Dr Maggioni and associates have reported an interesting case of intermittent angle-closure glaucoma masquerading as retinal migraine (1). However, there are points with which we cannot concur. First, the most common manifestation of intermittent angle-closure glaucoma is not headache but rather visual disturbance (2). Classical visual disturbance is not mere blurring of vision. It is highly characteristic and described by patients as ‘seeing halos around lights’, which actually represents diffuse corneal epithelial oedema due to elevated intraocular pressure (2). A careful history taking with specific questioning on this unique symptom may sometimes help achieve an early diagnosis and proper ophthalmic referral. Second, the authors mention presentations of acute angle closure glaucoma, which they believe should include mydiasis (2). This is astonishing. It is well known to every ophthalmologist that pupil block and iris bombe are the essential elements for acute attack of angle closure glaucoma (3). Clinically, these will be reflected as a non-reactive 3–4-mm pupil in ‘mid-dilated position’ with maximal irislenticular touch and pupil-blocking force (4). Physiologically speaking, this is completely different from the mydriatic pupil, which is devoid of pupilblocking force.
Intermittent angle-closure glaucoma in the presence of a white eye, posing as retinal migraine. Reply
ZANCHIN, GIORGIO;MAGGIONI, FERDINANDO
2006
Abstract
Dr Maggioni and associates have reported an interesting case of intermittent angle-closure glaucoma masquerading as retinal migraine (1). However, there are points with which we cannot concur. First, the most common manifestation of intermittent angle-closure glaucoma is not headache but rather visual disturbance (2). Classical visual disturbance is not mere blurring of vision. It is highly characteristic and described by patients as ‘seeing halos around lights’, which actually represents diffuse corneal epithelial oedema due to elevated intraocular pressure (2). A careful history taking with specific questioning on this unique symptom may sometimes help achieve an early diagnosis and proper ophthalmic referral. Second, the authors mention presentations of acute angle closure glaucoma, which they believe should include mydiasis (2). This is astonishing. It is well known to every ophthalmologist that pupil block and iris bombe are the essential elements for acute attack of angle closure glaucoma (3). Clinically, these will be reflected as a non-reactive 3–4-mm pupil in ‘mid-dilated position’ with maximal irislenticular touch and pupil-blocking force (4). Physiologically speaking, this is completely different from the mydriatic pupil, which is devoid of pupilblocking force.
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