Twelfth Edition - Review of Optometry

13.
22. Fujishima H, Toda I, Shimazaki J, Tsubota K.
Allergic conjunctivitis and dry eye. Br J Ophthalmol.
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23. Ishibashi T, Yokoi N, Kinoshita S. Comparison of
the short-term effects on the human corneal surface of
topical timolol maleate with and without benzalkonium
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24. Pisella PJ, Malet F, Lejeune S, et al. Ocular surface
changes induced by contact lens wear. Cornea.
2001;20(8):820-5.
25. Behrens A, Doyle JJ, Stern L, et al. Dysfunctional
tear syndrome study group. Dysfunctional tear syndrome:
a Delphi approach to treatment recommendations.
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26. Pflugfelder SC. Anti-inflammatory therapy for dry
eye. Am J Ophthalmol. 2003;1(1):31-6.
27. Sall K, Stevenson OD, Mundorf TK, et al. Two
multicenter, randomized studies of the efficacy and
safety of cyclosporine ophthalmic emulsion in moderate
to severe dry eye disease. CsA Phase 3 Study Group.
Ophthalmology. 2000;107(4):631-9.
28. Byun YJ, Kim TI, Kwon SM, et al. Efficacy of combined
0.05% cyclosporine and 1% methylprednisolone
treatment for chronic dry eye. Cornea. 2009. [Epub
ahead of print].
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effect on meibomian gland lipids in meibomianitis
patients. Exp Eye Res. 2003;76(4):417-20.
31. Macsai MS. The role of omega-3 dietary supplementation
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32. Papas AS, Sherrer YS, Charney M, et al. Successful
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33. Ono M, Takamura E, Shinozaki K, et al. Therapeutic
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THYGESON’S SUPERFICIAL
PUNCTATE KERATOPATHY
Signs and Symptoms
Thygeson’s superficial punctate
keratopathy (TSPK) is a bilateral, epithelial
keratitis of unknown etiology,
26A REVIEW OF OPTOMETRY APRIL 15, 2010
first described by Phillips Thygeson in
1950. 1 It is characterized by an insidious
onset of corneal inflammation with
a long duration of exacerbations and
remissions. The clinical presentation is
characterized by recurrent episodes of
photophobia, tearing, ocular burning
and foreign body sensation, typically
in both eyes. 1,2 Physical examination
reveals whitish fine granular “asteriskshaped”
or “dendriform” intraepithelial
opacities, sometimes creating an elevation
of the overlying corneal epithelium.
Characteristically, no conjunctival
inflammation is associated with the
keratitis, and the eye is otherwise white
and quiet.
Most lesions are central; however,
peripheral lesions do occur and may
be associated with delicate, peripheral
vascularization in chronic cases. Fine
filaments also may be associated with
the keratitis. 1-3 The disease may persist
from one month to decades, with
an average episodic duration of eight
years or longer. 4 Visual acuity may be
decreased by the subepithelial opacities,
but generally it returns to normal
following resolution of the keratitis. 3
Corneal sensation is usually normal,
but the physiologic climate for mild
hypoesthesia exists. 5
The onset of TSPK is most common
in the second and third decades with an
age range of 2.5 to 70 years. 5 No clear
sexual predilection exists, although a
female preponderance has been suggested.
1-5 Recurrence has been associated
with corneal surgical procedures. 7,8
Pathophysiology
Classically, there are five characteristic
features of TSPK: chronic,
bilateral punctate inflammation; long
duration with remissions and exacerbations;
healing without significant scarring;
absent clinical response to topical
antibiotics and striking symptomatic
response to topical corticosteroids. 3
No established cause for the disease
is known; however, allergic, viral and
toxic mechanisms that interrupt the
keratinization process (tissue drying)
have been proposed. 6,9 The clinical
manifestations of TSPK resemble a
combination of findings that meld the
signs of viral keratitis with the reaction
that is observed following an exposure
to a noxious agent. 2,3,6,10 The TSPK
lesions seem to possess the ability to
gain access to the deeper corneal epithelial
layers. 2,3,6,10 An altered immune
response to an unknown exogenous or
endogenous antigen may explain the
characteristic exacerbations and remissions
of the disease. 8,10,11 In some
patients, an increase in HLA-Dw3 and
HLA-DR3 expression, both of which
are HLA loci associated with immune
response genes, has been detected. 11,12
Recently, researchers were able
to determine that the number of
Langerhans cells (antigen-presenting
cells) in the cornea, normally located
in the peripheral cornea and to a lesser
extent, the central regions of the
healthy cornea, were greatly increased
within the basal cell layer of the corneal
epithelium and within Bowman’s layer
of affected eyes. 12 Most of the corneal
abnormalities in the eyes affected by
TSPK are confined to the basal cell
layer of the corneal epithelium, the
subepithelial nerve plexus, Bowman’s
membrane and the anterior stroma. 13
The middle and deep regions of the
stroma, Descemet’s membrane and
endothelial cells are spared from pathological
changes. 13
Corneal scrapings of the lesions
demonstrate nonspecific findings,
which include atypical and degenerated
epithelial cells and a mild mononuclear
and polymorphonuclear cell
infiltrate. 13 Focal cell destruction
without the cell-to-cell pattern, typical
of herpes simplex keratitis, has been
reported. However, the presence of