ICONIC EYECARE

Drugs

further metabolized to NO and the as primary choices or as an addition over and outflow resistance. Exp EyeRes. 2009; 88(4):676-682.
inactive 1,4-butanediol.45,46 NO to an established course of therapy 20. Tektas OY, Lutjen-Drecoll E. Structural changes of the tra-
reduces IOP by enhancing aqueous have shown great promise for reduc- becular meshwork in different kinds of glaucoma. Exp Eye Res.
outflow through the TM and SC. ing IOP in the setting of once-daily 2009;88(4):769-75.
Latanoprost acid, the active metabo- dosing with excellent safety profile. 21. Roy Chowdhury U, Hann CR, Stamer WD, Fautsch MP.
lite in latanoprost, increases the pres- Aqueous humor outflow: dynamics and disease. Invest Ophthal-
ence of matrix metalloproteinases Their ability to act on the conven- mol Vis Sci. 2015;56(5):2993-3003.
(MMPs). MMPs degrade collagen, tional and unconventional outflow 22. Overby DR, Zhou EH, Vargas-Pinto R, et al. Altered mecha-
specifically types I, III and IV. This mechanisms in addition to having nobiology of Schlemm’s canal endothelial cells in glaucoma.
degradation reduces outflow resis- other IOP-lowering mechanisms not Proc Natl Acad Sci USA. 2014;111(38):13876-81.
tance through the uveoscleral path- available with current topical treat- 23. Zhang M, Maddala R, Rao PV. Novel molecular insights into
way, ultimately lowering IOP.46 ment modalities makes them valu- RhoA GTPase-induced resistance to aqueous humor outflow
able and anticipated. ■ through the trabecular meshwork. Am J Physiol Cell Physiol.
The most notable clinical trial 2008;295(5):C1057-70.
for latanoprostene bunod was Dr. Rebar is coordinator of resi- 24. Brubaker RF. Introduction: three targets for glaucoma man-
Voyager.42 This Phase II clinical dency programs in Primary Care agement. Surv Ophthalmol. 2003;48(Suppl 1):S1-2.
trial demonstrated latanoprostene’s and Cornea & Contact Lens at 25. Kameda T, Inoue T, Inatani M et al. The effect of rho associ-
superiority over latanoprost.44,45 Salus University ated protein kinase inhibitor on monkey Schlemm’s canal endo-
Constellation, a Phase II, small-scale thelial cell. Invest Ophthalmol Vis Sci. 2012;53(6):3092-3103.
trial demonstrated superiority over Dr. Gurwood is a clinical director 26. Li T, Lindsley K, Rouse B, et al. Comparative effectiveness
timolol twice daily.45 Phase III trials and professor with the Eye Institute of first-line medications for primary open-angle glaucoma: A
include Apollo, Lunar and Jupiter. at Salus University. systematic review and network meta-analysis. Ophthalmology.
2016;123(1):129-140.
Apollo, a larger trial, compared 1. Quigley H. New paradigms in the mechanisms and manage- 27. Parrish RK, Palmberg P, Sheu WP, XLT Study Group. A com-
latanoprostene bunod with timolol ment of glaucoma. Eye. 2005;19(12):1241-8. parison of latanoprost, bimatoprost, and travoprost in patients
and demonstrated superiority in 2. Quigley H, Broman A. The number of people with glau- with elevated intraocular pressure: a 12-week, randomized,
overall IOP reduction. The study coma worldwide in 2010 and 2020. Br J Ophthalmol. masked-evaluator multicenter study. Am J Ophthalmol.
had a greater number of participants 2006;90(3):262-7. 2003;135(5):688-703.
with IOP less than or equal to 18mm 3. Tham Y, Li X, Wong T, et al. Global prevalence of glau- 28. Alm A, Villumsen J. PhXA34, a new potent ocular hypoten-
Hg and showed a higher percentage coma and projections of glaucoma burden through 2040: sive drug. A study on dose-response relationship and on aque-
of IOP reduction greater than or a systematic review and meta-analysis. Ophthalmology. ous humor dynamics in healthy volunteers. Arch Ophthlmol.
equal to 25%.44 These clinical tri- 2014;121(11):2081-90. 1991;109(11):1564-1568.
als show Vyzulta has the potential 4. Kapetanakis V, Chan M, Foster P, et al. Global variations and 29. Toris CB, Camras CB, Yablonski ME. Effects of PhXA41, a
to provide an additional 1mm Hg time trends in the prevalence of primary open angle glaucoma new prostaglandin F2, analog on aqueous humour dynamics on
to 3mm Hg drop in IOP, compared (POAG): a systematic review and meta-analysis. Br J Ophthal- human eyes. Ophthalmology. 1993;100(9):1297-304.
with the addition of latanoprost and mol. 2016;100(1):86-93. 30. Toris CB, Gabelt BT, Kaufman PL. Update on the mechanism
timolol.45 Twenty-two percent of 5. Weinreb R, Aung T, Medeiros FA. The pathophysiology and of action of topical prostaglandins for intraocular pressure
subjects reported at least one adverse treatment of Glaucoma:A Review. JAMA. 2014;311(18):1901-11. reduction. Surv Ophthalmol. 2008;53(S1):S107-20.
ocular event. These events were 6. Janssen SF, Gorgels TG, Ramdas WD, et al. The vast com- 31. Fung DS, Whitson JT. An evidence-based review of unopro-
mild, transient and consistent with plexity of primary open angle glaucoma: Disease genes, risks, stene isopropyl ophthalmic solution 0.15% for glaucoma: place
those seen caused by other topical molecular mechanisms and pathobiology. Prog Retin Eye Res. in therapy. Clin Ophthalmol. 2014;10(8):543-54.
glaucoma medications, including 2013 Nov;37:31-67. 32. Lee DA, Higginbotham EJ. Glaucoma and its treatment: A
conjunctival hyperemia, eye irrita- 7. Alm A, Nilsson SF. Uveoscleral outflow - a review. Experimen- Review. Am J Health Syst Pharm. 2005;62(7):691-9.
tion and eye pain.44,45 tal Eye Research. 2009;88(4):760-768. 33. Kopczynski CC, Epstein DL. Emerging trabecular outflow
8. Brubaker RF. Targeting outflow facility in glaucoma manage- drugs. J Ocul Pharmacol Ther. 2014;30(2-3): 85-7.
The incidence of glaucoma contin- ment. Surv Ophthalmol. 2003;48(Suppl 1):S17-20. 34. Webster AR, Luff AJ, Canning CR, Elkington AR. The effect
ues to rise and the more ammunition 9. Stamer WD, Braakman ST, Zhou EH, et al. Biomechanics of of pilocarpine on the glaucomatous visual field. Br J Ophthalmol.
provided to the armamentarium the Schlemm’s canal endothelium and intraocular pressure reduc- 1993;77(11):721-5.
better. Surgical interventions, such as tion. Prog Retin Eye Research. 2015;44(1):86-98. 35. Sihota R, Agarwal HC, Rajashekar YL. A comparative evalu-
cataract extraction, filtering proce- 10. Goel M, Picciani RG, Lee RK, Bhattacharya SK. Aque- ation of pilocarpine 1% and clonidine 0.125% versus timolol
dures and the placement of drainage ous humor dynamics: a review. Open Ophthalmol J. 2010 0.5%. Indian J Ophthalmol. 1996;44(2):87-9.
devices, increase risk to the patient. Sep;4:52–9. 36. Burr J, Azuara-Blanco A, Avenell A, Tuulonen A. Medical ver-
These new topical therapies, both 11. Kanski J. Clinical ophthalmology: a systematic approach, sus surgical interventions for open angle glaucoma. Cochrane
6th ed. Edinburgh: Elsevier Butterworth- Heinemann; 2007. Database Syst Rev. 2012;(9):CD004399.
12. McDougal DH, Gamli PD. Autonomic control of the eye. 37. Alm A, Camras CB, Watson PG. Phase III latanoprost studies
Compr Physiol. 2015;5(1):439–73. in Scandinavia, the United Kingdom and the United States. Surv
13. Gabelt BT, Kaufman PL. Aqueous humor hydrodynamics. Ophthalmol. 1997;41(Suppl 2):S105-110.
In: Hart WM, Ed. Adler’s Physiology of the Eye, 9th ed. St. Louis, 38. Aerie Pharmaceutical Products. http://aeriepharma.com/
MO: Mosby; 2003. products-at-a-glance/. Accessed April 22, 2017.
14. Johnson M. What controls aqueous humor outflow resis- 39. Ren R, Li G, Le TD, et al. Netarsudil increases outflow facility
tance? Exp Eye Res. 2006;82(4):545-57. in human eyes through multiple mechanisms. Invest Ophthal-
15. Tamm ER. The trabecular meshwork outflow path- mol Vis Sci. 2016;57:6197–209.
ways: structural and functional aspects. Exp Eye Res. 40. Lua LJ, Tsaib JC, Liua J. Novel pharmacologic candidates
2009;88(4):648-55. for treatment of primary open-angle glaucoma. Yale Journal of
16. Lutjen-Drecoll E. Functional morphology of the trabecular Biology and Medicine. 2017;90:111-8.
meshwork in primate. Prog Retin Eye Res. 1999;18(1):91-119. 41. Bacharach J, Dubiner HB, Levy B, et al. Double-masked,
17. Tian B, Gabelt BT, Geiger B, Kaufman P. The role of the randomized, dose-response study of AR-13324 versus latano-
actomyosin system in regulating trabecular fluid outflow. Exp prost in patients with elevated intraocular pressure. Ophthalmol-
Eye Res. 2009;88(4):713-17. ogy. 2015;122(2):302-7
18. Keller KE, Acott TS. The juxtacanalicular region of ocular 42. Perumal N, Manicam C, Steinicke M, et al. Characterization
trabecular meshwork: A tissue with a unique extracellular matrix of the human aqueous humour proteome: A comparison of the
and specialized function. J Ocul Biol. 2013;1(1):3-15. genders. PLoS One. 2017;12(3):e0172481.
19. Keller KE, Aga M, Bradley JM, et al. Extracellular matrix turn- 43. Kaufman PL. Latanoprostene bunod ophthalmic solution
0.024% for IOP lowering in glaucoma and ocular hypertension.
Expert Opinion on Pharmacotherapy. 2017;18(4):433-444.
44. Garcia GA, Ngai P, Mosaed S, Lin KY. Critical evaluation of
latanoprostene bunod in the treatment of glaucoma. Clinical
Ophthalmology. 2016 Oct;10:2035–50.
45. Krauss AH, Impagnatiello F, Toris CB, et al. Ocular hypo-
tensive activity of BOL-303259-X, a nitric oxide donating
prostaglandin F2α agonist, in preclinical models. Exp Eye Res.
2011;93(3):250–55.

REVIEW OF OPTOMETRY JULY 15, 2017 53

Diagnostics

23rd Annual Glaucoma Report

10-2 Visual Field Testing:

A Tool for All Glaucoma Stages

This diagnostic tool is a must for detecting paracentral and visual field defects close
to fixation in glaucoma, even the early-moderate stage. By Austin Lifferth, OD, Brian Fisher,

OD, April Stursma, OD, Sarah Cordes, OD, Stephanie Carter, OD, and Trina Perkins, OD

Advancing technol- glion cells and over 60% of
ogy has revolution- the visual cortex area.3
ized our toolbox
for detecting and By comparison, 10-2
threshold VF testing assesses

following glaucoma pro- 68 points, more than five

gression—but knowing times as many points in the

which tests provide the central 10 degrees com-

best diagnostic informa- pared with 24-2 and 30-2

tion is trickier than ever. testing. These points are all

Although 24-2 and 30-2 two degrees apart, just one

perimetry remain the degree from either side of

gold standard—despite the horizontal and vertical

advancements in retinal Fig. 1. As this comparison shows, 10-2 perimetry has greater meridians.4 As a result of

nerve fiber layer (RNFL) sensitivity and detects more points than 24-2 perimetry. this greater sensitivity, many

and ganglion cell analysis paracentral scotomas involv-

(GCA) optical coherence tomogra- using 10-2 VF testing to monitor ing only a small area of the visual

phy (OCT)—it may not be the most progression and change in advanced field at or near fixation may be

sensitive test to catch patients at visual field loss. missed with 24-2 and 30-2 perim-

the highest risk of functional visual Why 10-2? etry and are only detected with 10-2
impairment.1,2 Central 10-2 visual testing.5

field (VF) testing, however, may be The 24-2 and 30-2 threshold VF Early and Moderate Glaucoma
under-used in all stages of glaucoma. testing patterns assess a total of 54

These glaucoma cases—incor- and 74 points, respectively, each six Although central and paracentral

porating 10-2 and 24-2 perimetry, degrees apart (three degrees from glaucomatous VF damage more

RNFL and GCA OCT and optic the horizontal and vertical merid- commonly occurs in advanced

nerve head photos—highlight the ians) with only 12 points tested stages of glaucoma, such defects also

benefits of 10-2 perimetry in detect- within the central 10 degrees (Figure occur in patients with earlier stages

ing paracentral and VF defects close 1). Furthermore, only four of these of glaucoma and with relatively

to fixation in all stages of glaucoma, points are actually tested within the minimal peripheral VF loss.6 Recent

with special attention to the early- macular region (the central eight studies suggest these early central

moderate stage. In addition, these degrees)—the area that accounts for defects are usually more common in

cases also suggest the benefits of over 30% of the total retinal gan- the upper VF, deeper and generally

54 REVIEW OF OPTOMETRY JULY 15, 2017

Case 1 A

This 76-year-old patient has early-moderate primary open-angle glaucoma in the left eye and is a
high-risk glaucoma suspect in the right. His IOPs were stable with current topical ocular hypotensive
medications. Gonioscopy was normal OU and pachymetry measurements were thinner than average,
504µm OD and 508µm OS. Despite limited commitment to follow-up, his most recent 24-2 for his
left eye (B) confirmed overall stable superior paracentral defects, which were consistent with inferior
neuroretinal rim thinning (A) and moderate inferior/inferior-temporal RNFL loss on OCT testing (C). The
patient’s current 24-2 test pattern isn’t sufficient to fully understand his level of visual impairment and
reliably monitor for glaucomatous progression. Central 10-2 testing (D), however, can help reveal the
risk of potential visual impairment and better monitor for disease progression.

B CD

have an arcuate-like pattern that is Case 2
closer to fixation than those in the
inferior VF.7 This patient’s 24-2 VF testing shows apparent advanced structural and functional glauco-
matous damage with diffuse and deep superior central and paracentral damage (A). Such
Central and paracentral defects testing alone can lead clinicians to not only underestimate the extent of glaucomatous
in patients with early or moderate VF damage, but also overestimate the extent of damage and potentially miss the area of
glaucoma are more common than remaining superior temporal paracentral sensitivity (B).
you might expect. According to
one study, more than 50% of eyes AB
with mild-moderate glaucoma have
such defects within the central three 30-2 underestimated the level of VFs outside the central 10 degrees
degrees.8 Furthermore, research sug- glaucomatous damage in 13% of showed arcuate defects within the
gests macular damage evidenced the hemifields.10 Other researchers central 10 degrees with 10-2.11
on GCA OCT, with correlating found 11 eyes with normal 24-2
functional damage on 10-2 test- In a study published online May
ing, occurs almost as frequently as
peripheral defects in patients with
early glaucoma; approximately
16% of these patients may have
undetected functional central defects
when using 24-2 testing alone.4,9
Another study found 9% of normal
30-2 threshold VFs in glaucoma
suspects or early glaucoma patients
were actually classified as abnormal
with 10-2 testing.10 Additionally,

REVIEW OF OPTOMETRY JULY 15, 2017 55

Diagnostics

Case 3 B C
D E
This patient has detectable rim loss upon
optic nerve evaluation and OCT testing
(A) with correlating nasal step visual field
defects OU, more so in the right eye than
the left, and presumed minimal central
involvement on visual field 24-2 testing,
again more so in the right eye than the left
(B and C). Central 10-2 visual field testing
shows that 24-2 testing underestimates
these potential central defects (D and E).

A

24, 2017, researchers found that, in defect is greatly depressed relative to central visual acuities, clinicians
cases of normal 24-2 testing, 10-2 the mean deviation (MD) on 24-2; should regularly use 10-2 testing to
found abnormal central defects in or there are any abnormal points in better understand the significance
35% of the patients with ocular the central 12 points on 24-2 testing of the defect and better monitor
hypertension, 39% of glaucoma that spatially correlate to thinning in for progression.15,16 Furthermore,
suspects and 61% of the patients the macular ganglion cell inner plexi- researchers highly recommend all
with early glaucoma.12 An abnormal form layer (GCIPL) area.13 patients with advanced glaucoma
10-2 result was significantly associ- undergo a combination of 24-2 or
ated with at least one location on the Advanced Glaucoma 30-2 and 10-2 testing as close to one
total deviation or pattern deviation another as possible, or at least alter-
plot (p <0.5%) within the central 10 According to the Hodapp, Parrish, nated at future follow-up visits, to
degrees on 24-2 testing.12 They also and Anderson visual field classifica- help monitor for progression.6
found patients of African descent tion system, one of the criteria for
were more likely to have central VF advanced glaucoma is if the VF has For advanced cases, several stud-
defects.12 any points within the central five ies have found that 10-2 testing
degrees with a sensitivity less than or with non-standard V size stimulus
Key point: Armed with such equal to 0dB, or if both hemifields (as opposed to the standard III size
evidence, one group of research- have depressed points with sensitiv- stimulus) can more reliably measure
ers recommends 10-2 VF testing ity less than 15dB within the central visual function that was otherwise
always be considered if: there are five degrees of fixation—regardless undetected on 30-2 testing with
any depressed points in the central of the status of the rest of the visual standard III size and thus help moni-
12 degrees less than 0.5% on 24-2 field.14 For these patients in particu- tor progression of points with lower
or 30-2 VF testing; the paracentral lar, and even for patients with good sensitivity for a longer period.17,6

56 REVIEW OF OPTOMETRY JULY 15, 2017

Tonometry Done Right

D-KAT Digital
Keeler quality.

Pulsair Desktop
Smallest footprint and simple to use!

Purchase a Pulsair Desktop by
September 30, 2017 and get
a $1,326 Instant Rebate!

Intellipuff
The standard for hand held mobility.

Keeler Instruments, Inc. • 3222 Phoenixville Pike #50 • Malvern, PA 19355 • Tel: (800) 523-5620 • Fax: (610) 353-7814 • email: [email protected]

Up to 2017NEW TECHNOLOGIES

18 CE Eye Care&TREATMENTSIN

Credits*

Philadelphia REVIEW OF OPTOMETRY®

November 3-5, 2017 EDUCATIONAL MEETINGS OF CLINICAL EXCELLENCE

Join Review of Optometry’s New Technologies & Treatments
in Eye Care on November 3-5, 2017 in Philadelphia, PA.
This meeting provides up to 18* COPE CE credits including
interactive workshops!**

Loews Philadelphia Hotel EARLY BIRD SPECIAL

1200 Market Street, R$EG7IS5TROATFIOFN
Philadelphia, PA 19107 muSsetprte.g1is8t,e2r 0b1e7fore
Phone: (215) 627-1200
Photo: Loews Philadelphia Hotel
Discounted room rate: $189/night†

Program Chair:
Paul Karpecki, OD, FAAO

Registration Cost: $495

Receive $75 off if registered before September 18, 2017.

Three Ways to Register

Online: www.reviewofoptometry.com/philadelphia2017
E-mail: [email protected]
Phone: 866-658-1772

Administered by *Approval pending Partially supported by
unrestricted educational grants from
Review of Optometry ®
Shire Alcon

†Rooms limited. **Subject to change, separate registration required. See event website for complete details.

Case 4 A B
D E
This patient has superior rim thinning (A
and B) with correlating RNFL loss on OCT
testing (C and D). This corresponds to
associated inferior paracentral and nasal
visual field defects with variable central
defects in both eyes (D and E). Due to
these borderline defects and the spatially
correlating ganglion cell complex thinning
in the left eye (F), central 10-2 visual field
testing better documented the breadth
and depth of these defects (G and H).

C

F GH

Glaucoma Progression but the rate of MD change was lier, detect progression sooner and
significantly greater on 10-2 com- minimize the risk of under- or over-
Early evidence-based research shows pared with 24-2 testing for eyes with estimating the extent of the glauco-
10-2 perimetry detects central and advanced VF loss (-0.19dB/year for matous visual field damage—in all
paracentral glaucomatous progres- 24-2 testing and -0.26 dB/year for stages of glaucoma. ■
sion more frequently than 24-2 VF 10-2 testing).15
testing.18 In addition, one study Drs. Lifferth, Fisher, Cordes,
found the rate of MD change was By using central 10-2 VF test-
similar on 24-2 and 10-2 VF test- ing more routinely, clinicians can Carter and Perkins are attending
ing with mild to moderate VF loss, hopefully diagnose glaucoma ear-
optometrists at The Villages VA

Outpatient Clinic, in Fla.

REVIEW OF OPTOMETRY JULY 15, 2017 59

Diagnostics

Dr. Stursma is an attending 2014;55(2):632-49. 16. Rao HL, Begum VU, Khadka D, et al. Comparing glaucoma
optometrist at the Ocala Commu- 8. Schiefer U, Papageorgiou E, Sample PA, et al. Spatial pat- progression on 24-2 and 10-2 Visual field examinations. PLoS
nity Based VA Outpatient Clinic in tern of glaucomatous visual field loss obtained with regionally One. 2015;10(5):e0127233.
Ocala, Fla. condensed stimulus arrangements. Invest Ophthalmol Vis Sci. 17. Zalta A. Use of a central 10 degrees field and size V stimu-
2010;51(11):5685-9. lus to evaluate and monitor small central islands of vision in end
1. Khoury J, Donahue S, Lavin P, Tsai J. Comparison of 24-2 9. Teixeira IC, Bresciani-Battilana E, Barbosa D, et al. Cor- stage glaucoma. Br J Ophthalmol. 1991;75(3):151-4.
and 30-2 perimetry in glaucomatous and nonglaucomatous relation between the ganglion cell complex and functional 18. Park S, Kung Y, Ritch R, et al. Parafoveal scotoma progres-
optic neuropathies. J Neuroophthalmol. 1999;19(2):100-8. measures in glaucoma patients and suspects. Int Ophthalmol. sion in glaucoma: humphrey 10-2 versus 24-2 visual field
2. Heijl A, Bengtsson B, Chauhan B, et al. A comparison of 2015;35:81-7. analysis. Ophthalmol. 2013;120(8):1546-50.
visual field progression criteria of 3 major glaucoma trials 10. Langerhorst C, Carenini L, Bakker D, et al. Measurements
in early manifest glaucoma trial patients. Ophthalmology. for description of very early glaucomatous field defects. In: Wall Case 6
2008;115(9):1557-65. M, Heiji A, eds. Perimetry Update 1996/1997. New York, NY:
3. Schira MM, Wade AR, Tyler CW. Two-dimensional mapping of Kugler Publications;1997:67-73. This patient presented with severe
the central and parafoveal visual field to human visual cortex. J 11. Hood DC, Raza AS, de Moraes CG, et al. Initial arcuate inferior temporal glaucomatous structural
Neurophysiol. 2007;97(6):4284-95. defects within the central 10 degrees in glaucoma. Invest Oph- damage and has a corresponding superior
4. Traynis I, de Moraes CG, Raza AS, et al. Prevalence and thalmol Vis Sci. 2011;52(2):940-6. central and paracentral 24-2 VF defect
nature of early glaucomatous defects in the central 10 degrees 12. de Moraes C, Hood D, Liebmann J, et al. 24-2 visual fields (A). Central 10-2 testing reveals the
of the visual field. JAMA Ophthalmol. 2014;132(3):291-97. miss central defects shown on 10-2 tests in glaucoma sus- extent of this defect and better highlights
5. Hangai M, Ikeda H, Akagi T, et al. Paracentral scotoma in pects, ocular hypertensives, and early glaucoma. Ophthalmol- the possible progression that likely would
glaucoma detected by 10-2 but not by 24-2 perimetry. Jpn J ogy. May 24, 2017. [Epub ahead of print]. have been underestimated or missed on
Ophthalmol. 2014;58(2):188-96. 13. Park H, Hwang B, Shin H, et al. Clinical clues to predict the 24-2 testing alone (B and C).
6. de Moraes C, Liebmann J, Medeiros F, et al. Management presence of parafoveal scotoma on humphrey 10-2 visual field
of advanced glaucoma: characterization and monitoring. Surv using a humphrey 24-2 visual field. Am J Ophthalmol. 2016
Ophthalmol. 2016;61(5):597-615. Jan;161:150-9.
7. Hood D, Slobodnick A, Raza A, et al. Early glaucoma involves 14. Brusini P, Johnson C. Staging functional damage in glau-
both deep local, and shallow widespread, retinal nerve fiber coma: review of different classification methods. Surv Ophthal-
damage of the macular region. Invest Ophthalmol Vis Sci. mol. 2007;52(2):156-79.
15. Weinreb RN, Garway-Heath DF, Leung C, et al, eds. Progres-
sion of Glaucoma: The 8th Consensus Report of the World Glau-
coma Association. Amsterdam: Kugler Publications; 2011:15.

Case 5

Despite relatively mild inferior temporal neuroretinal rim loss in this patient’s right eye (A)

with confirmed RNFL loss on OCT (B), and regardless of the status of the rest of the visual

field, this patient has advanced visual field loss on 24-2 visual field testing (C). Due to

this deep central involvement, 10-2 visual field testing is critical to better understand the

significance of this defect and monitor for B
progression (D).

AA

CD B
C
60 REVIEW OF OPTOMETRY JULY 15, 2017

Prostaglandin Aqueous humor
analogues production
work better is highest in
at night1
the morning2

Classic beta blocker adjunctive therapy
for the right patient at the right time3

The concomitant use of two topical beta-adrenergic
blocking agents is not recommended4,5

Indications and Usage

ISTALOL® (timolol maleate ophthalmic solution) is a non-selective beta-adrenergic receptor blocking agent indicated in the treatment
of elevated intraocular pressure in patients with ocular hypertension or open-angle glaucoma.

Preservative-free TIMOPTIC® (timolol maleate ophthalmic solution) in OCUDOSE® (dispenser) is indicated in the treatment of elevated
intraocular pressure in patients with ocular hypertension or open-angle glaucoma. It may be used when a patient is sensitive to the
preservative in TIMOPTIC (timolol maleate ophthalmic solution), benzalkonium chloride, or when use of a preservative-free topical
medication is advisable.

Important Safety Information for Istalol® and Timoptic® in Ocudose®

• Both ISTALOL® (timolol maleate ophthalmic solution) and TIMOPTIC® (timolol maleate ophthalmic solution) in OCUDOSE® (dispenser)
are contraindicated in patients with: bronchial asthma; a history of bronchial asthma; severe chronic obstructive pulmonary disease;
sinus bradycardia; second or third degree atrioventricular block; overt cardiac failure; cardiogenic shock; hypersensitivity to any
component of the product.

• The same adverse reactions found with systemic administration of beta-adrenergic blocking agents may occur
with topical administration. Severe respiratory reactions and cardiac reaction, including death due to bronchospasm
in patients with asthma, and rarely death in association with cardiac failure, have been reported following systemic
or ophthalmic administration of timolol maleate.

• Patients with a history of atopy or severe anaphylactic reactions to a variety of allergens may be unresponsive to the usual doses
of epinephrine used to treat anaphylactic reactions.

• Timolol has been reported rarely to increase muscle weakness in some patients with myasthenia gravis or myasthenic symptoms.

• Beta-adrenergic blocking agents may mask signs and symptoms of acute hypoglycemia or certain clinical signs of hyperthyroidism.
Patients subject to spontaneous hypoglycemia, or diabetic patients receiving either insulin or oral hypoglycemic agents, or patients
suspected of developing thyrotoxicosis, should be managed carefully, with caution.

• In patients undergoing elective surgery, some authorities recommend gradual withdrawal of beta adrenergic receptor blocking agents
because these agents impair the ability of the heart to respond to beta-adrenergically mediated reflex stimuli.

• The most frequently reported adverse reactions have been burning and stinging upon instillation. This was seen in 38% of patients treated
with ISTALOL and in approximately one in eight patients treated with TIMOPTIC in OCUDOSE. Additional reactions reported with ISTALOL
at a frequency of 4 to 10% include: blurred vision, cataract, conjunctival injection, headache, hypertension, infection, itching and decreased
visual acuity.

Please see Brief Summary of Prescribing Information for ISTALOL and TIMOPTIC in OCUDOSE on the following pages.

For the patients who need incremental IOP For the patients who need incremental IOP
reduction in a preservative free form6 reduction in a once a day form6

References: 1. Alm A, Stjernschantz J. Effects on Intraocular Pressure and Side Effects of 0.005% Latanoprost Applied Once Daily, Evening or Morning. Ophthalmology. 1995;102:1743-1752. 2. Brubaker R. Flow of Aqueous Humor in
Humans. IOVS. 1991;32:(13)3145-3166. 3. Obstbaum S, Cioffi GA, Krieglstein GK, et al. Gold Standard Medical Therapy for Glaucoma: Defining the Criteria Identifying Measures for an Evidence-Based Analysis. Clin Ther.
2004;26(12)2102-2119. 4. Istalol [package insert]. Bridgewater, NJ: Bausch & Lomb Incorporated; 2013. 5. Timoptic in Ocudose [package insert]. Lawrenceville, NJ: Aton Pharma; 2009. 6. Stewart W, Day DG, Sharpe ED. Efficacy
and Safety of Timolol Solution Once Daily vs Timolol Gel Added to Latanoprost. Am J Ophthalmol. 1999;128(6)692-696.
Timoptic and Ocudose are trademarks of Valeant Pharmaceuticals International, Inc. or its affiliates.
Bausch + Lomb and Istalol are trademarks of Bausch & Lomb Incorporated or its affiliates.

©Bausch & Lomb Incorporated. US/TOP/14/0017(1)

BRIEF SUMMARY OF PRESCRIBING INFORMATION symptoms suggesting reduced cerebral blood flow develop following initiation of inrats, there were no adverse effects on postnatal development of offspring. Doses of
therapy with Istalol, alternative therapy should be considered. 1000 mg/kg/day (142,000 times the systemic exposure following the maximum
This Brief Summary does not include all the information needed to use 5.12 Choroidal Detachment: Choroidal detachment after filtration procedures recommended human ophthalmic dose) were maternotoxic in mice and resulted in an
ISTALOL® (timolol maleate ophthalmic solution) 0.5% safely and effectively. has been reported with the administration of aqueous suppressant therapy (e.g. increased number of fetal resorptions. Increased fetal resorptions were also seen in
See full prescribing information for ISTALOL. timolol). rabbits at doses of 14,000 times the systemic exposure following the maximum

Istalol®(timolol maleate ophthalmic solution) 0.5% ADVERSE REACTIONS recommended human ophthalmic dose, in this case without apparent maternotoxicity.
6.1 Clinical Trials Experience: Because clinical trials are conducted under There are no adequate and well-controlled studies in pregnant women.Istalolshould
Initial U.S.Approval: 1978 widely varying conditions, adverse reaction rates observed in the clinical trials of a be used during pregnancy only if the potential benefit justifies the potential risk to the

STERILE drug cannot be directly compared to rates in the clinical trials of another drug and fetus.
may not reflect the rates observed in practice. 8.3 Nursing Mothers: Timolol has been detected in human milk following oral and
INDICATIONS AND USAGE The most frequently reported adverse reactions have been burning and stinging ophthalmic drug administration. Because of the potential for serious adverse reactions
Istalol (timolol maleate ophthalmic solution) 0.5% is a non-selective beta-adrenergic upon instillation in 38% of patients treated with Istalol.Additional reactions reported from Istalol in nursing infants, a decision should be made whether to discontinue
receptor blocking agent indicated in the treatment of elevated intraocular pressure with Istalol at a frequency of 4 to 10% include: blurred vision, cataract, conjunctival nursing or to discontinue the drug, taking into account the importance ofthe drug to the
(IOP) in patients with ocular hypertension or open-angle glaucoma. injection, headache, hypertension, infection, itching and decreased visual acuity. mother.

CONTRAINDICATIONS The following additional adverse reactions have been reported less frequently with 8.4 Pediatric Use: Safety and effectiveness in pediatric patients have not been
4.1 Asthma, COPD: Istalol is contraindicated in patients with bronchial asthma; a ocular administration of this or other timolol maleate formulations. established.
history of bronchial asthma; severe chronic obstructive pulmonary disease (see 8.5 Geriatric Use: No overall differences in safety or effectiveness have been
WARNINGS AND PRECAUTIONS,5.1,5.3). Timolol (Ocular Administration): Body as a whole: Asthenia/fatigue and chest observed between elderly and younger patients.
pain; Cardiovascular: Bradycardia, arrhythmia, hypotension, syncope, heart
4.2 Sinus Bradycardia, AV Block, Cardiac Failure, Cardiogenic Shock: block, cerebral vascular accident, cerebral ischemia, cardiac failure, worsening OVERDOSAGE
Istalol is contraindicated in patients with sinus bradycardia; second or of angina pectoris, palpitation, cardiac arrest, pulmonary edema, edema, There have been reports of inadvertent overdosage with Istalol resulting in systemic
third degree atrioventricular block; overt cardiac failure DBSEJPHFOJD claudication, Raynaud’s phenomenon and cold hands and feet; Digestive: Nausea, effects similar to those seen with systemic beta-adrenergic blocking agents such as
TIPDL (see WARNINGS AND PRECAUTIONS, 5.2). diarrhea, dyspepsia, anorexia, and dry mouth; Immunologic: Systemic lupus dizziness, headache, shortness of breath, bradycardia, bronchospasm, and cardiac

4.3 Hypersensitivity Reactions: Istalol is contraindicated in patients who have erythematosus; Nervous System/Psychiatric: Dizziness, increase in signs and arrest. An in vitro hemodialysis study, using 14C timolol added to human plasma or
exhibited a hypersensitivity reaction to any component of this product in the past. symptoms of myasthenia gravis, paresthesia, somnolence, insomnia, nightmares, whole blood, showed that timolol was readily dialyzed from these fluids; however,
behavioral changes and psychic disturbances including depression, confusion, a study of patients with renal failure showed that timolol did not dialyze readily.
WARNINGS AND PRECAUTIONS hallucinations, anxiety, disorientation, nervousness and memory loss; Skin: NONCLINICALTOXICOLOGY
5.1 Potentiation of Respiratory Reactions Including Asthma: Istalol Alopecia and psoriasiform rash or exacerbation of psoriasis; Hypersensitivity: Signs 13.1 Carcinogenesis, Mutagenesis, Impairment of Fertility: In a two-year
contains timolol maleate; and although administered topically, it can be absorbed and symptoms of systemic allergic reactions, including angioedema, urticaria, study of timolol maleate administered orally to rats, there was a statistically
systemically. Therefore, the same adverse reactions found with systemic and localized and generalized rash; Respiratory: Bronchospasm (predominantly significant increase in the incidence of adrenal pheochromocytomas in male rats
administration of beta-adrenergic blocking agents may occur with topical in patients with pre-existing bronchospastic disease), respiratory failure, administered 300 mg/kg/day (approximately 42,000 times the systemic exposure
administration. For example, severe respiratory reactions and cardiac reactions dyspnea, nasal congestion, cough and upper respiratory infections; Endocrine: following the maximum recommended human ophthalmic dose).Similar differences were
including death due to bronchospasm in patients with asthma, and rarely death in Masked symptoms of hypoglycemia in diabetic patients (see WARNINGS AND not observed in rats administered oral doses equivalent to approximately 14,000
association with cardiac failure, have been reported following systemic or PRECAUTIONS, 5.6); Special Senses: Signs and symptoms of ocular irritation times the maximum recommended human ophthalmic dose. In a lifetime oral study in
ophthalmic administration of timolol maleate (see CONTRAINDICATIONS,4.1). including conjunctivitis, blepharitis, keratitis, ocular pain, discharge (e.g., crusting), mice, there were statistically significant increases in the incidence of benign and
5.2 Cardiac Failure: Sympathetic stimulation may be essential for support foreign body sensation, itching and tearing, and dry eyes; ptosis, decreased corneal malignant pulmonary tumors, benign uterine polyps and mammary adenocarcinomas in
of the circulation in individuals with diminished myocardial contractility, and its sensitivity; cystoid macular edema; visual disturbances including refractive changes female mice at 500 mg/kg/day, (approximately 71,000 times the systemic exposure
inhibition of beta-adrenergic receptor blockade may precipitate more severe failure. In and diplopia; pseudopemphigoid; choroidal detachment following filtration surgery following the maximum recommended human ophthalmic dose), but not at 5 or 50
patients without a history of cardiac failure, continued depression of the (see WARNINGS AND PRECAUTIONS, 5.12); Urogenital: Retroperitoneal fibrosis, mg/kg/day (approximately 700 or 7,000, respectively, times the systemic
myocardium with beta-blocking agents over a period of time can, in some cases, decreased libido, impotence, and Peyronie’s disease. exposurefollowing the maximum recommended human ophthalmic dose). In a
lead to cardiac failure. At the first sign or symptom of cardiac failure, Istalol should be 6.2 Postmarketing Experience subsequent study in female mice, in which post-mortem examinations were limited
discontinued (see CONTRAINDICATIONS,4.2). Oral Timolol/Oral Beta-blockers: The following additional adverse effects have
been reported in clinical experience with ORAL timolol maleate or other ORAL beta- to the uterusand the lungs, a statistically significant increase in the incidence of
5.3 Obstructive Pulmonary Disease: Patients with chronic obstructive blocking agents and may be considered potential effects of ophthalmic timolol pulmonarytumors was again observed at 500 mg/kg/day. The increased occurrence
pulmonary disease (e.g., chronic bronchitis, emphysema) of mild or moderate maleate: Allergic: Erythematous rash, fever combined with aching and sore throat, ofmammary adenocarcinomas was associated with elevations in serum prolactin which
severity, bronchospastic disease, or a history of bronchospastic disease [other than laryngospasm with respiratory distress; Body as aWhole: Extremity pain,decreased occurred in female mice administered oral timolol at 500 mg/kg/day, but not at doses
bronchial asthma or a history of bronchial asthma in which Istalol is contraindicated> exercise tolerance, weight loss; Cardiovascular: Worsening of arterial insufficiency, of 5 or 50 mg/kg/day. An increased incidence of mammary adenocarcinomas in
should, in general, not receive beta-blocking agents,including Istalol. vasodilatation; Digestive: Gastrointestinal pain, hepatomegaly, vomiting, mesenteric rodents has been associated with administration of several other therapeutic
5.4 Increased Reactivity to Allergens: While taking beta-blockers, patients arterial thrombosis, ischemic colitis; Hematologic: Nonthrombocytopenic agents that elevate serum prolactin, but no correlation between serum prolactin
with a history of atopy or a history of severe anaphylactic reactions to a variety of purpura; thrombocytopenic purpura, agranulocytosis; Endocrine: Hyperglycemia, levels and mammary tumors has been established in humans. Furthermore, in adult
allergens may be more reactive to repeated accidental, diagnostic, or therapeutic hypoglycemia; Skin: Pruritus, skin irritation, increased pigmentation, sweating; human female subjects who received oral dosages of up to 60 mg of timolol
challenge with such allergens. Such patients may be unresponsive to the usual Musculoskeletal: Arthralgia; Nervous System/Psychiatric: Vertigo, local weakness, maleate (the maximum recommended human oral dosage), there were no clinically
doses of epinephrine used to treat anaphylactic reactions. meaningful changes in serum prolactin. Timolol maleate was devoid of mutagenic

5.5 Potentiation of Muscle Weakness: Beta-adrenergic blockade has been diminished concentration, reversible mental depression progressing to catatonia, potential when tested in vivo (mouse) in the micronucleus test and cytogenetic
reported to potentiate muscle weakness consistent with certain myasthenic an acute reversible syndrome characterized by disorientation for time and place, assay (doses up to 800 mg/kg) and in vitro in a neoplastic cell transformation assay
symptoms (e.g., diplopia, ptosis, and generalized weakness). Timolol has been emotional lability, slightly clouded sensorium and decreased performance on (up to 100 mcg/mL). In Ames tests the highest concentrations of timolol employed,
reported rarely to increase muscle weakness in some patients with myasthenia neuropsychometrics; Respiratory: Rales,bronchial obstruction; Urogenital: Urination 5,000 or 10,000 mcg/plate, were associated with statistically significant elevations of
gravis or myasthenic symptoms. difficulties. revertants observed with tester strain TA100 (in seven replicate assays), but not in the

5.6 Masking of Hypoglycemic Symptoms in Patients with Diabetes DRUG INTERACTIONS remaining three strains. In the assays with tester strain TA100, no consistent dose
Mellitus: Beta-adrenergic blocking agents should be administered with caution in 7.1 Beta-Adrenergic Blocking Agents: Patients who are receiving a beta- response relationship was observed, and the ratio of test to control revertants did not
patients subject to spontaneous hypoglycemia or to diabetic patients (especially those adrenergic blocking agent orally and Istalol® should be observed for potential reach 2. A ratio of 2 is usually considered the criterion for a positive Ames test.
with labile diabetes) who are receiving insulin or oral hypoglycemic agents. Beta- additive effects of beta-blockade, both systemic and on intraocular pressure. Reproduction and fertility studies in rats demonstrated no adverse effect on male or
adrenergic receptor blocking agents may mask the signs and symptoms of acute The concomitant use of two topical beta-adrenergic blocking agents is not female fertility at doses up to 21,000 times the systemic exposure following the
hypoglycemia. recommended. maximumrecommended human ophthalmic dose.

5.7 Masking of Thyrotoxicosis: Beta-adrenergic blocking agents may mask 7.2 Calcium Antagonists: Caution should be used in the co-administration of PATIENT COUNSELING INFORMATION
certain clinical signs (e.g., tachycardia) of hyperthyroidism. Patients suspected of beta-adrenergic blocking agents, such as Istalol, and oral or intravenous calcium Patients with bronchial asthma, a history of bronchial asthma, severe chronic
developing thyrotoxicosis should be managed carefully to avoid abrupt withdrawal of antagonists because of possible atrioventricular conduction disturbances, left obstructive pulmonary disease, sinus bradycardia, second or third degree
beta-adrenergic blocking agents that might precipitate a thyroid storm. ventricular failure, and hypotension. In patients with impaired cardiac function, co- atrioventricular block, or cardiac failure should be advised not to take this product.

5.8 Contamination of Topical Ophthalmic Products After Use: There administration should be avoided. (see CONTRAINDICATIONS, 4.1, 4.2) Patients should also be instructed that ocular
have been reports of bacterial keratitis associated with the use of multiple-dose 7.3 Catecholamine-Depleting Drugs: Close observation of the patient solutions, if handled improperly or if the tip of the dispensing container contacts the
containers of topical ophthalmic products. These containers had been inadvertently is recommended when a beta blocker is administered to patients receiving eye or surrounding structures, can become contaminated by common bacteria known to
contaminated by patients who, in most cases, had a concurrent corneal disease or catecholamine-depleting drugs such as reserpine, because of possible additive cause ocular infections. Serious damage to the eye and subsequent loss of vision
a disruption of the ocular epithelial surface (see PATIENT COUNSELING effects and the production of hypotension and/or marked bradycardia, which may may result from using contaminated solutions. (see WARNINGS AND
INFORMATION,17). result in vertigo, syncope, or postural hypotension. PRECAUTIONS 5.8) Patients should also be advised that if they have ocular surgery or

5.9 Impairment of Beta-adrenergically Mediated Reflexes During Surgery: 7.4 Digitalis and Calcium Antagonists: The concomitant use of beta- develop an intercurrent ocular condition (e.g., trauma or infection), they should
The necessity or desirability of withdrawal of beta-adrenergic blocking agents prior to adrenergic blocking agents with digitalis and calcium antagonists may have additive immediately seek their physician’s advice concerning the continued use of the present
major surgery is controversial. Beta-adrenergic receptor blockade impairs the ability effects in prolonging atrioventricular conduction time. multidose container. If more than one topical ophthalmic drug is being used, the drugs
of the heart to respond to beta-adrenergically mediated reflex stimuli. This may 7.5 CYP2D6 Inhibitors: Potentiated systemic beta-blockade (e.g., decreased should be administered at least five minutes apart. Patients should be advised that Istalol®
augment the risk of general anesthesia in surgical procedures.Some patients receiving heart rate) has been reported during combined treatment with CYP2D6 inhibitors contains benzalkonium chloride which may be absorbed by soft contact lenses. Contact
beta-adrenergic receptor blocking agents have experienced protracted severe (e.g., quinidine) and timolol. lenses should be removed prior to administration of the solution. Lenses may be
hypotension during anesthesia. Difficulty in restarting and maintaining the heartbeat 7.6 Clonidine: Oral beta-adrenergic blocking agents may exacerbate the reinserted 15 minutes following Istalol® administration.
has also been reported. For these reasons, in patients undergoing elective surgery,
some authorities recommend gradual withdrawal of beta-adrenergic receptor rebound hypertension which can follow the withdrawal of clonidine. There have Rx Only
blocking agents. If necessary during surgery, the effects of beta-adrenergic blocking been no reports of exacerbation of rebound hypertension with ophthalmic timolol %JTUSJCVUFECZ
agents may be reversed by sufficient doses of adrenergic agonists. maleate. #BVTDI-PNC
BEJWJTJPOPG7BMFBOU1IBSNBDFVUJDBMT/PSUI"NFSJDB--$#SJEHFXBUFS

/+64"
5.10 Angle-Closure Glaucoma: In patients with angle-closure glaucoma, USE IN SPECIFIC POPULATIONS Under License from:
the immediate objective of treatment is to reopen the angle. This may require 8.1 Pregnancy SENJU Pharmaceutical Co.,Ltd
constricting the pupil. Timolol maleate has little or no effect on the pupil. Istalol Teratogenic Effects: Pregnancy Category C: Teratogenicity studies have been Osaka,Japan 541-0046
should not be used alone in the treatment of angle-closure glaucoma. performed in animals. Teratogenicity studies with timolol in mice, rats, and rabbits *TUBMPMJTBUSBEFNBSLPG#BVTDI-PNC*ODPSQPSBUFEPSJUTBGGJMJBUFT
5.11 Cerebrovascular Insufficiency: Because of potential effects of beta- at oral doses up to 50 mg/kg/day (7,000 times the systemic exposure following the © Bausch & Lomb Incorporated
adrenergic blocking agents on blood pressure and pulse, these agents should maximum recommended human ophthalmic dose) demonstrated no evidence of
be used with caution in patients with cerebrovascular insufficiency. If signs or fetal malformations. Although delayed fetal ossification was observed at this dose Based on 940150
,6786$ 5HYLVHG

BRIEF SUMMARY OF PRESCRIBING INFORMATION atrioventricular block, or cardiac failure should be advised not to take this product. phenomenon, and cold hands and feet.
This Brief Summary does not include all the information needed to use TIMOPTIC® (See CONTRAINDICATIONS.) DIGESTIVE: Nausea, diarrhea, dyspepsia, anorexia, and dry mouth.
0.25% AND 0.5% (timolol maleate ophthalmic solution) in OCUDOSE® (DISPENSER) Drug Interactions: Although TIMOPTIC (timolol maleate ophthalmic solution) used IMMUNOLOGIC: Systemic lupus erythematosus.
safely and effectively. See full prescribing information for TIMOPTIC in OCUDOSE. alone has little or no effect on pupil size, mydriasis resulting from concomitant therapy NERVOUS SYSTEM/PSYCHIATRIC: Dizziness, increase in signs and symptoms of
PRESERVATIVE-FREE STERILE OPHTHALMIC SOLUTION with TIMOPTIC (timolol maleate ophthalmic solution) and epinephrine has been myasthenia gravis, paresthesia, somnolence, insomnia, nightmares, behavioral changes
in a Sterile Ophthalmic Unit Dose Dispenser reported occasionally. and psychic disturbances including depression, confusion, hallucinations, anxiety,
disorientation, nervousness, and memory loss.
TIMOPTIC® 0.25% AND 0.5% Beta-adrenergic blocking agents: Patients who are receiving a beta-adrenergic SKIN: Alopecia and psoriasiform rash or exacerbation of psoriasis.
blocking agent orally and Preservative-free TIMOPTIC in OCUDOSE should be observed HYPERSENSITIVITY: Signs and symptoms of systemic allergic reactions including
(TIMOLOL MALEATE OPHTHALMIC SOLUTION) for potential additive effects of beta-blockade, both systemic and on intraocular anaphylaxis, angioedema, urticaria, and localized and generalized rash.
pressure. The concomitant use of two topical beta-adrenergic blocking agents is RESPIRATORY: Bronchospasm (predominantly in patients with pre-existing
in OCUDOSE®(DISPENSER) not recommended. bronchospastic disease), respiratory failure, dyspnea, nasal congestion, cough and upper
respiratory infections.
INDICATIONS AND USAGE Calcium antagonists: Caution should be used in the coadministration of beta- ENDOCRINE: Masked symptoms of hypoglycemia in diabetic patients (see WARNINGS).
Preservative-free TIMOPTIC in OCUDOSE is indicated in the treatment of elevated adrenergic blocking agents, such as Preservative-free TIMOPTIC in OCUDOSE, and oral SPECIAL SENSES: Signs and symptoms of ocular irritation including conjunctivitis,
or intravenous calcium antagonists, because of possible atrioventricular conduction blepharitis, keratitis, ocular pain, discharge (e.g., crusting), foreign body sensation,
intraocular pressure in patients with ocular hypertension or open-angle glaucoma. disturbances, left ventricular failure, and hypotension. In patients with impaired cardiac itching and tearing, and dry eyes; ptosis; decreased corneal sensitivity; cystoid
Preservative-free TIMOPTIC in OCUDOSE may be used when a patient is sensitive function, coadministration should be avoided. macular edema; visual disturbances including refractive changes and diplopia;
pseudopemphigoid; choroidal detachment following filtration surgery (see PRECAUTIONS,
to the preservative in TIMOPTIC (timolol maleate ophthalmic solution), benzalkonium Catecholamine-depleting drugs: Close observation of the patient is recommended General); and tinnitus.
chloride, or when use of a preservative-free topical medication is advisable. when a beta blocker is administered to patients receiving catecholamine-depleting UROGENITAL: Retroperitoneal fibrosis, decreased libido, impotence, and Peyronie’s disease.
drugs such as reserpine, because of possible additive effects and the production of
CONTRAINDICATIONS hypotension and/or marked bradycardia, which may result in vertigo, syncope, or The following additional adverse effects have been reported in clinical experience
Preservative-free TIMOPTIC in OCUDOSE is contraindicated in patients with (1) postural hypotension. with ORAL timolol maleate or other ORAL beta blocking agents, and may be considered
potential effects of ophthalmic timolol maleate: Allergic: Erythematous rash, fever
bronchial asthma; (2) a history of bronchial asthma; (3) severe chronic obstructive Digitalis and calcium antagonists: The concomitant use of beta-adrenergic blocking combined with aching and sore throat, laryngospasm with respiratory distress; Body
pulmonary disease (see WARNINGS); (4) sinus bradycardia; (5) second or third degree agents with digitalis and calcium antagonists may have additive effects in prolonging as a Whole: Extremity pain, decreased exercise tolerance, weight loss; Cardiovascular:
atrioventricular block; (6) overt cardiac failure (see WARNINGS); (7) cardiogenic shock; or atrioventricular conduction time. Worsening of arterial insufficiency, vasodilatation; Digestive: Gastrointestinal pain,
(8) hypersensitivity to any component of this product. hepatomegaly, vomiting, mesenteric arterial thrombosis, ischemic colitis; Hematologic:
CYP2D6 inhibitors: Potentiated systemic beta-blockade (e.g., decreased heart rate, Nonthrombocytopenic purpura; thrombocytopenic purpura; agranulocytosis; Endocrine:
WARNINGS depression) has been reported during combined treatment with CYP2D6 inhibitors (e.g., Hyperglycemia, hypoglycemia; Skin: Pruritus, skin irritation, increased pigmentation,
As with many topically applied ophthalmic drugs, this drug is absorbed systemically. quinidine, SSRIs) and timolol. sweating; Musculoskeletal: Arthralgia; Nervous System/Psychiatric: Vertigo, local
The same adverse reactions found with systemic administration of weakness, diminished concentration, reversible mental depression progressing to
Clonidine: Oral beta-adrenergic blocking agents may exacerbate the rebound catatonia, an acute reversible syndrome characterized by disorientation for time and
beta-adrenergic blocking agents may occur with topical administration. For hypertension which can follow the withdrawal of clonidine. There have been no reports of place, emotional lability, slightly clouded sensorium, and decreased performance
example, severe respiratory reactions and cardiac reactions, including death exacerbation of rebound hypertension with ophthalmic timolol maleate. on neuropsychometrics; Respiratory: Rales, bronchial obstruction; Urogenital:
due to bronchospasm in patients with asthma, and rarely death in association Urination difficulties.
with cardiac failure, have been reported following systemic or ophthalmic Injectable epinephrine: (See PRECAUTIONS, General, Anaphylaxis) OVERDOSAGE
administration of timolol maleate (see CONTRAINDICATIONS). Carcinogenesis, Mutagenesis, Impairment of Fertility: In a two-year oral study
Cardiac Failure: Sympathetic stimulation may be essential for support of the circulation of timolol maleate administered orally to rats, there was a statistically significant There have been reports of inadvertent overdosage with Ophthalmic Solution
in individuals with diminished myocardial contractility, and its inhibition by beta- increase in the incidence of adrenal pheochromocytomas in male rats administered TIMOPTIC (timolol maleate ophthalmic solution) resulting in systemic effects similar
adrenergic receptor blockade may precipitate more severe failure. 300 mg/kg/day (approximately 42,000 times the systemic exposure following the to those seen with systemic beta-adrenergic blocking agents such as dizziness,
maximum recommended human ophthalmic dose). Similar differences were not headache, shortness of breath, bradycardia, bronchospasm, and cardiac arrest (see
In Patients Without a History of Cardiac Failure continued depression of the observed in rats administered oral doses equivalent to approximately 14,000 times the also ADVERSE REACTIONS).
myocardium with beta-blocking agents over a period of time can, in some cases, lead to maximum recommended human ophthalmic dose.
cardiac failure. At the first sign or symptom of cardiac failure, Preservative-free TIMOPTIC Overdosage has been reported with Tablets BLOCADREN* (timolol maleate tablets). A
in OCUDOSE should be discontinued. In a lifetime oral study in mice, there were statistically significant increases in 30 year old female ingested 650 mg of BLOCADREN (maximum recommended oral daily
Obstructive Pulmonary Disease: Patients with chronic obstructive pulmonary disease the incidence of benign and malignant pulmonary tumors, benign uterine polyps and dose is 60 mg) and experienced second and third degree heart block. She recovered
(e.g., chronic bronchitis, emphysema) of mild or moderate severity, bronchospastic mammary adenocarcinomas in female mice at 500 mg/kg/day (approximately 71,000 without treatment but approximately two months later developed irregular heartbeat,
disease, or a history of bronchospastic disease (other than bronchial asthma or times the systemic exposure following the maximum recommended human ophthalmic hypertension, dizziness, tinnitus, faintness, increased pulse rate, and borderline first
a history of bronchial asthma, in which TIMOPTIC in OCUDOSE is contraindicated dose), but not at 5 or 50 mg/kg/day (approximately 700 or 7,000 times, respectively, the degree heart block.
[see CONTRAINDICATIONS]) should, in general, not receive beta-blockers, including systemic exposure following the maximum recommended human ophthalmic dose). In
Preservativefree TIMOPTIC in OCUDOSE. a subsequent study in female mice, in which post-mortem examinations were limited to An in vitro hemodialysis study, using 14C timolol added to human plasma or whole
Major Surgery: The necessity or desirability of withdrawal of beta-adrenergic blocking the uterus and the lungs, a statistically significant increase in the incidence of pulmonary blood, showed that timolol was readily dialyzed from these fluids; however, a study of
agents prior to major surgery is controversial. Beta-adrenergic receptor blockade impairs tumors was again observed at 500 mg/kg/day. patients with renal failure showed that timolol did not dialyze readily.
the ability of the heart to respond to beta-adrenergically mediated reflex stimuli. This DOSAGE AND ADMINISTRATION
may augment the risk of general anesthesia in surgical procedures. Some patients The increased occurrence of mammary adenocarcinomas was associated with
receiving beta-adrenergic receptor blocking agents have experienced protracted severe elevations in serum prolactin which occurred in female mice administered oral timolol Preservative-free TIMOPTIC in OCUDOSE is a sterile solution that does not contain
hypotension during anesthesia. Difficulty in restarting and maintaining the heartbeat has at 500 mg/kg/day, but not at doses of 5 or 50 mg/kg/day. An increased incidence a preservative. The solution from one individual unit is to be used immediately after
also been reported. For these reasons, in patients undergoing elective surgery, some of mammary adenocarcinomas in rodents has been associated with administration opening for administration to one or both eyes. Since sterility cannot be guaranteed after
authorities recommend gradual withdrawal of beta-adrenergic receptor blocking agents. of several other therapeutic agents that elevate serum prolactin, but no correlation the individual unit is opened, the remaining contents should be discarded immediately
between serum prolactin levels and mammary tumors has been established in humans. after administration.
If necessary during surgery, the effects of beta-adrenergic blocking agents may be Furthermore, in adult human female subjects who received oral dosages of up to 60 mg
reversed by sufficient doses of adrenergic agonists. of timolol maleate (the maximum recommended human oral dosage), there were no Preservative-free TIMOPTIC in OCUDOSE is available in concentrations of 0.25 and
Diabetes Mellitus: Beta-adrenergic blocking agents should be administered with clinically meaningful changes in serum prolactin. 0.5 percent. The usual starting dose is one drop of 0.25 percent Preservative-free
caution in patients subject to spontaneous hypoglycemia or to diabetic patients TIMOPTIC in OCUDOSE in the affected eye(s) administered twice a day. Apply enough
(especially those with labile diabetes) who are receiving insulin or oral hypoglycemic Timolol maleate was devoid of mutagenic potential when tested in vivo (mouse) in gentle pressure on the individual container to obtain a single drop of solution. If the
agents. Beta-adrenergic receptor blocking agents may mask the signs and symptoms the micronucleus test and cytogenetic assay (doses up to 800 mg/kg) and in vitro in clinical response is not adequate, the dosage may be changed to one drop of 0.5 percent
of acute hypoglycemia. a neoplastic cell transformation assay (up to 100 mcg/mL). In Ames tests the highest solution in the affected eye(s) administered twice a day.
Thyrotoxicosis: Beta-adrenergic blocking agents may mask certain clinical signs (e.g., concentrations of timolol employed, 5,000 or 10,000 mcg/plate, were associated with
tachycardia) of hyperthyroidism. Patients suspected of developing thyrotoxicosis should statistically significant elevations of revertants observed with tester strain TA100 (in Since in some patients the pressure-lowering response to Preservative-free
be managed carefully to avoid abrupt withdrawal of beta-adrenergic blocking agents that seven replicate assays), but not in the remaining three strains. In the assays with tester TIMOPTIC in OCUDOSE may require a few weeks to stabilize, evaluation should include
might precipitate a thyroid storm. strain TA100, no consistent dose response relationship was observed, and the ratio of a determination of intraocular pressure after approximately 4 weeks of treatment with
test to control revertants did not reach 2. A ratio of 2 is usually considered the criterion Preservative-free TIMOPTIC in OCUDOSE.
PRECAUTIONS for a positive Ames test.
General: Because of potential effects of beta-adrenergic blocking agents on blood If the intraocular pressure is maintained at satisfactory levels, the dosage schedule
pressure and pulse, these agents should be used with caution in patients with Reproduction and fertility studies in rats demonstrated no adverse effect on male may be changed to one drop once a day in the affected eye(s). Because of diurnal
cerebrovascular insufficiency. If signs or symptoms suggesting reduced cerebral blood or female fertility at doses up to 21,000 times the systemic exposure following the variations in intraocular pressure, satisfactory response to the once-a-day dose is best
flow develop following initiation of therapy with Preservative-free TIMOPTIC in OCUDOSE, maximum recommended human ophthalmic dose. determined by measuring the intraocular pressure at different times during the day.
alternative therapy should be considered. Pregnancy: Teratogenic Effects — Pregnancy Category C. Teratogenicity studies with
timolol in mice, rats and rabbits at oral doses up to 50 mg/kg/day (7,000 times the Dosages above one drop of 0.5 percent TIMOPTIC (timolol maleate ophthalmic
Choroidal detachment after filtration procedures has been reported with the systemic exposure following the maximum recommended human ophthalmic dose) solution) twice a day generally have not been shown to produce further reduction in
administration of aqueous suppressant therapy (e.g. timolol). demonstrated no evidence of fetal malformations. Although delayed fetal ossification was intraocular pressure. If the patient’s intraocular pressure is still not at a satisfactory
observed at this dose in rats, there were no adverse effects on postnatal development level on this regimen, concomitant therapy with other agent(s) for lowering intraocular
Angle-closure glaucoma: In patients with angle-closure glaucoma, the immediate of offspring. Doses of 1000 mg/kg/day (142,000 times the systemic exposure pressure can be instituted taking into consideration that the preparation(s) used
objective of treatment is to reopen the angle. This requires constricting the pupil. Timolol following the maximum recommended human ophthalmic dose) were maternotoxic concomitantly may contain one or more preservatives. The concomitant use of two
maleate has little or no effect on the pupil. TIMOPTIC in OCUDOSE should not be used in mice and resulted in an increased number of fetal resorptions. Increased fetal topical beta-adrenergic blocking agents is not recommended. (See PRECAUTIONS, Drug
alone in the treatment of angle-closure glaucoma. resorptions were also seen in rabbits at doses of 14,000 times the systemic exposure Interactions, Beta-adrenergic blocking agents.)
following the maximum recommended human ophthalmic dose, in this case without ---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
Anaphylaxis: While taking beta-blockers, patients with a history of atopy or a apparent maternotoxicity.
history of severe anaphylactic reactions to a variety of allergens may be more reactive By: Laboratories Merck Sharp & Dohme-Chibret
to repeated accidental, diagnostic, or therapeutic challenge with such allergens. There are no adequate and well-controlled studies in pregnant women. Preservative- 63963 Clermont-Ferrand Cedex 9, France
Such patients may be unresponsive to the usual doses of epinephrine used to treat free TIMOPTIC in OCUDOSE should be used during pregnancy only if the potential benefit Based on PI - 514266Z/069A-03/09/9689-9690
anaphylactic reactions. justifies the potential risk to the fetus. US/TOP/14/0018 Issued February 2009
Nursing Mothers: Timolol maleate has been detected in human milk following oral and
Muscle Weakness: Beta-adrenergic blockade has been reported to potentiate muscle ophthalmic drug administration. Because of the potential for serious adverse reactions
weakness consistent with certain myasthenic symptoms (e.g., diplopia, ptosis, and from timolol in nursing infants, a decision should be made whether to discontinue
generalized weakness). Timolol has been reported rarely to increase muscle weakness in nursing or to discontinue the drug, taking into account the importance of the drug to
some patients with myasthenia gravis or myasthenic symptoms. the mother.
Information for Patients: Patients should be instructed about the use of Preservative- Pediatric Use: Safety and effectiveness in pediatric patients have not been established.
free TIMOPTIC in OCUDOSE. Geriatric Use: No overall differences in safety or effectiveness have been observed
between elderly and younger patients.
Since sterility cannot be maintained after the individual unit is opened, patients should
be instructed to use the product immediately after opening, and to discard the individual ADVERSE REACTIONS
unit and any remaining contents immediately after use. The most frequently reported adverse experiences have been burning and stinging

Patients with bronchial asthma, a history of bronchial asthma, severe chronic upon instillation (approximately one in eight patients).
obstructive pulmonary disease, sinus bradycardia, second or third degree The following additional adverse experiences have been reported less frequently with
-------------------------------------
* Registered trademark of ATON PHARMA, INC. ocular administration of this or other timolol maleate formulations:
BODY AS A WHOLE: Headache, asthenia/fatigue, and chest pain.
COPYRIGHT © 2009 ATON PHARMA, INC. CARDIOVASCULAR: Bradycardia, arrhythmia, hypotension, hypertension, syncope, heart
All rights reserved block, cerebral vascular accident, cerebral ischemia, cardiac failure, worsening of angina
pectoris, palpitation, cardiac arrest, pulmonary edema, edema, claudication, Raynaud’s

Cornea

Be a Hero toYour
HSVK Patients

It is important for ODs to have a thorough understanding of this sight-threatening
disease. By Shannon Leon, OD, and Joseph J. Pizzimenti, OD

Herpes simplex virus (HSV) Photo: Lisa Martén, MD involvement, as well as intraocular
is a major health concern. infections and retinitis.2,5 Approxi-
This is evidenced by the epi- Advanced dendritic lesions during mately 72% of ocular HSV disease
demic of genital herpes and involves the corneal epithelium;
the enhanced acquisition of human HSV epithelial keratitis can result in 41% involves the lid or conjunctiva;
immunodeficiency virus (HIV) asso- 12% affects the corneal stroma; and
ciated with HSV.1 Its prevalence in geographic ulcers (green arrow). These 9% involves the iris and associated
the ocular world is just as strong, uveal tract.
with HSV keratitis (HSVK) stand- defects are more diffuse in appearance,
ing as the leading infectious cause of Primary ocular HSV infections
corneal blindness among developed but still maintain branched features typically involve rapidly spreading
nations, primarily because of its corneal dendrites or geographic
recurrent nature.2 Here, you’ll find along their borders. ulcers in the epithelium, as there is
a review of HSVK, including proper no antibody in the tear film to act
differential diagnosis and contempo- or retinitis based on the specific against the virus. In these cases,
rary antiviral medical management. ocular tissues affected. there is no associated immune reac-
tion to cloud the stroma or deeper
Assessing the Eye HSVK is classified by the loca- ocular tissues.6,7
tion of the principal site of corneal
Humans are the only known natural involvement. This includes HSVK of Those undergoing chemotherapy,
reservoir for HSV. Along with the the epithelium (HSV epithelial kera- recipients of bone marrow or organ
nose and mouth, the eyes are a main titis), HSVK of the stroma (HSV transplants and people with HIV
access point (Table 1).3 Systemic stromal keratitis with or without infection can develop multiple and
viral infections from other areas of ulceration) and HSVK of the endo- extensive lesions. In some cases, vis-
the body may also manifest in the thelium (HSV endothelial keratitis).4 ceral spread may occur.2,3,5
ocular tissues, resulting in potential-
ly sight-threatening complications. Ocular complications of HSV HSV-1 or HSV-2?
include lid, conjunctival and corneal
HSV-related ocular disease is clas- An estimated 3.7 billion people
sified as either primary or recurrent. under age 50 worldwide have
It is also classified as blepharitis, HSV-1 infection.8 HSV-1 is trans-
conjunctivitis, HSVK, iridocyclitis mitted primarily through direct
contact with infected secretions

64 REVIEW OF OPTOMETRY JULY 15, 2017

(i.e., saliva or tears) or Table 1. Major Viruses of Ophthalmic Significance3 is frequently present
lesions. Complications in an HSV dendrite.
of HSV-1 infection DNA Conversely, there is fre-
occur mainly in the oro- quently minimal or no
facial and ocular areas, Family Ophthalmic Involvement ulceration or epithelial
but they can also include defect in a VZVK
genital herpes.5,8,9 Adenoviridae • Epidemic keratoconjunctivitis (most commonly pseudodendrite.

HSV-2 is less preva- associated serotypes are adenovirus 8, 19 and 37) It is also prudent
lent, with an estimated to evaluate corneal
417 million people Herpesviridae • Herpes simplex ocular disease sensitivity bilaterally.9

• Varicella-zoster ophthalmicus

• Cytomegalovirus retinitis (human herpes virus 5)

Papoviridae • Human papilloma virus of lids, adnexa, conjunctiva

ages 15 to 49 affected Poxviridae • Molluscum contagiosum of lids, adnexa Unlike other microbial

worldwide.8 It is sexu- RNA infections and cor-

ally transmitted and Togaviridae • Rubella retinopathy neal abrasions, where

causes genital herpes. Retroviridae • HIV – affects many ocular tissues corneal sensitivity is

The decreasing preva- heightened, patients

lence of HSV-1 before puberty in detailed history. Optometrists with HSVK often present with

affluent and developed countries, should elicit the exact clinical course decreased sensitivity in the involved

and the increase in orogenital sexual of the patient’s symptoms. Some eye relative to the fellow eye.11 To

practice, have led to a change in the history items to probe include HSV test this, gently apply a cotton swab

epidemiology of HSV-1 and HSV-2. recurrence, contact lens wear, medi- to the patient’s cornea and evaluate

HSV-1 is now causing disease in a cal and systemic history, nasal and the blink reflex. You should test the

territory formerly inhabited exclu- oral cold sore history, recent topi- uninvolved eye first so the patient

sively by HSV-2 and vice-versa.9 cal or systemic steroid treatment can use it as a basis for comparison.

Recurrences of HSV may be trig- and recent fever or ultraviolet light A higher or lower sensitivity in one

gered by fever, hormonal changes, exposure.4,11 The clinician should eye may manifest as a subjective

ultraviolet exposure, psychological ask also about recent ocular surgery increase or decrease of feeling, touch

stress, ocular surgery, ocular trauma or trauma, previous corneal abra- or sensitivity.

and trigeminal nerve manipula- sions and recurrent erosions. This HSV has the ability to establish

tion.5,8 Although pregnant women will help to narrow down the list of a latent infection. This allows it to

do not fit the traditional definition differential diagnoses. live in the host without inducing

of immunosuppressed, the changes During the clinical examination, pathology. As a result, it is difficult

in immune response due to the if the patient presents with skin to detect. While laboratory testing

pregnancy increase the risk of both vesicles, note their distribution. For is generally not needed to establish

primary and recurrent HSV infec- example, vesicles on the forehead, a diagnosis of HSVK, it can help

tions.10 HSV-1 tends to recur in the scalp and nose that respect the verti- to provide confirmation in the rare

orofacial area but not in the genital cal midline are more suggestive of complicated case where the diag-

area after primary infection; con- varicella-zoster (VZV) than HSV.11 nosis is in doubt. The standard in

versely, HSV-2 tends to recur in the The slit lamp examination should diagnosis of HSVK is viral isolation

genital area but not in the orofacial include a detailed evaluation of in a culture.13 Due to potentially

area after primary infection.9 the cornea. Vital dye staining with lengthy turnaround time, standard

Both HSV-1 and HSV-2 infections fluorescein and either rose bengal or HSV culture is not useful for rapid

are lifelong. Vaccines have been inef- lissamine green should also be per- clinical diagnosis.

fective to date, but researchers con- formed. The typical epithelial lesion Additional tests that can be con-

tinue to study the possibilites.8 in HSVK presents as a true dendritic ducted include Giemsa stains of the

Making the Diagnosis ulcer with terminal endbulbs.12 This cornea and skin scrapings, enzyme-

is different from the presentation linked immunosorbent assay testing,

HSVK is often diagnosed without of VZV keratitis (VZVK), which HSV antibody titers and polymerase

the need for laboratory testing, usually presents as a pseudoden- chain reaction assays.4,11,13 Serology

so an understanding of the clini- drite without terminal bulb stain- is of limited use because there is a

cal signs and symptoms is critical. ing. In differentiating HSVK from high prevalence of antibodies in the

Proper diagnosis begins with a VZVK, remember that ulceration normal population. These tests are

REVIEW OF OPTOMETRY JULY 15, 2017 65

Education: September 13-16 2017 PQCYVM8VaQKkUKOeQPGyGo'VuZrYRaQKVpJ9pCoGPinUVGtmZReGnTtV
Exhibition: September 14-16, 2017
Location: Sands Expo | Las Vegas, NV

Are you wasting
time and money
using outdated

VGEJPQNQI[!

It’s time to upgrade your lens processing.

Invest in the latest lens processing software and equipment to make an exponential difference
in your bottom line. Save time and money while preparing your business for the future of the

eyewear industry.
Need convincing? Visit with more than 40 industry-leading organizations at International Vision
Expo West 2017 – view the latest lens technologies in person, get hands-on demonstrations, and

talk to industry experts about the best solutions for your business.
#EEGUUCEQORNGVGNKDTCT[QHOGODGTEQORCPKGUƂPFVJGKT8KUKQP'ZRQDQQVJNQECVKQPU

CPFIGVHTGG8KUKQP'ZRQTGIKUVTCVKQPCVNRVVJGXKUKQPEQWPEKNQTI.

Cornea

Photos: Lisa Martén, MD

At left, significant scarring from deep corneal inflammation, which is one of the most common causes of vision loss in HSVK. At
right, keratic precipitates with anterior chamber reaction and stromal haze, which are hallmarks of HSV endothelial keratitis.

only positive when a live virus is keratitis. Infectious masqueraders coidosis.4,12 When diagnosing HSV
present (as seen in HSV epithelial include Acanthamoeba kerati- stromal keratitis with ulceration,
keratitis) and cannot be used to tis, VZVK, adenovirus epithelial consider all forms of microbial kera-
diagnose, or exclude, active disease keratitis, Epstein-Barr epithelial titis as well as exposure and neuro-
caused by immunologic reactions keratitis, chlamydial keratitis and tropic keratopathy.4,12
against HSV triggered by prior other varying microbial keratitis.4,12
infections, which is typically the case Non-infectious differentials include Of the different types of HSVK,
for HSV stromal keratitis. Thygeson’s superficial punctate endothelial is the least common. The
keratopathy, exposure keratopathy, presence of stromal and epithelial
HSVK or a Masquerader? epithelial defects from topical medi- edema with inflammation at the
cations (i.e., antivirals and beta- level of the endothelium, signified
The initial presentation of ocular blockers), epithelial defects due to by keratic precipitates in the absence
HSV may or may not represent pri- contact lens wear, epithelial regen- of significant anterior uveitis, is clas-
mary infection by the virus. In one eration lines, epithelial basement sified as endothelial keratitis. The
study of 108 adult patients with pri- membrane disease and recurrent list of differential diagnoses for HSV
mary ocular HSV, 84% of patients corneal erosions.4,12 Appropriate endothelial keratitis is the same as
had moderate to severe conjuncti- patient history, demographics and that for stromal keratitis, in addi-
vitis, 38% had moderate to severe a comprehensive workup will help tion to any form of keratouveitis,
blepharitis, 35% had a concomitant you sift through masqueraders. Posner-Schlossman syndrome, cyto-
upper respiratory infection and megalovirus endothelial keratitis
31% had generalized symptoms. There are several differential and corneal graft rejection.4,12 These
Only 15% of patients had dendritic diagnoses for both HSV stromal differential diagnoses frequently
ulcers, while 2% had HSV endothe- keratitis and HSV endothelial kera- present with raised intraocular pres-
lial keratitis and 19% had bilateral titis. Differentials for HSV stromal sure (IOP). Herpetic eye disease
disease.14 keratitis include an exhaustive list of should be considered the cause
interstitial and microbial keratitides. of acute-onset, unilateral corneal
Because of its variable presenta- In diagnosing HSV stromal kera- edema unless proven otherwise.
tion and ability to affect all corneal titis without ulceration, consider
layers, HSVK has several masquer- other interstitial keratitides such The wide variety of conditions
aders and differential diagnoses. as that caused by syphilis, Cogan’s that can masquerade as HSVK
For example, any keratitis that syndrome, Lyme disease, leprosy, makes the history and work-up vital
creates a dendriform lesion could lymphoma, tuberculosis and sar- to a correct diagnosis. In any case
be mistaken for HSV epithelial of epithelial, stromal or endothelial

REVIEW OF OPTOMETRY JULY 15, 2017 67

Cornea

Photo: Lisa Martén, MD mised patients with HSV epithelial processing (i.e., metabolism, excre-

keratitis, as the prevalence of acyclo- tion) of these agents. Available oral

vir-resistant (ACVR) HSV-1 isolates formulations include Zovirax (acy-

is much higher (4.3% to 14%) than clovir, GlaxoSmithKline), Valtrex

that in immunocompetent patients (valacyclovir, GlaxoSmithKline) and

(0.1% to 0.6%).16 This difference Famvir (famciclovir, Novartis).

is likely due to longer mucosal per- Oral antivirals tend to be the

sistence of ACVR HSV variants. treatment of choice for HSV epithe-

Therefore, it may be prudent to lial keratitis because they are often

treat immunocompromised patients less expensive than topical agents,

HSV epithelial keratitis doesn’t always with HSVK both systemically and and the dosing schedule is more

present with the classic corneal topically. adaptable to daily use (Table 2).

dendrite. Sometimes, the epithelial HSV epithelial keratitis is usually In addition to prescribing antivi-

defect will be more coalesced in treated with antiviral medication, ral therapy, clinicians should stabi-

appearance. which may be topically applied lize the ocular surface by prescribing

or systemically administered. The preservative-free tear supplements.

keratitis, if the patient’s story does two most common topical antiviral Topical immunomodulatory medi-

not fit the clinical findings, then agents include Viroptic (trifluridine cations may be added for increased

HSVK should be at the top of your 1%, Pfizer) and Zirgan (ganciclovir tear production and anti-inflam-

differentials. 0.15%, Bausch + Lomb). Both of matory support. Lacrimal plugs

Treatment these agents are FDA approved for and bandage contact lenses may be
treating HSVK. Viroptic is gener- implemented in long-term ocular

Once a diagnosis has been made, ally dosed one drop nine times daily surface management.

focus should shift to treatment. in the affected eye until the ulcer is HSV stromal keratitis without

HSV epithelial keratitis is resolved, whereas Zirgan is dosed epithelial ulceration is the more

thought to account for 50% to 80% one drop five times daily until the common of the two HSV stromal

of all ocular herpes infections.13 ulcer is resolved, then three times infections. As its name implies,

HSV epithelial keratitis is the result daily for seven additional days. stromal keratitis without ulceration

of the virus’ destruction of corneal Viroptic is effective, but also known is thought to occur due to viral pro-

epithelial cells secondary to viral for its toxicity, which can delay teins that remain in the cornea even

replication.13 Patients often present corneal healing. As a result, Zirgan after the infection has resolved.17

with the classic symptoms of HSV is often the topical treatment of In response to these remaining pro-

ocular infection such as redness, choice. teins, the body produces an inflam-

tearing, foreign body sensation, Unlike topical antivirals, oral matory response, which results in a

pain, photophobia and blurred antiviral medications should be used stromal keratitis without necrosis.

vision.11,12,15 with caution in patients with kidney Patients will generally present with

The cornea generally shows dif- or liver disease due to the internal symptoms of blurry vision, photo-

fuse punctate areas that even- Photo: Lisa Martén, MD phobia and halos around lights

tually coalesce into a distinct brought on by edema of the

dendritic lesion with terminal stroma.15

bulbs.12 If the ulcer is more Clinical signs include stro-

advanced, a more diffuse epi- mal edema, anterior chamber

thelial lesion, known as a geo- reaction, stromal opacity and

graphic ulcer, will be present. neovascularization.13 This sig-

The Herpetic Eye Disease nificant inflammatory response,

Study (HEDS) I showed no in combination with recurrent

benefit in combining both oral disease, often makes stromal

and topical antivirals, so choose keratitis the instigator of irre-

one course of treatment.15 One versible damage and significant

exception to this may be pre- Here is an example of the classic HSVK epithelial scarring. Stromal keratitis

scribing for immunocompro- dendrite with terminal bulbs. without ulceration requires the

68 REVIEW OF OPTOMETRY JULY 15, 2017

Up to 2018NEW TECHNOLOGIES

18-28 CE Eye Care&TREATMENTSIN

Credits*

2018 REVIEW OF OPTOMETRY®

EDUCATIONAL MEETINGS OF CLINICAL EXCELLENCE

MEETINGS

FEBRUARY 16-20, 2018

Winter Ophthalmic Conference

ASPEN, CO

Westin Snowmass
Conference Center

Program Chairs: Murray Fingeret, OD & Leo Semes, OD

APRIL 6-8, 2018

NASHVILLE, TN

Nashville Marriott at Vanderbilt

Program Chair: Paul Karpecki, OD

APRIL 26-29, 2018

SAN DIEGO, CA

Program Chair: Paul Karpecki, OD

MAY 17-20, 2018

ORLANDO, FL

Disney’s Yacht & Beach Club

Program Chair: Paul Karpecki, OD

NOVEMBER 2-4, 2018

PHILADELPHIA, PA

Program Chair: Paul Karpecki, OD

Visit our website for the latest information:

www.reviewofoptometry.com/events

email: [email protected] | call: 866-658-1772

Administered by *Approval pending

Review of Optometry ®

Review of Optometry® partners with Salus University for those ODs who are licensed in states that require university credit.
See Review website for any meeting schedule changes or updates.

Cornea

use of a topical corticosteroid Table 2. Oral Antiviral Therapy Dosing4 Post-HSVK eyes should
be carefully monitored for
along with an oral antiviral. Dendritic Epithelial Keratitis (Seven to 10 days) IOP rise secondary to trabe-
HSV stromal keratitis with culitis.17 In some cases, long-
Antiviral Dosage
ulceration is, fortunately, less
common than stromal kera- Acyclovir 400mg five times daily
term use of topical steroids

titis without ulceration. Stro- Valacyclovir 500mg three times daily is needed to prevent future

mal keratitis with ulceration Famciclovir 250mg two or three times daily flare-ups and scarring. When-
is also an immune-mediated ever corticosteroids are used
response to the proteins left Geographic Epithelial Keratitis (14 to 21 days) with a patient with previous

behind in the stroma.12 How- Acyclovir 800mg five times daily history of HSV ocular infec-

ever, instead of producing Valacyclovir 1g three times daily tion, antivirals are needed to

inflammation, the cells signal Famciclovir 500mg three times daily prevent recurrence.
tissue necrosis, resulting in For patients with significant
ulceration and, ultimately, Stromal Keratitis Without Ulceration* (At least 10 weeks)
stromal bed destruction. corneal scarring from recur-
Acyclovir 400mg two times daily rent HSVK episodes, consider

Clinical symptoms are Valacyclovir 500mg once daily use of an amniotic membrane

similar between the two types Famciclovir 250mg two times daily to boost corneal repair.
of stromal keratitis. Patients Although not considered a
with HSV stromal keratitis Stromal Keratitis With Ulceration** (Seven to 10 days) first-line treatment for HSVK,
with ulceration present with amniotic membranes can help
Acyclovir 800mg three to five times daily

necrosis of the stromal tissue. Valacyclovir 1g three times daily decrease inflammation and

This results in an opacifica- Famciclovir 500mg two times daily provide the building blocks

tion of the stroma, which can Endothelial Keratitis*** (Variable) to heal corneal tissue. Even
lead to thinning of the tissue when scarring appears to be
and increased risk of corneal Acyclovir 400mg three to five times daily beyond repair, these devices

perforation.12 Valacyclovir 500mg two times daily may be able to improve the

The treatment of stromal Famciclovir 250mg two times daily corneal appearance and give

keratitis with ulceration is Prophylaxis of Recurrent HSVK (At least one year) the ocular surface a second
still commonly debated. A chance.
limited number of studies Acyclovir 400mg two times daily
Surgical intervention is
Valacyclovir 500mg once daily
exist regarding treatment; seldom necessary in the man-

thus, a well-established Famciclovir 250mg two times daily agement of HSVK. Progres-

protocol does not exist. It is *Antiviral treatment is prophylactic since patients are also treated with a thera- sive stromal thinning with
thought, however, that simi- peutic dose of topical steroid. impending or actual perfora-
lar to stromal keratitis with- **Limited dose of topical steroid plus therapeutic dose of antiviral. tion may occur, although it
out ulceration, a combination ***Therapeutic dose of topical steroid and therapeutic dose of antiviral. Oral anti- is rare. Conservative surgical
of topical corticosteroids and viral agent is reduced to prophylactic dose after seven to 10 days and maintained intervention with applica-
as long as steroid is in use.

oral antivirals is best suited tion of cyanoacrylate glue is

to treat stromal keratitis with ulcer- precipitates and, occasionally, usually sufficient, although tectonic

ation.4 elevated IOP.12 The elevation of IOP keratoplasty may be required to

HSV endothelial keratitis is a common sign of endotheliitis preserve the integrity of the globe.

stems from inflammation due to and should never be overlooked. Adjunctive temporary or permanent

viral proteins within the corneal Much like its stromal counterpart, tarsorrhaphy is recommended in

endothelium.13 Patients with HSV HSV endothelial keratitis is thought such cases.

endothelial keratitis present with to respond well to a combination of
symptoms similar to other forms of oral antivirals and topical corticoste- When Acute Becomes Chronic
HSVK, including pain, redness, pho- roids. Because Zirgan and Viroptic A maintenance dose of systemic

tophobia and blurry vision. HSV do not penetrate the cornea deeply, antiviral therapy may help some

endothelial keratitis is also marked oral antivirals are the preferred patients with HSVK. In the HEDS II

by a deep stromal opacification with method of treating HSV endothelial study, a maintenance dose of either

anterior chamber reaction, keratic keratitis.4 400mg of acyclovir BID or 500mg

70 REVIEW OF OPTOMETRY JULY 15, 2017

valacyclovir QD for 12 months Dr. Leon is an optometrist at the Eye Res. 2006;2(4):355-80.
after resolution of the initial episode South Texas Eye Institute. She is a 6. Pavan-Langston D. Part one: the research perspective.
significantly decreased the prob- graduate of the Rosenberg School Advances in the management of ocular herpetic disease.
ability of recurrence.18 Patients who of Optometry at the University Candeo Clin Sci Comm. 2011;1-9.
have had more than one episode of of the Incarnate Word, where she 7. Toma HS, Murina AT, Areaux RG Jr, et al. Ocular HSV-1
HSVK and those with HSV stromal completed a residency in primary latency, reactivation and recurrent disease. Semin Ophthalmol.
keratitis are prime candidates for care optometry. 2008;23(4):249-73.
a maintenance course of antiviral 8. World Health Organization fact sheet on herpes simplex
medication, which can often spare Dr. Pizzimenti is a full-time virus. www.who.int/mediacentre/factsheets/fs400/en/. Janu-
patients significant scarring and loss faculty member at the University of ary 2017. Accessed June 15, 2017.
of vision. the Incarnate Word in San Antonio, 9. Azher TN, Yin XT, Tajfirouz D, et al. Herpes simplex keratitis:
Texas, where he coordinates the challenges in diagnosis and clinical management. Clin Oph-
HSVK is the most frequent Primary Care Residency Program. thalmol. 2017;11:185-191.
cause of corneal blindness in the He is also a contributing editor for 10. Langford KS. Infectious disease and pregnancy.
United States and the most com- Review of Optometry. Obsestrics, Gynaecology and Reproductive Medicine.
mon source of infectious blindness 2002;12(3):125-30.
in the Western world.2 A detailed, 1. Freeman EE, Weiss HA, Glynn JR, et al. Herpes simplex 11. Rabinowitz MP. Herpes simplex virus. Wills Eye Manual
targeted history and meticulous virus 2 infection increases HIV acquisition in men and women: Office and Emergency Room Diagnosis and Treatment of Eye
clinical work-up are essential to systematic review and meta-analysis of longitudinal studies. Disease. 6th ed. Philadelphia: Lippincott Williams & Wilkins;
proper diagnosis, effective treatment Aids. 2006;20(1):73-83. 2012.
and preservation of visual function. 2. Farooq AV, Shukla D. Herpes simplex epithelial and stro- 12. Hill GM, Ku ES, Dwarakanathan S. Herpes simplex kerati-
With timely, aggressive treatment, mal keratitis: an epidemiologic update. Surv Ophthalmol. tis. Disease-a-Month. 2014;60(6):239-46.
the prognosis in HSVK is generally 2012;57(5):448–62. 13. Zhu L, Zhu H. Ocular herpes: the pathophysiology, man-
favorable. ■ 3. Harding SP. Viral infections of the eye. Reviews in Medical agement and treatment of herpetic eye diseases. Virologica
Virology. 1993:161-71. Sinica. 2014;29(6):327-42.
4. White ML, Chodosh J. Herpes simplex virus keratitis: a 14. Liesegang, TJ. Herpes simplex virus epidemiology and
treatment guideline. The American Academy of Ophthalmology ocular importance. Cornea. 2001;20(1):1-13.
Clinical Guidelines. June 2014. 15. Murphy C, Shahnazaryan D. Managing herpes simplex
5. Kaye S, Choudhary A. Herpes simplex keratitis. Prog Retin keratitis. Iris Medical Times. 2011;45(16):35.
16. Duan R, de Vries RD, Osterhaus ADME, et al. Acyclovir-
resistant corneal HSV-1 isolates from patients with herpetic
keratitis. J Infect Dis. 2008;198(5):659-63.
17. Adams MJ, Carstens EB. Ratification vote on taxonomic
proposals to the International Committee on Taxonomy of
Viruses. Arch Virol. 2012;157(7):1411–22.
18. Wilhelmus KR, Beck RW, Moke PS, et al. Acyclovir for
the prevention of recurrent herpes simplex virus eye disease.
N Engl J Med. 1998;339:300-6.

Unlocking the Future of Healthcare Analytics

ARE YOU KEEPING UP WITH THE COMPETITION?

Quickly identify missed revenue
opportunities
Create your own metric dashboard
Complete accuracy customized to
your billing habits
Have fun and engage your team
with Gamification

PLEASE CONTACT GLIMPSE TO JOIN | [email protected] | 904.503.9616 EXT. #1 | GLIMPSELIVE.COM

2 CE
Credits

(COPE approved)

Caring for Patients

With Brain Injury

More often than not, TBI affects a patient’s vision, and ODs must be prepared to

evaluate and manage this population. By Aaron K. Tarbett, OD
A“silent epidemic.”1
That’s how traumatic Photo: Ann McKee, MD Given the strong prevalence and
brain injury (TBI) was impact on vision, optometrists
described in the 1990s. should be familiar with the basics
of TBI and its management.

Today, with conservative estimates Terminology
of 2.8 million Americans suffering

a TBI every year and accounting for The terminology currently

10% of Americans with disabilities, employed in brain injury often

it’s hardly silent anymore.2,3 From leads to confusion. The three com-

sports-related concussion to mili- mon terms used to describe brain

tary TBI, it’s better recognized and injury are concussion, mild trau-

often covered in the lay media.4 It’s matic brain injury (mTBI) and,

also more prevalent in optometric Fig. 1. A focus of perivascular neurofibrillary most recently, chronic traumatic

practice. tangles (black) and neurites at the depth encephalopathy (CTE). Concussion

Approximately 50% of the of sulcus in the dorsolateral frontal and mTBI are used interchangeably

brain’s neural circuitry is dedicated cortex consistent with stage I/IV CTE, in medical literature and by medi-

to vision, and 75% of TBI patients AT8 immunostaining for p-tau, original cal professionals (as is the case in

will experience visual symptoms.5,6 magnification×100.63 this article). However, specialists

Release Date: July 2017 Faculty/Editorial Board: Aaron K. Tarbett, OD
Expiration Date: July 15, 2020 Credit Statement: This course is COPE approved for 2 hours of CE
Goal Statement: Because 75% of patients sustaining a traumatic brain credit. Course ID is 54094-NO. Check with your local state licensing
injury (TBI) will experience visual symptoms, eye care providers should board to see if this counts toward your CE requirement for relicensure.
be familiar with the basics of TBI and its management. This article Disclosure Statements:
provides the foundation of knowledge necessary to alleviate any trepi- Authors: The author has no relationships to disclose.
dation practitioners may have in diagnosing and managing this patient
population. Editorial staff: Jack Persico, Rebecca Hepp, William Kekevian, Michael
Riviello and Michael Iannucci all have no relationships to disclose.

72 REVIEW OF OPTOMETRY JULY 15, 2017

OPTOMETRIC STUDY CENTER

suggest concussion and mTBI should Table 1. Glasgow Coma Scale
be separate entities with concussion
referring to a neurological syndrome Behavior Response Score
involving head trauma and subse-
quent symptoms, while mTBI is an Eye opening Spontaneously 4
identifiable injury to brain tissue.7 response To speech 3
Currently, this differentiation is dif- To pain 2
ficult, given our common screening No response 1
and neuroimaging techniques are
not sensitive enough to detect such Best verbal Oriented to time, place and person 5
microstructural and physiological response Confused 4
changes in the brain. Inappropriate words 3
Best motor Incomprehensible sounds 2
Classification response No response 1

Following head trauma, clinical diag- Obeys commands 6
nosis and classification of severity is Moves to localized pain 5
typically done by either the Glasgow Flexion withdrawal from pain 4
Coma Scale (Table 1) or one or a Abnormal flexion to pain (also termed decorticate) 3
combination of: loss of consciousness Abnormal extension to pain (also termed decerebrate) 2
(LOC), alteration of consciousness No response 1
(AOC) such as disorientation or ‘see-
ing stars’ or post-traumatic amnesia Pathophysiology potential, is often disrupted, as well
(PTA).8 Both concussion and mTBI as other cytoskeletal elements. Pos-
are often defined as any LOC or The pathophysiology in mTBI is sible axon rupture and excitotoxicty
AOC less than 30 minutes or amne- complex, not fully understood and (unchecked neurotransmitter release)
sia lasting less than 24 hours (Table involves physiological, structural and follow, leading to an interruption in
2).4,9 More often than not, concus- vascular processes. Two pathological signal transmission.15,16 Areas com-
sions are without loss of conscious- mechanisms are notable: traumatic monly affected include the midline
ness and diagnosed by the variable axonal injury and microvascular regions such as the corpus callosum,
degrees of AOC.10 Any momentary damage.8 brainstem and thalamus—all heavily
disorientation will qualify as a diag- involved in vision.17
nosis of mTBI, while any identifiable Traumatic axonal injury. Dur-
tissue damage or intracranial hemor- ing a rapid acceleration of or blow Microvascular damage. Consider-
rhage (subdural, epidural, etc.) on to the head, the brain shifts within ing the brain contains 400 miles of
neuroimaging is considered moderate the skull, causing stretching and capillaries, microvascular damage
to severe brain injury.11,12 twisting of the axons, which are in mTBI is a primary mechanism of
responsible for signal transmission tissue injury.18 Pial vessels surround
CTE has driven much discus- and can course great distances across and penetrate brain parenchyma,
sion recently due to its notoriety in the brain. With their viscoelastic supplying oxygen and other metabol-
sports-related concussion.13 CTE is a nature and large surface-to-volume ically needed nutrients. Violent head
progressive, pathological deteriora- ratio, the axons are fragile and acceleration can shear these vessels
tion of the brain caused by repeti- prone to damage. The axolemma, or cause rupture during impact with
tive head trauma. It is due only to the outer membrane containing bony protuberances of the cranium.
head trauma with pathognomonic, ion channels that create membrane
perivascular accumulations of hyper-
phosphorylated tau (p-tau) present Table 2. Severity Rating for TBI Post-traumatic Amnesia
in neurofibrillary tangles located at
the sulcus of brain folds (Figure 1). Severity Glasgow Alteration of Loss of ≤ 24 hrs
Current theory speculates the sulci Coma Scale Consciousness Consciousness > 24 hrs
absorb the compressive force of < 7 days
brain movement during injury and Mild 13-15 ≤ 24 hrs 0 to 30 min ≥ 7 days
consequently accumulate p-tau.14 Moderate 9-12 > 24 hrs > 30 min
< 24 hrs
Severe 3-8 > 24 hrs ≥ 24 hrs

REVIEW OF OPTOMETRY JULY 15, 2017 73

OPTOMETRIC STUDY CENTER

Photo: Charles Shidlofsky, OD ber of nonspecific symptoms (fatigue, sically photosensitive retinal ganglion
depression, irritability, etc.) that cells (ipRGC) and their interaction
Fig. 2. FL-41 tinted lenses can help affect their daily living and quality with the thalamus.22 The recent
of life (Table 3). The official ICD-10 discovery of retinal cells, other than
patients with brain injury cope with diagnosis for this neurological syn- rods and cones, that detect light has
drome is postconcussion syndrome caused quite a shift in current theory
photosensitivity. (PCS), although patients are anec- about the detection of light and the
dotally referred to as the “miserable perception of vision.23 Approximate-
The decrease in cerebral autoregula- minority.”21 Here is a look at the ly 1% of ganglion cells detect light,
tory capacity, in addition to the phys- most common mTBI sequelae and thought to be primarily background-
ical vessel injury, leads to hypoxia, the treatment options that can help: related illumination, with the ipRGC
edema and blood toxicity.16,19 axons projecting directly to the
Headache. This is the most com- thalamus—the primary signal weigh
Sequelae and Treatment mon symptom following mTBI, station of the brain that regulates
and whether the headache is visu- perceptual sensations.24 Brain injury
Patients with acute concussion or ally related is the primary concern results in thalamic damage and dys-
mTBI (within one month post-injury) for clinicians.21,22 The most reliable regulation of the incoming signal.
can experience a variety of physical, indication of visual involvement is Principally, upregulation or poor
emotional and cognitive sequelae the association with visually related suppression of light intensity (par-
that will typically resolve without tasks. Although headaches take ticularly background lighting) results
intervention over three months. on many forms following mTBI, in an enhanced sensitivity to light,
migraine and cervical headache are and a threshold of pain stimulus is
However, approximately 15% of predominant, and these will be man- reached as the sensitivity increases.24
patients will have symptoms that aged medically, surgically or with
persist beyond one year.11,20 This physical therapy. Treatment of photosensitivity out-
group of patients may retain a num- doors logically consists of sunglasses
Clinicians must rule out or treat and a brimmed hat; but treatment of
visual etiologies, while continued debilitating indoor photosensitivity is
management for chronic headache is more controversial. While a patient
typically handled by other specialists wearing sunglasses indoors has long
coordinated by the patient’s primary been thought to be an indication
care provider. of non-organic or psychologically
related conditions, merit for such a
Photosensitivity. This remains one diagnosis may be lacking in the case
of the most common and enigmatic of brain injury. This patient likely
symptoms in PCS. Current theory on experiences true light sensitivity
the pathophysiology involves intrin- unrelated to a functional or conver-
sion disorder. However, there is con-
Sheard’s Criterion cern that sunglasses for indoor use
3 ∆ BI 10∆ will establish a “habit-forming ten-
dency” and may actually prevent the
7∆ resolution of visual or psychological
symptoms.25 In this regard, clinicians
Exophoria Base Out Vergence could recommend titration of tints
10∆ 11∆ over a period of time.

7∆ A number of studies indicate the
usefulness of different tints, such as
0∆ 21∆ FL-41 for patients with migraine and
blepharospasm (Figure 2).26,27 Inter-
Total Fusional Vergence estingly, FL-41 filters 480nm light,
the peak activation range of photo-
Fig. 3. This criterion can help ECPs diagnose and manage decompensated exophoria. sensitive retinal ganglion cells.28

74 REVIEW OF OPTOMETRY JULY 15, 2017

Oculomotor dysfunction. This Table 3. Postconcussion Symptoms
affects approximately 30% to 50%
of mTBI patients at some point.5,29,30 Physical Cognitive Emotional
The most common issues are eye
tracking (saccades and pursuits), con- Headache Memory deficits Irritability
vergence insufficiency and accommo- Dizziness Attention/concentration deficits Depression
dative dysfunction.31,32 Fatigue Executive function deficits Anxiety
Visual disturbance
Accommodative dysfunction is of Noise sensitivity
particular concern for optometrists, Light sensitivity
as roughly 50% of pre-presbyopic Insomnia
TBI patients show accommodative
dysfunction following TBI vs. 6% defined as the presence of a positive visual symptoms.40 However, without
in the normal population.33,34 Most fusional ability twice that of the pho- large scale, prospective studies, it is
clinicians can use Donder’s push up ria.38 For example, if a patient pre- not a universally recommended treat-
method or minus lenses and address sented with near exophoria of 10pd, ment; clinicians should first consider
those results with Hofstetter’s formu- the positive fusional ability to satisfy a brief trial of vision rehabilitation.
la to assess age-related accommoda- Sheard’s criterion would be 20pd. The 2016 Department of Defense
tive ability. Hofstetter’s formula for and Veterans Affairs guidelines for
the minimum amplitude for a given In addition to determining wheth- traumatic brain injury issues a word
age is defined as: 15 - 1/4 age.35 er an exophoria should be symptom- of caution for all rehabilitative thera-
atically relevant, Sheard’s criterion pies, including vision rehabilitation.39
Reading glasses are an effective also provides a recommendation for A prolonged course of therapy (three
treatment since asthenopic symptoms judicious use of prism in patients to six months) without significant
may be short-lived. Considering with CI. Prism is a recommended improvement will considerably influ-
latent hyperopia is a concern when treatment practice, particularly con- ence a patient’s perception of their
dealing with accommodative short- sidering postconcussion CI symp- ability to recover from a TBI, foster-
ages, a cycloplegic refraction is an toms could be transitory.39 According ing negative expectations.41,42
absolute necessity in those with age- to Sheard’s criterion, the needed
remaining accommodative ability. prism to help carry the load of the Dizziness, disequilibrium and
overburdened vergence system will imbalance. These commonly occur
Convergence insufficiency (CI). be equal to the amount of prism to after mTBI and are an indicator of a
This occurs when the near exophoria place a patient’s phoria within a third potentially long recovery process in
overrides the positive fusional ver- of their overall vergence ability. For PCS.43,44 Vestibular dysfunction, both
gence ability of the patient to main- example, a patient with 10pd exo- peripheral (inner ear) and central
tain comfortable binocular vision. phoria and 11pd base-out vergence (cerebellar), is a common etiology.
Research suggests the prevalence of at near would need 3pd of base-in After ruling out obvious oculomo-
CI in the non-TBI population ranges prism applied to their spectacles, tor deficiencies, (e.g., muscle palsies,
up to 7.7%, while it can be 42% or moving the image toward apex. decompensated phorias and espe-
higher in the post-TBI population.5,33 cially mild vertical phorias) impair-
The disruption of integrated neuro- This formula will also provide the ment of the vestibulo-ocular reflex
logic circuitry following brain injury practitioner with the recommended (VOR) is one of the leading concerns
reduces the ability to compensate for prism: 2/3(phoria) - 1/3(positive for optometrists. The vestibulo-
an existing exophoria. Diagnostic fusional vergence).36 ocular system is responsible for
criteria for CI is provided by the gaze stability (non-pursuit) during
Convergence Insufficiency Treatment Resultant prism from Sheard’s cal- high frequency and velocity-related
Trial (CITT) (Table 4).36 culations should be trial framed for head movements. When the VOR is
patient approval. However, Sheard’s disrupted, oscillopsia and dizziness
Sheard’s criterion, used in the criterion is only a recommendation, ensue.45 Its counterpart, the vestibu-
CITT, remains useful in the diagnosis and they may be successful with less lospinal system, is responsible for
and management of decompensated prism than indicated. postural control with consequences
exophoria (Figure 3).37 It establishes of disrupted balance.46,47 The integri-
the needed positive fusional vergence Small studies and anecdotal expe- ty of the vestibulo-ocular system can
(base out) to control exophoria rience attest to the effectiveness of
without symptoms. The criterion is vision therapy/rehabilitation as a
treatment modality for TBI-related

REVIEW OF OPTOMETRY JULY 15, 2017 75

OPTOMETRIC STUDY CENTER

Table 4. CITT Convergence mTBI is increased visual motion sen- perceived imbalance. Similarly, if the
Insufficiency Criteria sitivity (VMS). With increased VMS, patient tends to lean forward, yoked
a patient will report imbalance, nau- base down prism (also 2pd to 6pd,
Near exophoria at least 4pd greater than sea and disorientation in situations but could vary depending on the
with significant peripheral motion case) could be trialed for improve-
at distance such as walking through a shopping ment in posture.
mall or riding in a car.50
Plus Additional Signs: TBI and PTSD
Research shows binasal occlusion
• Insufficient positive fusional (BNO) is an effective treatment, both Post-traumatic stress disorder
subjectively and objectively. Clini- (PTSD) is frequently associated with
convergence meeting Sheard's cians can add partial occluders to the TBI. While approximately 50% of
patient’s spectacle lenses to suppress military service members that have
Criterion excessive visual motion in the periph- sustained an mTBI have associated
eral visual field. The occlusion can PTSD, it is not unique to military
• Failure to reach normative values for be done using scotch tape, bangerter members. Those who have sustained
foils or electrical tape placed nasal to an mTBI from motor vehicle acci-
positive fusional vergence (≤15 pd the pupillary-limbal margin and ori- dents also have a 50% chance of
blur or break) ented with a 15° superior-temporal developing PTSD.55,56 Patients with
tilt (Figure 4).51,52 more violent or anxiety-laden brain
• Receded near point of convergence injury events logically have higher
Patients with TBI may also expe- rates of PTSD development.
(≥6 cm) rience a shift in their perception of
• CI Symptom Score ≥16 midline. Known as abnormal egocen- Current theory suggests damage to
tric localization, visual midline shift the rational thinking medial prefron-
be evaluated by assessing VOR with or optic ataxia (misreaching to visual tal cortex (mPFC) causes an inability
dynamic visual acuity (DVA). targets), it can cause a patient to lean to regulate the fear response. Espe-
to one side, forward or backward, cially damaging is the evolutionary
When performing DVA testing, resulting in difficulties with balance juxtaposition of the amygdala, the
clinicians establish a baseline with during ambulation. center of the brain for fear, and the
best-corrected visual acuity and hippocampus, the region for memory
then rotate the head from side to To diagnose and manage these development (Figure 5). Situated
side, managing one complete cycle shifts, clinicians must first determine next to each other, without mPFC
(left, right and back left) with two where the shift occurs (right, left, for- tempering, the exaggerated fear
cycles per second. At this rate, VOR ward or backward) and then attempt response becomes inextricably linked
dysfunction may exist if the patient to correct the misperception with with a memory, thus generating the
reads worse than two lines below prism.53,54 For example, a patient associated PTSD symptoms.57
their baseline acuity.48 notes when you hold a pen directly
in front of them that it appears to the Post-concussion symptoms such
Research suggests vestibular left of center. Shifting the patient’s as headache, lack of concentration
therapy that involves gaze stabiliza- midline back toward the center with and poor sleep, among others, may
tion exercises is effective in these base left yoked prism (approximately be more related to PTSD than PCS.58
patients.49 It is common to work 2pd to 6pd) may help correct the Although the high rates of anxiety
with an interdisciplinary team com- and depressive disorders related to
prised of neurology, ENT, audiology PTSD exacerbate visual symptoms,
and physical therapy with patients in no studies indicate visual symptoms
need of vestibular rehabilitation. are directly linked to PTSD.

Visuospatial disruptions in TBI
are more perplexing, since they are
higher-order dysfunctions of the
brain and are poorly understood. A
commonly encountered symptom in

Photo: Marc Taub, OD

Fig. 4. Binasal occlusion can help TBI patients overcome visual motion sensitivity in Malingering and
the peripheral visual field. Stereotype Threat

Managing a patient with TBI usually
goes beyond clinical medicine. The
social and psychological ramifica-
tions of brain injury can lead to other
complications such as malingering

76 REVIEW OF OPTOMETRY JULY 15, 2017

and stereotype threat. mPFC 9. Mild Traumatic Brain Injury Committee of the Head Injury Interdisci-
Malingering. This is a major plinary Special Interest Group of the American Congress of Rehabilitation
Amygdala Medicine. Definition of mild traumatic brain injury. J Head Trauma
dilemma with mTBI since it is dif- Rehabil. 1993;8(3):86-87.
ficult to tell if symptoms are truly Hippocampus 10. Collins MW, Grindel SH, Lovell MR, et al. Relationship between con-
related to injury. Survey data suggest cussion and neuropsychological performance in college football players.
20% to 40% of mTBI patients pres- Fig. 5. Because the amygdala and the JAMA. 1999;282(10):964-70.
ent with exaggerated or fabricated hippocampus are situated next to each 11. Carroll LJ, Cassidy JD, Peloso PM, et al. Prognosis for mild
neuropsychological deficits.59 A other, the exaggerated fear response traumatic brain injury: results of the WHO Collaborating Centre Task
number of complicating factors exist becomes inextricably linked with a Force on Mild Traumatic Brain Injury. J Rehabil Med. 2004 Feb;(43
with TBI-related malingering, such as memory, creating symptoms of PTSD. Suppl):84-105.
the difficult distinction between pre- 12. Narayan R, Wilberger, JE, Povlishock, JT, eds. Neurotrauma. New
TBI abilities and post-TBI deficits. prolonged courses of ineffective York, NY: McGraw-Hill; 1996.
Researchers found that, for many treatment or communicating with a 13. Fainaru-Wada M, Avila J, Fainaru S. Doctors: Junior Seau's
patients, complaints following mTBI despondent bedside manner could brain had CTE. January 11, 2013. www.espn.com/espn/otl/story/_/
were more a reflection of a pre-TBI set patients back substantially in id/8830344/study-junior-seau-brain-shows-chronic-brain-damage-
condition that was brought to the recovery. found-other-nfl-football-players. Accessed April 20, 2017.
fore by the TBI.60,61 14. McKee AC, Stern RA, Nowinski CJ, et al. The spectrum of disease in
With a high prevalence and an chronic traumatic encephalopathy. Brain. 2013;136(Pt 1):43-64.
There is also the matter of voli- increasing community awareness 15. Bauer D, Tung ML, Tsao JW. Mechanisms of traumatic brain injury.
tion, or the degree to which a behav- of brain injury, it is not a question Semin Neurol. 2015;35:e14-22.
ior is both conscious and deliberate. of whether optometrists will see 16. Choe MC. The pathophysiology of concussion. Curr Pain Headache
Optometrists should look to neuro- these patients, but when. Having an Rep. 2016;20:42.
psychological personnel to assess an adequate foundation of understand- 17. Grossman EJ, Inglese M. The role of thalamic damage in mild trau-
individual’s volition in malingering ing will alleviate any trepidation and matic brain injury. J Neurotrauma. 2016;33(2):163-7.
and other disorders. In addition, mystique in managing them. ■ 18. Cipolla M. The Cerebral Circulation. San Rafael, CA: Morgan &
malingering and legitimate neuro- Claypool Life Sciences; 2009.
logic deficit from concussion are not Dr. Tarbett is the former chief of 19. Junger EC, Newell DW, Grant GA, et al. Cerebral autoregulation fol-
mutually exclusive, possibly compel- the Optometry Service at Walter lowing minor head injury. J Neurosurg. 1997;86(3):425-32.
ling providers to attempt to manage Reed Army Medical Center. He 20. Alexander MP. Mild traumatic brain injury: pathophysiology, natural
nonorganic or fictitious ailments. is currently on staff at the Hefner history, and clinical management. Neurology. 1995;45(7):1253-60.
VAMC in Salisbury, NC. 21. Ruff RM, Crouch JA, Troster AI, et al. Selected cases of poor outcome
Stereotype Threat. This social following a minor brain trauma: comparing neuropsychological and
psychology theory purports that a 1. Goldstein M. Traumatic brain injury: a silent epidemic. Ann Neurol. positron emission tomography assessment. Brain Inj. 1994;8:297-308.
stereotyped individual, when placed 1990;27(3):327. 22. Noseda R, Constandil L, Bourgeais L, et al. Changes of meningeal
in a situation that risks validation of 2. Centers for Disease Control and Prevention. Get the stats on traumatic excitability mediated by corticotrigeminal networks: a link for the endog-
that stereotype, performs poorly due brain injury in the United States. www.cdc.gov/traumaticbraininjury/pdf/ enous modulation of migraine pain. J Neurosci. 2010;30(43):14420-9.
to “performance pressure,” thus sup- bluebook_factsheet-a.pdf. Accessed April 13, 2017. 23. Xue T, Do MT, Riccio A, et al. Melanopsin signalling in mammalian
porting the stereotype.62 3. Taylor CA, Bell JM, Breiding MJ, Xu L. Traumatic brain injury-related iris and retina. Nature. 2011;479(7371):67-73.
emergency department visits, hospitalizations, and deaths-United States, 24. Digre KB, Brennan KC. Shedding light on photophobia. J Neurooph-
Stereotype threat is a proven phe- 2007 and 2013. MMWR Surveill Summ. 2017;66:1-16. thalmol. 2012;32(1):68-81.
nomenon in mTBI patients, as soci- 4. Centers for Disease Control and Prevention. Report to Congress on 25. Truong JQ, Ciuffreda KJ, Han MH, Suchoff IB. Photosensitivity in
ety does hold specific maladaptive traumatic brain injury in the United States: epidemiology and rehabilita- mild traumatic brain injury (mTBI): a retrospective analysis. Brain Inj.
beliefs regarding the cognitive effects tion. National Center for Injury Prevention and Control; Division of 2014;28(10):1283-7.
of brain injury.61 Thus, patients diag- Unintentional Injury Prevention. 2015. 26. Good PA, Taylor RH, Mortimer MJ. The use of tinted glasses in child-
nosed with mTBI may do poorly on 5. Brahm KD, Wilgenburg HM, Kirby J, et al. Visual impairment and dys- hood migraine. Headache. 1991;31(8):533-6.
cognitive or memory testing simply function in combat-injured servicemembers with traumatic brain injury. 27. Blackburn MK, Lamb RD, Digre KB, et al. FL-41 tint improves blink
because they have been diagnosed Optom Vis Sci. 2009;86(7):817-25. frequency, light sensitivity, and functional limitations in patients with
with mTBI, not due to any associ- 6. Felleman DJ, Van Essen DC. Distributed hierarchical processing in the benign essential blepharospasm. Ophthalmol. 2009;116(5):997-1001.
ated sequelae. primate cerebral cortex. Cereb Cortex. 1991;1(1):1-47. 28. Lucas RJ, Douglas RH, Foster RG. Characterization of an ocular
7. Keener AB. Tackling the brain: Clues emerge about the pathology of photopigment capable of driving pupillary constriction in mice. Nat
Optometrists must be aware of sports-related brain trauma. Nat Med. 2016;22(4):326-9. Neurosci. 2001;4(6):621-6.
this during the exam but, more 8. Kushner D. Mild traumatic brain injury: toward understanding mani- 29. Lew HL, Otis JD, Tun C, Kerns RD, Clark ME, Cifu DX. Prevalence of
importantly, on treatment recom- festations and treatment. Arch Intern Med. 1998;158(15):1617-24. chronic pain, posttraumatic stress disorder, and persistent postconcus-
mendations and patient interaction. sive symptoms in OIF/OEF veterans: polytrauma clinical triad. J Rehabil
Stigmatizing or fostering nega- Res Dev. 2009;46(6):697-702.
tive expectations for patients with 30. Kontos AP, Elbin RJ, Schatz P, et al. A revised factor structure for the
post-concussion symptom scale: baseline and postconcussion factors.
Am J Sports Med. 2012;40(10):2375-84.
31. Master CL, Scheiman M, Gallaway M, et al. Vision diagnoses
are common after concussion in adolescents. Clin Pediatr (Phila).
2016;55(3):260-7.
32. Goodrich GL, Kirby J, Cockerham G, et al. Visual function in patients
of a polytrauma rehabilitation center: A descriptive study. J Rehabil Res
Dev. 2007;44(7):929-36.
33. Porcar E, Martinez-Palomera A. Prevalence of general binocular
dysfunctions in a population of university students. Optom Vis Sci.
1997;74(2):111-3.
34. Stelmack JA, Frith T, Van Koevering D, et al. Visual function in
patients followed at a Veterans Affairs polytrauma network site: an elec-
tronic medical record review. Optometry. 2009;80(8):419-24.
35. Scheiman M, Wick B. Clinical Management of Binocular Vision:
Heterophoric, Accommodative and Eye Movement Disorders. 3rd ed.
Philadelphia, PA: Lippincott Williams and Wilkens; 2008.
36. Convergence Insufficiency Treatment Trial Study G. Randomized
clinical trial of treatments for symptomatic convergence insufficiency in
children. Arch Ophthalmol. 2008;126(10):1336-49.
37. Gray L. The prescribing of prisms in clinical practice. Graefes Arch
Clin Exp Ophthalmol. 2008;5(5):627-9.
38. Sheard C. Zones of ocular comfort. Am J Optom. 1930;7:9-25.
39. Heinmiller L, Gunton KB. A review of the current practice in diagnosis
and management of visual complaints associated with concussion and
postconcussion syndrome. Curr Opin Ophthalmol. 2016;27(5):407-12.

REVIEW OF OPTOMETRY JULY 15, 2017 77

OPTOMETRIC STUDY CENTER

40. Thiagarajan P, Ciuffreda KJ. Effect of oculomotor rehabilitation on 48. Rakozcy C. Brain Injury Electronic Resource Manual: Vol 1 A: Trau- traffic accident victims. Three-year follow-up of a randomised controlled
accommodative responsivity in mild traumatic brain injury. J Rehabil Res matic Brain Injury. American Optometric Association. 2013. trial. Br J Psychiatry. 2000;176:589-93.
Dev. 2014;51(2):175-91. 49. Hall CD, Heusel-Gillig L, Tusa RJ, Herdman SJ. Efficacy of gaze 57. Rauch SL, Shin LM, Phelps EA. Neurocircuitry models of posttrau-
41. VA/DoD Clinical Practice Guideline for the Management of Concus- stability exercises in older adults with dizziness. J Neurol Phys Ther. matic stress disorder and extinction: human neuroimaging research-past,
sion-mild Traumatic Brain Injury. 2016. www.guideline.gov/summaries/ 2010;34(2):64-9. present, and future. Biol Psychiatry. 2006;60(4):376-82.
summary/50140/vadod-clinical-practice-guideline-for-the-management- 50. Winkler PA, Ciuffreda KJ. Ocular fixation, vestibular dysfunction, and 58. Schneiderman AI, Braver ER, Kang HK. Understanding sequelae of
of-concussionmild-traumatic-brain-injury. Accessed March 29, 2017. visual motion hypersensitivity. Optometry. 2009;80(9):502-12. injury mechanisms and mild traumatic brain injury incurred during the
42. Kay T. Neuropsychological treatment of mild traumatic brain injury. 51. Padula WV, Argyris S, Ray J. Visual evoked potentials (VEP) evaluat- conflicts in Iraq and Afghanistan: persistent postconcussive symptoms
Journal of Head Trauma Rehabilitation. 1993;8:74-85. ing treatment for post-trauma vision syndrome (PTVS) in patients with and posttraumatic stress disorder. Am J Epidemiol. 2008;167:1446-52.
43. Alsalaheen BA, Mucha A, Morris LO, et al. Vestibular rehabilitation traumatic brain injuries (TBI). Brain Inj. 1994;8(2):125-33. 59. Dominic Carone DA, Bush SS, eds. Mild Traumatic Brain Injury:
for dizziness and balance disorders after concussion. J Neurol Phys Ther. 52. Yadav NK, Ciuffreda KJ. Effect of binasal occlusion (BNO) and base- Symptom Validity Assessment and Malingering. New York, NY: Springer
2010;34(2):87-93. in prisms on the visual-evoked potential (VEP) in mild traumatic brain Publishing Company; 2012.
44. Ellis MJ, Cordingley D, Vis S, et al. Vestibulo-ocular dysfunc- injury (mTBI). Brain Inj. 2014;28(12):1568-80. 60. Greiffenstein FM, Baker JW. Comparison of premorbid and postinjury
tion in pediatric sports-related concussion. J Neurosurg Pediatr. 53. Ciuffreda KJ, Ludlam DP, Yadav NK, Thiagarajan P. Traumatic brain mmpi-2 profiles in late postconcussion claimants. Clin Neuropsychol.
2015;16(3):248-55. injury: visual consequences, diagnosis, and treatment. In: Advances in 2001;15(2):162-70.
45. Grossman GE, Leigh RJ, Abel LA, et al. Frequency and velocity Ophthal and Optom. Yanoff M, ed. Philadelphia: Elsevier; 2016:307-33. 61. Kit KA, Mateer CA, Tuokko HA, Spencer-Rodgers J. Influence of
of rotational head perturbations during locomotion. Exp Brain Res. 54. Padula WV, Nelson CA, Padula WV, et al. Modifying postural adapta- negative stereotypes and beliefs on neuropsychological test perfor-
1988;70(3):470-6. tion following a CVA through prismatic shift of visuo-spatial egocenter. mance in a traumatic brain injury population. J Int Neuropsychol Soc.
46. Cullen KE. The vestibular system: multimodal integration and encod- Brain Inj. 2009;23(6):566-76. 2014;20(2):157-67.
ing of self-motion for motor control. Trends Neurosci. 2012;35(3):185-96. 55. Hoge CW, McGurk D, Thomas JL, et al. Mild traumatic brain injury in 62. Steele CM, Aronson J. Stereotype threat and the intellectual test per-
47. Khan S, Chang R. Anatomy of the vestibular system: a review. Neuro- U.S. Soldiers returning from Iraq. N Engl J Med. 2008;358(5):453-63. formance of African Americans. J Pers Soc Psychol. 1995;69(5):797-811.
Rehabilitation. 2013;32(3):437-43. 56. Mayou RA, Ehlers A, Hobbs M. Psychological debriefing for road 63. McKee, et al. The neuropathology of traumatic brain injury. Handb
Clin Neurol. 2015;127:45–66.

You can obtain transcript-qual- OSC QUIZ c. Amygdala.
ity continuing education credit d. Thalamus.
through the Optometric Study resolve by?
Center. Complete the test form and return a. Two weeks. 9. Besides photoreceptors, what other
it with the $35 fee to: Jobson Medical b. One month. retinal cell has been shown to detect light?
Information, Dept.: Optometric CE, 440 9th c. Three to six months. a. Bipolar.
Avenue, 14th Floor, New York, NY 10001. d. One year. b. Mueller.
To be eligible, please return the card c. Ganglion.
within one year of publication. 4. What are two of the main mechanisms in d. Amacrine.
the pathophysiology of TBI?
You can also access the test form and a. Demyelination and vascular dysregulation. 10. What is the Hofstetter’s formula for age-
submit your answers and payment via b. Traumatic axonal injury and microvascular related accommodative ability?
credit card at Review of Optometry online, damage. a. 15 - ¼ age.
www.reviewofoptometry.com/ce. c. Microvascular damage and ossification. b. 12 - ¼ age.
d. DNA and RNA disruption. c. 8 + ¼ age.
You must achieve a score of 70 or d. 18 - ¼ age.
higher to receive credit. Allow eight to 10 5. Chronic traumatic encephalopathy is
weeks for processing. For each Optometric characterized by: 11. Which of the following is not a criterion
Study Center course you pass, you earn a. Repetitive head trauma and DNA used in the CITT?
2 hours of transcript-quality credit from mutation. a. Near exophoria at least 4pd greater than
Pennsylvania College of Optometry and b. DNA mutation and vascular dysregulation. at distance.
double credit toward the AOA Optometric c. Repetitive head trauma and perivascular b. Insufficient positive fusional convergence
Recognition Award—Category 1. p-tau deposition. meeting Sheard’s Criterion.
d. Neurofibrillary tangles and Alzheimer’s c. Failure to reach normative values for
Please check with your state licensing disease. positive fusional vergence (≤15pd blur or
board to see if this approval counts toward break).
your CE requirement for relicensure. 6. Chronic traumatic encephalopathy is d. All are used in the CITT.
differentiated from mTBI by:
1. A concussion or mild TBI is a blow or a. Chronic progressive tissue degeneration. 12. What is an absolute necessity when
acceleration to the head with: b. Cranial impact trauma. evaluating refractive error in pre-presbyopic
a. Loss of consciousness for 24 to 36 hours. c. Glasgow Coma Scale score of five or less. TBI patients?
b. Loss of consciousness for less than 30 d. Loss of consciousness. a. Red-green balance.
minutes. b. Cycloplegic refraction.
c. Alteration of consciousness for less than 7. Following acute head trauma, tissue c. Monocular fogging.
30 minutes. damage on CT imaging indicates: d. 1.00D Jackson cross cylinder testing.
d. Both b and c. a. Mild TBI.
b. Concussion. 13. Sheard’s criteria establishes:
2. What is the most common symptom c. Moderate to severe TBI. a. Needed fusional vergence to control
following a TBI? d. PTSD. heterophoria without symptoms.
a. Photophobia. b. Likelihood of developing photosensitivity.
b. Headache. 8. Pathophysiology of TBI-related c. Residual accommodative function.
c. Diplopia. photosensitivity is associated with disruption d. Needed fusional ability to converge to the
d. Blurred vision. of the: nose.
a. Hippocampus.
3. Following concussion, when should b. Medial prefrontal cortex.
concussion-related symptoms typically

78 REVIEW OF OPTOMETRY JULY 15, 2017

OSC QUIZ Examination Answer Sheet

14. Vestibular dysfunction in TBI can occur: Caring for Patients with Brain Injury
a. Centrally.
b. Peripherally. Valid for credit through July 15, 2020
c. Both a and b.
d. Vestibular dysfunction does not occur. Online: This exam can be taken online at www.reviewofoptometry.com/ce. Upon passing the exam, you can
view your results immediately and download a real-time CE certificate. You can also view your test history at
15. Vestibular dysfunction commonly any time from the website.
involves disruption of the: Directions: Select one answer for each question in the exam and completely darken the appropriate circle. A
a. Spinal-cephalic pathway. minimum score of 70% is required to earn credit.
b. Vestibulo-ocular reflex. Mail to: Jobson Medical Information, Dept.: Optometric CE, 440 9th Avenue, 14th Floor, New York, NY 10001.
c. Babinski reflex. Payment: Remit $35 with this exam. Make check payable to Jobson Medical Information LLC.
d. King-Smith Purkinje reflex. Credit: This course is COPE approved for 2 hours of CE credit. Course ID is 54094-NO.
Sponsorship: This course is joint-sponsored by the Pennsylvania College of Optometry.
16. The vestibulo-ocular reflex can be Processing: There is an eight- to 10-week processing time for this exam.
measured by:
a. Dynamic visual acuity. Answers to CE exam: Post-activity evaluation questions:
b. Von Graefe vergence assessment. 1. A B C D
c. Park’s three-step test. 2. A B C D Rate how well the activity supported your achievement of these learning objectives:
d. Maddox rod test. 3. A B C D 1=Poor, 2=Fair, 3=Neutral, 4=Good, 5=Excellent
4. A B C D
17. Which of the following can be a useful 5. A B C D 21. Improve my clinical ability to diagnose and manage 12345
treatment for patient suffering from 6. A B C D ocular effects of traumatic brain injury.
increased visual motion sensitivity? 7. A B C D
a. Sunglasses. 8. A B C D 22. Become familiar with the key definitions related to 12345
b. Yoked vertical prism. 9. A B C D traumatic brain injury.
c. Progressive addition lenses.
d. Binasal occlusion. 10. A B C D 23. Increase my understanding of the pathophysiology of 1 2 34 5
11. A B C D traumatic brain injury.
18. PTSD and TBI commonly occur due to 12. A B C D
the anatomical position in the brain of the: 13. A B C D 24. Better understand the connection between PTSD, 12345
a. Occipital lobe and hippocampus. 14. A B C D malingering stereotype and brain injury.
b. Corpus callosum and amygdala. 15. A B C D
c. Cerebellum and occipital lobe. 16. A B C D 25. Increase my knowledge of the signs and symptoms of 12345
d. Amygdala and hippocampus. 17. A B C D brain injury.
18. A B C D
19. Determination of patient malingering is 19. A B C D 26. Improve my ability to communicate with patients about
best done by: 20. A B C D the nature of their brain injury and any treatment needed. 1 2 3 4 5
a. The eye care provider.
b. Neuropsychological personnel. Rate the quality of the material provided:
c. Family members. 1=Strongly disagree, 2=Somewhat disagree, 3=Neutral, 4=Somewhat agree, 5=Strongly agree
d. None of the above.
27. The content was evidence-based. 12345
20. Awareness of stereotype threat is 28. The content was balanced and free of bias. 12345
useful: 29. The presentation was clear and effective. 12345
a. In analyzing patient exam data. 30. Additional comments on this course:
b. Patient interaction.
c. Treatment recommendations. Please retain a copy for your records. Please print clearly.
d. All of the above.
First Name
TAKE THE TEST ONLINE TODAY!
www.reviewofoptometry.com/ Last Name

continuing_education/ E-Mail

The following is your: Home Address Business Address

Business Name

Address

City State

ZIP

Telephone # --

Fax # --

By submitting this answer sheet, I certify that I have read the lesson in its entirety and completed the self-
assessment exam personally based on the material presented. I have not obtained the answers to this exam
by any fraudulent or improper means.

Signature Date
Lesson 114851 RO-OSC-0717

REVIEW OF OPTOMETRY JULY 15, 2017 79

Neuro Clinic

Every Picture Tells a Story

Studies suggest imaging is fruitful in cases of isolated palsies, regardless of whether

neurological symptoms are present. By Michael DelGiodice, OD, and Michael Trottini, OD
It’s debatable whether all acute
isolated oculomotor cranial
neuropathies, in patients older
than 50 with or without vascular

factors, should undergo neuroim-

aging.1-3 Here, we review cranial

nerve (CN) three, four and six

palsies and provide reasons for This patient presented with an acute partial pupil-involved third nerve palsy from an

neuroimaging all isolated cranial aneurysm. The picture shows compete restriction of the right eye on upgaze.

mononeuropathies.

CN Three numerous case reports exist isolated FNPs have trochlear
implicating midbrain infarction, nerve schwannomas.18 Addition-

The major functions of the third neoplasm, infection, vasculitis, ally, one study describes a patient

nerve are oculomotor and pupil- pituitary apoplexy, aneurysm and with an isolated FNP secondary

lomotor. Partial and complete carotid artery occlusion as causes to a cavernous meningioma, a

third nerve palsies (TNPs) can be of isolated and complete TNP.7 second reports a patient with an

manifestations of ischemia in the Our recommendation is to intracavernous carotid artery aneu-

setting of diabetes, hypertension obtain emergent CT/CTA or MRI/ rysm and a third study describes a

and hyperlipidemia.4 Non-ischemic MRA in all TNPs. In cases where patient with a carotid-cavernous

pathologies involving the oculo- noninvasive neuroimaging is nega- fistula.19,20,13 Given these findings,

motor nerve include hemorrhagic tive and aneurysm is highly sus- it is certainly prudent to consider

stroke, primary and secondary pected, such as in partial TNP with obtaining contrast-enhanced MRI

neoplasm, aneurysm, cavernous pupil involvement, cerebral angi- of the brain with special attention

malformation, infection and demy- ography should be performed and to the cavernous sinus, since there

elinating disease.5 interpreted by a neuroradiologist seems to be an increased preva-

Third nerve palsies are clini- before discounting an aneurysm. lence of cavernous sinus disease in

cally differentiated as either partial CN Four non-ischemic FNPs.
or complete and pupil-sparing
vs. pupil-involving. According to The most common causes of fourth CN Six

one study, aneurysms are likely nerve palsies (FNPs) are congeni- Sixth nerve palsy (SNP) is the

to affect pupillomotor fibers in tal, traumatic and vasculopathic. most common ocular motor nerve

complete TNP, but spare its func- While isolated fourth nerve palsies palsy due to its long subarachnoid

tion in superior division palsies.6 in older individuals, especially with course.21 According to researchers,

With regards to microvascular vascular disease, are most often the etiology of unilateral SNP is

TNP, up to 20% of cases had pupil ischemic in nature, additional often attributed to ischemia, trau-

involvement.6 And, according to a etiologies include midbrain hemor- ma, demyelinating disease, metas-

second study, the relative presence rhage, pituitary macroadenoma, tasis, aneurysm and intracranial

of aneurysm as a cause of isolated posterior fossa tumor, dural fistula, hypertension, the latter of which

TNP ranged from 14% to 56%.7,8 schwannoma and cavernoma of can occur bilaterally.22

Finally, while evidence supports the fourth nerve.9-17 Because hypertension and diabe-

observation in complete isolated According to researchers, a tes are known etiologies of isolated

TNP without pupil involvement, small number of patients with SNPs in up to 35% of patients,

80 REVIEW OF OPTOMETRY JULY 15, 2017

some researchers argue 5. Bruce BB, Biousse V, Newman NJ.
that monthly follow-up Third nerve palsies. Semin Neurol 2007;
27:257–68.
is the best approach.23 6. Trobe JD. Managing oculomotor nerve
The main disadvantage palsy. Arch Ophthalmol. 1998; 116:798-802.
7. Lee AG, Hayman LA, Brazis PW. The evalu-
ation of isolated third nerve palsy revisited:
of these studies is the an update on the evolving role of magnetic
lack of brain MRI con- resonance, computed tomography, and cath-
eter angiography. Surv Ophthalmol. 2002;
ducted during follow-up. 47:137-157.
Furthermore, one study 8. Mathew MR, Teasdale E, McFadzean RM.
Multidetector computed tomographic angiog-
concludes that sig- raphy in isolated third nerve palsy. Multide-
nificant evidence doesn’t tector computed tomographic angiography in
isolated third nerve palsy.
exist in the literature to 9. Galetta SL, Balcer LJ. Isolated fourth nerve
warrant observation- palsy from midbrain hemorrhage: case report.
J Neuroophthalmol. 1998; 18:204- 205.
only management.24 A 10. Petermann SH, Newman NJ. Pituitary
Medline literature search macroadenoma manifesting as an isolated
fourth nerve palsy. Am J Ophthalmol. 1999;
conducted by research- 127:235-236.
ers reported 199 patients 11. Krohel GB, Mansour AM, Petersen WL, et
al. Isolated trochlear nerve palsy secondary
with isolated SNPs; to a juvenile pilocytic astrocytoma. J Clin
31 were traumatic, 42 Neuroophthalmol. 1982; 2:119-123.
12. Mielke C, Alexander MS, Anand N.
vasculopathic, 43 “idio- Isolated bilateral trochlear nerve palsy as the
first clinical sign of a metastatic [correction
pathic;” 50 cases were This is an MRI of a 71-year-old white male who presented with of metastasic] bronchial carcinoma. Am J
Ophthalmol. 2001; 132(4):593-4.
related to tumors and an acute isolated right fourth nerve palsy. The MRI shows dural 13. Selky AK, Purvin VA. Isolated trochlear
the remainder were from thickening abutting the cavernous sinus and possible compression nerve palsy secondary to dural carotid-
cavernous sinus fistula. J Neuroophthalmol.
miscellaneous causes of the fourth nerve within the cavernous sinus.

(e.g., lumbar puncture, 1994; 14:52-54.
14. Feinberg AS, Newman NJ. Schwannoma in patients with
multiple sclerosis, immunization, with TNPs, two of which were isolated unilateral trochlear nerve palsy. Am J Ophthalmol.

infection, aneurysm, sarcoidosis, pupil-involving, one patient with 1999; 127:183-188.
15. Maurice-Williams RS. Isolated schwannoma of the fourth
inflammatory, orbital amyloidosis FNP, and four patients with SNPs. cranial nerve: case report. J Neurol Neurosurg Psychiatry. 1989;

and diverticulum of the cavernous Excluding pupil-involving TNP, 52:1442-1443.2001; 132:593-594.
16. Leibovitch I, Pakrou D, Selva D, et al. Neuro-ophthalmic
sinus).25 A second study reported which is suggestive of aneurysm manifestations of intracranial cavernous hemangiomas. Eur J

spontaneous recovery of SNPs in and routinely imaged, 11% of Ophthalmol. 2006; 16:148-152.
17. Surucu O, Sure U, Mittelbronn M, et al. Cavernoma of the
the presence of extramedullary patients were identified as having trochlear nerve. Clin Neurol Neurosurg. 2007; 109:791-793.

compression by a tumor at the a significant etiology, which were 18. Feinberg AS1, Newman NJ. Schwannoma in patients with
isolated unilateral trochlear nerve palsy. Am J Ophthalmol. 1999
base of the brain.26 defined by the study as neoplasm, Feb; 127(2):183-8.

Ultimately, it’s our opinion that brainstem infarct, demyelinating 19. Slavin M. Isolated trochlear nerve palsy secondary to cav-
ernous sinus meningioma. Am J Ophthalmol. 1987; 104:433-4.
not enough evidence exists to sup- disease and pituitary apoplexy. 20. Arruga J, de Rivas P, Espinet H, Conesa G. Chronic isolated

port observation alone in isolated Subsequently, these patients were trochlear nerve palsy produced by intracavernous internal carot-
SNPs. It is reasonable to consider offered early medical and surgical id artery aneurysm. J Clin Neuro-ophthalmol. 1991; 11:104-8.
21. Rosenberg RN. Comprehensive Neurology. New York: Raven
ordering contrast-enhanced MRI management.28 It’s our opinion Press, 1991.
of the brain in patients with acute that sufficient data supports imag- 22. Richards BW, Jones FR Jr, Younge BR. Causes and
prognosis in 4,278 cases of paralysis of the oculomotor,
isolated SNPs; a previous study ing all acute, isolated cranial nerve trochlear, and abducens cranial nerves. Am J Ophthalmol. 1992;
shows CT is not diagnostically palsies regardless of the lack of 113(5):489–496.
23. Patel S. V., Mutyala S., Leske D. A. et al. Incidence, associa-
beneficial.27 associated neurologic symptoms. ■ tions, and evaluation of sixth nerve palsy using a population-
Until recently, no well-designed, based method. Ophthalmology. 2004; 111:369-75.
24. Moster ML, Savino PJ, Sergott RC, et al. Isolated sixth-
randomized, prospective, con- nerve palsies in younger adults. Arch Ophthalmol. 1984;
trolled studies or prospective 1. Patel SV, Mutyala S, Leske DA, et al. Incidence, associations, 102:1328-30.
and evaluation of sixth nerve palsy using a population-based 25. Miller RW et al. A Practice Pathway for the Initial Diagnostic
method. Ophthalmology. 2004;111:369–75. Evaluation of Isolated Sixth Cranial Nerve Palsies. Med Decis
case series have been conducted. 2. Bendszus M, Beck A, Koltzenburg M, et al. MRI in isolated Making. 1999; 19:42–48.
One study included patients with sixth nerve palsies. Neuroradiology. 2001;43:742–5. 26. Volpe NJ, Lessell S. Remitting sixth nerve palsy in skull
3. Tamhankar MA, Biousse V, Ying GS, et al. Isolated third,
fourth, and sixth cranial nerve palsies from presumed microvas- base tumors. Arch Opthalmol. 1993; 111:1391–5.
acute, non-traumatic, isolated cular versus other causes: a prospective study. Ophthalmology. 27. Nolan J. Diplopia. Br J Ophthalmol. 1968; 52:166-71.
ocular motor nerve palsies. Of the 2013; 120(11):2264–2269. 28. Volpe N. The Work Up of Isolated Ocular Motor Palsy:
4. Jacobson DM, McCanna TD, Layde PM. Risk factors Who to Scan and Why. http://content.lib.utah.edu/utils/getfile/
66 patients followed, nine had for ischemic ocular motor nerve palsies. Arch Ophthalmol. collection/ehsl-nam/id/116/filename/7.pdf. 2009. Accessed
significant causes; four patients 1994;112:961-6. Jun7, 2015.

REVIEW OF OPTOMETRY JULY 15, 2017 81

WEST COAST Up to

12 CE

Credits*

2017 Optometric Glaucoma
Symposium

DECEMBER 15-16, 2017

Join our faculty of renowned ODs, MDs and PhDs
for a highly interactive meeting covering the
most up-to-date information in glaucoma care.
Up to 12 CE credits for only $275.

HILTON HOTEL
HUNTINGTON BEACH

21100 Pacific Coast Highway
Huntington Beach, CA 92648

Discounted room rate: $227/night + applicable taxes and fees.
Please call the hotel directly at 714-845-8000 and mention
“WCOGS” for group rate.

MEETING CO-CHAIRS:

Murray Fingeret, OD Robert Weinreb, MD

SPEAKERS: Alex Huang, MD Ben Gaddie, OD
Richard Madonna, OD
Sameh Mosaed, MD

THREE WAYS TO REGISTER

www.reviewofoptometry.com/WCOGS2017
Email: [email protected]
Call Lois DiDomenico: 877-451-6514

Administered by *Approval pending

Review of Optometry®

The Essentials

Lymphocytes on the Loose

Most anterior uveitis arises from systemic causes. Make the connection and you’ll be
better equipped to quickly and accurately distginuish etiologies. By Bisant A. Labib, OD

We all know the geminal nerve.2
classic presenta- Tearing, a result of tri-
tion of uveitis:
geminal nerve stimulation

cells and flare, pain, photo- and irritation, is another

phobia and reduced vision. commonly reported symp-

But because a multitude tom.2 Other possible symp-

of events can trigger such toms include redness and,

a response, we sometimes less commonly, floaters.2

lose sight of how these Exam Intricacies

processes occur and what

they signify about our AU presents, anatomically,

patient. Myriad underly- in three forms:

ing systemic conditions • iritis (involving only

can cause anterior uveitis the iris);

(AU); it is often the ocular • anterior cyclitis (ante-

sequela of an autoimmune Deposition of keratic precipiates on the inferior corneal rior portion of the ciliary

condition or infection, endothelium. body); and

and many of the potential • iridocyclitis (a combi-
causes lead to significant morbidity AU Common Symptoms
nation of iris and anterior ciliary

if left unmanaged.1-3 The patient’s The most commonly reported body).1-3

systemic and ocular health rely symptom of AU is blurred vision, Though the clinical findings that

on you, the optometrist, to care- caused by the infiltration of cells lead to a general diagnosis of AU

fully and strategically undertake into the otherwise clear anterior are fairly similar, a few key intrica-

a systemic review and work-up chamber and anterior vitreous cav- cies exist that can help determine

of AU patients, to investigate and ity.1,2,5,6 In cases of Fuchs’ uveitis the subsequent systemic question-

potentially uncover, an infectious, syndrome (FUS), blur is often the naire and work-up, after you’ve

autoimmune or inflammatory only reported symptom; this is a confirmed a case.

underlying etiology. key feature to help you differenti- Conjunctival injection. The

Historically, the majority of ate between FUS and other types dilation of the episcleral blood

AU cases were thought to be idio- of AU. For FUS, treatment with vessels in response to inflamma-

pathic; now we know that a prop- corticosteroids is sufficient and tion causes prominent vasculature

erly executed work-up, combined work-up is unnecesary.5,6 and hyperemia to appear around

with more recent and advanced Pain is a common complaint of the limbus.1,4 The conjunctival

diagnostic techniques, yields an AU with an as-yet undisclosed sys- injection may also be diffuse.1,2

underlying systemic diagnosis in temic etiology. Pain as a response Both FUS and Posner-Schlossman

70% of cases.4 The need is clear to light, and described as worsen- syndrome (PSS) present with low-

for a careful ocular evaluation and ing at near, is caused by ciliary and grade inflammation, and these

review of histopathological and iris sphincter muscle spasms.1,2 It diagnoses should be considered in

immunological mechanisms to can vary in severity and may be the absence of prominent conjunc-

further narrow down the systemic described as midly as a dull ache tival injection.5-7

work-up. This month, we will or as extreme as referred pain that Keratic precipitates (KPs).

focus on the steps to achieve this. spans the area supplied by the tri- These deposits of various cell

REVIEW OF OPTOMETRY JULY 15, 2016 83

The Essentials

Table 1. Systemic Etiologies of Uveitis (mainly lymphocytes, and neutro-
phils to a lesser degree) that have
Granulomatous Non-ganulomatous leaked into the anterior chamber
as a result of the breakdown in the
Herpes viruses: simplex, zoster, cytomega- HLA-B27 conditions: ankylosing spondylitis, blood-aqueous barrier.1,2,4 These
cells are amelanotic and must be
lovirus, Epstein-Barr Reiter’s syndrome, Crohn’s disease, ulcerative differentiated from the brownish
pigment that is released in cases of
colitis pigment dispersion syndrome or
following pupillary dilation.4 The
Sarcoidosis exudation of protein (albumin) into
the anterior chamber comprises
Behcet’s syndrome flare.2

Tuberculosis The quantity of cells and flare
in the anterior chamber is helpful
Juvenile idiopathic arthritis in differentiating purely ocular vs.
systemic etiologies. Systemic causes
Lyme disease of cells or flare are typically more
significant, as they are caused by
Tubulointerstitial nephritis more severe extraocular inflam-
matory diseases. If seen in trace
Syphilis quantities, PSS and FUS should be
excluded before assuming systemic
Multiple sclerosis work-up.5-7 By contrast, if cells are
seen in dense quantities, forming a
Table 2. Summary of Clinical Features of PSS and FUS hypopyon or fibrinous clot, these
typically suggest AU secondary to
Symptoms Posner-Schlossman Fuchs’ Uveitis Syndrome HLA-B27-related conditions such
Blur or haloes Blur or haloes as juvenile idiopathic arthritis (JIA)
no pain no pain or Behcet’s disease.1,4

Signs Unilateral presentation Unilateral presentation Iris changes. Inflammatory cells
Low grade cells Low grade cells may also deposit onto the surface
Fine KPs Diffuse fine or mutton fat KPs of the iris in granulomatous forms
No injection Iris hypochromia/diffuse atrophy of uveitis. When they are located
Significantly elevated IOP No injection on the pupillary border, they are
called Koeppe’s nodules. These
Treatment Anti-hypertensives Not usually responsive to corticosteroids nodules, when located elsewhere
Corticosteroids No systemic work-up indicated on the iris body stroma, are called
No systemic work-up indicated Busacca’s nodules.1,4

types on the surface of the corneal KPs helps distinguish some con- Iris atrophy may also be seen
endothelium serve as perhaps the in FUS and AU that is second-
most important clinical finding ditions. The normal convection ary to herpetic disease. Diffuse
in narrowing the potential cause iris atrophy and hypochromia
of a patient’s AU. Fine, stellate current of the aqueous is created are seen more commonly in FUS,
and diffuse KPs are made up of whereas sectoral atrophy is more
lympho-plasmocytic inflammatory by a temperature gradient, where characteristic of AU caused by the
cells and indicate a non-granulo- herpes virus.5,6,9 Though the exact
matous etiology, which may be cells are moved upwards towards mechanism is unknown, research-
allergic inflammatory in nature; on ers believe that the herpes virus
the other hand, medium to large the lens where the temperature invades the pigment epithelium
“mutton fat” KPs consist of both of the iris, causing these atrophic
lympho-plasmocytic inflammatory is warmer, and then downwards
and epitheloid cells and point to
granulomatous inflammation.1,2,4,8 towards the cornea where the
Pigmented KPs are often indicative
of a previous episode or episodes temperature is cooler, depositing
of AU, in contrast to fresh KPs that inferiorly on the endothelium.2 The
appear round, white and fluffy.1-3
pattern of this deposition, known
Paying close attention to the
exact location and deposition of as “Arlt’s triangle,” is displayed as

a base-down triangle at the inferior
corneal endothelium.2,3 KPs depos-

ited outside of this triangle, in a

diffuse pattern, are suggestive of
FUS and herpetic etiologies.2,3,5,9

Anterior chamber cells and
flare. This clinical manifestation is
pathognomonic for AU. Aqueous

cells consist of inflammatory cells

84 REVIEW OF OPTOMETRY JULY 15, 2017

patches in previous or active bouts trast to lower IOP in the affected physician or rheumatologist. ■
of AU.10 In contrast, researchers eye, which is more suggestive of an
etiology, such as HLA-B27-related 1. Agrawal RV, Murthy S, Sangwan V, et al. Current approach
believe the etiology of FUS (also uveitides from ciliary body isch- in diagnosis and management of anterior uveitis. Ind J
emia and less aqueous production.4 Ophthalmol. 2010;58(1):11-19.
not completely understood) is a 2. Kelkar AS, Arora ER, Sowkath B, et al. Uveitis: clas-
Putting the Pieces Together sification, etiologies, and clinical signs. Del J Ophthalmol.
sympathetic dysfunction; as such, 2016;26(4):264-71.
Carefully examining the clinical 3. Guney E, Tugal-Tutkun I. Symptoms and signs of anterior
the hypochromic iris—indicating manifestations on initial presenta- uveitis. Touch Medical Media. 2013;6(1):33-7.
tion of AU alone can significantly 4. Herbort CP. Appraisal, work-up and diagnosis of anterior
the affected eye—may be a result reduce the clinician’s list of differ- uveitis: A practical approach. Middle East Afr J Ophthalmol.
ential diagnoses. This also elimi- 2009;16(4):159-67.
of decreased innervation to the iris nates the “shotgun” approach of 5. Nalcacioglu P, Ozdel PC, Simsek M. Clinical charac-
stroma.11 non-systematic, overly laborious teristics of fuchs’ uveitis syndrome. Turk J Ophthalmol.
medical work-up; rather, it pro- 2016;46:52-7.
Intraocular pressure (IOP). In motes a more targeted approach 6. Mocan MC, Kadayificilar S, Irkec M. In vivo confo-
AU, patients may present with to help determine a management cal microscopic evaluation of keratic precipitates and
plan. Of course, given the pos- endothelial morphology in Fuchs’ uveitis syndrome. Eye.
abnormal IOP, which can be either sible, and often probable, systemic 2012;26(1):119-25.
underpinnings, anticipate that this 7. Green RJ. Posner-Schlossman syndrome. Clin Exp Optom.
significantly higher or lower than plan will be carried out in conjunc- 2007;90(1):53-6.
tion with the patient’s primary care 8. Kanavi MR, Soheilian M. Confocal scan features of keratic
the non-affected eye. Unilateral precipitates in granulomatous versus nongranulomatous
uveitis. J Ophthalmic Vis Res. 2011;6(4)255.
IOP spikes on initial presentation 9. Kardes E, Bozjurt K, Akcay BI, et al. Clinical features and
prognosis of herpetic anterior uveitis. Turk J Ophthalmol.
are characteristic of herpes sim- 2016;46(3):109-13.
plex/zoster or PSS.4,7,9 Studies show 10. Marsh RJ, Easty DL, Jones BR. Iritis and iris atro-
phy in herpes zoster ophthalmicus. Am J Ophthalmol.
both the herpes virus and PSS to 1974;78(2):255-61.
11. Mohamed Q, Zamir E. Update of Fuchs’ uveitis syn-
cause damage or inflammation drome. Curr Opin Ophthalmol 2005;16(6):356-63.

that is localized to the trabecular

meshwork, which explains the
elevation in IOP.4,7,9 This is in con-

HIRE THE BEST
in Optometry

>>>>>>>

We provide you with the tools to recruit &
hire the best Optometrists in the industry.

Find out how easy recruiting can be.

localeyesite.com/hire/ods

Review of Systems

Not Just Another Headache

Migraine is the most common disabling brain disorder. Are you ready to help these

patients? By Carlo J. Pelino, OD, and Joseph J. Pizzimenti, OD

Headache is one of the Image: Grey’s Anatomy Public Domain • Neck stiffness
most common patient • Increased thirst and urination
symptoms and a fre- • Frequent yawning

quent condition encountered by The Stats
optometrists and other health

care providers. Millions of More than 30 million people in

Americans are living with the the United States experience one

complex, recurrent headache or more migraines per year, the

disorder known as migraine.1 majority (75%) of whom are

The name migraine is derived women.1,2 The overall prevalence

from the Greek word hemikra- of migraine is 18% in women

nia, meaning half of the head, and 6% in men.2-4 About 70% of

representing one of the most patients have a first-degree rela-

striking features of the condi- tive with a history of migraine,

tion: In many cases the pain suggesting a genetic component

is unilateral.1,2 Migraine often Fig. 1. The trigeminovascular system may be a exists.3,4
comes with visual signs and prominent component in the circuitry of migraine. The Women’s Health Study,
symptoms, and patients will
which included professional

present to your office looking for The typical chief symptom is a women older than 45, shows that

relief. Knowing what to look for is severe, unilateral, throbbing head any history of migraine is associated

the first step in properly diagnosing pain or pulsing sensation, which with a higher incidence of major

migraine and starting patients on the may be preceded or accompanied by cardiovascular disease.4,5 Those with

path to better control. visual alterations, difficulty speak- a history of migraine with aura have

Headache Basics ing, numbness of the face, nausea, the highest cardiovascular risk with
vomiting and extreme sensitivity to a 2.3-fold risk of cardiovascular

The term primary headache light and sound.1-3 About 20% of death and a 1.3-fold risk of coro-

describes head pain due to the head- migraine sufferers experience aura— nary vascularization.4,5

ache condition itself, and not a result a complex of neurological symptoms Chronic migraine, characterized

of another cause. A secondary head- that occurs usually before the head- by the experience of migrainous

ache is one that is present because of ache. Most aura is visual, consisting headache on at least 15 days per

another condition such as sinusitis, of a combination of positive visual month, is highly disabling and may

for example. phenomena (floaters, flashes, zig-zag impair a person’s ability to accom-

The three types of primary head- patterns) and negative phenomena plish everyday activities.

ache are migraine, tension and clus- (loss of vision causing blind spots). The Pathways

ter. Migraine headache is recognized Some patients experience a pro-

as a distinct neurological disease of drome. One or two days before Migraine etiology was previously

complex pathophysiology and is the attack, they may notice subtle considered a vascular issue resulting

considered the most common dis- changes, including: from intracranial vasoconstriction

abling brain disorder.1,2 • Constipation followed by rebound vasodilation.

Migraine is further classified into • Mood changes, from depres- However, this contradicts the effi-

migraine with aura, migraine with- sion to euphoria cacy of pharmacotherapies that have

out aura and chronic migraine.1,2 • Food cravings no effect on blood vessels.2,3,5

86 REVIEW OF OPTOMETRY JULY 15, 2017

Table 1. When It’s Not cranial vessels is quite painful.2-4 1. At least five attacks fulfilling
Migraine: Red Flags1,2 Researchers now propose that criteria two through four

• First or worst headache ever brainstem activation may be the 2. Attacks lasting four to 72 hours
• New onset initiating factor.2,3 Functional brain (untreated or unsuccessfully
• Onset after age 50 imaging with positron emission treated)
• Change in pattern of headache tomography (PET) scans performed
• Worsening headache during migraine without aura has 3. At least two of the following
• Acute or sudden onset shown activation of the dorsal mid- four characteristics:
• Sudden onset during exertion (e.g., brain, including the periaqueductal a. Unilateral location
grey and in the dorsal pons, near b. Pulsating quality
coughing, sneezing, sexual activity) the locus coeruleus.2,3 Investigators c. Moderate or severe pain
• With postural link believe the most important recep- d. Aggravation by or causing
• In a setting of malignancy or HIV tor in the headache pathway is the avoidance of routine physical
• Systemic symptoms (e.g., fever, serotonin receptor (5-hydroxytryp- activity (e.g., walking or climb-
tamine [5-HT]). Immunohistochemi- ing stairs)
weight loss, cough) cal studies have detected 5-HT1D
• Neurologic symptoms or signs receptors in trigeminal sensory 4. During headache, at least one of
neurons, while 5-HT1B receptors the following:
More appropriately, studies sug- are present on smooth muscle cells a. Nausea, vomiting or both
gest the origin of a migraine attack found in meningeal vessels.2,3 b. Photophobia/phonophobia
is associated with neuronal activa-
tion, during which a series of central The Triggers 5. Cannot be attributed to another
and peripheral neural and vascular medical condition
events initiate the migraine.3,4 Propo- As there is no known cure for
nents describe migraine as primarily migraine, patients most often rely on Some signs and symptoms, how-
a neurogenic process with secondary avoiding triggers whenever possible.5 ever, should lead you to suspect a
changes in cerebral perfusion.2,3 For many patients, anything from secondary headache such as a “thun-
stress, caffeine, chocolate and alco- derclap” or persistent worsening
A plexus of largely unmyelinated hol to hormonal changes during the headache caused by a more serious
fibers from the ophthalmic divi- menstrual cycle and foods that con- medical problem (Tables 1 and 2).
sion of the trigeminal nerve and the tain nitrates, tyramine, monosodium
upper cervical dorsal roots surround glutamate or aspartame can initiate It is not uncommon for patients to
the large cerebral vessels, pial ves- or aggravate the migraine.1,2 Avoid- exhibit characteristics of more than
sels, large venous sinuses and dura ing such triggers may help to reduce one subtype of migraine, in which
mater of the meninges (Figure 1).2,3 their frequency or severity.5 case all subtypes that present should
When the trigeminal fibers inner- be diagnosed. For example, a patient
vating these vessels are activated, a Diagnostic Guidelines may have frequent attacks with aura
stimulation of nociceptive neurons but also some attacks without aura.
releases plasma proteins and pain- The diagnosis of migraine is based
generating substances such as calci- on patient history. The International Stay tuned for our next column,
tonin gene-related peptide, substance Classification of Headache Disor- which will discuss the various man-
P, vasoactive intestinal peptide and ders diagnostic criteria is as follows:6 agement strategies you can employ
neurokinin A.2,3 These substances to help these patients overcome the
eventually produce blood vessel disabling effects of migraine. ■
dilation, protein extravasation and
inflammation. Stimulation of these 1. Hildreth CJ, Lynm C, Glass RM. Migraine headache. JAMA.
2009;301(24):2608.
Table 2. Conditions Associated with Secondary Headache2 2. Weatherall MW. The diagnosis and treatment of chronic
migraine. Therapeutic Advances in Chronic Disease.
“Thunderclap” Headache Persistent Worsening Headache 2015;6(3):115-23.
3. Goadsby PJ. Pathophysiology of migraine. Ann Indian Acad
• Subarachnoid hemorrhage • Raised cerebrospinal fluid (CSF) Neurol. 2012;15(Suppl S1):15-22.
• Cerebral venous sinus thrombosis (CVST) pressure (tumor, abscess, CVST, 4. Van den Maagdenberg AM, Haan J, Terwindt GM, Ferrari MD.
• Reversible cerebral vasoconstriction idiopathic intracranial hypertension) Migraine: Gene mutations and functional consequences. Curr
Opin Neurol. 2007;20:299-305.
syndrome • Low CSF volume (post-lumbar 5. Estemalik E, Tepper S. Preventive treatment in migraine
• Carotid/vertebral artery dissection puncture, spontaneous CSF leak) and the new US guidelines. Neuropsychiatr Dis Treat.
• Pituitary apoplexy 2013;9:709–20.
• Intracerebral hemorrhage/hematoma • Meningitis (acute/chronic) 6. Headache Classification Committee of the International
• Hypertensive encephalopathy • Hypoxia/hypercapnia Headache Society. The International Classification of Head-
• Idiopathic thunderclap hemorrhage • Substance abuse/withdrawal ache Disorders, 3rd edition. 2013. www.ihs-headache.org/
• Systemic inflammatory conditions, binary_data/1437_ichd-iii-beta-cephalalgia-issue-9-2013.pdf.
(Call–Fleming syndrome) Accessed June 5, 2017.
including temporal arteritis

REVIEW OF OPTOMETRY JULY 15, 2017 87

Find your inspiration
for excellence.

&72%(5©g`©!© È© &250,&.©/$&(
Find your inspiration for
excellence at Academy 2017
Chicago. Join us in Chicago
for four days of brilliant
speakers, clinically-relevant
CE sessions, the latest
products and technology in
the exhibit hall, captivating
papers and posters and
cherished social events.

Early bird registration ends August 7! Register today at www.aaopt.org.

Therapeutic Review

Prescribe with Laser Focus
Know how to pair drugs with associated procedures.

By Alan G. Kabat, OD, and Joseph W. Sowka, OD

Laser procedures represent
the next frontier in opto-
metric scope expansion for
many states. Knowing the risks,
benefits and indications for these
procedures is critically important for
doctors who would perform them.
Yet, understanding the periproce-
dural management of laser surgical
patients is equally crucial for success
in these endeavors.

This month, we review some of
the more common laser procedures
for the anterior segment, focusing
on pre- and postoperative care to
ensure the best possible outcomes.

Techniques This one-day postoperative cataract surgery patient displays redness indicating
inflammation, similar to the inflammation laser procedure patients face.
Currently, certified optometrists in
Kentucky, Louisiana and Oklahoma dures (e.g., focal or panretinal laser terior capsular bag.2,3 Symptoms
can perform laser procedures, but photocoagulation), laser in situ of posterior capsule opacification
only procedures that involve struc- keratomileusis (LASIK) and other (PCO) may not become manifest
tures of the anterior segment. Three refractive or cosmetic surgeries. for months or even years after
specific techniques account for the the initial surgery, but can include
vast majority of laser procedures by YAG Capsulotomy such diverse complaints as blurred
ODs. They are: vision, decreased contrast sensitivity,
• Laser capsulotomy for posterior Opacification of the posterior cap- increased glare and even monocu-
capsular fibrosis, sometimes referred sule is a common complication of lar diplopia.1 The only remedy for
to as “after-cataract.” phacoemulsification surgery for this problem is laser capsulotomy.2
• Laser peripheral iridotomy (LPI) cataracts, with estimates as high as Essentially, this involves using the
for those at risk for or suffering 18% of cases.1 Researchers believe it Nd:YAG laser to create an opening
from angle closure glaucoma. occurs because of postoperative pro- in the posterior capsule, eliminating
• Laser trabeculoplasty using liferation and migration of residual obscuration of the visual axis.
either the argon laser (ALT) or the lens epithelial cells within the pos-
Nd:YAG laser (selective laser tra-
beculoplasty or SLT).

Less frequently, lasers may be
used to perform iridoplasty on nar-
row angles, or to remove lesions
from the ocular adnexa. Techniques
that are expressly forbidden in these
states include retinal laser proce-

REVIEW OF OPTOMETRY JULY 15, 2017 89

Therapeutic Review

Dr. Sowka’s Personal Perspective formed as a therapeutic measure for
those in acute or chronic ACG, or
We detailed in an earlier column how we encountered a printed brochure extolling that SLT as a prophylactic measure for those
creates no side effect.1 However, risks are associated with any procedure and laser proce- determined to be at increased risk
dures are no exceptions. I am personally aware of a situation where a patient with ocular (i.e., anatomically narrow angles).8
hypertension underwent a so-called benign SLT, only to develop an intractable IOP spike The Nd:YAG laser is typically the
into the 40s necessitating bilateral trabeculectomy. I myself recently underwent one of the device of choice for this procedure,
above-mentioned laser procedures without complications, until I awoke the next morn- although in dark irides both argon
ing with hazy vision, steamy corneal edema, and an IOP spike into the 50s! Fortunately, and Nd:YAG lasers may be used
the complication was short-lived and easily managed, but had I been a fragile glaucoma sequentially.8
patient, the outcome could have been poor.
The risks associated with LPI
1. Sowka J, Kabat A. Irresponsible education. Rev. of Optom. 2016 April;153(4):88-9. are similar to those encountered
with laser capsulotomy, includ-
Discharging laser energy into the eye For these individuals, recheck the ing postprocedural IOP elevation
can result in a host of undesirable IOP one to four hours after the pro- and anterior uveitis. Less common
sequelae. These commonly consist cedure; if elevated, the continued sequelae include burns to the cornea
of transiently elevated intraocular use of a topical IOP-lowering agent or retina, or both, macular edema
pressure (IOP), postoperative inflam- during the postoperative period is and retinal detachment.9 To prevent
mation (i.e., mild anterior uveitis) recommended.4 an associated IOP spike, one drop
and an increase in floaters.1 Less of apraclonidine or brimonidine is
frequent, but more serious, compli- Corticosteroid drops are also instilled about 20 minutes before
cations include retinal detachment, commonly given postoperatively the procedure.10 In addition to
cystoid macular edema, pitting or after laser capsulotomy to curb lowering IOP, pilocarpine is also
displacement of the lens implant, iris associated inflammation. Pred- used to induce miosis, stretching
hemorrhage and vitreous prolapse.1,4 nisolone acetate 1% QID remains the iris and facilitating penetration
To minimize these complications, the standard for most physicians, of the tissue with less laser energy.10
the physician must make appropri- although some practitioners prefer IOP should be checked roughly 30
ate use of perioperative medications loteprednol 0.5% QID or even minutes to 60 minutes after the pro-
and perform careful postoperative difluprednate 0.05% BID-TID. Fol- cedure. As with laser capsulotomy,
assessment. low-up is usually at one week fol- the use of topical corticosteroids is
lowing surgery, at which point IOP helpful in minimizing post-proce-
To guard against a pressure spike, is measured and the anterior cham- dural inflammation. The one-week
it is customary to instill an IOP- ber assessed. If normal, drops can follow up involves inspection of the
lowering agent prophylactically sev- be discontinued at this point. Obvi- iridotomy site to ensure patency,
eral minutes before or immediately ously, if pain, reduced vision, newly IOP measurement and assessment
after performing laser capsuloto- observed flashes or floaters occur at of intraocular inflammation. Phy-
my.1,4 Historically, 1% apracloni- any point postoperatively, urge the sicians may also complete a one-
dine was the drug of choice, but patient to return immediately. Rou- month follow-up, which includes a
today 0.2% brimonidine is often tine dilation following capsulotomy dilated fundus examination. If IOP
used in a similar fashion.5 Stud- is generally not necessary unless is elevated with dilation after LPI,
ies show these agents can help symptoms dictate otherwise. the clinician should suspect alter-
minimize IOP spikes.5,6 The greatest native mechanisms of glaucoma
incidence of IOP elevation occurs Peripheral Iridotomy (e.g., plateau iris or other non-pupil
within three hours of the procedure block conditions).
and tends to return to normal with- This procedure, which seeks to alle-
in 24 hours.1 Those in whom higher viate pupil-block, results in deepen- Laser Trabeculoplasty
amounts of laser energy are used ing of the anterior chamber angle
during the procedure have a greater and alleviating or preventing angle- In this procedure, the laser is
tendency toward more severe or closure glaucoma (ACG) by creating directed at the pigmented epithe-
prolonged IOP elevation, as do a pathway for aqueous egress from lium of the TM via a gonioscopy
those with a prior diagnosis of the posterior to the anterior chamber lens. Although the exact therapeutic
glaucoma or ocular hypertension.7 and into the trabecular meshwork mechanism remains incompletely
(TM). This technique can be per-

90 REVIEW OF OPTOMETRY JULY 15, 2017

Advertisers Index

understood, the successful result is diminished IOP by Alcon Laboratories ..........................................13, 27, 28, 100
way of enhanced outflow through Schlemm’s canal.11 Phone ................................................................(800) 451-3937
ALT acts through thermal alteration of the TM while SLT Fax.....................................................................(817) 551-4352
enhances biologic activity in this structure.11 Because SLT
induces far less structural damage to the TM than ALT, Allergan, Inc. ........................................................................ 25
SLT can potentially be repeated once if IOP control falters Phone ................................................................(800) 347-4500
over time.12
Bausch + Lomb .......................................10, 31, 32, 61, 62-63
As with LPI and YAG capsulotomy, the main complica- Phone ................................................................(800) 323-0000
tions of SLT include a postprocedural IOP spike and sec- Fax.....................................................................(813) 975-7762
ondary inflammation.9 This paradoxical IOP spike seems
to happen more commonly in heavily pigmented angles Beaver-Visitec International, Inc.......................................... 9
such as those encountered in exfoliative and pigmentary Phone ................................................................(866) 906-8080
glaucoma.13 The use of apraclonidine or brimonidine Fax.....................................................................(866) 906-4304
before and immediately after SLT helps to blunt this ............................................................ www.beaver-visitec.com
effect.9,11
CooperVision ....................................................................... 99
Postoperative corticosteroid use remains controversial, Phone ................................................................(800) 341-2020
although a symptomatic anterior chamber reaction is not
uncommon following SLT. While some continue to advo- Icare USA ............................................................................. 21
cate for steroids, others suggest that their use may hinder Phone ................................................................(888) 389-4022
the subsequent IOP-lowering effect.11 A randomized, ....................................................................www.icare-usa.com
controlled study evaluating the use of anti-inflammatory
agents following SLT revealed little difference between Katena .................................................................................. 19
groups using 1% prednisolone acetate, 0.5% ketorolac or Phone ................................................................(800) 225-1195
artificial tears QID for five days postoperatively.14 ........................................................................www.katena.com

An ancient Greek philosopher once proclaimed, Keeler Instruments.......................................................... 5, 57
“Change is the only constant in life.” Our profession has Phone ................................................................(800) 523-5620
changed dramatically since its inception, and it will con- Fax.....................................................................(610) 353-7814
tinue to evolve. As we prepare for surgical privileges in
optometry, we must be certain that we first comprehend Lombart Instruments .......................................................... 51
the impact of our actions and can manage the potential Phone ................................................................(800) 446-8092
complications effectively. ■ Fax.....................................................................(757) 855-1232

1. Boucher K, Ellis B, Lighthizer N. Capping off cataract surgery. Rev of Optom. 2015 Jun;152(6):44-52. Mentholatum Company ........................................................ 7
2. Sharon Y, Livny E, Mimouni M, et al. Laser capsulotomy following cataract surgery: comparing time Phone ................................................................(877) 636-2677
to capsulotomy with implantation of two broadly used intraocular lenses. Indian J Ophthalmol. 2017 ......................................... [email protected]
Feb;65(2):144-7. ..............................................................www.mentholatum.com
3. Wormstone IM, Eldred JA. Experimental models for posterior capsule opacification research. Exp Eye Res.
2016 Jan;142:2-12. Reichert Technologies .......................................41, 43, 45, 47
4. Steinert RF. Nd:YAG laser posterior capsulotomy. American Academy of Ophthalmology. www.aao.org/ Phone ................................................................(888) 849-8955
munnerlyn-laser-surgery-center/ndyag-laser-posterior-capsulotomy-3. November 4, 2013. Accessed May Fax.....................................................................(716) 686-4545
20, 2017. ...................................................................... www.reichert.com
5. Singhal D, Desai R, Desai S, et al. Use of topical brimonidine to prevent intraocular pressure elevations fol-
lowing Nd: YAG-laser posterior capsulotomy. J Pharmacol Pharmacother. 2011 Apr-Jun; 2(2):104-6. S4OPTIK ....................................................................35, 37, 39
6. Kaur M, Singh A, Kailwoo S. Apraclonidine 1% to prevent post Nd:Yag laser capsulotomy rise of intraocu- Phone ................................................................(888) 224-6012
lar pressure. JARMS. 2012;4(3):237-42.
7. Bhargava R, Kumar P, Phogat H, Chaudhary KP. Neodymium-yttrium aluminium garnet laser capsulotomy Shire Ophthalmics ................................................... 14-15, 16
energy levels for posterior capsule opacification. J Ophthalmic Vis Res. 2015 Jan-Mar;10(1):37-42. ...........................................................................www.shire.com
8. de Silva DJ, Gazzard G, Foster P. Laser iridotomy in dark irides. Br J Ophthalmol. 2007 Feb;91(2):222-5.
9. Van Alstine A, Caruso JM. Managing the post-op glaucoma patient. Rev of Optom. 2016 Oct;153(10):58- Transitions Optical .............................................................. 23
65. Phone ................................................................(800) 848-1506
10. Shetler J, Miller J, Lighthizer N. Breaking down barriers: iridotomy in optometric practice. Rev of Optom. Fax.....................................................................(813) 546-4732
2016 May;153(5):74-82.
11. Leahy KE, White AJ. Selective laser trabeculoplasty: current perspectives. Clin Ophthalmol. 2015 May Vistakon .............................................................................. 2-3
11;9:833-41. Phone ................................................................(800) 874-5278
12. Latina MA, Tumbocon JA. Selective laser trabeculoplasty: a new treatment option for open angle glau- Fax.....................................................................(904) 443-1252
coma. Curr Opin Ophthalmol. 2002 Apr;13(2):94-6.
13. Zhou Y, Aref A. A review of selective laser trabeculoplasty: recent findings and current perspectives. Oph- This advertiser index is published as a convenience and not as part of the advertising contract.
thalmol Ther. 2017 Mar 3. doi: 10.1007/s40123-017-0082-x. [Epub ahead of print] Every care will be taken to index correctly. No allowance will be made for errors due to
14. Jinapriya D, D’Souza M, Hollands H, et al. Anti-inflammatory therapy after selective laser trabeculoplasty: spelling, incorrect page number, or failure to insert.
a randomized, double-masked, placebo-controlled clinical trial. Ophthalmology. 2014 Dec;121(12):2356-61.

REVIEW OF OPTOMETRY JULY 15, 2017 91

Meetings + Conferences

August 2017 Optometric Association and Delaware Optometric Association.
CE hours: 14. To register, email Cheryl Frazier at
■ 3-6. VT4. OEP National Headquarters, Baltimore. Host: [email protected], call (410) 486-9662 or go to
Optometric Extension Program Foundation. Key faculty: Robin www.marylandoptometry.org.
Lewis. CE hours: 35. To register, email Karen Ruder at ■ 9-10. Primary Eye Care Update. Oklahoma College of
[email protected], call (410) 561-3791 or go to www.oepf.org. Optometry Academic Wing, Tahlequah, OK. Host: Oklahoma
■ 4-6. SWFOA Educational Retreat. South Seas Island College of Optometry. CE hours: 10. To register, email Callie
Resort, Captiva Island, FL. Host: Southwest Florida Optometric McAtee at [email protected], call (918) 444-4033 or go to
Association. Key faculty: Nate Lighthizer, Leo Semes, Ron www.optometry.nsuok.edu/continuingeducation.aspx.
Foreman. CE hours: 16. To register, email Brad Middaugh at ■ 9-10. MBKU Pathology Conference Featuring USC & VA
[email protected], call (239) 481-7799 or go to www.swfoa.com. Faculty. Marshall B. Ketchum University, Fullerton, CA. Host:
■ 5-6. End of Summer Seminar. IU School of Optometry, Marshall B. Ketchum University. CE hours: 16. To register, email
Bloomington, IN. Host: IU School of Optometry. CE hours: 16. To Antoinette Smith at [email protected], call (714) 872-5684 or
register, email Cheryl Oldfield at [email protected], call (812) go to www.ketchum.edu/ce.
856-3502 or go to www.optometry.iu.edu/continuing-education. ■ 11-13. 2017 World Congress of Optometry. Hyderabad
■ 6. Breakfast and Learn — New Technology. SUNY College of International Convention Centre, Hyderabad, India. Host: India
Optometry, New York City. Host: SUNY Office of CE. CE hours: Vision Institute & World Council of Optometry. To register, email
4. To register, email Betsy Torres at [email protected], call (212) [email protected] or go to
938–5830 or go to www.sunyopt.edu/cpe. www.worldcongressofoptometry.org.
■ 9. Annual Summer Seminar. Jumping Brook Country Club, ■ 13. OD Excellence Information Meeting. Office of Terry Chan,
Neptune, NJ. Host: NJ Academy of Optometry. Key faculty: Vipul San Francisco. Host: OD Excellence. Key faculty: Terry Chan.
Lahkani. CE hours: 6. To register, email Dennis Lyons at CE hours: 2. To register, email Anthony Senander at
[email protected] or call (732) 920-0110. [email protected], call (707) 433-5542 or go to
■ 9. OD Excellence Information Meeting. Office of Steve Chander, www.odexcellence.com.
Chicago. Host: OD Excellence. Key faculty: Steve Chander. CE ■ 13-16. International Vision Expo West. Sands Expo and
hours: 2. To register, email Anthony Senander at Convention Center, Las Vegas. Host: International Vision Expo.
[email protected], call (707) 433-5542 or go to Key faculty: Ben Gaddie, Mark Dunbar. CE hours: 310+ total, 27
www.odexcellence.com. per OD. To register, email Diane at [email protected], call
■ 18-20. UABSO CE & Alumni Weekend. UAB School of (203) 840-5436 or go to www.visionexpowest.com.
Optometry, Birmingham, AL. Host: University of Alabama ■ 13-16. COVD at Int’l Vision Expo West. Sands Expo and
Birmingham School of Optometry. CE hours: 18. To register, email Convention Center, Las Vegas. Host: College of Optometrists in
Katherine Clore at [email protected], call (205) 934-5700 or go to Vision Development. Key faculty: Robin Price. CE hours: 12. To
www.uab.edu/optometry/home/uabso-ce. register, email Penny at [email protected], call (330) 995-0718 or
■ 20. Annual Optometry Academe. UMSL JC Penney Conference go to www.covd.org.
Center, St. Louis. Host: UMSL College of Optometry. Key faculty: ■ 15-16. Alumni Weekend. IU School of Optometry,
Joseph Pizzimenti, Carlo Pelino. CE hours: 8. To register, email Lis Bloomington, IN. Host: IU School of Optometry. CE hours: 16. To
Ellerbusch at [email protected], call (314) 516-5615 or go to register, email Cheryl Oldfield at [email protected], call (812)
http://optometry.umsl.edu. 856-3502 or go to www.optometry.iu.edu/continuing-education.
■ 24-27. 110th SCOPA Annual Meeting. Myrtle Beach Marriott ■ 17. Central Pennsylvania Optometric Society Annual Meeting.
Resort and Spa at Grande Dunes, Myrtle Beach, SC. Host: South Hotel Hershey, Hershey, PA. Host: Central Pennsylvania
Carolina Optometric Physicians Association. CE hours: 21. To reg- Optometric Society. Key faculty: Ron Melton, Randall Thomas. To
ister, email Jackie Rivers at [email protected], call (877) register, email [email protected].
799-6721 or go to www.sceyedoctors.com.
To list your meeting, please send the details to:
September 2017 Michael Iannucci
Associate Editor
■ 8-10. VOA Fall Conference. Essex Resort and Spa, Essex, Email: [email protected]
VT. Host: Vermont Optometric Association. CE hours: 17. To reg- Phone: (610) 492-1043
ister, email Rebecca Hogan at [email protected].
■ 8-10. i.CE on the Shore MOA/DOA Fall Conference. Hyatt
Regency Chesapeake Bay, Cambridge, MD. Host: Maryland

92 REVIEW OF OPTOMETRY JULY 15, 2017

Up to

20 CE

Credits*

ANNUAL

A REVIEW OF OPTOMETRY ® MEETING OF CLINICAL EXCELLENCE
CE AT ITS PEAK! WORLD CLASS EDUCATION BY LEADING OPTOMETRIC EDUCATORS

THE LONGEST RUNNING WINTER
CE MEETING IN EYE CARE!

February 16-20, 2018

LOCATION: Aspen, Colorado
WESTIN SNOWMASS
EARLY BIRD
CONFERENCE CENTER SPECIAL

100 Elbert Lane $75 OFF

Snowmass Village, CO 81615 before Dec. 15, 2017

Phone: (970) 923-8200

Discounted room rates:
$219 - $429 per night

CONTINUING EDUCATION:

• Earn up to 20 hours of COPE CE* Credits
• Registration Cost - $650

Early Bird Special: Receive $75 off before Dec. 15, 2017

• See website for meeting agenda

MEETING CO-CHAIRS:

Murray Fingeret, OD, FAAO
Leo Semes, OD, FAAO

3 WAYS TO REGISTER

E-MAIL: [email protected] PHONE: (866) 730-9257
WEBSITE: WWW.SKIVISION.COM

See event website for all accommodations and rates.

Review of Optometry® partners with Salus University for those
ODs who are licensed in states that require university credit.

Administered by *Approval pending

Review of Optometry ®

Review Classifieds

Merchandise Offered

NËŗµrɳŷȕNJǢËŷɟNJŷŷō
NŷĵŷNJŷŗ^rōŗ^

ÝŘǼNjŸ_ȖOÞض

ĵ r ^ ǢËrĵəÝŗµƻŗrĵǢ

ĵʳrʳ^ʳǢËrĵəÝŗµƻŗrĵǢNjsǼǼNjOǼÞɚsʪŸǼÞضǣÌsĶɚsǣ
¯ŸNjĶÞ¶ÌǼɠsÞ¶ÌǼŎsNjOÌŘ_ÞǣsʱÞŘOĶȖ_ÞضsɴsɠsNjʳǻÌsǣÌsĶ¯
ƼNjŸʩĶsǣNjsŎsNjs˨ŎÞĶĶÞŎsǼsNjǣÞŘǼÌÞOĨŘsǣǣŘ_
ǣsŎĶsǣǣĶɴOŸŘŘsOǼǼŸǼÌsEOĨƼŘsĶʰONjsǼÞضǣsNjsŘs
Ř_OÌNjŎÞضƼNjŸ_ȖOǼ_ÞǣƼĶɴʳNJsOŸŎŎsŘ_s_ÞǣǼÌs
ĵʳrʳ^ʳÞĶĶȖŎÞŘǼÞŸŘǣɴǣǼsŎɠÌÞOÌÞǣɚÞĶEĶsÞŘEŸǼÌɠÌÞǼs
Ř_NjsŎŸǼs_ĠȖǣǼEĶsŎȖĶǼÞ˚OŸĶŸNjNJµDʳ

ĵʳrʳ^ʳǢËrĵəÝŗµƻŗrĵǢǣǼNjǼǼĠȖǣǼ̱˨˨˨ʳəÞǣÞǼȖǣŸŘĶÞŘs
ŸNjOĶĶǼÌsŘȖŎEsNjĶÞǣǼs_EsĶŸɠ¯ŸNjŎŸNjsÞŘ¯ŸNjŎǼÞŸŘʳ

ɠɠɠʳ¯NjŎs_ÞǣƼĶɴǣʳOŸŎ

Merchandise Offered

94 REVIEW OF OPTOMETRY JULY 15, 2017

Review Classifieds

Contact Lenses

FACULTY

ASSISTANT PROFESSOR POSITIONS: CONTACT LENSES, PRIMARY CARE, AND PEDIATRICS

F CC O AC O

R:

TS S

: :I CA O ,P I E
O
C ,D , D M L , P
D M:

REVIEW OF OPTOMETRY JULY 15, 2017 95

Review Classifieds Practice For Sale

Continuing Education PRACTICE SALES
& APPRAISAL
MEDICAL OPTOMETRISTS
Expert Services for:
The American Board of Certification in Buying or Selling a Practice
Medical Optometry (ABCMO) is recognized at Practice Appraisal
Joint Commission (JC) accredited medical Practice Financing
facilities as issuing board certification in the Partner Buy-in or Buy-out
specialty of medical optometry and those Call for a Free Consultation
ABCMO certifies are eligible for credentialing
at these facilities as specialists rather than (800) 416-2055
general optometry practitioners.^
www.TransitionConsultants.com
The Joint Commission, the accepted
national Gold Standard, reviews and accredits MONTEREY PARK, CA
over 21,000 federal, state and local-chartered
medical facilities. PRACTICE FOR SALE Practice Opportunity
To Be Eligible for ABCMO board certification:
WHIDBEY ISLAND, WA PRACTICE FOR SALE
1. Complete an accredited residency
in medical optometry Established practice for W W , WI
sale on beautiful south WI
2. Pass the national Advanced Competence r. nutson
in Medical Optometry Examination Whidbey Island WA.
Annual gross revenue is
3. Practice in a medical setting for a
minimum of two years.# 685K.Owner retiring.

www.abcmo.org [email protected]

Visit www.abcmo.org to understand how
JC accredited medical facilities credential
specialists and why specialty certification can
enhance the careers of optometrists who
complete residencies in medical optometry.

For Application procedures see
www.abcmo.org

or contact [email protected]

^ At this time, 127 JC accredited hospitals, clinics and teaching institutions
recognize ABCMO specialist certification.

* www.jointcommission.org
# Waived for two years after residency

Equipment and Supplies

Targeting Optometrists?

CLASSIFIED ADVERTISING WORKS

Contact us today for
classified advertising:
Toll free: 888-498-1460
E-mail: [email protected]

It’s What the Best
Pretest on!

(800) 522-2275

www.optinomics.com
[email protected]

Contact us today
for classified advertising:
Toll free: 888-498-1460
E-mail: [email protected]

96 REVIEW OF OPTOMETRY JULY 15, 2017

Career Opportunities Review Classifieds
OPTOMETRIST OPPORT NITY
F LL TIME OPTOMETRIST
A ,T

A ,A F O O

A PREMIER E C

P A E C C , APC

A

O

O

A ,T

C :D D ,

A D M DN N
F
, :

A EC C

A ,A ,A

Looking to C :D F ,A
increase
sales? F OPTOMETRY ASSOCIATE
: LP
Place Your
Ad here. Staff Optometrist Wanted E:

Contact us today for Bard Optical is a family owned full-service Place Your
classified advertising: retail optometric practice with 22 offices (and Ad Here!
growing) throughout Central Illinois. Bard
888-498-1460 Optical prides itself on having a progressive Toll free: 888-498-1460
optometric staff whose foundation is based on E-mail: [email protected]
E-mail: [email protected] one-on-one patient service. We are currently
accepting CV/resumes for Optometrists to join REVIEW OF OPTOMETRY JULY 15, 2017 97
our medical model optometric practice that
includes extended testing. The practice
includes but is not limited to general optometry,
contact lenses and geriatric care. Salaried,
full-time positions are available with excellent
base compensation and incentive programs
and benefits. Some part-time opportunities
may also be available.

Current positions are available in
Bloomington/Normal, Decatur/Forsyth,
Peoria, Sterling and Canton as we continue
to grow with new and established offices.

Please email your information to
[email protected] or call
Mick at 309-693-9540 ext 225.
Mailing address if more convenient is:

Bard Optical
Attn: Mick Hall, Vice President

8309 N Knoxville Avenue
Peoria, IL 61615

Bard Optical is a proud
Associate Member of the
Illinois Optometric Association.

www.bardoptical.com

Diagnostic Quiz

Beginner’s Luck

By Andrew S. Gurwood, OD

History

An 11-year-old Caucasian
male reported to the office
for a routine eye examina-
tion. He explained that his
general practitioner wanted
him to get his first eye exam
after reporting some blur
in his left eye over the last
month. His systemic and
ocular histories were unre-
markable and he denied hav-
ing allergies of any kind.

Diagnostic Data
His best-corrected entering

visual acuities were 20/20

OD and 20/25 OS at distance

and near. His external exam-

ination was normal with no

evidence of afferent pupillary

defect. The biomicroscopic

examination of the anterior

segment was normal in every This 11-year-old patient appeared for his first eye exam with blurry vision in his left eye,

way. Goldmann applanation shown in the bottom fundus image. Can you identify the cause?

tonometry measured 15mm Your Diagnosis diagnosis? What is the patient’s
Hg OU. The pertinent fun-

dus finding is demonstrated in the Does this case require any addi- likely prognosis? To find out,

photographs and optical coherence tional tests? How would you please visit us online at

tomography. manage this patient? What is your www.reviewofoptometry.com. ■

Next Month in the Mag • What Corneal Topography Reveals About Your Contact Lens
Patients
In August, Review of Optometry is proud to present its Also in this issue:
41st annual contact lens report. • Time to Update Your Plaquenil Toxicity Screening Protocol
Topics include: (earn 2 CE credits)
• Fitting Irregular Cornea Patients in Scleral Contact Lenses • Parsing Dry Eye Symptoms
• Are You Up to Date on the Newer Contact Lens Materials? • Horner’s Syndrome: So, You’ve Got A Positive Apraclonidine
• The Case for Daily Disposable-only Practice vs. Other Drop Test, Now What?
Replacement Modalities

REVIEW OF OPTOMETRY (ISSN 0147-7633) IS PUBLISHED MONTHLY, 12 TIMES A YEAR BY JOBSON MEDICAL INFORMATION LLC, 440 9TH AVENUE, 14TH FLOOR, NEW YORK, NY
10013-1678. PERIODICALS POSTAGE PAID AT NEW YORK, NY AND ADDITIONAL MAILING OFFICES. POSTMASTER: SEND ADDRESS CHANGES TO REVIEW OF OPTOMETRY, PO
BOX 81, CONGERS, NY 10920-0081. SUBSCRIPTION PRICES: US: ONE YEAR $56; TWO YEARS $97, CANADA: ONE YEAR $88, TWO YEARS $160, INT’L: ONE YEAR $209, TWO YEARS
$299. FOR SUBSCRIPTION INFORMATION CALL TOLL-FREE (877) 529-1746 (USA); OUTSIDE USA, CALL (845) 267-3065. OR EMAIL US AT [email protected].
PUBLICATIONS MAIL AGREEMENT NO: 40612608. CANADA RETURNS TO BE SENT TO BLEUCHIP INTERNATIONAL, P.O. BOX 25542, LONDON, ON N6C 6B2.

98 REVIEW OF OPTOMETRY JULY 15, 2017



START YOUR PATIENTS ON A

HEALTHY ROUTINE TODAY

ALCON DAILIES®

CH ICE
PROGRAM

Now, you can upgrade your weekly and monthly replacement
lens wearers with the ALCON DAILIES® CHOICE PROGRAM

Recommend a healthy choice Reduce the price barrier with A convenient alternative to weekly
for your patients and practice $200 savings* on a year’s supply and monthly replacement lenses

DAILIESCHOICE.com

*Via mail-in or online rebate on an annual supply of DAILIES TOTAL1® or
DAILIES® AquaComfort Plus® contact lenses. Rebate is in the form of an Alcon Visa
Prepaid Card. Must be a new patient to DAILIES TOTAL1® or DAILIES® AquaComfort Plus®
contact lenses and must purchase an annual supply of the lenses within 90 days of eye
exam and/or contact lens fitting. Applies to purchases from participating retailers only.
Visit DAILIESCHOICE.COM for full terms and conditions. Offer ends 12-31-17.

See product instructions for complete wear, care and safety information.

© 2016 Novartis 12/16 US-DAL-16-E-4914