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We read, with interest the article published in the BJO by Tomsak et al.1 Interest in the Charles-Bonnet syndrome (CBS) has escalated of late, highlighting the probable 15% incidence of the condition in patients with significant visual impairment coupled with a clear sensorium.2
The authors implied that CBS was induced in four patients by brimonidine tartrate on the basis of patient age and the instigation of brimonidine therapy, with discontinuation resulting in eventual resolution of the hallucinations. Firstly, the diagnostic criteria proposed by Gold and Rabins3 and Podell et al,4 quite rightly made no reference to age being indicative of CBS, although incidence certainly increases with age. Schwartz and Vahgei5 found that CBS also occurred in children following profound visual loss. This suggests that the high incidence in the elderly population is possibly attributable to the increased incidence of acquired visual loss occurring with age; therefore, age is not a criterion for diagnosis. Further, although the Snellen acuity of all four patients was reasonably good in at least one eye of each patient, it may be surmised that severe visual impairment may have been due to visual field loss secondary to glaucomatous damage. Although this is not clear from the article, the cause of visual impairment and bilaterality are important in the diagnosis of CBS. Indeed, bilateral advanced visual field defects induced by glaucoma and homonymous hemianopia have resulted in CBS.6,7 A prevailing theory suggests sensory visual deprivation as an integral causative factor in CBS. Interestingly, and supportive of this theory, musical pseudohallucinations have been documented in cases of acquired deafness.8 Sensory deprivation in the presence of a clear sensorium will be necessary bilaterally to induce CBS, although no lower limit of Snellen visual acuity has been defined as a level for which CBS symptoms are stimulated. In the article case 4 seems to have sufficiently adequate visual function in the right eye to justify a definite misdiagnosis of CBS.
Secondly, as mentioned by the authors, α-2 agonists have been shown to cause systemic and neuropsychiatric phenomena.9 As with the discontinuation of any medication, the expectation would be resolution of induced symptoms, and as such we believe the hallucinations may easily be explained as a side effect of the medication. Brimonidine is a known lipophilic compound able to penetrate the blood-brain barrier. Through the accompanying package insert, neurological side effects such as depression and dizziness are well known. There is, therefore, little doubt that in the aged population in whom pharmacokinetics is often unpredictable, the likelihood of greater systemic absorption and distribution may well lead to neuropsychiatric phenomena. Consequently, we believe that CBS was not the cause of the complex visual hallucinations experienced by these patients but may be attributed to a rarer side effect of brimonidine, which should now be included in the patient information leaflet.
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