Abstract
We read with great interest the paper from Choi et al. (1). The authors reported an angle-closure glaucoma patient whose presenting sign was unilateral orthostatic headache and was successfully treated by glaucoma drainage implant surgery. They presumed that increased intraocular pressure (IOP) was exacerbated by the possible mydriasis resulting from ‘hyperadrenergic’ presentation of the severe orthostatic hypotension due to diabetic autonomic neuropathy. This is a reasonably acceptable explanation for the elevation of IOP in an eye with predisposition to angle closure because such autonomic factors may influence the onset or severity of pupil block. Systemic autonomic dysfunction has been reported in patients with primary angle-closure glaucoma (PACG) (2,3), although Yong and co-workers failed to identify systemic autonomic dysfunction in 16 patients with PACG (4). However, there are some issues that need to be clarified.
First, it is well-known that the IOP increases in healthy eyes on assumption of the supine position from the seated upright position (5). Increased episcleral venous pressure and increased ophthalmic artery pressure with the posture change have been suggested as contributory mechanisms for this phenomenon. Such IOP increases with postural alteration were reported to be greater in eyes with glaucoma or diabetes (5,6). In addition, some studies investigated the effect of posture on IOP in patients with systemic autonomic dysfunction and demonstrated larger IOP decreases than normal on upright position in such patients (7,8). Interestingly, the presumed changes of the IOP in this case contrast with the findings of the previous studies.
Second, the authors provided only the precipitating factor for the IOP rise and did not explain the mechanism by which the headache and ocular pain were relieved by the postural change. Common clinical scenarios of intermittent (or subacute) angle closure are as follows: angle closure attacks often occur at night or in dim light and disappear later during sleep or after exposure to bright light, both of which are thought to induce miosis.9 However, this case showed relatively quick relief of the symptoms within 10–15 s upon assumption of the supine position. Mere postural shift to the supine position does not lead to immediate miosis. It seems that other factors such as the gravity and/or the crystalline lens may (if the patient had not undergone cataract surgery) have played a role in relieving the spike of IOP. Gravity may have pulled the peripheral iris and/or the crystalline lens posteriorly, thereby alleviating the appositional closure between the peripheral iris and the trabecular meshwork.