Concussion Management Option: Learning Objectives Vision ... › Documents › PA › 2016-POA-Kapoor... · TBI/Concussion: Commonalities •Commonalities between mild/moderate TBI

Neera Kapoor, OD, MS

POA Congress 05/14/16 1

Concussion Management Option: Vision Rehabilitation

Neera Kapoor, O.D., M.S., F.A.A.O.,F.C.O.V.D.-A.

Associate Clinical Professor at NYU’s Langone Medical Center

RUSK Institute of Rehabilitation Medicine

Email: [email protected]

*Dr. Kapoor has no financial disclosures.

1

Learning Objectives •To increase familiarity and understanding with respect to:

1) why sensorimotor vision function may be impaired following concussion/mild traumatic brain injury (mTBI)

2) the members of the inter-professional health care management team

3) the vision provider’s associated role in managing such vision deficits

2

Learning Objectives •To increase familiarity and understanding with respect to the:

4) behavioral and visual considerations when evaluating patients with concussion/mTBI

5) high-yield vision examination for patients with mTBI/concussion and evidence-based medicine support regarding the occurrence of and treatment for vision problems

6) typical residual vision disturbances (amenable to non-surgical treatment interventions) evident following concussion/mTBI along with:

neurological correlates

associated symptoms

possible treatment options

3

VISION AND CONCUSSION/mTBI

4

TBI/Concussion

• According to the Centers for Disease Control and Prevention (CDC):

• “A TBI is caused by a bump, blow, or jolt to the head or a penetrating head injury that disrupts the normal function of the brain. Not all blows or jolts to the head result in a TBI. The severity of a TBI may range from “mild” (i.e., a brief change in mental status or consciousness) to “severe” (i.e., an extended period of unconsciousness or memory loss after the injury). ”

http://www.cdc.gov/TraumaticBrainInjury/get_the_facts.html,

accessed on January 30, 2016 5

TBI/Concussion

• According to the CDC:

• “A concussion is a type of traumatic brain injury—or TBI—caused by a bump, blow, or jolt to the head or by a hit to the body that causes the head and brain to move rapidly back and forth. This sudden movement can cause the brain to bounce around or twist in the skull, stretching and damaging the brain cells and creating chemical changes in the brain.”

http://www.cdc.gov/headsup/basics/concussion_whatis.html,

accessed on January 30, 2016 6

mailto:[email protected]

http://www.cdc.gov/TraumaticBrainInjury/get_the_facts.html

http://www.cdc.gov/headsup/basics/concussion_whatis.html



TBI/Concussion: Epidemiology ▶ According to the CDC, current U.S. civilian statistics from 2006-

2010 reveal that: • ~2.5 million people present at hospital (emergency room,

hospitalization, fatality) with TBI in 2010, with most being concussions or other forms of mild TBI

• for non-fatal TBI-related hospitalizations: gender bias towards males evident those aged 65 years and older have the highest

hospitalization rates children aged 0-4 years have the highest rates of ED visits the greatest reason was: a fall for 0-4 years of age and > 45 years of age. motor vehicle accident for 15-44 years of age.

http://www.cdc.gov/traumaticbraininjury/get_the_facts.html ; accessed

on January 30, 2016 7


2010 reveal that: • TBI-related deaths:

• due to any cause: three-fold gender bias towards males evident

• highest rates for persons 65 years and older. • Leading cause varied by age.

• Falls for those >65 years of age.

• Assaults for children ages 0-4 years of age.

• Motor vehicle crashes:

a) for children and young adults ages 5-24 years of age

b) were the second leading cause of TBI-related deaths, accounting for 26% in 2006-2010

http://www.cdc.gov/traumaticbraininjury/get_the_facts.html ;

accessed on January 30, 2016

8


2010 reveal that the common causes of TBI (in order) are:

1. falls (40%) –bimodal age distribution for TBIs being due to falls: for persons under 15 years of age (55%) and over 65 years of age (~81%)

2. unintentional blunt trauma (15%)-TBI was due to blunt trauma in ~24% of persons under 15 years of age

3. motor vehicle accident (14.3% of TBI), which were the third leading cause of TBI among all age groups

4. assault (10.7%)-~75% of all assault-related TBI occurred in persons 15 to 44 years of age.

http://www.cdc.gov/traumaticbraininjury/get_the_facts.html; accessed on

January 30, 2016 9

TBI/Concussion: Epidemiology ▶ According to the CDC, current U.S. civilian statistics regarding

concussion and sports/recreational injuries reveal that:

• ~248,418 persons under 19 years of age were treated in U.S. emergency departments (EDs) in 2009

• from 2001-2009, rate of ED visits associated with concussion/sports injuries in those under 19 years of age rose by 57%

http://www.cdc.gov/traumaticbraininjury/get_the_facts.html; accessed on January 30, 2016

10

TBI/Concussion: Epidemiology Military Statistics

▶Between January 2000 through December 8, 2015, 339,462 servicemembers were identified as having suffered a TBI, based on the most recent update from the Defense and Veterans Brain Injury Center (web-link: http://www.dvbic.org/dod-worldwide-numbers-tbi, accessed on 01/25/16). From January 1, 2000 through December 8, 2015, ~82.5% of these TBIs were classified as mild TBIs or concussions.

• Operation Enduring Freedom (Afghanistan)

• Operation Iraqi Freedom (Iraq, primarily)

• Operation New Dawn (working with Iraqi forces to develop their internal security and infrastructure)

11

TBI/Concussion: Closed Head Injuries

• With the cranium in tact, typically cause a more diffuse or global insult:

• Coup (acceleration) insult

• Contre-coup (deceleration) insult

12

http://www.cdc.gov/traumaticbraininjury/get_the_facts.html




http://www.dvbic.org/dod-worldwide-numbers-tbi










• With the cranium in tact, typically cause a more diffuse or global insult:

• Percussive event/blast injury/shock trauma (evident more recently with returning veterans of the Iraq/Afghanistan wars)

13


• Shearing forces which may lead to:

• Breakage of blood vessels (epidural or subdural hematomas)

• Diffuse axonal injury (DAI)

14

TBI/Concussion: Sequence of Brain Damage

• Primary injury:

• Occurs at moment of injury/insult as:

• Lacerations

• Contusions

• Fractures

• Diffuse axonal shearing

15

TBI/Concussion: Sequence of Brain Damage

Secondary brain injury (from where functional changes associated with the TBI/Concussion arise)

May Occur Hours to Weeks Post-Injury and Alter:

May Result in:

auto-regulatory physiological mechanisms

hemorrhages

neurotoxin release hypoxia

cascade of biochemical reactions increased intracranial pressure

build-up of the protein tau infection

16

TBI/Concussion: Severity • Severity of TBI/Concussion is determined by

the:

• Glasgow Coma Score (GCS)

• Neuro-imaging

• Loss of consciousness (LOC)

• Alteration of consciousness (AOC) or mental state

• Post-traumatic amnesia (PTA)

• Neuro-psychological testing, when possible (typically performed on those with mild TBI)

17

TBI/Concussion: Commonalities

• Commonalities between mild/moderate TBI and concussion are evident in the: • Presenting categories of symptoms

• Parameters of the grading scales

Bodin D, Yeates KO, and Klamar K (2012). Definition and classification of

concussion, in “Pediatric and Adolescent Concussion: Diagnosis, Management,

and Outcomes”, Eds Apps JN and Walter KD, New York: Springer, pp 9-19.

Cantu, R. C. (2001). Posttraumatic retrograde and anterograde amnesia:

Pathophysiology and implications in grading and safe return to play. Journal of

Athletic Training, 36 (3), 244–248.

18



TBI: Severity Scale Using Neuro-imaging, LOC, AOC, PTA, and GCS

Parameter Mild Moderate Severe

Structural

Neuro-

imaging

normal normal OR

abnormal

abnormal

LOC 0-30 mins 30 mins to

24 hours

>24 hours

AOC 1 min-

24 hours

>24 hours >24 hours

PTA 0-1 day 1-7 days >7 days

GCS 13-15 9-12 <9

Based on guidelines from the American Congress of Rehabilitation Medicine

19

Concussion Grading Scales Concussion

Grading Scales

Grade 1 Grade 2 Grade 3

Colorado

Medical Society

-confusion with no

amnesia

-no loss of

consciousness (LOC)

-confusion with

amnesia

-no LOC

-any LOC

American

Academy of

Neurology

-transient confusion

-symptoms or mental

status abnormalities

(<=15 minutes to

resolve)

-no LOC

-transient confusion

-symptoms or

mental status

abnormalities (> 15

minutes to resolve)

-no LOC

-any LOC

Cantu (revised) -post-traumatic

amnesia (PTA) and

post-concussive

symptoms (PCSS)

(<30 minutes to

resolve)

-no LOC

-PTA

<30minutes<24

hours

-PCSS <30

minutes<7 days

-LOC (< 1 minute)

-PTA >=24h

-PCSS>7 days

-LOC>=1min

Bodin D, Yeates KO, and Klamar K (2012). Definition and classification of concussion, in “Pediatric and Adolescent Concussion: Diagnosis, Management, and Outcomes”, Eds

Apps JN and Walter KD, New York: Springer, pp 9-19.

Cantu, R. C. (2001). Posttraumatic retrograde and anterograde amnesia: Pathophysiology and implications in grading and safe return to play. Journal of Athletic Training, 36 (3),

244–248

20

TBI/Concussion: Typical Signs Observed and Symptoms Reported

Signs Observed Symptoms Reported

Poor recall of events prior to or subsequent to a hit or fall

Headache or head pressure

Appears dazed or stunned Nausea and/or vomiting

Forgets an instruction/ confused about an assignment or position/unsure of game, score, or opponent

Confused, problems concentrating, or problems with memory

Clumsy movements Balance problems, dizziness, and/or vision problems (commonly blur/diplopia)

Slow to answers questions Feel sluggish, foggy, or groggy

Loses consciousness (even if brief) Increased sensitivity to light and/or noise

Mood, behavior, or personality changes

Just not “feeling right,” or “feeling down”

Modified from information on:

http://www.cdc.gov/headsup/basics/concussion_symptoms.html, accessed January 30,

2016

21

TBI/Concussion: Functional Impact

• Encompasses possible changes in:

• Cognitive abilities

• Mood/affect

• Sleep

• Sensorimotor abilities --- including vision

22

Typical Vision Deficits/Primary Associated Symptoms Evident Following TBI/Concussion

Deficit of: Primary Associated Symptom:

Accommodation Constant/intermittent blur

Tear Film Integrity Distorted clarity/gritty sensation, which

varies with blinking

Versional Ocular Motility Slower, less accurate reading /difficulty

sustaining gaze, shifting gaze, or tracking

targets

Vergence Ocular Motility Constant/intermittent eyestrain / diplopia

eliminated with monocular occlusion

Visual-Vestibular

Interaction

Vestibular symptoms exacerbated in

multiply, visually-stimulating environments

Light-Dark Adaptation Elevated light sensitivity

Visual processing Slower speed/impaired visual memory and

visual-spatial processing

**The above is also referred to as “Post-trauma vision syndrome” (PTVS)

23

TBI/Concussion: Informational Web-based Documents from the CDC

• http://www.cdc.gov/traumaticbraininjury/get_the_facts.html, accessed January 30, 2016

• http://www.cdc.gov/headsup/index.html, accessed January 30, 2016

• http://www.cdc.gov/concussion/signs_symptoms.html, accessed January 30, 2016

• http://www.cdc.gov/headsup/providers/index.html, accessed January 30, 2016

24

http://www.cdc.gov/headsup/basics/concussion_symptoms.html



TBI/Concussion: Informational Web-based Documents from the CDC’s Heads Up Site

http://www.cdc.gov/headsup/schools/index.html , accessed January 30, 2016

http://www.cdc.gov/headsup/youthsports/index.html, accessed January 30, 2016

http://www.cdc.gov/headsup/highschoolsports/index.html, accessed January 30, 2016

http://www.cdc.gov/headsup/highschoolsports/parents.html, accessed January 30, 2016

25

Inter-Professional Neuro-Rehabilitation Team

• Usual team leaders –one of the following:

• Physiatrist (MDs specializing in physical medicine and rehabilitation)

• Neurologist

• Neuropsychologist (specializing in evaluation and rehabilitation of cognitive impairments)

• Sports medicine (coaches, physical education teachers, and engaged parents/caregivers are also involved and frequently refer to a internist or team leader)

• Internal medicine- internists, physician’s assistants, and registered

nurses

• Psychologist/psychiatrist

26

Inter-Professional Neuro-Rehabilitation Team • Typical therapies

• Physical Therapist

• Occupational Therapist

• Vestibular therapy (depending upon the rehab department) by one of the following:

• Physical Therapist

• Occupational Therapist

• Cognitive rehab – one of the following:

• Speech/Language Therapist

• Neuropsychologist

• Vision therapy – one of the following:

• OT

• PT

• Optometrist

27

Inter-Professional Neuro-Rehabilitation Team • Management approaches:

• Refer for/provide EBM services within that particular center/rehab department/hospital

• Refer to/recommend needed services (regardless of location) as long as they are EBM

• Refer for/provide any potentially beneficial services (even if not EBM) within that particular center/rehab department/hospital

• Refer to/recommend needed services (regardless of location and even if not EBM)

28

Vision and the Brain • Starting with the brainstem:

• 50% of the cranial nerves impact vision function directly or indirectly:

• Direct:

• CN II, III, IV, and VI

• Indirect:

• CN V and VII

• Moving on to cortex:

• Primary and associated neurons relating to these brainstem cranial nerve nuclei traverse all 4 cortical lobes (not just occipital). 29

Role of Optometry/Ophthalmology • To diagnose and/or treat (optically and/or with vision

rehabilitation) vision disturbances to optimize vision function for use in a patient’s:

• Overall rehabilitation regimen

• Activities of daily independent living (ADLs), thereby impacting overall quality of life (QOL)

• Finding an optometrist specializing in neuro-optometric rehabilitation near you:

• www.covd.org

• www.nora.cc 30

http://www.covd.org/

http://www.nora.cc/



Behavioral and Visual Considerations with Concussion

31

What to be Aware of When Examining Those with Concussion/mTBI • Those with concussion/mTBI typically report sensorimotor symptoms:

• Related to sensory stimulation overload with the perception that,

in most places (aside from their home and other controlled quiet,

dim environments), there are too many:

• visual stimuli/movements

• sounds

• smells

• NOTE: the sensory stimulation overload may be due to difficulty

selecting the stimulus from the noise- i.e., often, everything feels

like a stimulus 32

What to be Aware of When Examining Those with Concussion/mTBI

• Those with concussion/mTBI may have sensorimotor deficits such as:

• Hearing deficits

• loss

• hyperacusis

• tinnitus

• Speech impairments

• Dizziness/nausea 33


• Those with concussion/mTBI (*this is more likely with mild to moderate TBI rather than classical concussion*) may have motor disturbances such as:

• Restricted neck movements

• Restricted lateralized mobility of upper and/or lower extremities

• Gait disturbance

• Tremors

34


• Those with concussion/mTBI may have affect disorders such as:

• Increased emotional lability

• Anger control (as evident with frontal lobe injuries)

• Impulsivity (as evident with frontal lobe injuries)

• Inappropriate behavior (as evident with frontal lobe injuries)

• Perseveration

35


• Those with concussion/mTBI may have cognitive deficits such as:

• Slower speed of processing (in varying degrees), frequently across all modes of processing

• auditory

• verbal

• visual

36




• Those with concussion/mTBI may have cognitive deficits such as:

• Impairment of:

• short- and/or long-term memory

• word-retrieval and/or language processing (i.e., as aphasia, expressive/receptive/mixed)

• organizational abilities/prioritization

• executive control

37

Factors Exacerbating Symptoms (Including Vision) Following Concussion/mTBI

• Illness (fever/flu/virus) and/or Pain

• Note for those with vestibular dysfunction, changes in barometric pressure exacerbates their symptoms

• Fatigue (over-exertion/lack of rest OR aerobic respiration)

• Use of controlled substances (alcohol, nicotine, narcotics, etc.)

38

Pearls When Examining Those with Concussion/mTBI

• Minimize movements (i.e., gesticulation, rapid movements in front of or around the patient)

• Keep the room illumination relatively dim (use incandescent,

rather than fluorescent, lighting when possible) • Speak clearly and slightly more slowly than you may normally

speak • Slowly change the lens/prism magnitudes when performing

refractive/ accommodative/ heterophoria/ vergence testing • Have the patient close their eyes in between tests

39

Visual Appearance of Text to Our Patients

Ideal, Clear and Single Vision How it May Look….

40

Optometric Examination: High Yield

History and Testing

41

Elements of High Yield Vision Exam

• Very good paper supporting high yield case history questions and diagnostic tests for mild TBI: Goodrich, Martinsen, Flyg, Kirby, Asch, Brahm, Brand,

Cajamarca, Cantrell, Chong, Dziadul, Hetrick, Huang, Ihrig, Ingalla, Meltzer, Rakoczy, Rone, Schwartz, and Shea (2013). Development of a mild traumatic brain injury-specific vision screening protocol: A Delphi study. JRRD Vol 50 (6): 757-768

Goodrich, Martinsen, Flyg, Kirby, Asch, Brahm, Brand, Cajamarca, Cantrell, Chong, Dziadul, Hetrick,

Huang, Ihrig, Ingalla, Meltzer, Rakoczy, Rone, Schwartz, and Shea (2013). Development of a mild

traumatic brain injury-specific vision screening protocol: A Delphi study. JRRD Vol 50 (6): 757-768.

42



Elements of High Yield Vision Exam • Case History

• Trauma history: date/nature of neurological insult

• Traditional ocular history PLUS onset/nature of any of the following **vision symptoms:

• blur (constant/intermittent)

• reading difficulties (slower speed/loss of place/skipping lines)

• diplopia or overlapping images (constant/intermittent)

• increased sensitivity in multiply visually-stimulating environments in conjunction with dizziness/ nausea/ vertigo/ disequilibrium

• increased sensitivity to light (fluorescent versus all types of light)

• missing one half of their vision/bumping into objects on one side of space

• visual perceptual processing (visual recognition, visual memory, visual spatial relations, visual spatial memory, speed of visual processing)



traumatic brain injury-specific vision screening protocol: A Delphi study. JRRD Vol 50 (6): 757-768.

43


PTVS

Survey =>

44

Elements of High Yield Vision Exam:

Management of Refractive Status • **For those with signs or symptoms of gait,

vestibular, or cognitive dysfunction:

• multi-focal spectacle lenses are:

• 1) typically contraindicated for ambulation

• 2) appropriate for non-ambulatory tasks

• prescribe single vision distance correction for

ambulation and single vision near (or flat-

top/round-segment computer top/reading bottom

bifocal) correction for prolonged

reading/computer use

45

Elements of High Yield Vision Exam • **Accommodative assessment for pre-presbyopes

• Monocular amplitudes

• Monocular (or binocular) lags

• **Vergence ocular motor assessment

• Cover test at far and near, as well as near point of convergence (NPC)

• **Versional ocular motor assessment

• Monocular and binocular motilities

• Relative accommodation, especially when prescribing near vision corrections

• ** denotes high yield diagnostic tests in those with TBI/ concussion



traumatic brain injury-specific vision screening protocol: A Delphi study. JRRD Vol 50 (6): 757-768

46

Elements of High Yield Vision Exam • Visual field assessment

• Confrontation visual field testing

• Automated visual field testing when possible

• Ocular health assessment

• Pupils

• Anterior segment evaluation

• Tonometry

• Posterior segment evaluation with dilation

• As indicated:

• contrast testing

• color vision

• OCT 47


• Case Disposition

• 10-15 minutes at the close of the examination to:

• Summarize findings, outlining remarkable ones in terms of:

• diagnosis

• relation to ADLs

• treatment options

• prognosis

• Report-writing

• Send to referring physician with a copy to the patient 48



OPTOMETRIC EVALUATION:

ADDITIONAL TESTING PERFORMED BY NEURO-

OPTOMETRY

49

Elements of Vision Exam- Additional Testing Performed by Neuro-optometry

• Sensorimotor vision testing:

• Cover test, NPC, phoria and vergence ranges

• Accommodative amplitudes, facility, and lag

• Keystone Visual Skills

• Cheiroscopic tracing

• Van Orden Star

• Vectograms

• King-Devick or DEM

• Visagraph

• Visual-perceptual testing:

• Visual memory

• simultaneous (Tachistoscope)

• sequential (Visual Span)

• Speed of visual processing

• Visual-spatial processing

• block design

• visual spatial relations

• visual spatial memory

50


• **For patients with vestibular symptoms:

• Dynamic visual acuity (DVA) –an assessment of VA performed while the head is in motion

• re-check monocular/binocular acuity at far or near while head is slowly (50-60 rotations per minute, if possible and patient has no neck issues) moving horizontally

• if DVA is more than 2 lines poorer than static VA (SVA), then there is a visual-vestibular problem

51


• For vestibular patients:

• Check for opticokinetic response (if possible or warranted) –helpful to rule out malingering for visual-vestibular symptomatology

52

Elements of Vision Exam- Additional Testing Performed by Neuro-optometry • Visual evoked potential

assessment

53

EVIDENCE-BASED MEDICINE ON OCCURRENCE OF SENSORIMOTOR

VISION DEFICITS IN TBI

54



Clinical Research on Vision and TBI: OCCURRENCE OF OCULAR MOTILITY (INCLUDING ACCOMMODATIVE) DEFICITS

• Ciuffreda KJ, Kapoor N, Rutner D, Suchoff IB, Han ME, Craig S (2007). Occurrence of oculomotor dysfunctions in acquired brain injury: a retrospective analysis. Optometry, 78(4): 155-61.

• PURPOSE: To report the percentage of ocular motor (including accommodative) diagnoses evident in a selected, visually-symptomatic out-patient sample with TBI (n=160) and CVA (n=60) of patients seen 10/01/2000 to 10/07/2003.

55

Clinical Research on Vision and TBI

Parameter TBI (n=160)

Age range (years) 8 to 91

Mean age (years) 44.9

#of males 73

# of females 87

Years post-injury (range) 0.1-42.0

Mean years post-injury 4.5

PATIENT PROFILE

Ciuffreda KJ, Kapoor N, Rutner D, Suchoff IB, Han ME, Craig S (2007).

Occurrence of oculomotor dysfunctions in acquired brain injury: a retrospective

analysis. Optometry, 78: 155-61

56

Results of Ciuffreda et al. (2007)

Ocular motor

dysfunction

TBI

(%)

Most common anomaly

(TBI)

Accommodation 41.1 Accommodative insufficiency

Versional 51.3 Deficits of saccades

Vergence 56.3 Convergence insufficiency

Strabismus 25.6 Strabismus at near

CN palsy 6.9 CN III

Ciuffreda KJ, Kapoor N, Rutner D, Suchoff IB, Han ME, Craig S (2007). Occurrence of oculomotor dysfunctions in acquired brain injury: a retrospective analysis. Optometry, 78: 155-61.

**NOTE- regarding accommodation: 51 (out of 160) persons with

TBI were pre-presbyopic and were included in the accommodative

statistics. 57

Clinical Research on Vision and TBI OCCURRENCE OF OCULAR MOTILITY (INCLUDING ACCOMMODATIVE) DEFICITS

• SO WHAT?

• In a visually-symptomatic TBI/concussion sample, over 50% may present with deficits of:

• versional ocular motility (51.3%)

• vergence ocular motility (56.3%)

• Most common anomalies were convergence insufficiency and deficits of saccades

58


• RECENT STUDIES –reporting on non-selected patient samples with TBI

• Regarding the military, studies by Drs. Gregory Goodrich and Glenn Cockerham also support a high occurrence of vision dysfunctions in TBI => Goodrich GL, Kirby J, Cockerham G, Ingalla SP, Lew HL; JRRD 2007; 44 (7) :929-936

• Investigated the occurrence of sensorimotor vision deficits on patients at their center whether symptomatic or not and then compared blast-related TBI to non-blast-related TBI 59


• Goodrich et al. JRRD 2007 –RESULTS:

Common Deficits Total TBI sample (n=46)

Blast-related TBI (n=21)

Non-Blast-related TBI (n=25)

Convergence 30.4% 23.8% 36%

Accommodation 21.7% 23.8% 20%

Saccades/ pursuit

19.6% 4.8% 32%

60




• RECENT STUDIES –reporting on non-selected patient samples with TBI

• Cockerham GC, Goodrich GL, Weichel ED, Orcutt JC, Rizzo JF, Bower KS and Schuchard RA; JRRD 2009 46(6): 811-818

• Compared the occurrence of vision dysfunctions for in-(n=108) versus out-(n=125) patient TBI.

61

Clinical Research on Vision and TBI OCURRENCE OF OCULAR MOTILITY (INCLUDING ACCOMMODATIVE) DEFICITS

• Cockerham et al., JRRD 2009 -RESULTS:

Common Vision Deficit In-patient TBI (n=108)

Out-patient TBI (n=125)

Strabismus 32% 8%

Accommodative insufficiency

31% 47%

Convergence insufficiency 40% 48%

Pursuit/saccade deficits 29% 23%

Diplopia 19% 6%

62


• Beneficial to know that when evaluating patients in a non-selected, TBI sample, over 20% of patients may present with symptoms/signs of deficits of:

• Convergence (36-48%)

• Accommodation (20-47%)

• Saccades/pursuit (23-32%)

63

Clinical Research on Vision and Concussion: Application of Saccadic Testing in Sideline Concussion Evaluation

• At least 10-15 papers since 2010 have been published demonstrating that the King-Devick test is effective at identifying neurologic deficits following concussion:

• Saccadic eye movement deficits

• Associated impairment of visual attention

• The simplicity, rapidity, validity, and reliability of the test lend itself for use as part of sideline testing for concussion

64

Clinical Research on Vision and TBI TREATMENT OF OCULAR MOTILITY (INCLUDING ACCOMMODATIVE) DEFICITS

• Doble JE, Feinberg DL, Rosner MS, Rosner AJ (2010) Identification of binocular vision dysfunction (vertical heterophoria) in traumatic brain injury patients and effects of individualized prismatic spectacle lenses in the treatment of postconcussive symptoms: a retrospective analysis. Physical Medicine and Rehabilitation 2010 Apr;2(4):244-53.

• Identified a series of patients with TBI who had vertical deviations. They gave a survey pre- and post-prescribing prism glasses and found a 71.8% reduction in symptoms with the prism glasses.

65

Clinical Research on Vision and TBI: TRAINING OF OCULAR MOTILITY

(INCLUDING ACCOMMODATIVE) DEFICITS

• Ciuffreda KJ, Rutner D, Kapoor N, Suchoff IB, Craig S, Han ME (2008). Vision therapy for oculomotor dysfunctions in acquired brain injury: a retrospective analysis. Optometry, 79:18-22.

• PURPOSE: To report the efficacy of conventional in-office vision therapy in in our selected, visually-symptomatic, out-patient sample with TBI (n=33) and CVA (n=7).

66





• Ciuffreda et al., Optometry, 2008- METHODS: The patient sample included those who had started and completed their vision therapy in the proposed time period (10/2000 through 10/2003):

• 33 (out of 160) persons with TBI

• Symptoms and signs noted for each subgroup, with some patients having multiple symptoms or signs.

• Success=reduction of at least 1 primary symptom and normalization of at least 1 clinical sign.

67



• Ciuffreda et al., Optometry 2008-RESULTS:

• 30/33 of those with TBI improved with vision therapy

Sub-

group

Total

completing

vision

therapy

Total

improving

after vision

therapy

Number of sessions

10-14 15-20 21-25 26-30

TBI 33 30 4 7 10 12

68



Vision Symptom # TBI reporting the

symptom

Ocular motility difficulty when reading 27

Eyestrain 18

Diplopia (at near more so than far

viewing distances)

18

Headaches 11

Visual fatigue 5

Near blur 3

Sliding together of text words 1

Increased sensitivity to visual motion 1

Avoidance of near tasks 1

69



Vision Sign #TBI reporting

the sign

Receded near point of convergence 23

Abnormal DEM test 23

Reduced near positive relative vergence

(NBO) range

16

Reduced near vergence ranges 9

Binocular suppression during testing 3

Impaired versional ocular motility 2

Nausea during testing 1 70



# of vision

symptoms

Pre-Therapy (# TBI

reporting

symptoms)

Post-Therapy (#

TBI reporting

symptoms)

5 1 0

4 7 0

3 11 1

2 11 1

71



# of vision

signs

Pre-Therapy(# of

TBI manifesting

vision signs)

Post-Therapy(# of

TBI manifesting

vision signs)

3 12 1

2 15 1

1 2 1

72



Clinical Research on Vision and ABI: TREATMENT OF OCULAR MOTILITY (INCLUDING ACCOMMODATIVE) DEFICITS

• Kapoor N, Ciuffreda KJ, Han Y. Arch Phys Med Rehab 2004.

• two case reports (one TBI and one CVA) showing pre-/post-therapy objective eye movement recordings and subjective symptoms.

• Ciuffreda KJ, Han Y, Kapoor N, et al. NeuroRehabilitation 2006.

• a series of 9 TBI and 5 CVA showing pre-/post-therapy objective eye movement recordings and subjective symptoms.


• Doble JE, Feinberg DL, Rosner MS, Rosner AJ. Identification of binocular vision dysfunction (vertical heterophoria) in traumatic brain injury patients and effects of individualized prismatic spectacle lenses in the treatment of postconcussive symptoms: a retrospective analysis. Physical Medicine and Rehabilitation 2010 Apr;2(4):244-53.

73

Clinical Research on Vision and TBI: TREATMENT OF OCULAR MOTILITY (INCLUDING ACCOMMODATIVE) DEFICITS

• Thiagarajan P, Ciuffreda KJ. Effect of oculomotor rehabilitation on vergence responsivity in mild traumatic brain injury. J Rehabil Res Dev. 2013;50(9):1223-40.

• Thiagarajan P, Ciuffreda KJ. Effect of oculomotor rehabilitation on accommodative responsivity in mild traumatic brain injury. J Rehabil Res Dev. 2014;51(2):175-91.

• Thiagarajan P, Ciuffreda KJ. Versional eye tracking in mild traumatic brain injury (mTBI): effects of oculomotor training (OMT). Brain Inj. 2014;28(7):930-43.

74

Clinical Research on Vision and TBI: TREATMENT OF OCULAR

MOTILITY (INCLUDING ACCOMMODATIVE) DEFICITS

• Bigsby K, Mangine RE, Clark JF, Rauch JT, Bixenmann B, Susaret AW, Hasselfeld KA, Colosimo AJ. Effects of postural control manipulation on visuomotor training performance: comparative data in healthy athletes. The International Journal of Sports Physical Therapy, Volume 9, Number 4, August 2014, Pages 436-446.

• Clark JF, Graman P, and Ellis JK. Depth perception improvement in collegiate baseball players with vision training. Optometry & Visual Performance, 2015, Volume 3, Issue 2, pages 106-115.

• Clark JF, Graman P, Ellis JK, Mangine RE, Rauch JT, Bixenmann B, Hasselfeld KA, Divine JG, Colosimo AJ, and Myer GD. An exploratory study of the potential effects of vision training on concussion incidence in football. Optometry & Visual Performance, 2015, Volume 3, Issue 2, pages 116-125.

• Clark JF, Colosimo A, Ellis JK, Mangine R, Bixenmann B, Hasselfeld K, Graman P, Elgendy H, Myer G, Divine J. Vision training methods for sports concussion mitigation and management. J Vis Exp. 2015 May 5;(99): e52648. doi: 10.3791/52648.

75

Clinical Research on Vision and TBI OCULAR MOTILITY


• SO WHAT?

• Beneficial to know that vision therapy (for those with TBI) can:

• reduce vision symptoms

• normalize vision signs using standard clinical testing AND objective eye movement testing

76


• The Ciuffreda et al. 2007 retrospective, Goodrich et al. 2007, and Cockerham et al. 2009 papers:

• Concurred (in general) with a report of an elevated occurrence in TBI (relative to a normal, non-neurologically-impaired reference population) of ocular motor deficits (convergence insufficiency, deficits of saccades, accommodative insufficiency)

77


• In the future, investigate efficacy of treatment (with vision therapy) for accommodative/ocular motility conditions using:

• Larger sample sizes

• Multicenter

• Non-selected patient samples (civilian and/or military) should involve larger samples of:

• TBI

• Concussion

78



TYPICAL VISION DEFICITS FOLLOWING CONCUSSION/mTBI

79

Optical Management Options • Place patient with single vision spectacle lenses due to lens

design and try to address small magnitudes of:

• Astigmatism

• Hyperopia

• Anisometropia-contact lenses can be helpful

• Esophoria/Exophoria/Hyperphoria/Fixation disparity

• Increased sensitivity to light is often present in this patient population. Consider prescribing a light tint and/or anti-reflective coating

• *When these optical issues are not compensated for, visual and visual-vestibular symptoms are worse*

80

Rehabilitation Treatment Options

• Habituation/Adaptive

• Compensatory

• Restorative

• Some combination of the above 81

Common Vision Deficits/Their Primary Associated Symptoms Evident Following Concussion/mTBI Deficit of: Primary Associated Symptom:


Tear Film Integrity Distorted clarity/gritty sensation, which varies

with blinking

Versional Ocular

Motility

Slower, less accurate reading /difficulty


targets

Vergence Ocular

Motility

Constant/intermittent eyestrain / diplopia


Visual-Vestibular

Interaction

Disequilibrium exacerbated in multiply,

visually-stimulating environments



visual-spatial processing 82

Accommodation: Neurological Correlates

• Pre-motor neural components:

• mediated by the autonomic nervous system (ANS)

• primarily the parasympathetic system to stimulate or increase the accommodative response

• secondarily the sympathetic system to inhibit or reduce the accommodative response 83


• Retinal cones stimulated by defocus blur

• Summated blur signals transmitted through magnocellular layer of lateral geniculate nucleus (LGN) to primary visual cortex (V1)

• Contrast-related neurons in V1 alter signal and send signal to parieto-temporal (PT) area to the Edinger-Westphal (EW) nucleus in the pre-tectum

• At the EW nucleus, autonomic input (from parasympathetic fibers) is received to form the combined motor command 84




• Combined autonomic and motor neurons travel via the oculomotor nerve from the EW nucleus to the ciliary ganglion (where sympathetic fibers join CN III without synapsing) to the short ciliary nerve and then to the ciliary muscle

• End result:

• a change in the contraction of the ciliary muscle

• consequent change in crystalline lens shape and effective state of accommodation

85

Accommodative Deficits: Associated Symptoms

• Constant/intermittent blur at far or near

• Intermittent blur due to infacility

• Near-far blur

• Far-near blur

• Symptoms associated with near vision tasks (i.e., reading/ using computer/ handicrafts):

• Eyestrain/ eye fatigue/browaches

• Dizziness/nausea/motion sickness 86

Accommodative Deficits: Compensatory Treatment Options

• Lenses may be prescribed for near vision tasks either:

• In lieu of restorative accommodative training

• In conjunction with restorative accommodative training

• Following restorative accommodative training 87

Accommodative Deficits: Restorative Treatment Options

• Equalize accommodative amplitudes

• Work on improving the weaker aspect of focusing; i.e., if a patient cannot:

• Relax the accommodative state, work on near-far focusing

• Increase the accommodative state, work on far-near focusing

88

Accommodative Deficits: Restorative Treatment Options

• Work on maintaining the ability to:

• Rapidly change focus on command and repeatedly over time

• Sustain focus for extended periods of time

• Training may be performed:

• Using lenses

• In free space regarding targets at different viewing distances 89







targets



Visual-Vestibular

Interaction








Dry Eye: Etiology

OLD THEORY- Dry eye in TBI is related to:

• Poor lid hygiene

• Side effects of anti-depressant, anti-hypertensive, and anti-anxiety medications

• Prior refractive surgery, contact lens wear, facial nerve, and/or meibomian gland dysfunction

NEW THEORY (Cockerham et al., 2013 in Ocular Surface) -Dry eye in TBI:

• Is not apparently associated with meds or prior issues

• Still requires assessment and should almost be viewed as a new condition

• May persist for months or years post-TBI

Cockerham GC, Lemke S, Glynn-Milley C, Zumhagen L, and Cockerham KP.

(2013) Visual performance and the ocular surface in traumatic brain injury. Ocul

Surf Jan 11 (1): 25-34.

91

Dry Eye Associated Symptoms

• Intermittent lack of visual clarity that varies with blinking

• “gritty”, foreign body sensation

Treatment Options (depending upon the nature of dry eye):

•Mild dry eye, over the counter artificial tears TID/QID OU (in conjunction with lid hygiene) may suffice

•Moderate to severe dry eye: a) liquigels (Refresh,

Systane, etc.) b) Restasis (if autoimmune

component evident, as with Sjogren’s)

c) insertion of punctal plugs

92

Common Vision Deficits/Their Primary Associated Symptoms Evident Following Concussion/mTBI







targets



Visual-Vestibular

Interaction





visual-spatial processing

93

Versional Ocular Motility: Neurological Correlates

• Integrated pre-motor neural activity occurs in similar areas for vertical saccades, horizontal saccades, and horizontal pursuit:

• Frontal lobe (frontal eye fields, supplemental eye fields, dorsolateral prefrontal cortex, and cingulate eye field)

• parietal lobe

• basal ganglia

• superior colliculus

• cerebellum

94

Versional Ocular Motility: Neurological Correlates • Vertical Saccades pre-motor neural area:

• rostral mesencephalon

• Horizontal pre-motor neural components:

• saccade: excitatory burst neurons in the paramedian pontine reticular formation (PPRF)=> project directly to the oculomotor neuron for horizontal saccades

• pursuit: pursuit neurons in the medial vestibular nuclei and prepositus hypoglossi => project directly to the oculomotor neuron for horizontal pursuit 95

Versional Ocular Motility: Neurological Correlates

• Integrated pre-motor neural components for fixation include:

• frontal eye fields

• supplemental eye fields

• parietal eye fields

• right prefrontal cortex (for attention)

• right posterior parietal cortex (for attention)

96



Versional Ocular Motility: Associated Symptoms

• Reading-related difficulties

• Slower reading speed

• Loss of place/skipping or missing lines or words

• Re-reading/misreading words or lines

• Print seems to “swim” / “jumble” on the page

• Difficulty shifting to/tracking objects

• Dizziness/nausea/motion sickness

97

Versional Ocular Motility Deficits: Compensatory/Adaptive Treatment Options

• Encourage a typoscopic approach (i.e., create an aperture/window highlighting the text of regard while obscuring non-pertinent text)

98

Versional Ocular Motility Deficits: Restorative Treatment Options

• Basic scanning and searching exercises

• Concentrate on accuracy

• Gradually build up speed

• Text size is often not the issue:

• The space between the lines is often more critical.

99

Versional Ocular Motility Deficits: Restorative Treatment Options

• Examples of versional oculomotor restorative treatment techniques:

• Small-angle (i.e., Ann Arbor/Michigan tracking, pencil/paper tracings and mazes, Pegboard Rotator, Groffman computer scan/search/coding/ perceptual speed)

• Medium-angle (i.e., Hart Chart, Pegboard Rotator, Keystone Rotator, Groffman computer pegboard/visual motor integration/visual tracings)

• Large-angle (i.e., 4-corner saccades, Keystone Rotator) 100

Versional Ocular Motor Deficits: Restorative Treatment Options

101

Versional Ocular Motor Deficits: Restorative Treatment Options

102









targets



Visual-Vestibular

Interaction






Vergence Ocular Motility: Neurological Correlates

• Pre-motor neural innervation lies in the mesencephalic reticular formation, with three of the better-studied types of vergence cells being:

• tonic: respond to change in vergence angle

• burst: respond to change in vergence velocity

• burst-tonic: respond to changes in both vergence angle and velocity

104

Vergence Ocular Motility: Neurological Correlates

• Pre-motor neural innervation (continued):

• medial longitudinal fasciculus

• cerebellum

• frontal eye fields

• Role in generating vergence response of the abducens and oculomotor interneurons: not clearly elucidated

105

Vergence Ocular Motility Deficits: Associated Symptoms

Diplopia/overlapping images/eyestrain which is eliminated with monocular occlusion

• Constant or intermittent

• At far or near

• More evident in one position of gaze than another

• After a brief (<10-15 minutes) time period of performing a visually-based task

Closing one eye or squinting when performing a prolonged visual task

Avoidance of prolonged vision-related tasks

Dizziness/nausea/motion sickness

106

Vergence Ocular Motor Deficits: Compensatory Treatment Options

To compensate for constant diplopia, decompensated phoria, or fixation disparity, incorporate:

fusional prism, if possible

◦ varying degrees of occlusion may be required if fusion is

not achievable: selective (to insure peripheral fusion, while inhibiting

central simultaneous perception)

graded (i.e., using Bangerter foils or other such translucent materials to blur/degrade image)

complete (i.e., with an opaque eyepatch) 107

Vergence Ocular Motor Deficits: Restorative Treatment Options • Once person presents with fusion (even if

intermittent), then:

• Stabilize vergence in primary gaze (ramp and step) at far and near viewing distances

• Work on facility and sustainability of fusional vergence at far and near viewing distances

108



Vergence Ocular Motor Deficits: Restorative Treatment Options

• Integration with other modalities is important, including:

• Visual motor integration

• Auditory visual integration

109







targets



Visual-Vestibular

Interaction






Vestibular Function

• Afferent systems

• Vestibular

• Somatosensory/ proprioception

• Visual- which is a significant contributing component!

• Efferent systems

• Musculoskeletal

• Ocular motor

111

Visual-Vestibular Interaction

• CN III and VI communicate with CN VIII via the medial longitudinal fasciculus to generate the horizontal vestibulo-ocular reflex (VOR, also referred to as gaze stabilization)

112

Visual-Vestibular Interaction: Purpose

VOR

◦ Stabilizes the visual world while the head is in motion

◦ Is utilized in most vestibular rehabilitation regimens

◦ May be impaired in the presence of ocular motor deficits

Improving and stabilizing any ocular motor deficit may facilitate vestibular rehabilitative progress

113

Videonystagmography (VNG)

• A series of objective recordings to evaluate/aid in diagnosing patients who report dizziness or other balance problems

• Uses goggles that can detect the smallest eye movements using infrared cameras

• Computer analyzes video images to track movements of the pupil

114



Hearing Evaluation

• Certain vestibular conditions are accompanied by auditory symptoms

• Need to know if patient experiences:

• Hearing loss (unilateral, asymmetric bilateral, symmetric bilateral, progressive, or fluctuating)

• Aural fullness (constant or intermittent, unilateral, asymmetric bilateral, symmetric bilateral)

• Tinnitus (constant or intermittent, unilateral, asymmetric bilateral, symmetric bilateral)

115

Visual-Vestibular Dysfunction: Associated Vision Symptoms

Similar for vergence and versional ocular motility, emphasizing:

1)Vestibular symptoms (often accompanied by nausea, vomiting, and/or headache), such as:

a) Dizziness

b)Lightheadedness

c) Vertigo

116

Visual-Vestibular Dysfunction: Associated Vision Symptoms

• Similar for vergence and versional ocular

motility, emphasizing:

2) *Increased dizziness and/or

disequilibrium in/sensitivity to multiply-

visually stimulating environments.

Examples of stimulating

environments/tasks include:

a) Supermarkets

b)Malls

c) Motion sickness in a moving vehicle

d)Scrolling on a computer

e)Watching television or movies

117

Visual-Vestibular Dysfunction: Associated Vision Symptoms • Similar for vergence and versional

ocular motility, emphasizing:

3) Difficulty with eye/head dissociation

4) Foreground/background discrimination difficulty

NOTE: ask about hypertension, heart

problems, sinus problems, tinnitus,

changes or asymmetry in audition, as well

as aural fullness or pain.

118

Versional Ocular Motility Deficits and Vestibular Dysfunction: Treatment Options

• Same as for versional oculomotor deficits without vestibular dysfunction, except:

• Start at a slower velocity and lower number of repetitions of saccades and pursuit, while patient is seated and minimal targets in the background

• Systematically and gradually increase the:

• velocity of the ocular motility

• number of targets in the background

• Build to having the patient marching in place while performing these tasks in front of a multiply, visually-stimulating background

119

Vergence Ocular Motility Deficits and Vestibular Dysfunction: Treatment Options

• Same as for vergence ocular motility deficits without vestibular dysfunction, except:

• After stabilizing fusional vergence in primary gaze under static conditions, then stabilize:

• vergence 30 degrees right gaze (ramp, step) and then 30 degrees left gaze (ramp, step)

• dynamic vergence while the patient is performing a slow horizontal VOR (approximately 40-60 rotations per minute)

120



Vergence Ocular Motility Deficits and Vestibular Dysfunction: Treatment Options

• After stabilizing horizontal fusional vergence and a slow horizontal VOR, then stabilize:

• vergence 25 degrees upgaze (ramp, step) and then 25 degrees downgaze (ramp, step)

• dynamic vergence while the patient is performing a slow vertical VOR (approximately 40-60 rotations per minute)

121

Vergence Ocular Motor Deficits and Vestibular Dysfunction: Treatment Options

122




with blinking



targets



Visual-Vestibular

Interaction






Photosensitivity: Neurological Correlates • Elevated light sensitivity (to all lights OR specifically to

fluorescent lights) despite unremarkable ocular health:

• No evident ocular inflammation or infection

• Current hypothesis for neural mechanism:

• Cortical or subcortical substrates resulting in anomalous dark and light adaptation and associated filtering/processing deficits when in very bright or very dim lighting

• Precise location of neural substrate: not yet localized

124

Photosensitivity

Associated Symptoms

• Increased light sensitivity

• General- to all types of light

• Selective- to fluorescent lighting

• more common in the “dizzy” patient

• may be related to anomalous thresholds to critical flicker fusion and anomalous coherent motion

Compensatory

Treatment Options

• Incorporation of tints with spectacle correction (30-40% tint for indoors, 80-85% tint for outdoors) for photosensitivity that is:

• General to all lights (using either brown or gray tints)

• Selective/specific for fluorescent lighting (using either FL41, blue or gray tints)

• Wearing brimmed hats/caps

125

Common Vision Deficits/Their Primary Associated Symptoms Evident Following Concussion/mTBI




with blinking



targets



Visual-Vestibular

Interaction








Visual Processing: Neurological Correlates

More than just occipital cortex

Multiple areas of the brain with two principal, parallel interacting pathways:

◦ Ventral stream (a.k.a. the “what is it?”)

◦ Dorsal stream (formerly the “where is it?” or “how is it?”)

127

Ventral Stream

Pathway • Ventral stream pathway:

• V1 in the occipital cortex moving anteriorly through V2, the ventral posterior aspect of V3, V4, and finally reaching the posterior inferior temporal lobe for processing

• Changes in ventral stream processing directed by the ventral lateral prefrontal cortex (VLPFC)

Purpose Uses a representational system

that is rich and detailed, but not precise metrically, for: • form perception • object identification (i.e.,

examines the visual array and identifies different objects in the scene)

128

Dorsal Stream

Pathway ▶V1 in the occipital cortex moving

anteriorly through V2, the dorso-medial area of V3, the middle temporal area (V5/MT), and finally reaching the parietal lobe for final processing.

▶Changes in dorsal stream processing directed by the dorso-lateral prefrontal cortex (DLPFC)

Purpose ▶Uses precise egocentric coding

of location & orientation of goal object for:

• spatial representation via the inferior parietal lobule

• visually-guided action and motion perception of objects, as well as ocular and limb motility, in the superior parietal lobule

129

Visual Processing: Dorsal-Ventral Stream Mis-communication

• Example in which patient presents with blur, eyestrain, and difficulty tracking when reading/ambulating/using a computer:

• Unremarkable (involves more ventral stream processing):

• visual acuity

• perimetry

130

Visual Processing: Dorsal-Ventral Stream Mis-communication • Example in which patient presents with blur, eyestrain, and

difficulty tracking when reading/ambulating/using a computer:

• Impaired ocular motility (involves more dorsal stream processing):

• vergence, accommodation

• pursuit

• saccades

• fixation

• Sometimes, the patient has difficulty computing the location of the object in visual space (dorsal stream issue), which impedes basic ocular motility (i.e., vergence, accommodation, pursuit, saccades, fixation)

131

Summary The purpose of today’s presentation was to increase familiarity

and understanding with respect to:

1) Why sensorimotor vision function may be impaired following concussion/mTBI

2) The members of the inter-professional health care management team

3) The vision provider’s associated role in managing such vision deficits. To find an optometrist specializing in neuro-optometric rehabilitation near you:

www.covd.org

www.nora.cc

132

http://www.covd.org/

http://www.nora.cc/



Summary • The purpose of today’s presentation was to increase familiarity

and understanding with respect to the:

4) behavioral and visual considerations when evaluating patients with concussion/mTBI

5) high-yield vision examination for patients with mTBI/concussion and evidence-based medicine support regarding the occurrence of and treatment for vision problems

6) typical residual vision disturbances (amenable to non-surgical treatment interventions) evident following concussion/mTBI along with:

neurological correlates

associated symptoms

possible treatment options

133

Some (not all!) Evidence-Based References For Vision and Rehab

134

Accommodation: Relevant Publications


Ciuffreda KJ, Rutner D, Kapoor N, Suchoff IB, Craig S, Han ME (2008). Vision therapy for oculomotor dysfunctions in acquired brain injury: a retrospective analysis. Optometry, 79:18-22.

Green W, Ciuffreda KJ, Thiagarajan P, Szymanowicz D, Ludlam DP, Kapoor N. (2010) Accommodation in mild traumatic brain injury. Journal Rehabilitation Research and Development 47(3):183-200.

Greenwald, BD, Kapoor N, Singh AD. (2012) Visual impairments in the first year

after traumatic brain injury. Brain Injury 26(11):1338-59. Thiagarajan P, Ciuffreda KJ. Effect of oculomotor rehabilitation on

accommodative responsivity in mild traumatic brain injury. J Rehabil Res Dev. 2014;51(2):175-91.

135

Clinical Research on Vision and Concussion: Saccadic Function: Sideline Testing for Concussion

• Kutcher JS, Giza CC. (2011) Sideline assessment of sports concussion: the lure of simplicity. Neurology 76: 1450-1.

• King D, Clark T, Gissane C. (2012) Use of a rapid visual screening tool for the assessment of concussion in amateur rugby league: a pilot study. J Neurol Sci 320: 16-21.

• King D, Brughelli M, Hume P, and Gissane C. (2013) Concussions in amateur rugby union identified with the use of a rapid visual screening tool. J Neurol Sci 326: 59-63. 136

Clinical Research on Vision and Concussion: Saccadic Function: Sideline Testing for Concussion

• Galetta MS, Galetta KM, McCrossin J, Wilson JA, Moster S, Galetta SL, and Balcer LJ, Dorshimer GW, and Master CL. (2013) Saccades and memory: baseline associations of the King-Devick and SCAT2 SAC tests in professional ice hockey players. J Neurol Sci 328: 28-31.

• King D, Brughelli M, Hume P, and Gissane C. (2014 epub ahead of print) Assessment, management and knowledge of sport-related concussion: systematic review. Sports Med Jan 9

137

Versional Ocular Motility: Relevant Publications

• Kapoor N, Ciuffreda KJ, and Han Y. (2004) Oculomotor rehabilitation in acquired brain injury: a case series. Arch Phys Med Rehabil, 85(10): 1667-1678.

• Ciuffreda KJ, Han Y, Kapoor N, and Ficarra AP (2006) Oculomotor rehabilitation for reading in acquired brain injury. NeuroRehabil, 21(1): 9-21.

• Ciuffreda KJ, Kapoor N, Rutner D, Suchoff IB, Han ME, Craig S (2007). Occurrence of oculomotor dysfunctions in acquired brain injury: a retrospective analysis. Optometry, 78: 155-61.


• Thiagarajan P, Ciuffreda KJ. Versional eye tracking in mild traumatic brain injury (mTBI): effects of oculomotor training (OMT). Brain Inj. 2014;28(7):930-43. 138



Versional Ocular Motility: Relevant Publications

• Bigsby K, Mangine RE, Clark JF, Rauch JT, Bixenmann B, Susaret AW, Hasselfeld KA, Colosimo AJ. Effects of postural control manipulation on visuomotor training performance: comparative data in healthy athletes. The International Journal of Sports Physical Therapy, Volume 9, Number 4, August 2014, Pages 436-446.

• Clark JF, Graman P, and Ellis JK. Depth perception improvement in collegiate baseball players with vision training. Optometry & Visual Performance, 2015, Volume 3, Issue 2, pages 106-115.

• Clark JF, Graman P, Ellis JK, Mangine RE, Rauch JT, Bixenmann B, Hasselfeld KA, Divine JG, Colosimo AJ, and Myer GD. An exploratory study of the potential effects of vision training on concussion incidence in football. Optometry & Visual Performance, 2015, Volume 3, Issue 2, pages 116-125.

• Clark JF, Colosimo A, Ellis JK, Mangine R, Bixenmann B, Hasselfeld K, Graman P, Elgendy H, Myer G, Divine J. Vision training methods for sports concussion mitigation and management. J Vis Exp. 2015 May 5;(99): e52648. doi: 10.3791/52648.

139

Vergence Ocular Motility: Relevant Publications


Ciuffreda KJ, Rutner D, Kapoor N, Suchoff IB, Craig S, Han ME (2008). Vision therapy for oculomotor dysfunctions in acquired brain injury: a retrospective analysis. Optometry, 79:18-22

Thiagarajan P, Lakshminarayanan V, Bobier WR. (2010) Effect of vergence adaptation and positive fusional vergence training on oculomotor parameters. Optom Vis Sci 87 (7): 487-93.

Szymanowicz D, Ciuffreda KJ, Thiagarajan P, Ludlam DP, Green W, Kapoor N. (2012) Vergence in mild traumatic brain injury: a pilot study. Journal Rehabilitation Research and Development 49 (7): 1083-1100.

Thiagarajan P, Ciuffreda KJ. Effect of oculomotor rehabilitation on vergence responsivity in mild traumatic brain injury. J Rehabil Res Dev. 2013;50(9):1223-40.

140

Visual-Vestibular Dysfunction: Relevant Publications

• Bronstein AM. (2004) Vision and vertigo: some visual aspects of vestibular disorders. Journal of Neurology 251:381-387.

• Bucci, M.P., Kapoula, Z., Yang, Q., Wiener-Vacher, S., & Bremond-Gignac, D. (2004). Abnormality of vergence latency in children with vertigo. Journal of Neurology, 251, 204-213.

• Leigh RJ, Zee DS. (2006) The Neurology of Eye Movements, 4th Ed. New York: Oxford University Press.

• Chandrasekhar S, Kapoor N (2007) Neuro-optometric evaluation and rehabilitation as a useful adjunct in the management of the complex dizzy patient. Annual meeting of the American Neurotology Society in San Diego, CA April 28, 2007.

141

Visual-Vestibular Dysfunction: Relevant Publications

• Sambur I, Chandrasekhar S, Kapoor N (2010) Migraine-associated dizziness: neuro-optometric findings and treatment. Annual meeting of the American Neurotology Society in Las Vegas, NV on May 2, 2010.

• Kapoula Z, Gaertner C, Yang Q, Denise P, Toupet M (2013) Vergence and Standing Balance in Subjects with Idiopathic Bilateral Loss of Vestibular Function. PLoS ONE 8(6): e66652.

• Cohen AH. Vision rehabilitation for visual-vestibular dysfunction: The role of the neuro-optometrist. NeuroRehabilitation 32 (2013) 483–492

142

Visual Processing Relevant Publications

Lowell L, Cohen AH, Kapoor N. (2010) Optometric management of visual sequelae of frontal lobe-related traumatic brain injury. Journal of Behav Optom 21(1): 3-11.

Iskander D, Cohen AH, Kapoor N. (2011) Optometric management of a patient with parietal lobe injury. Journal of Behav Optom 21(6): 143-149.

Chang A, Cohen A.H., Kapoor N (2013) Top-down visual framework for optometric vision therapy for those with traumatic brain injury, Optometry and Visual Performance: Vol. 1, Issue 2, 82-93

Kravitz D, Saleem KS, Baker CI, Mishkin M. A new neural framework for visuospatial processing. Nature Reviews volume 12. April 2011.

143

Dry Eye: Relevant Publications

• Cockerham GC, Lemke S, Glynn-Milley C, Zumhagen L, and Cockerham KP. (2013) Visual performance and the ocular surface in traumatic brain injury. Ocul Surf Jan 11 (1): 25-34.

• Han ME, Craig SB, Rutner D, Kapoor N, Ciuffreda KJ, and Suchoff IB (2008) Medications prescribed to brain injury patients: a retrospective analysis. Optometry, 79: 252-8.

• Rutner D, Kapoor N, Ciuffreda KJ, Craig S, Han ME, Suchoff IB (2006) Occurrence of ocular disease in traumatic brain injury in a selected sample: a retrospective analysis. Brain Injury, 20 (10): 1079-86. 144



Photosensitivity: Relevant Publications

• Du T, Ciuffreda KJ, and Kapoor N. (2005) Elevated dark adaptation thresholds in traumatic brain injury. Brain Injury 19: 1125-38.

• Chang TT, Ciuffreda KJ, and Kapoor N. (2007) Critical flicker frequency and related symptoms in mild traumatic brain injury. Brain Injury 21: 1055-1062.

• Schrupp L, Ciuffreda K, Kapoor N. (2009) Foveal versus eccentric retinal critical flicker frequency in mild traumatic brain injury. Optometry, 80 (11): 642-650.

• Patel R, Ciuffreda KJ, Tannen B, Kapoor N. (2011) Elevated coherent motion thresholds in mild traumatic brain injury. Optometry 82 (5): 284-9.

145

Seminal References • Ciuffreda KJ, Kapoor N, Rutner D, Suchoff IB, Han ME, Craig S (2007).

Occurrence of oculomotor dysfunctions in acquired brain injury: a retrospective analysis. Optometry, 78(4): 155-61.


• Cockerham GC, Goodrich GL, Weichel ED, Orcutt JC, Rizzo JF, Bower KS and Schuchard RA. (2009) Eye and visual function in traumatic brain injury. JRRD, 46(6): 811-818.

• Convergence Insufficiency Treatment Trial Study Group (2008) Randomized clinical trial of treatments for symptomatic convergence insufficiency in children. Arch Ophthalmol 126:1336-1349.

146

Seminal References • Craig SB, Kapoor N, Ciuffreda KJ, Suchoff IB, Han ME, and Rutner D. (2008)

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