The question concerns a patient diagnosed with trigeminal neuralgia in 1991. He has been treated fo

Fråga: The question concerns a patient diagnosed with trigeminal neuralgia in 1991. He has been treated for this disease with carbamazepine (dose unknown) for a period of about three months. A few months ago, he was referred to an opthalmologist because of decreased central vision. Carbamazepine was discontinued some months before the patient was referred to the opthalmologist. Is there any documentation concerning macula changes or optic nerve damage as a side-effect of carbamazepine?

Sammanfattning: Visual disturbances, such as diplopia, blurred vision and decreased accomodation, have been reported as side-effects of carbamazepine treatment. These adverse effects are assumed to be dose-dependent and reversible. One article was found, reporting two cases in which the development of retinopathy was possibly related to carbamazepine. Disturbances in vision reversed after discontinuation of the drug. Despite an extensive literature search, considering also the widespread use of carbamazepine, no other reports concerning retinal or optic nerve damage in connection with carbamazepine could be found.

Svar: Visual disturbances, such as diplopia, blurred vision and decreased accomodation, belong to the more common observed side-effects of carbamazepine (1). These kinds of ocular adverse reactions will occur in most patients when the daily dosage exceeds 1200 mg. Most ocular side-effects seem to be reversible and may spontaneously clear up even without reduction of the drug dosage (1). However, cataract has been reported as a rare side-effect of carbamazepine (2).

Despite a thorough literature search, reports relating any retinal, macular or optic nerve damage to carbamazepine seem very scarce; only one article could be found presenting two cases of retinopathy, possibly caused by carbamazepine (3). The first case describes a 41-year-old woman treated with phenytoin and phenobarbital since 1961 and treated since 1969 with carbamazepine (600-1000 mg daily). Ten years later she developed a sudden reduction of visual acuity and investigations disclosed extensive lesions of the retinal pigment epithelium, including the macular regions. Discontinuation of carbamazepine led to an improvement of the morphological changes and to a normalisation of visual function. The second case concerned a 35-year-old woman, treated with phenobarbital and diphenylhydantoin for 16 years, and treated from 1973 to 1983 with carbamazepine 1000 mg daily. In 1982 she developed blurred vision and a subjective paracentral scotoma in one eye. Investigation showed discrete lesions of the retinal pigment. After discontinuation of the drug, her visual disturbances disappeared one month later. It was concluded that carbamazepine might have had a possible retinotoxic effect, especially on the retinal pigment epithelium, causing a decreased visual acuity that reversed after discontinuation of the drug.

Of interest may be a study investigating visual contrast sensitivity (VCS), comparing a group of 27 epileptic patients treated with carbamazepine (200-1800 mg/day) with an age-matched control group (4). Visual contrast sensitivity was found to be significantly lower in the patient group compared with the control group. However, all patients had a normal visual acuity. It was not possible in this study to distinguish whether the drug treatment, the epilepsy, an underlying brain disorder or a combination of these factors was causing the decrease in VCS. A reduction in VCS may be found in many disorders, among these refractive disorders, macular or other retinal disorders (4). However, none of the patients showed any sign of retinopathy.

Ten reports of ocular side-effects possibly related to carbamazepine have been received by the Swedish Adverse Drug Reactions Advisory Committee since 1965: one case of conjunctivitis, one case of cataract and eight cases of diplopia.