rehabilitative optometric management

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Patients with traumatic brain injury (TBI) frequently exhibit visual symptomology characterised by diplopia,

intermittent blurriness, asthenopia, photophobia, and spatial disorientation. Clinical findings on this patient

population commonly include accommodative and binocular dysfunctions, refractive error shifts and

oculomotor dysfunction. Resultant visual field loss in many of these patients also impacts visual performance.

medications. She was taking Depacote(250mg) and Ibuprofen. Family history ofprevious eye or head trauma and the socialhistory was unremarkable.

Visual evaluationVisual evaluation of the patient is basedupon the standard optometric primary careexamination. However, tests are added toprobe pertinent areas for the TBI patient.Consequently, additional testing includescontrast sensitivity, Goldmann visual fieldsand perceptual/motor tests. Eletrodiagnostictesting, which can objectively documentvisual system deficit, including visuallyevoked cortical potential (VECP) and thefocal and full-field electroretinogram (ERG)are also performed. The VECP reflects notonly the neural representation of retinalfunction, but also indicates the functional

integrity of the visual pathway from theretina to and including the visual cortex. Thefull-field ERG represents an overall score ofretinal function and the focal ERG responseindicates macular receptor integrity. Theinitial clinical findings follow.

Ocular healthExternal examination: Unremarkable for

both eyes and adnexa.Pupils: Equal, round and respond to light

and accommodation; no Marcus Gunnresponse.

Slit lamp biomicroscopy: Unremarkable forboth eyes.

Intraocular pressures: 12mmHg OU byapplanation tonometry.

Dilated fundus examination: Cup/discration of 0.2 OU, normal macular andfoveal areas, intact vascualar tree OU, nopathology in retinal peripheries.

Rehabilitative optometric management

of a traumatic brain injury patient - Part 2

Lynn Fishman Hellerstein OD and Sieglinde Freed MS

We present a case history of a TBI patientwith associated visual dysfunction.Treatment modalities included lenses, prismsand rehabilitative vision therapy.Improvements in function and visualprocessing were noted and clinically

documented in the visual evaluation andvisual electrodiagnostics.

Traumatic Brain Injury (TBI) patients showmany types of visual dysfunction, includingaccommodative, binocular and oculomotordysfunction, refractive error shift and visualfield loss1-16. These visual problems havegreat impact on everyday functioning anddaily living activities, etc. Much of theliterature regarding visual dysfunction in TBIconcentrates on moderate to severe injuries.A patient with a mild TBI, as diagnosed by aneurologist or neuropsychologist, can showsignificant frunctional deficit, even in the

absence of loss of consciousness at time ofinjury17. In fact, whiplash or cervical straincan cause visual dysfunctions without adocumented TBI18-20. Mild TBI encompasses adiffuse injury which can disrupt the overallspeed, efficiency and integration of mentaland central nervous system function.

Optometrists have historically treated

functional and visual perceptual problems inchildren and adults2,12,21. Therefore, it isappropriate for optometric services to beincluded in the rehabilitation of the TBIpatient with visual problems1,2.

We present a case history of a patient

with a mild TBI. This 32-year-old whitefemale had been evaluated by severalophthalmologists prior to our evaluation.She received no vision treatment other thanthe recommendation to buy a pair ofmagnifiers at the drug store.

HistoryThe patient presented for examinationapproximately two and a half years after afall, which resulted in a mild traumatic braininjury, whiplash, and cervical strain, asdiagnosed by her neurologist. Shecomplained of frequent frontal headacheswhich occurred one or two times per week,

horizontal intermittent diplopia, blurredvision, motor function decrease, poorbalance, attention/concentration andorganisational deficits. She stated that sheexperienced difficulties with performance ofdaily tasks, i.e. grocery shopping, cookingand writing. General medical health wasunremarkable, with no known allergies to

Figure 1

Initial contrast

sensitivity

findings


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Visual acuityDistance: OD 20/20, OS 20/25.Near: OD 20/30, OS 20/60 at 16 inches.

It is important to note that by the end ofthe examination, the visual acuity of the lefteye decreased to 20/200.

Distance refractionStatic retinoscopy: OD +2.50 D and

OS +2.00 D.Subjective: There was a variable

acceptance from plano to +1.00 D (20/20)for the OD. The refraction of the OS wasplano (20/25-). Because of the variabilityin refraction, the patient was given+1.00 D spheres OU to wear for fiveminutes and then was retested. Delayedsubjective (gross findings) was OD +1.50

D (20/20), OS +1.00 D (20/25-).Cycloplegic testing utilising 1%cyclopentolate revealed: Retinoscopy: OD+2.50, OS +2.00 D. Subjective: OD+2.75 D (20/20), OS +2.25 D (20/25).

Sensorimotor examination Cover test distance: Orthophoria. Cover test near: 10 prism dioptres of

intermittent alternating exotropia. Nearpoint of convergence: 10/14. Distance vergences: Convergence

X/6/2, Divergence 12/6. Near vergences: Testing not possible

because of diplopia at near.

Accommodative status: Positive andnegative relative accommodation -testing not accomplished because ofdiplopia.

Dynamic near retinoscopy: OD variablereflex, +2.00 D to +3.00 D; PS +0.75D(dull reflex).

Flexibility: Inability to clear 2.00flipper, monocularly - binocular testingimpossible because of diplopia.

Cheiroscopic tracings, Van Ordent Star,and Brock String Testing: All of thesetests revealed fragile binocularintegration because of alternating centralto complete suppression.

Fixation disparity (utilising WessonFixation Disparity Card a: 8.6 to 12.9minutes of arc, exo deviation, withinstability and alternating suppression.While base-in prism reduced the exodeviation, the associate phoria could notbe determined because of the instabilityand suppressions.

Ocular motilities: Pursuits and saccadicfixations: Concomitant with fullexcursions in all fields of gaze, but withfrequent demonstrated tearing anddiscomfort during this testing andsaccades could not be performed withouthead movement.

Contrast sensitivity testingContrast sensitivity testing was performedutilising the Vistech CTS 6500 System b:Initial contrast sensitivity functionabnormalities was found to be subnormal in

low, middle and high spatial frequencies forboth eyes (Figure 1).

Visual perceptual/motor testingDevelopmental test of visual motorintegration c: The patient could adequatelycopy 21 of the 24 forms. The patient took aninordinate amount of time to complete thistest. Observations of the patients behaviourincluded blinking, squinting and bodyreadjustments to move closer and furtherfrom the paper.

Test of Visual Perceptual Skills d: Unable

to complete testing at the time due toocular discomfort and fatigue.

Localisation: The patient could notaccurately grasp or point to objects withinarms reach. Her grasp was consistentlyseveral inches behind the object.

Walking/balance: The patient neededassistance in walking long distances becauseof fatigue and poor balance. She could notwalk heel-toe on a straight line.

Goldmann visual field testingInitial Goldmann visual field testing resultsshowed a generalised constriction of the

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Figure 2a

Initial Goldmann visual field, OD

Figure 2b

Initial Goldmann visual field, OS


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peripheral isopters for both eyes utilising theIII/4e target. There was a homonymous,incongruous lower right quadrantanopsia withIII/4e, I/4e and I/2e target intensities. Therewas also baring of the physiological blindspoton the left side (Figures 2a and 2b).

Visual electrodiagnostictestingVisual electrodiagnistic testing wasperformed using pattern - reversalstimulation from a television monitor at anintensity of between 68 and 96 nit/seconds.Stimulations were performed binocularly and

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to each eye independently. The stimulussubtended a visual angle of 0-14 radiuswith a variety of check sizes from 1 56minutes to 11 minutes. The visually evokedcortical potential (VECP) was alwaysrecorded from both hemispheres usingstandard bi-polar linkage 02-C4 and 01-C3

and midline recording as well as using FpZto Cz to Oz. This technique allowslateralisation of the evoked potential overthe visual cortex contralateral to the fieldilluminated22-24. The resulting signal wasrecorded and averaged using computer andclinical averages.

Three trials of 100 rps were performed forthe purposes of waveform reproducibilityand to determine processing stability and

conduction quality in this patient. In thenormal VECP recording, multiple trialsgenerally reveal reproducible and consistentwaveform responses. TBI patients candemonstrate loss of conduction speed andquality over time in multiple trials. Thelatency was defined as a measure of thetime it takes for visual information to beprocessed from the eye to the visual cortex.The interwave amplitude represented thequality of conduction through the anteriorvisual pathways.

Initial VECP findings for this patientshowed normal waveform values for bothsides in the first trial. The second trial

showed P100 latency delays with decreasedinterwave amplitude responses for the leftside and normal latency values and adecreased interwave amplitude for the right.The third trial demonstrated no consistent ororganised waveform responses for the leftside and delays in P100 latency values andfurther decreased interwave amplituderesponses for the right (Figure 3). Full-fieldERG and focal ERG findings were found to beunremarkable for both eyes.

Diagnoses1. Mild traumatic brain injury, by history.2. Hyperopia.

3. Intermittent near exotropia.4. Accommodative dysfunction.5. Binocular dysfunction.6. Oculomotor dysfunction.7. Normal retinal and macular function.8. Homonymous, incongruous, lower right

quadrantanopsia.9. Abnormal conduction through the

anterior visual pathways. The abnormalitywas greater on the left side than theright.

ManagementWe prescribed +1.00D OU for distance. Equalspheres were prescribed because of the

variability in refraction and because thepatient was most comfortable with thisprescription. A near prescription of +2.00D,combined with two prism dioptres base-inOU, were given, based on near retinoscopyand patient acceptance. Because of logisticsand personal issues for the patient,rehabilitative vision therapy was commencedapproximately one year after initialexamination. Rehabilitative vision therapywas initiated on a one-time-per-week basis,with home therapy activities given. Thetherapy plan progressed from equalisingmonocualar oculomotor skills to improvingfusions vergences, increasing accommodativeflexibility and eliminating suppression. Inorder to improve ocular motor control, tasksrequiring proprioceptive responses wereutilised. Spatial awareness, localisation andbalance/movement activities were alsoemphasised. Yoked prisms, walking rails,

Figure 3

Initial VECP

findings

Figure 4

Follow-up

contrast

sensitivity

findings

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balance beams, and mini trampolines wereused cautiously to allow her to exploremovement through space under different

conditions and demands. Due to her balanceand movement difficulties, consultationswith an occupational therapist and referralto a physical therapist were made.Visualisation activities includingtachistoscope flash and parquetry blockseries were utilised. Once vision therapy wasinitiated, she was consistent in attendanceand worked well on home therapy activitieswith her husbands guidance and support.

Throughout the therapy, yoked prismswere investigated and found to be useful,especially in aiding localisation ability andspatial awareness. The yoked prisms arebased on number of factors, especially

central/peripheral processing, and are wornduring visual motor performances todetermine effectiveness21,25,26. Both distanceand near prescriptions were changed toinclude two prism dioptres of base-up yokedprisms.

Diagnostic re-evaluation approximatelyeight months after therapy revealed thefollowing: Improvement in subjectivesymptomology; less visual confusion andblurriness, less diplopia, and a decrease inheadache frequency and severity. Clinicalfindings at that time revealed the following:

Visual acuityDistance and Near: 20/20 consistently witheither eye or binocularly.

Sensorimotor examination Cover test distance: Orthophoria. Cover test near: 8-10 prism dioptres

exophoria. Nearpoint of convergence: 5/8 inches. Distance vergencies: Convergence

16/20/6, Divergence 10/6. Near vergences: Convergence 14/3,

Divergence 24/17. Accommodative status: Positive relative

accommodation 1.00 dioptre, Negativerelative accommodation 2.00 dioptre.

Contrast sensitivity testingFollow-up contrast sensitivity findingsshowed normal low spatial frequencyresponse, subnormal middle spatialfrequency responses and a high spatialfrequency response which was found to bewith normal limits for both eyes (Figure 4).

Goldmann visualfield testingSubsequent Goldmann visual field resultsdemonstrated negligible peripheral fieldconstriction using the III/4e targetintensity. The homonymous, incongruous,lower, right quadrantanopsia was still foundwith all target intensities (III4/e, I/4e,I/3e, and I/2e) but no baring of thephysiological blindspot was found for theleft eye (Figures 5a and 5b).

Visual electrodiagnostictestingVECP follow-up evaluation demonstrated firstand second trials to be within normal limitsfor both sides. Third trials showed loss ofP100 conduction with decreased interwaveamplitude responses for both sides. Findingsshowed waveform improvement whencompared to the initial VECP evaluation forthis patient (Figure 6). Retinal function wasfound to be unchanged and still withinnormal limits for both eyes.

Rehabilitative vision therapy wascontinued for another 18 months withsporadic interruptions due to patientcompliance problems. At the last optometric

progress evaluation, the patient reportedbeing able to read comfortably forapproximately 45 minutes. She can drive andperform most daily tasks. She stated thatshe is still unable to work outside the home,mainly due to her fatigue. She reports thather visual complaints have drasticallydecreased, but are more noticeable when sheis fatigued. The patient still utilises herdistance and near prescriptions.

ConclusionIt has been well-documented that visualsystem dysfunction is frequently found inpatients with TBI1-16. In-depth visionevaluation and examination are critical when

Figure 5a

Follow-up on Goldmann visual field, OD

Figure 5b

Follow-up on Goldmann visual field, OS

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assessing the injury extent to the visualsystem in this population. In patients withmild to moderate TBI, the probability ofchiasmal compressions or damage is low, butthe possibility of post-chiasmal and, moreusually, cortical damage is higher. Byrecording from right and left occiputsindependently, it is possible to identify post-chiasmal damage27,28. We found an initialbreakdown in visual processing in thispatient over three trials for each side withsubsequent improvement in follow-up

electrophysiological evaluation. This patientssubjective visual complaints had a correlate

Figure 6 Follow-up on VECP findings

in documented and verified VECP pathwayabnormalities. VECP findings demonstratedwaveform improvement on both sides afterapproximately eight months of rehabilitativevision therapy. VECP assessment of thispatient with TBI was of significant clinicaluse in determination of visual pathwayprocessing integrity.

The presented case history is consistentwith symptomology encountered in thispopulation. The term mild TBI is verymisleading and does not necessarily translate

to mild functional loss, as these injuriescan have a devastating impact on function.

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trauma on the visual system; the doctor ofoptometry as a member of therehabilitation team.J Am Optom Assoc,1992; 63:530-536.

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11. Beck RW. Ocular deviation after headinjury.Am Orthop J1985; 103-107.

12. Aksionoff EB, Falk NS. The differentialdiagnosis of perceptual deficits intraumatic brain injury patients.J AmOptom Assoc1992;63:554-558.

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1983; 3(1):43-48.14. Vogel MS. An overview of head trauma for

the primary care practitioner: Part 11 ocular damage associated with headtrauma.J Am Optom Assoc1992; 63:542-546.

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16. Fowler MS, Richardson AJ, Stein JF.Orthoptic investigation of neurologicalpatients undergoing rehabilitation.J BrOrthop 1991; 48.

17. Kay T. Minor head injury: an introductionfor professionals. National Head InjuryFound Inc., 1986; 1-12.

18. Burke JP, Orton HP et al. Whiplash and itseffect on the visual system. GrailsArchClin Exp Ophthalmol 1992; 230:335-339.

19. Wiesinger H, Guerry D. The ocular aspectsof whiplash. Virginia Med Monthly1962;89:165-168.

20. Oosterveid WJ, Kortschot HW, Kingma GG,et al. Electronystagmographic findingsfollowing cervical whiplash injuries.ActaOtolaryngol (Stockh) 1991; 111:201-205.

21. Berne SA. Visual therapy for the traumaticbrain-injured.J Optom Vis Devel., 12/90;21:13-16.

22. Blumhardt LD, Barrett G, Halliday AM. Theasymmetries of visual evoked potentials topattern reversal inone half field an ditssignificance for the analyses of visual fielddefects, Brit J Ophthal, 1977; 61:454-461.

23. Halliday AM, Harding GFA, Holder GF:Discussion of lateralisation of patternVECP in homonymous field defects. MTPPress: Evoked Potentials, 1980: 292-298.

24. Harding GFA. The use of the visual fieldpotential to flash stimuli in the diagnosisof visual field defects. Visual evoked

potentials in man: new developments.Oxford: Clarenden Press, 1987: 500-508.

25. Kaplan M. Verticaql yoked prisms. OptomExtension Prog., CII; 51:1.

26. Kraskin RA. Lens power in action. OptomExtension Prog., CII; 54-55:12.

27. Rubenstein MP, Harding GFA. The scalptopography of the human visual evokedsubcortical potential.Invest Ophthal Vis

Sci, 1980; 19:318-321.28. Rubenstein MP, Harding GFA. Components

of the visually evoked subcorticalpotential to flash stimulation in man inEEF and clinical neurophysiology. ExcerptaMedica.International Congress Series,1986:464-474.

Sourcesa. Wesson Fixation Disparity Card. University

Alabama at Birmingham, School ofOptometry.

b. Vistech Contrast Sensitivity Testing.Consultants, Inc., Dayton, Ohio, 1983.

c. Beery KE, Buktenica NA. The developmentaltest of visual motor integration. Cleveland,Ohio: Modern Curriculum Press, 1989.

d. Gardner MF. Test of visual perceptual skills(non-motor). Seattle, WA: Special ChildPublications, 1982.

Corresponding authorLynn Fishman Hellerstein, 7180 East OrchardRoad, Suite 103, Englewood, Co 80111, USA.

PermissionReprinted with permission from Hellerstein LF,Freed S. Maples WC. Vision profile of patients

with mild brain injury.Journal of the AmericanOptometric Association 1995;66:634-39.

It is also interesting to note that treatmentwas initiated approximatelytwo and a half years after injury and

eliminates spontaneous recovery as anexplanation for improvement in this patientsvisual system deficits. The treatment wasfound to yield improvement in visual andoverall functioning for this patient. Theimprovements were not only documented inoptometric clinical findings, but also in theelectrodiagnostic and contrast sensitivitytest results as well.

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