‐dependent

Hoane MR, 2007

Magnesium (Headaches)

• Oral supplementation with magnesium oxide and L‐carnitine and concurrent supplementation of Mg‐L‐carnitine could be effective in migraine prophylaxis (TarighatEsfanjan A et al, 2012)

Resveratrol for Neuroprotection(Zhuang et al, 2006)

• Seen in grapes and seeds

• Serves as an anti‐oxidant

• Why might it work?

– May block free radicals

– Decreases clotting

– May decrease the infarct size

25

Resveratrol

• Administration of resveratrol can increase cell survival

• Resveratrol may serve as a potential therapeutic agent in the treatment of TBI

Lin CJ et al, 2014

Green Tea – Polyphenols – 500 mg

• Green tea improved cerebral function following TBI in rats

• Drinking green tea may be an effective therapy for persons post concussion

Itoh T et al, 2011; 2012; 2013

Curcumin (500 mg BID)

• Curcumin possesses strong antioxidant properties

• Improved the neurological status evaluated 2 weeks after brain injury in rats

• There appears to be neuroprotection with use of curcumin in the rat traumatic brain injury model

Samini F et al, 2011

Acupressure

Sea Bands

• PC6 acupressure for the treatment of migraine‐associated nausea may be of value (Allais G et al, 2012)

Melatonin

• It is considered a sleep aid• No associations between melatonin levels and cognitive function were observed in a 36 hour endurance activity with humans (Davis GR et al, 2014)

• Melatonin is a safe and well‐tolerated agent • A double‐blind, placebo‐controlled intervention trial of 3 and 10 mg sublingual melatonin has begun to determine if melatonin is a useful treatment for children with post‐concussion syndrome (Barlow KM et al, 2014)

26

Peppermint oil

Amato A et al, 2014

Hyperbaric Oxygen Therapy (Wolf EG et al, 2012; 2012)

• 50 military persons diagnosed with TBI were randomized to either a sham or hyperbaric O2

• 48 people completed 30 treatments

• Persons experienced ear blockage, sinus squeezing, and claustrophic symptoms

• HBO₂ at 2.4 ATA pressure had no effect on post‐concussive symptoms after mild TBI

Hyperbaric Oxygen Therapy

• Bennett et al (2013) said it was no better than sham

• In people with prolonged PCS, might work in the chronic stage (Boussi‐Gross et al, 2013)

Light Sensitivity

Treating symptoms may be critically important

• Studies of management of concussion were so poor that conclusions that rest was not helpful or that exercise might be beneficial are premature

• Better evidence showed that individualized treatment of long‐standing symptoms may allow earlier return to sport than rest and exercise alone

Brolinson PG, 2014

Use of Complimentary Medicine for Concussion

• The jury is out as to if complimentary medicine works, what to use, and when to use it

• Alternative supplements are being used all the time with children with concussion

• Parents are often afraid to try standard medical interventions with their young children

27

What is best?Department of Physical Therapy

Concussion Management??

Exertion:

• Student athletes who engaged in high levels of activity in the weeks following concussion had increased symptoms and worsened neurocognitive data

• They also had significantly longer recovery time

Majerske et al., 2008


Strict rest versus usual care• 11 to 22 y/o kids presenting to a pediatric

ED within 24 hours of concussion were included

• Randomized to strict rest for 5 days versus usual care (1–2 days rest, followed by stepwise return to activity)

• Strict rest immediately after concussion offered no added benefit over the usual care Thomas DG et al, 2015

Negative Effects of Prolonged Rest:• Deconditioning

• Fatigue

• Reactive depression

Benefits of Exercise:• Exercise has positive effects on mental health

• Athletes can have adverse psychological responses when unable to participate in sports

• Exercise improves performance in spatial learning and memory tasks (Griesbach et al, 2004)

• Exercise promotes neuroplasticity and enhances neuroprotectiveproperties (Griesbach et al, 2008)

Exertion following Concussion: Striking a Balance?

It may be in the Timing . . . Animal studies:• Voluntary exercise within first week impaired cognitive

performance

• Aerobic exercise performed 14-21 days after concussive injury improved cognitive performance (Griesbach GS, et al 2004)

Human studies:• Uncontrolled activity too soon after concussion can have

negative effects on recovery (Majerske et al, 2008)

• But . . . in the same study, student athletes who were the most sedentary following injury also had a poorer outcome

28


Are the International Guidelines Enough?

Evidence for more intensive Return to Play testing . . .

McGrath et al 2013

How do you feel?

Fine!

How do you feel? Fine!

Are asymptomatic athletes really back to normal?

Study Protocol (N= 55 concussed)

BASELINE

ImPACT,symptoms

POST-CONCUSSIO

N (P1)ImPACT,

symptoms

RETURN TO BASELINE

(RTB)ImPACT,

symptoms

POST-EXERTION

(PE)ImPACT,

symptoms

Moderate Exertion20 min of :

Stationary CyclingTreadmill or

Elliptical

M= 3.15 days(SD= 2.45)

M= 13.23 days(SD= 8.82)

M= 18.78 days(SD = 14.57)

16 FAIL (1+ RCI)

and39 PASS (NO RCI)

McGrath N et al, 2013


Results

• Nearly 30% of athletes who were back to baseline on ImPACT and reported no symptoms at rest FAILED a post-exertion (PE) ImPACT test in spite of reporting no symptoms (after exertion)


465…458…451…

Serial 7s Cognitive Dual-Task

*p<.05 Kontos, Ortega, Larson (2011)

Dual-task eyes-closed differentiated concussed from controls

BESS Error Scores across Four Conditions for Recent (1 month) Concussion v. Controls (N= 86)

29

Medication Management in ConcussionGeneral principles:

• There is no 1 medication for management of concussion

• Pharmacological intervention is regulated via physician with recommendations from the therapeutic team

• Considered when symptoms do not subside spontaneously & interfere with rehabilitation and recovery

• OFF Label use of most medications


Headaches

• Most common post concussive symptom (71% in sports related concussion)– Lovell 2004

• Types based on etiology:– Cognitive Fatigue

– Migrainous

– Musculoskeletal/Cervicogenic

– Medication Induced

Cognitive Fatigue Headaches

Scenarios:

• High school student sustains concussion in a game. Feels dazed, groggy, but awakes next day feeling minimal to no symptoms. Goes to school; by the end of the third period has to go to nurse’s office because of severe headache. Unable to remain in school; parents called to take home.

• 15 year old student experiences concussion. Asymptomatic at rest, but gets headaches when he goes up stairs.

Potential Medications: Neurostimulants(amantadine, methylphenidate, etc.)

Management – Headaches

• Migraine HA’s:

• Abortive agents (zolmitriptan, sumatriptan)

• Prophylactic migraine medication:

• Antidepressants:

• SSRI’s (eg, sertraline)

• Tricyclics (eg, amitriptyline, imipramine)

• Anticonvulsants (topiramate, depakote, etc)

• Beta blockers

• Calcium channel blockers


Medication Overuse Headache (MOH)/Rebound Headache

• Among those individuals with chronic daily headache, approximately one-third meet the criteria for medication overuse (Colas 2004)

• Largest culprits for MOH – Acetaminophen & aspirin combined with caffeine, opiods, triptans, NSAIDS (lower risk) (Bigal 2004)

Management - Headaches

• Along with pharmacotherapy, the VA/DoD Clinical Practice Guidelines in March 2009 recommend the following:

• Assessment of cervical spine for musculoskeletal contributions

• history taking of pre-existing headache

• assessment of visual acuity issues

• sleep review

• physical examination for sinus infection or CSF leak

30

Management – Sleep Disturbances

• Medication Options:

• Ambien: First line agent for sleep as recommended by VA/DoD Clinical Practice Guidelines, 2009

• Trazodone - efficacious in depressed patients with insomnia (Willer, 2006)

• Other medications: melatonin (over the counter), amitriptyline, trazadone, Prazosin, Seroquel (more for disturbed sleep, nightmares),

• Benzodiazepines generally avoided due to risk of addiction & negative impact on cognitive recovery

• Non medication management: avoid daytime naps, avoid caffeine, regular sleep schedule, etc.

Management – Cognitive Impairment

• Neuro-stimulants: classifications of medications most commonly to improve concentration/attention

• amantadine (Symmetrel)• Reddy 2012 (sport-related concussion)

• Giacino 2012 (severe TBI)

• modafinil (Provigil)

• methylphenidate (Ritalin)

• amphetamine/dextroamphetamine (Adderall)

• Cholinergics: ?

• Aricept – shown in severe TBI to have +effect on memory & mood (Willer 2006)

• No studies in mild TBI

Management – Mood Issues

• SSRI’s – used frequently with head injury–associated depression due to:

• Perceived clinical efficacy

• Relatively few side effects

• Possible contributions to assist in reducing cognitive deficits (Willer 2006, Fann 2000)

• VA/DoD Clinical Practice Guidelines suggest Zoloft (sertraline) and Celexa (citalopram) as first line agents for depression/mood

Conclusion

• Concussion is a functional, rather than a structural injury to the brain, which is extremely prevalent across the life span

• Recovery time following concussion is variable

• Several known factors contribute to protracted recovery following concussion

• Vestibular and ocular motor findings are common following concussion, and appear to be amenable to intervention

The Balance Error Scoring System (BESS) Obtain Preseason Baseline Score; Compare with Post-Concussion Score33-34

The Balance Error Scoring System33-34 provides a portable, cost-effective and objective method of assessing static postural stability. The BESS can be used to assess the effects of mild head injury on static postural stability. Information obtained from this clinical balance tool can be used to assist clinicians in making return to play decisions following mild head injury. The BESS can be performed in nearly any environment and takes approximately 10 minutes to conduct.

The balance-testing regime consists three stances on two different surfaces. The three stances are double leg stance, single leg stance and tandem stance. The two different surfaces include both a firm (ground) and foam surface. Athletes’ stance should consist of the hands on the iliac crests, eyes closed and a consistent foot position depending on the stance. Shoes should not be worn.

Errors: •Moving the hands off the hips •Opening the eyes •Step, stumble or fall •Abduction or flexion of the hip beyond 30˚ •Lifting the forefoot or heel off of the testing surface •Remaining out of the proper testing position for greater than 5 seconds

The maximum total number of errors for any single condition is 10.

If a subject commits multiple errors simultaneously, only one error is recorded.

In the double leg stance, the feet are flat on the testing surface approximately pelvic width apart.

In the single leg stance position, the athlete is to stand on the non-dominant leg with the contralateral limb held in approximately 20° of hip flexion, 45° of knee flexion and neutral position in the frontal plane.

In the tandem stance testing position, one foot is placed in front of the other with heel of the anterior foot touching the toe of the posterior foot. The athlete’s non-dominant leg is in the posterior position. Leg dominance should be determined by the athlete’s kicking preference.

Scoring the BESS: Each of the trials is 20 seconds. Count the number of errors (deviations) from the proper stance. The examiner should begin counting errors only after the individual has assumed the proper testing position.

Double Leg Stance Firm Surface

Single Leg Stance Firm Surface

Tandem Stance Firm Surface

Double Leg Stance Foam Surface

Single Leg Stance Foam Surface

Tandem Stance Foam Surface

B.E.S.S. SCORECARD Count Number of Errors max of 10 each stance/surface

FIRM Surface

FOAM Surface

Double Leg Stance (feet together)

Single Leg Stance (non-dominant foot)

Tandem Stance (non-dominant foot in back)

TOTAL SCORES: total each column

B.E.S.S. TOTAL: (Firm+Foam total)

Administering the BESS: Establish baseline score prior to the start of the athletic season. After a concussive injury, re-assess the athlete and compare to baseline score. Only consider return to activity if scores are comparable to baseline score. Use with Standardized Symptom Scale Checklist.

Airex™ Foam Balance Pads available at www.power-systems.com or through most sporting goods stores.

1

Evaluation of the Oculomotor System

Eye movement system: Neurological pathologies may lesion the optic pathways in the brain or areas of the brain that control vision and eye movements. Therefore, it is critical to test for impairments in the visual system that may impact postural control. Eye movement abnormalities occur as a result of:

Cranial nerve lesions Weakness of extraocular muscles Lesions of the medial longitudinal fasciculus Lesions in vestibular system or cerebellum (pathological nystagmus) Lesions of eye fields in cortex

o Frontal eye fields Temporary ipsilateral gaze deviation Inability to move eyes to a new target (saccades)

o Parieto-occipital eye field Inadequate smooth pursuit (must use catch up saccades) Poor ability of the eyes to generate nystagmus when an object is

moving in front of them (OKN – see below). Smooth pursuit: Hold the patient’s head or chin stationary. Have the person follow your slowly moving finger (or sticker on a pen) horizontally (from center 30 degrees right and then to 30 degrees left), and then vertically (center to 30 degrees up to 30 degrees down). You may need to hold the eyelids up in order to see the downward eye movement clearly. Normal response: Smooth, conjugate eye movement. The key is to move your finger at the correct speed (20 deg/sec or so). If you move your finger too fast, the eye movement will become jerky. Also, do not move the finger past 30 degrees. Abnormal response: Saccadic or jerky eye movement. Note the direction of pursuit when it occurred. Normal vertical eye pursuit is often interrupted by a saccade. Saccadic eye movements: Hold your finger approx. 15 degrees to one side of your nose. Ask the patient to look at your nose, then at your finger, repeating several times. Do this from the left, right, up and down. You are looking for the number of eye movements it takes for the patient’s eyes to reach the target.

2

Eye movement ROM: Can be done in conjunction with the smooth pursuit test. Looking for the ability to fully move the eyes. Bring the finger out to the side or up/down. Watch for the eyes to move conjugately. I like the 9 points. Vergence: Hold your finger (or sticker) 2 feet away from the person’s face. Ask him/her to focus on the finger while you move it forward toward the nose. Normal response: convergence of the eyes with papillary constriction. Vergence is usually done 3 times. Normal is less than 6 cm. You are asking them when they see double and then measuring the distance in cm. We also measure “recovery” which is moving it away from the eyes and when do the see one object again. Static visual acuity: Ideally use a DVA chart (Lighthouse):

a. Have the patient wear corrective lenses if usually worn. b. Place the patient at whatever distance required of the chart you are using (our

chart is for testing at 3 meters or 9.84 feet). c. Have the patient read the optotypes until they miss the majority of letters on a

line (3/5 symbols) d. The line above this (or the line where all are correct – just be consistent) is

considered their visual acuity. e. Snellen notation: 20/10 is interpreted as: Most people view that line at 20’ /

the patient has to be at 10’ to view the line. f. logMAR notation: allows for use in statistics since each line differs by .1

logMAR. It is calculated by taking the log10 of the fraction. For example, 20/20=1 and the log of this is 0.

Dynamic Visual Acuity: Static visual acuity is determined as above. Then the person’s head is moved at 2 Hz (240 beats/min) as they are asked to read the optotypes. If they lose more than 2 lines from baseline, it is considered to be an abnormal test. This test DOES NOT provide a diagnosis—it can be abnormal for many different reasons in both persons with peripheral or central vestibular pathology but does provide you with information of the functioning of the VOR. Optokinetic nystagmus: OKN tests the ability of the pursuit system. It is NOT a vestibular test, but a test of how well the eyes follow moving objects. If you look at the eyes of someone who is watching a train go by, you might see nystagmus. Test this by slowly moving a striped cloth in front of the eyes. Instruct your patient to look forward and “count the stripes”. The eyes will follow a stripe, then when they get to the end of the socket, will jump back to follow the next stripe. If your patient does not have this, it means a deficit somewhere in the

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pathway from the retina to the visual cortex and back to the eye muscles (OKN involves many neural substrates). Eye alignment: The ability to look straightforward is the job of intact cranial nerves and ocular musculature. Tropia is deviation of one eye from forward gaze when both eyes are open (always present). Phoria is deviation from forward gaze, apparent when only when the person is looking forward with one eye (the other eye is covered). The cover test and the cover/uncover test can help you to identify a phoria or trophia. Both are negative predictors of recovery (Pavlou et al, 2015) Cover test: Tell your patient to look at a distant object. Cover one eye and observe the uncovered eye. If the uncovered eye moves, it is indicative of tropia. Tropia is often difficult to see unless you cover one eye. Cover-uncover test: Cover one of the subject’s eyes for about 10 seconds, watch the covered eye for movement as it is quickly uncovered. An abnormal response is movement of the uncovered eye. This may be indicative of an otolith or central problem.

Head Impulse Test The persons head is moved quickly about 15 degrees towards the center from the side while you watch to see if they can stay focused on your nose throughout the fast head movement. Movement of the eyes (a saccade) is considered abnormal. You must make sure that they are paying attention to the task as it can be miss read as abnormal when in fact they just were not paying attention. The stop with the nose straight ahead must also be done quickly. One is looking for a “catch up” saccade as with VOR involvement, the eyes cannot remain focused on the nose as the VOR gain is low. Some PTs move the head to the right or left in order to make it less likely that the person can predict which direction their head will be moved. One can move the head in towards center or you can move it quickly 15-20 degrees from the center quickly. The direction that you are moving quickly is the ear that you are testing. Many people flex the head slightly in order to put the horizontal canal in the horizontal plane. If you see the saccadic “jump” after the end of the head movement that is called an overt saccade (you saw it). Some people have “covert” saccades, which means that they had a saccadic correction but that it occurred DURING the head movement. You will not be able to see a covert saccade but with a vHIT system (about 14,000-15,000 dollar system) it can be recorded. The HIT was developed by Halmalghi. The HINTS paper (Kattah JC et al, 2009) is useful in identifying central (stroke) pathology from peripheral pathology.

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Head Shake Test The persons head is flexed 20-30 degrees and rotated rapidly to the right and left 20 times (10 times in each direction) with infrared goggles in place. They are to close their eyes. Upon opening the eyes, there will be nystagmus if it is not normal. The nystagmus noted is abnormal but the direction of the nystagmus does not tell you which the involved side is. Goggles with light on and off If you have infrared goggles, it is important to assess for nystagmus with the light on and off. If the person has nystagmus and you turn on the light and it gets worse, it is most likely a central problem. With fixation and the nystagmus becomes less intense, it is a peripheral problem. Subjective visual vertical (Bucket test)

Put the bucket over the persons face so that they cannot see anything in the periphery except for the bucket. Start the bucket at about 30 degrees to the right or left of earth vertical. Do not look at the goniometer as you move the bucket but ask the patient to tell you when the bucket is straight. Record the reading. Do this to the right and left approximately 10 times in each direction. Greater than 2 degrees off is considered to be abnormal.

VOR Exercises (change the gain of the VOR) VOR x 1 The patient is to focus on a target at varying distances. They need to be able to see the target clearly as they move their head to the right and left at approximately 2 Hz (approximately 240 beats/min on a metronome). Target size, body position, and backgrounds can be varied as the patient improves. This can be done in the pitch, yaw and roll directions. VOR x 2 The patient is to move the target to the left while the head moves to the right as they focus on the target in the moving hand. They then move the head and hand in the opposite direction as they remain focused on the target. This is done in the pitch and yaw directions.

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Substitution Exercises Imaginary Target (Remembered target) The patient is to focus on a target in front of them, remember where it was, close their eyes and then move their head to the right or left. When they open their eyes, it is hoped that their eyes remain on the target. This exercise is most commonly given to persons with bilateral vestibular loss (Dandy’s syndrome). Eye Head saccadic exercise The patient is to have 2 cards in their hands (one in each) with letters on the cards. They are to look at one card and face their nose to the target. Then they are to move their eyes to the second target and follow with their head. Then eyes, head, eyes first, head. This is a form of substitution exercise done to help people learn how to use the saccadic eye system to substitute for a damaged VOR. Examples of habituation exercises Wii balance system Disco balls URLs the include busy environments Repeated performance of an activity Virtual reality Viewing complex patterns with visual searches

Vestibular/Ocular-Motor Screening (VOMS) for Concussion

Vestibular/Ocular Motor Test: Not Tested

Headache0‐10

Dizziness0‐10

Nausea0‐10

Fogginess 0‐10

Comments

BASELINE SYMPTOMS: N/A

Smooth Pursuits

Saccades – Horizontal

Saccades – Vertical

Convergence (Near Point) (Near Point in cm):Measure 1: ______ Measure 2:______ Measure 3:______

VOR – Horizontal

VOR – Vertical

Visual Motion Sensitivity Test

Tester:__________________________________________Date of Screen:______________________ Name: DOB: Circle: Male Female

VOMS Instructions: Interpretation: This test is designed for use with subjects ages 9-40. When used with patients outside this age range, interpretation may vary. Abnormal findings or provocation of symptoms with any test may indicate dysfunction – and should trigger a referral to the appropriate health care professional for more detailed assessment and management. Equipment: Tape measure (cm); Metronome; Target w/ 14 point font print. Baseline Symptoms – Record: Headache, Dizziness, Nausea & Fogginess on 0-10 scale prior to beginning screening

Smooth Pursuits - Test the ability to follow a slowly moving target. The patient and

the examiner are seated. The examiner holds a fingertip at a distance of 3 ft. from the patient. The patient is instructed to maintain focus on the target as the examiner moves the target smoothly in the horizontal direction 1.5 ft. to the right and 1.5 ft. to the left of midline. One repetition is complete when the target moves back and forth to the starting position, and 2 repetitions are performed. The target should be moved at a rate requiring approximately 2 seconds to go fully from left to right and 2 seconds to go fully from right to left. The test is repeated with the examiner moving the target smoothly and slowly in the vertical direction 1.5 ft. above and 1.5 ft. below midline for 2 complete repetitions up and down. Again, the target should be moved at a rate requiring approximately 2 seconds to move the eyes fully upward and 2 seconds to move fully downward. Record: Headache, Dizziness, Nausea & Fogginess ratings after the test.

Saccades – Test the ability of the eyes to move quickly between targets. The

patient and the examiner are seated. Horizontal Saccades: The examiner holds two single points (fingertips)

horizontally at a distance of 3 ft. from the patient, and 1.5 ft. to the right and 1.5 ft. to the left of midline so that the patient must gaze 30 degrees to left and 30 degrees to the right. Instruct the patient to move their eyes as quickly as possible from point to point. One repetition is complete when the eyes move back and forth to the starting position, and 10 repetitions are performed. Record: Headache, Dizziness, Nausea & Fogginess ratings after the test.

Vertical Saccades: Repeat the test with 2 points held vertically at a distance of 3 ft. from the patient, and 1.5 feet above and 1.5 feet below midline so that the patient must gaze 30 degrees upward and 30 degrees downward. Instruct the patient to move their eyes as quickly as possible from point to point. One repetition is complete when the eyes move up and down to the starting position, and 10 repetitions are performed. Record: Headache, Dizziness, Nausea & Fogginess ratings after the test.

Convergence – Measure the ability to view a near target without double vision. The patient is seated and wearing corrective lenses (if needed). The examiner is seated front of the patient and observes their eye movement during this test. The patient focuses on a small target (approximately 14 point font size) at arm’s length and slowly brings it toward the tip of their nose. The patient is instructed to stop moving the target when they see two distinct images or when the examiner observes an outward deviation of one eye. Blurring of the image is ignored. The distance in cm. between target and the tip of nose is measured and recorded. This is repeated a total of 3 times with measures recorded each time. Record: Headache, Dizziness, Nausea & Fogginess ratings after the test. Abnormal: Near Point of convergence ≥ 6 cm from the tip of the nose.

Vestibular-Ocular Reflex (VOR) Test – Assess the ability to stabilize vision as the head moves. The patient and the examiner are seated. The examiner holds a target of approximately 14 point font size in front of the patient in midline at a distance of 3 ft.

Horizontal VOR Test: The patient is asked to rotate their head horizontally while maintaining focus on the target. The head is moved at an amplitude of 20 degrees to each side and a metronome is used to ensure the speed of rotation is maintained at 180 beats/minute (one beat in each direction). One repetition is complete when the head moves back and forth to the starting position, and 10 repetitions are performed. Record: Headache, Dizziness, Nausea and Fogginess ratings 10 sec after the test is completed.

Vertical VOR Test: The test is repeated with the patient moving their head vertically. The head is moved in an amplitude of 20 degrees up and 20 degrees down and a metronome is used to ensure the speed of movement is maintained at 180 beats/minute (one beat in each direction). One repetition is complete when the head moves up and down to the starting position, and 10 repetitions are performed. Record: Headache, Dizziness, Nausea and Fogginess ratings after the test.

Visual Motion Sensitivity Test – Test visual motion sensitivity and the ability to

inhibit vestibular-induced eye movements using vision. The patient stands with feet shoulder width apart, facing a busy area of the clinic. The examiner stands next to and slightly behind the patient, so that the patient is guarded but the movement can be performed freely. The patient holds arm outstretched and focuses on their thumb. Maintaining focus on their thumb, the patient rotates, together as a unit, their head, eyes and trunk at an amplitude of 80 degrees to the right and 80 degrees to the left. A metronome is used to ensure the speed of rotation is maintained at 50 beats/min (one beat in each direction). One repetition is complete when the trunk rotates back and forth to the starting position, and 5 repetitions are performed. Record: Headache, Dizziness, Nausea & Fogginess ratings after the test.

(Mucha A et al, 2014)

TEST PURPOSE EQUIPMENT TECHNIQUE RESULTS

C O V E R T E S T S

Cover Test

Test for eye misalignment (TROPIA)

Visual occluder, Distant Visual Target (6 meters)

Patient focuses on a distant object

Cover one eye – observe for movement of the UNCOVERED EYE

NORMAL:

ABNORMAL: (LEFT EXOTROPIA)

a) Initially L eye positioned laterally. b) When R eye is occluded, L eye moved medially to focus target on fovea. INTERPRETATION: Positive Cover Test indicative of tropia (eso/exo/hyper) – Refer for further workup

Uncover Test

Test for eye misalignment (PHORIA OR TROPIA)



Cover one eye, wait 5-10 seconds

Uncover that eye

Observe for saccadic correction of the eye that was uncovered

NORMAL

ABNORMAL (LEFT EXOPHORIA)

a) Initially L eye is positioned laterally (image from L eye is suppressed) b) When R eye is occluded, the L eye moves medially to pickup target, the R eye moves laterally due to yoked movement c) When occluder is removed the R eye moves back to center to pick up image on fovea INTERPRETATION: Positive Uncover can be indicative of tropia or phoria; in presence of negative Cover Test indicative of phoria – Refer for further workup

* Examiner should focus attention on the eye that is shaded in grey

Alternate (Cross) Cover Test

Test for abnormal eye alignment (PHORIA OR TROPIA) This test brings out maximal eye movement for tropia or phoria



Cover one eye with occlude, several seconds

Rapidly move occlude to opposite eye

Continue 10-20 sec

NORMAL

ABNORMAL (RIGHT EXOPHORIA)

a) Initially both eyes appear aligned and fixed on target b) When R eye is occluded L eye maintains fixation, R eye drifts slowly to resting position c) Occluder quickly moved to L eye – R eye refixates, L eye moves behind occluder due to yoked movement d) Occluder moved back to R eye, L eye refixates INTERPRETATION: Positive Alternate Cover Test can be indicative of tropia or phoria; in presence of negative Cover Test indicative of phoria – Refer for further workup

Maddox Rod

Tests for abnormal eye alignments

Maddox Rod, Pen Light, Eye Alignment Card (if available)

Test Horizontal Alignment:

Maddox Rod held in front of RIGHT eye horizontally

Hold Pen Light 16 inches from patient

Patient describes what they see (vertical red line and white dot)

Test Vertical Alignment:

Maddox Rod held in front of right eye vertically

Patient should see white light

INTERPRETATION: Red Line and White dot are ≤ 1 inch apart from each other ABNORMAL RESULTS: (IF MR held over RIGHT eye)

- Horizontal Alignment: Red Line and White dot are > 1 inch apart – Exo or Esophoria are defined by position of the red line/white dot

o If line is to RIGHT of light - Esophoria (uncrossed diplopia) o If line is to LEFT of light - Exophoria (crossed diplopia)

- Vertical Alignment – Any amount of deviation o If line is below light – right Hyperphoria o If line above light – left Hyperphoria

ATYPICAL RESULTS: - Patient sees only red line or white light but not both (SUPPRESSION) - Patient sees the red line moving (UNSTABLE ACCOMODATION) - Red line is diagonal – examiner is not holding the Maddox Rod in

proper alignment Refer for further workup *If an Eye Alignment card is used, patient will indicate which line on the card is bisected by the red line – refer to Card specifics for interpretation

and red horizontal line

Convergence Test

Tests ability of both eyes to work together to maintain binocular fusion

Visual Target

Hold target 16” from bridge of patients nose

Slowly move closer to bridge of nose while observing for bilateral eye adduction – ask patient to tell you when they begin to see target as two objects

INTERPRETATION: NORMAL near point of convergence < 4inches from bridge of nose in individuals < 40 years old If abnormal, refer for further workup; Treat with Brock String Exercises, Two Targets, etc

Subjective Visual Vertical Test (Bucket Test)

Tests individual’s perception of verticality – otolith dysfunction

SVV Bucket

Patient sits upright

Bucket randomly rotated right or left and is slowly rotated back to 0 position by examiner

Patient signals when they estimate line to be vertical

INTERPRETATION: NORMAL: ≤2.3 degrees from true vertical (binocular) ≤ 2.5 degrees from vertical (monocular) ABNORMAL: >2.3 degrees from vertical (binocular) >2.5 degrees from vertical (monocular)

Documents

3/27/2017...3/27/2017 1 Concussion and TBI: Dizziness and Balance Issues Susan L. Whitney, DPT, PhD, NCS, ATC, FAPTA School of Health & Rehabilitation Sciences Department of Physical