Neuroradiology DOI 10.1007/s00234-015-1528-2
LETTER TO THE EDITOR
Re: Guillain Barré syndrome-related posterior reversible encephalopathy syndrome Fuldem Yildirim Donmez 1
Received: 26 March 2015 / Accepted: 1 April 2015 # Springer-Verlag Berlin Heidelberg 2015
Dear Editor, I have read the article BGuillain Barré syndrome-related posterior reversible encephalopathy syndrome^ by Zuccoli G et al. with interest [1]. The authors reported the unique case of posterior reversible encephalopathy syndrome (PRES) in a child with Epstein-Barr virus (EBV) infection-related Guillain Barré syndrome (GBS). Their patient had a positive result for EBV viral capsid and antigen IgG and IgM antibodies and developed progressive difficulty standing and walking with evidence of dysarthria and dysphagia which turned out to be compatible with GBS. During hospitalization, he had high blood pressure and decreased responsiveness. MRI showed bilateral frontal and parietooccipital edema, suggestive of PRES. The pathophysiology of PRES is still not well known; there are two contradicting theories favoring either hypoperfusion or hyperperfusion. However, these theories are not capable of explaining all the cases; therefore recently, some of the cases are thought to be affected by endothelial injury which may be a result of infection, inflammation, or sepsis [2, 3]. Marra et al. offer a common pathogenetic mechanism for every PRES-related condition, either hypertensive or not, which is the activation of immune system and consequent endothelial activation, starting a molecular cascade causing the production of cytokines and
VEGF. This may alter the homeostasis of the blood-brain barrier and allow fluid leakage and edema [4]. Although not very common, infection was found as the underlying etiology of PRES. In an article published by Sweany et al., it is indicated that viral infection may trigger the immune reaction and lead to the development of PRES [2, 5]. Since immune system activation is now discussed as the etiological factor for PRES, infection-related PRES cases, which were underestimated earlier, will be more commonly encountered. In the case of Zuccoli et al., the EBV infection may be the cause of both GBS and PRES rather than the GBS being an independent risk factor for PRES as the authors suggested. Moreover, the elevated arterial blood pressure which could be seen in GBS patients may be the underlying factor for PRES, which is independent of all. Given the clinical and laboratory results, it is hard to conclude a direct relationship between GBS and PRES; in my opinion, it may be explained as a coincidence rather than an independent risk factor, as it is now stated that infection itself is the risk factor. The article is interesting as it is quite rare; however, more evidence is needed to suggest a relationship between the two clinical scenes. Ethical standards and patient consent I declare that this manuscript does not contain clinical studies or patient data. Conflict of interest I declare that I have no conflict of interest.
* Fuldem Yildirim Donmez [email protected] 1
References 1.
Department of Radiology, Baskent University Faculty of Medicine, 44. Sokak No:11/8, Bahcelievler, Ankara, Turkey
Zuccoli G, Nardone R, Hoda AH (2015) Guillain Barré syndromerelated posterior reversible encephalopathy syndrome. Neuroradiology. doi:10.1007/s00234-015-1499-3
Neuroradiology 2.
3.
Bartynski WS (2008) Posterior reversible encephalopathy syndrome, part 2: controversies surrounding pathophysiology of vasogenic edema. AJNR Am J Neuroradiol 29(6):1043–1049 McCoy B, King M, Gill D, Twomey E (2011) Childhood posterior reversible encephalopathy syndrome. Eur J Paediatr Neurol 15(2): 91–94
4.
5.
Marra A, Vargas M, Striano P, Del Guercio L, Buonanno P, Servillo G (2014) Posterior reversible encephalopathy syndrome: the endothelial hypotheses. Med Hypotheses 82(5):619–622 Sweany JM, Bartynski WS, Boardman JF (2007) BRecurrent^ posterior reversible encephalopathy syndrome, report of 3 cases—PRES can strike twice! J Comput Assist Tomogr 31(1):148–156
LETTER TO THE EDITOR
Re: Guillain Barré syndrome-related posterior reversible encephalopathy syndrome Fuldem Yildirim Donmez 1
Received: 26 March 2015 / Accepted: 1 April 2015 # Springer-Verlag Berlin Heidelberg 2015
Dear Editor, I have read the article BGuillain Barré syndrome-related posterior reversible encephalopathy syndrome^ by Zuccoli G et al. with interest [1]. The authors reported the unique case of posterior reversible encephalopathy syndrome (PRES) in a child with Epstein-Barr virus (EBV) infection-related Guillain Barré syndrome (GBS). Their patient had a positive result for EBV viral capsid and antigen IgG and IgM antibodies and developed progressive difficulty standing and walking with evidence of dysarthria and dysphagia which turned out to be compatible with GBS. During hospitalization, he had high blood pressure and decreased responsiveness. MRI showed bilateral frontal and parietooccipital edema, suggestive of PRES. The pathophysiology of PRES is still not well known; there are two contradicting theories favoring either hypoperfusion or hyperperfusion. However, these theories are not capable of explaining all the cases; therefore recently, some of the cases are thought to be affected by endothelial injury which may be a result of infection, inflammation, or sepsis [2, 3]. Marra et al. offer a common pathogenetic mechanism for every PRES-related condition, either hypertensive or not, which is the activation of immune system and consequent endothelial activation, starting a molecular cascade causing the production of cytokines and
VEGF. This may alter the homeostasis of the blood-brain barrier and allow fluid leakage and edema [4]. Although not very common, infection was found as the underlying etiology of PRES. In an article published by Sweany et al., it is indicated that viral infection may trigger the immune reaction and lead to the development of PRES [2, 5]. Since immune system activation is now discussed as the etiological factor for PRES, infection-related PRES cases, which were underestimated earlier, will be more commonly encountered. In the case of Zuccoli et al., the EBV infection may be the cause of both GBS and PRES rather than the GBS being an independent risk factor for PRES as the authors suggested. Moreover, the elevated arterial blood pressure which could be seen in GBS patients may be the underlying factor for PRES, which is independent of all. Given the clinical and laboratory results, it is hard to conclude a direct relationship between GBS and PRES; in my opinion, it may be explained as a coincidence rather than an independent risk factor, as it is now stated that infection itself is the risk factor. The article is interesting as it is quite rare; however, more evidence is needed to suggest a relationship between the two clinical scenes. Ethical standards and patient consent I declare that this manuscript does not contain clinical studies or patient data. Conflict of interest I declare that I have no conflict of interest.
* Fuldem Yildirim Donmez [email protected] 1
References 1.
Department of Radiology, Baskent University Faculty of Medicine, 44. Sokak No:11/8, Bahcelievler, Ankara, Turkey
Zuccoli G, Nardone R, Hoda AH (2015) Guillain Barré syndromerelated posterior reversible encephalopathy syndrome. Neuroradiology. doi:10.1007/s00234-015-1499-3
Neuroradiology 2.
3.
Bartynski WS (2008) Posterior reversible encephalopathy syndrome, part 2: controversies surrounding pathophysiology of vasogenic edema. AJNR Am J Neuroradiol 29(6):1043–1049 McCoy B, King M, Gill D, Twomey E (2011) Childhood posterior reversible encephalopathy syndrome. Eur J Paediatr Neurol 15(2): 91–94
4.
5.
Marra A, Vargas M, Striano P, Del Guercio L, Buonanno P, Servillo G (2014) Posterior reversible encephalopathy syndrome: the endothelial hypotheses. Med Hypotheses 82(5):619–622 Sweany JM, Bartynski WS, Boardman JF (2007) BRecurrent^ posterior reversible encephalopathy syndrome, report of 3 cases—PRES can strike twice! J Comput Assist Tomogr 31(1):148–156
