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Cortically visually impaired children
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  1. M P CLARKE,
  2. K W MITCHELL
  1. Department of Ophthalmology
  2. University of Newcastle
  3. Royal Victoria Infirmary
  4. Newcastle upon Tyne NE1 4LP
    1. CREIG S HOYT,
    2. DOUGLAS R FREDRICK
    1. San Francisco, California

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      Editor,—While Hoyt and Fredrick rightly state the heterogeneous aetiology of cortical visual impairment (CVI) in children,1 we were disappointed in their bland and unjustified dismissal of the value of electrophysiological studies in these cases. They fail to quote any electrophysiological studies more recent than 1979 in their review, of which there have been a not inconsiderable number. As for our own work we have found that a normal flash VEP indicates statistically and clinically a better prognosis in blind babies with non-ocular visual impairment even though we would concede that in some cases flash VEPs can be normal in CVI.2 It is therefore clinically useful to perform evoked potential studies in these children, a position endorsed by the commentary in the same issue ofBJO,3 which states that electrophysiological investigations are mandatory in the investigation of babies with poor visual contact. We endorse this sentiment and although accepting the limitations of the technique, feel that VEP investigations provide valuable objective information in the assessment of these infants. Hoyt and Frederick rightly point out that further work is required in the evaluation of infant CVI but not even to attempt any review of work within the past 20 years—never mind the most recent—is at best misleading and at worst scientifically unacceptable.

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      Reply

      Editor,—We thank Clarke and Mitchell for their thoughtful comments on our editorial on cortical visual impairment (CVI). We are somewhat bemused by the notion that the passage of time invariably invalidates good clinical studies. Our editorial did not go into detail about VEPs and CVI because of space limitations and the focus of that editorial. We meant only to imply that VEPs had been less useful than we all hoped they would be in evaluating this difficult group of visually impaired children. We do not disagree with Clarke and Mitchell that intact flash VEPs usually imply a better visual outcome than if the VEPs are abnormal or absent. Similar results have been reported by Taylor and McCulloch. Regrettably, in our studies of children with cortical visual impairment the group of patients with intact flash VEPs represents only a small portion of those we care for. In the remaining larger group of patients with abnormal VEPs we have not found good correlation with the ultimate visual outcome. Moreover, in children with neurological disorders, flash VEPs are often abnormal even when the patient is well sighted. The problem then is how to interpret an abnormal VEP in a child with CVI. This is where VEPs have been disappointing and frequently misleading. VEP mapping may be a significant improvement over standard flash VEPs. Witing et al  reported that VEP mapping in 50 children with permanent CVI was always abnormal and showed good correlation with computed tomography results, whereas the conventional VEP recordings were abnormal in only 50% of cases and with much less good correlation. We, therefore, look forward to further studies of VEPs demonstrating improved techniques that provide better prognostic value when evaluating the abnormal VEP in a child with CVI.

      We apologise for any confusion caused by the terseness of our discussion. We encourage Clarke and Mitchell to continue their VEPs of children with CVI and look forward to reading their results in the future.

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