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It was with much interest that we read the recent article by Severn et al1 regarding the first documented report of topiramate maculopathy secondary to an increase in dose. In contrary, in
2014 we shared our experience of acute myopia syndrome secondary to topiramate discontinuation, a dose decrease.2 Therefore, we assume that an increase as well as decrease of dosing may have
a common physiological mechanism through which both ocular adverse effects are mediated.
We previously hypothesized that the change in topiramate plasma levels was the likely culprit of the ocular effects rather than the administration itself—a theory that corroborates findings
of Severn et al. A sudden change in plasma levels of topiramate may result in abnormal carbonic anhydrase activity and subsequent fluid accumulation within the uveal tissue, suprachoroidal
space and the vitreous body. The anticipated accumulation of H+ in the uveal tissue and consequently altered permeability of choriocapillaris could also account for the etiology of choroidal
folds. Interestingly, we also found choroidal folds as a feature of advanced acute myopia syndrome suggesting that topiramate maculopathy may be one of the early signs or an incomplete
manifestation of acute myopia syndrome.
We believe that the crux for ocular adverse effects of topiramate could be in its pharmacokinetics, which is known to be unbalanced as it accumulates disproportionately in erythrocytes in
blood.3 Therefore, we suspect that the fluctuation in dosing could be responsible for abrupt changes in plasma levels and thus, disproportionate carbonic anhydrase activity in susceptible
individuals. Similarly, it implies that any insult to the red cells could result in an unexpected change of topiramate plasma levels.
In our opinion, the sudden changes in the plasma levels of topiramate should be avoided if possible and its mode of titration be reviewed in conjunction with both neurologists and
pharmacologists.
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