- Email: [email protected]
Bilateral posterior cortical diffusion restriction due to electrocution
G Model
ARTICLE IN PRESS
CLINEU-4537; No. of Pages 1
Clinical Neurology and Neurosurgery xxx (2016) xxx–xxx
Contents lists available at ScienceDirect
Clinical Neurology and Neurosurgery journal homepage: www.elsevier.com/locate/clineuro
Correspondence Bilateral posterior cortical diffusion restriction due to electrocution To the Editor, Chauhan et al. reported an extremely interesting patient presenting with reversible cortical blindness following electrocution in the subacute period [1]. The patient had admitted with sudden onset headache and bilateral visual blurring which had suddenly developed one week later electrocution. Concurrently performed cranial MRI had showed bilateral cortical diffusion restriction in parieto-occipital regions. However, I would like to comment the article in some aspects. First, I agree that the lesion sites did not correspond to any vascular territories. In addition, T2 and FLAIR sequences showed subtle hyperintensity in the corresponding areas which were incompatible with stroke. Nonetheless, considering that neuroimaging results showed diffusion restriction (reflection cytotoxic edema), but not vasogenic edema; a major question may be that why steroid treatment was administered and did it be efficient in the clinical recovery of the patient or otherwise, the following recovery was rather due to its natural course. I think that, based on the cranial MRI findings, there is not a rationale indication for administering steroid in this patient. I think that follow-up MRI recordings might give substantial contributions regarding the pathophysiology and nature of the diffusion restricted lesions. Another more interesting point may be that is the clinical manifestations primarily associated with electrocution or it is only a factor inducing this, or it is only a co-existence? The authors discussed other possible diagnosis of PRES and delayed clinical manifestation of anoxic injury. I think that the delayed clinical manifestation of this patient does not correspond to clinical evolution of anoxic injury. However, PRES can be considered as the most likely diagnosis. Although blood pressure was within normal range, normotensive PRES patients have been reported many times in literature [2–4]. Rabistein et al. reported that %15–20 of the PRES patients are not hypertensive. Taken together, I think that presenting this case as a patient with PRES in the background of electrocution as an inducer would be more suitable. In accordance with this consideration, the only other case (as also referred by Chauhan et al.) reported by Gans et al. had presented with visual deterioration 4 day after electrocution and cranial BT had showed
hypodensity in the left occipital region which were compatible with PRES. Of note, tension values were high in this patient [5]. At this point, a major topic of discussion may be that what was the pathophysiologies underlying this effect of electrocution as an inducer of PRES. I think that the most probable explanation may be glutamate increment and its excitotoxic effect underlying neuroimaging abnormalities. However, although the patient by Chauhan et al. can be evaluated as PRES, this case constitutes a very crucial report illustrating this presentation occurring in the background of electrocution. Future studies focusing on the neurological side effects of electrocution as well as pathomechanisms of PRES need to be conducted to clarify these arguments. Conflict of interests None. Funding None. References [1] B. Chauhan, V.J. Philip, U.C. Shankar, Late onset reversible cortical blindness following electrocution, Clin. Neurol. Neurosurg. 139 (2015) 311–313. [2] K. Vakharia, I. Siasios, V.G. Dimopoulos, J. Pollina, Posterior reversible encephalopathy syndrome resolving within 48 hours in a normotensive patient who underwent thoracic spine surgery, J. Clin. Med. Res. 8 (3) (2016) 263–266. [3] O. Abbas, A. Shamseddin, S. Temraz, A. Haydar, Posterior reversible encephalopathy syndrome after bevacizumab therapy in a normotensive patient, BMJ Case Rep. 2013 (2013). [4] A.A. Rabinstein, J. Mandrekar, R. Merrell, O.S. Kozak, O. Durosaro, J.E. Fugate, Blood pressure fluctuations in posterior reversible encephalopathy syndrome, J Stroke Cerebrovasc. Dis. 21 (4) (2012) 254–258. [5] M. Gans, J.S. Glaser, Homonymous hemianopia following electrical injury, J. Clin. Neuroophthalmol. 6 (4) (1986) 218–223.
Halil Onder Yozgat State Hospital, Department of Neurology, Yozgat, 66000, Turkey E-mail address: [email protected] 1 October 2016 Available online xxx
http://dx.doi.org/10.1016/j.clineuro.2016.10.005 0303-8467/© 2016 Published by Elsevier B.V.
Please cite this article in press as: H. Onder, Bilateral posterior cortical diffusion restriction due to electrocution, Clin Neurol Neurosurg (2016), http://dx.doi.org/10.1016/j.clineuro.2016.10.005
ARTICLE IN PRESS
CLINEU-4537; No. of Pages 1
Clinical Neurology and Neurosurgery xxx (2016) xxx–xxx
Contents lists available at ScienceDirect
Clinical Neurology and Neurosurgery journal homepage: www.elsevier.com/locate/clineuro
Correspondence Bilateral posterior cortical diffusion restriction due to electrocution To the Editor, Chauhan et al. reported an extremely interesting patient presenting with reversible cortical blindness following electrocution in the subacute period [1]. The patient had admitted with sudden onset headache and bilateral visual blurring which had suddenly developed one week later electrocution. Concurrently performed cranial MRI had showed bilateral cortical diffusion restriction in parieto-occipital regions. However, I would like to comment the article in some aspects. First, I agree that the lesion sites did not correspond to any vascular territories. In addition, T2 and FLAIR sequences showed subtle hyperintensity in the corresponding areas which were incompatible with stroke. Nonetheless, considering that neuroimaging results showed diffusion restriction (reflection cytotoxic edema), but not vasogenic edema; a major question may be that why steroid treatment was administered and did it be efficient in the clinical recovery of the patient or otherwise, the following recovery was rather due to its natural course. I think that, based on the cranial MRI findings, there is not a rationale indication for administering steroid in this patient. I think that follow-up MRI recordings might give substantial contributions regarding the pathophysiology and nature of the diffusion restricted lesions. Another more interesting point may be that is the clinical manifestations primarily associated with electrocution or it is only a factor inducing this, or it is only a co-existence? The authors discussed other possible diagnosis of PRES and delayed clinical manifestation of anoxic injury. I think that the delayed clinical manifestation of this patient does not correspond to clinical evolution of anoxic injury. However, PRES can be considered as the most likely diagnosis. Although blood pressure was within normal range, normotensive PRES patients have been reported many times in literature [2–4]. Rabistein et al. reported that %15–20 of the PRES patients are not hypertensive. Taken together, I think that presenting this case as a patient with PRES in the background of electrocution as an inducer would be more suitable. In accordance with this consideration, the only other case (as also referred by Chauhan et al.) reported by Gans et al. had presented with visual deterioration 4 day after electrocution and cranial BT had showed
hypodensity in the left occipital region which were compatible with PRES. Of note, tension values were high in this patient [5]. At this point, a major topic of discussion may be that what was the pathophysiologies underlying this effect of electrocution as an inducer of PRES. I think that the most probable explanation may be glutamate increment and its excitotoxic effect underlying neuroimaging abnormalities. However, although the patient by Chauhan et al. can be evaluated as PRES, this case constitutes a very crucial report illustrating this presentation occurring in the background of electrocution. Future studies focusing on the neurological side effects of electrocution as well as pathomechanisms of PRES need to be conducted to clarify these arguments. Conflict of interests None. Funding None. References [1] B. Chauhan, V.J. Philip, U.C. Shankar, Late onset reversible cortical blindness following electrocution, Clin. Neurol. Neurosurg. 139 (2015) 311–313. [2] K. Vakharia, I. Siasios, V.G. Dimopoulos, J. Pollina, Posterior reversible encephalopathy syndrome resolving within 48 hours in a normotensive patient who underwent thoracic spine surgery, J. Clin. Med. Res. 8 (3) (2016) 263–266. [3] O. Abbas, A. Shamseddin, S. Temraz, A. Haydar, Posterior reversible encephalopathy syndrome after bevacizumab therapy in a normotensive patient, BMJ Case Rep. 2013 (2013). [4] A.A. Rabinstein, J. Mandrekar, R. Merrell, O.S. Kozak, O. Durosaro, J.E. Fugate, Blood pressure fluctuations in posterior reversible encephalopathy syndrome, J Stroke Cerebrovasc. Dis. 21 (4) (2012) 254–258. [5] M. Gans, J.S. Glaser, Homonymous hemianopia following electrical injury, J. Clin. Neuroophthalmol. 6 (4) (1986) 218–223.
Halil Onder Yozgat State Hospital, Department of Neurology, Yozgat, 66000, Turkey E-mail address: [email protected] 1 October 2016 Available online xxx
http://dx.doi.org/10.1016/j.clineuro.2016.10.005 0303-8467/© 2016 Published by Elsevier B.V.
Please cite this article in press as: H. Onder, Bilateral posterior cortical diffusion restriction due to electrocution, Clin Neurol Neurosurg (2016), http://dx.doi.org/10.1016/j.clineuro.2016.10.005