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• REPLY TO: "RETINAL NERVE FIBRE LAYER THINNING IS ASSOCIATED WITH DRUG RESISTANCE IN EPILEPSY: PROMISING YET OPEN ENDED"
  Simona Balestrini
  Published on: 13 May 2016
• A radiological curiosity of hyperammonaemia!
  Michael Kinney
  Published on: 13 April 2016

• Published on: 13 May 2016

  REPLY TO: "RETINAL NERVE FIBRE LAYER THINNING IS ASSOCIATED WITH DRUG RESISTANCE IN EPILEPSY: PROMISING YET OPEN ENDED"

  • Simona Balestrini
  • Other Contributors:
    • Sanjay M Sisodiya

  Sir, We thank Kumar et al. for their interest in our recent article on retinal nerve fibre layer thickness (RNFL) in people with epilepsy. In their letter they raise a few points that we would like to address.

  1. Comparison between people with epilepsy and healthy controls. They suggest that a comparison between people with drug-resistant versus non- resistant epilepsy might have been more appropriate. However, a...

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  Sir, We thank Kumar et al. for their interest in our recent article on retinal nerve fibre layer thickness (RNFL) in people with epilepsy. In their letter they raise a few points that we would like to address.

  1. Comparison between people with epilepsy and healthy controls. They suggest that a comparison between people with drug-resistant versus non- resistant epilepsy might have been more appropriate. However, as described in the paper itself, in Methods - Statistics, we first compared cases versus controls and then tested for differences in the distribution of average RNFL thickness as a continuous variable according to each demographic and clinical factor, including drug-resistance. The results of this comparison are presented in Results - Average RNFL thickness across all quadrants and exposure to AEDs or non-medical treatments, and showed thinner average RNFL in people with drug-resistant epilepsy compared with non-resistant epilepsy.

  2) Kumar et al. state that the aetiological spectrum of epilepsy is not described. We report the epilepsy aetiology in Supplementary material, Table S2, classified according to the "Commission on Classification and Terminology of the International League Against Epilepsy, 1989". We also tested for difference in the distribution of RNFL thickness according to the epilepsy type (see Results - Average RNFL thickness and clinical characteristics--univariate associations). This information was all present in the publication.

  3) We agree with the fact that age is a major factor determining the RNFL thickness. We analysed correlation of average RNFL thickness with age in both cases and controls. We included only epilepsy duration in the regression models because of high collinearity with age. We did not consider age group distribution as this would have significantly limited the sample size.

  4) We recognise that refractive errors may affect RNFL thickness. For this reason, we excluded people with a distance refractive error of >4.50 dioptres mean sphere/>2.5 dioptres cylinder.

  5) We attempted to account for all known factors known to be associated with changes in RNFL (exposure to vigabatrin, diabetes, glaucoma or other known ocular disease, concurrent diagnosis of multiple sclerosis, history of trauma or surgery to the eye or orbit, refractive errors, brain MRI evidence of visual pathway involvement), as stated in Methods, Participants.

  The points raised by Kumar et al. were therefore all already addressed in the original paper.

  Conflict of Interest:

  None declared

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  Conflict of Interest:
  None declared.

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• Published on: 13 April 2016

  A radiological curiosity of hyperammonaemia!

  • Michael Kinney, Neurology doctor
  • Other Contributors:
    • Dr. Eugene McKenna

  We would like to draw attention to one important point in regard to hyperammonaemic encephalopathy which was not mentioned in the recent excellent article by Sutter and Kaplan discussing the imaging features of encephalopathy.

  The cases of hyperammonaemic encephalopathy with neuroimaging features number less than 10 in the reported literature. As the authors stated they can develop cortical signal abnormalitie...

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  We would like to draw attention to one important point in regard to hyperammonaemic encephalopathy which was not mentioned in the recent excellent article by Sutter and Kaplan discussing the imaging features of encephalopathy.

  The cases of hyperammonaemic encephalopathy with neuroimaging features number less than 10 in the reported literature. As the authors stated they can develop cortical signal abnormalities.

  However having recently had experience with three cases of hyperammonaemia we noted despite the very diffuse cortical signal change, the signal change didn't involve the perirolandic cortex, in each of the three cases. This was noted in all but one of the reported cases in the literature.

  It is worth drawing attention to this, as this radiological feature may be a feature which is quite specific to hyperammonaemia. Clearly this is observation is based on a very small number of patients, but is worth bearing in mind when assessing patients with cortical signal change, which may spare the perirolandic cortex.

  As an explanation for this process, it is possible that this is related to cortical cytoarchitecture (perineuronal nets-abundent in perirolandic cortex [1])/receptor characteristics leading to a differential sensitivity to the toxic insult of elevated ammonia.

  Reference:

  [1] Karaarslan E, Arslan A. Perirolandic cortex of the normal brain. Low signal intensity on turbo FLAIR MR images. Radiology. 2003;227:538-541

  Conflict of Interest:

  None declared

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  Conflict of Interest:
  None declared.

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