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Articles by Kruize et al and Tsubota et alin this issue of the BJO (pp 435 and 439), emphasise two important clinical aspects of dry eye or keratoconjunctivitis sicca (KCS). Not all dry eye symptoms are due to a dry eye and dry symptoms and findings do not necessarily worsen over time, and in fact may improve.
The symptoms are always the same—a sandy, gritty, burning feeling. Unfortunately, the causes of the dry eye are not. There are many different aetiologies of KCS.1 All too often we associate dry eye symptoms with a disorder of the tear film or tear secretion. In the article by Tsubota et al another important cause of dry eye symptoms is reported, Meige’s syndrome,2characterised by involuntary eye closure (blepharospasm) with middle or lower facial dystonia. In a subgroup of patients with dry eye who failed to respond to topical lubricant therapy, the authors found that more than half of these patients had Meige’s syndrome. In patients with blepharospasm, it can be difficult determining whether dry eye causes blepharospasm (secondary) or blepharospasm (primary) causes the dry eye. In general, patients with primary blepharospasm do not show significant improvement in dry eye symptoms with topical lubricants. Therefore, a therapeutic trial of artificial lubricants is a useful diagnostic test to distinguish blepharospasm from other causes of dry eye as the source of symptoms. Meige’s syndrome along with dermatochalasis3 represent conditions which can be characterised by severe eye symptoms with minimal abnormalities of tear secretion, the film, and the ocular surface. In both groups, patient symptoms are ill defined, usually dryness rather than foreign body sensation, grittiness, or burning. Often, there is a complaint of a feeling of watery eyes, but without frank epiphora. The source of the dry eye symptoms in these patients is not known. Patients with Meige’s syndrome and essential blepharospasm respond well to botulinum A toxin which may relieve dry eye symptoms as well as blepharospasm.
KCS in primary Sjögren’s syndrome (PSS) may not lead to a progressive deterioration in lacrimal gland function. Those of us who follow patients with PSS find that the onset of symptoms and clinical findings occur over a relatively short period of time, often associated with inflammation of the ocular surface. After several years, symptoms and clinical findings often appear to stabilise without continued progression. The study by Kruize et al lends support to this clinical observation. They suggest that PSS patients remain relatively stable after an initial active disease phase.
Patients with secondary Sjögren’s syndrome (SSS) were found to have their lacrimal gland function return to normal, perhaps related to remission of the underlying disease process. Non-Sjögren’s syndrome patients showed marked improvement in tear function factors after 10–12 years. The authors rightly suggest that the term ‘age-related’ dry eye be avoided as age-related changes in the lacrimal gland do not necessarily cause a dry eye.
PSS is characterised by an active inflammatory stage followed by a chronic stage. Most of the signs and symptoms are probably due to residual lacrimal gland damage from the initial active disease process. Intervention in the active stage with systemic, or perhaps topical, immunomodulating agents may reduce the severity of the eye disease and improve the long term quality of life of patients with PSS.4
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