| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Boston, MA
To the Editor:
The editorial by Dr. Miller1 regarding the retinal toxicity of anticonvulsants is timely and informative. However, some clarification would be helpful. It appears that Dr. Miller is suggesting that patients taking any of the gamma-aminobutyric acid (GABA)-ergic antiepileptic drugs should have electroretinograms (ERG) before initiation of the drug and during the course of therapy. Although Dr. Miller states that preliminary data indicate that tiagabine has similar effects on the visual system as vigabatrin, no peer-reviewed references are provided. This is an important issue and before advocating ERG in patients taking tiagabine, it would be helpful to provide readers with documentation that tiagabine, which has a different mechanism of action than vigabatrin, can lead to retinal toxicity. Likewise, because many of the other commonly used antiepileptic drugs such as phenobarbital, divalproex sodium, benzodiazepines, felbamate, and topiramate have GABA-ergic effects, it is necessary to provide convincing evidence that the incidence of retinal toxicity is sufficiently high to justify routine ERG. Although Dr. Miller states that "further studies are needed to determine the optimum interval for monitoring the visual effects of other GABA-ergic drugs," the more relevant question is whether any monitoring is necessary at all.
Baltimore, MD
To the Editor:
Dr. Miller1 recently noted the possibility that antiepileptic drugs other than vigabatrin, specifically tiagabine, might produce retinal damage. Dr. Miller is, however, a blinded investigator in a study of visual function during tiagabine treatment, which is sponsored by Abbott Laboratories (Abbott Park, IL). Our preliminary evidence shows that tiagabine does not cause visual abnormalities. Other findings support our results. Kalvianinen et al.2 reported no visual field defects in 15 patients treated with tiagabine monotherapy. Conversely, Beran et al.3 reported that six of 12 patients treated with tiagabine had visual field defects. These conflicting findings are important, but unpublished. I feel that these differences are due to methodologic problems that I encountered in a number of recent vigabatrin studies. Common problems with studies of visual function and antiepileptic drugs include the following:
Patients are often unaware of even major impairments in their vision, and so it is important that visual function be measured accurately in patients taking antiepileptic drugs to determine whether a neurotoxicologic effect is present. At this point, however, there is no evidence that GABA-ergic agents, as a class, produce retinal toxicity.
Baltimore, MD
Reply from the Author:
I appreciate the opportunity to clarify the remarks I made concerning the known and potential effects of GABA-ergic drugs on the visual system. The only peer-reviewed articles on this subject of which I am aware concern vigabatrin. At the time I wrote my editorial,1 I was aware of the abstract by Beran et al.,2 in which the authors stated that six of 12 patients taking tiagabine "had definite field defects similar to that [sic] seen with vigabatrin."2 It was my opinion that this information was sufficient to warrant a mention in the editorial, particularly when one compares the potential effects on quality of life from visual sensory deficits compared with the relative ease of monitoring visual function, clinically or electrophysiologically, in patients taking GABA-ergic drugs. Since this editorial was written, however, Sills et al.6 have shown that tiagabine does not accumulate in the retina of rats as does vigabatrin, and a number of investigators have concluded from unblinded studies that long-term use of tiagabine does not cause visual field defects or other visual sensory defects.2,7-9 In addition, as noted by Dr. Krauss, our group at Johns Hopkins University Hospital is currently performing a clinical and electrophysiologic study of patients taking tiagabine versus control patients. I am performing the clinical assessments of these patients, and am blinded to which patients are taking tiagabine and which are not, as is Dr. Mary Johnson, who is performing the electrophysiologic studies. Although the study has not been completed, I can state that I have not been impressed with any visual sensory deficits in any of the patients I have examined, as I was during our studies of patients taking vigabatrin.5,10 Thus, although none of these studies, including our own, has yet been published as a peer-reviewed article, I do not believe that patients taking GABA-ergic drugs—other than vigabatrin—require electrophysiologic monitoring, although there is no downside to monitoring such patients clinically.
Footnotes
Copyright © 2001 by AAN Enterprises, Inc.
References
This article has been cited by other articles:
|
|
 |
|
  G L Krauss, M A Johnson, S Sheth, and N R Miller A controlled study comparing visual function in patients treated with vigabatrin and tiagabine J. Neurol. Neurosurg. Psychiatry, March 1, 2003; 74(3): 339 - 343. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
