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Wernicke Encephalopathy Due to Thiamine Deficiency After Surgery on a Child With Duodenal Stenosis
Pediatric Neurology 51 (2014) 840e842
Contents lists available at ScienceDirect
Pediatric Neurology journal homepage: www.elsevier.com/locate/pnu
Clinical Observations
Wernicke Encephalopathy Due to Thiamine Deficiency After Surgery on a Child With Duodenal Stenosis Elif Acar Arslan MD a, *, Saniye Ekinci MD b, Pınar Zengin Akkus¸ MD a, lu MD a Rahs¸an Göçmen MD c, Göknur Halilog a
Department of Pediatric Neurology, Hacettepe University Children’s Hospital, Ankara, Turkey Department of Pediatric Surgery, Hacettepe University Children’s Hospital, Ankara, Turkey c Department of Radiology, Hacettepe University, Ankara, Turkey b
abstract BACKGROUND: Wernicke encephalopathy is rare in children and is caused by thiamine deficiency. It is characterized
by acute or subacute ataxia, altered consciousness, and ophthalmoparesis. Gastroenterological surgery, total parenteral nutrition for short bowel syndrome, and alcoholism are common risk factors for Wernicke encephalopathy. Typical magnetic resonance imaging features include selective symmetrical signal changes in the mammillary bodies, medial thalamus, tectum, periaqueductal region, cranial nerves, cerebellum, red nucleus, dentate nucleus, fornix, splenium, cerebral cortex, and putamen. If left undiagnosed and untreated, the disease may be fatal. PATIENT DESCRIPTION: We describe a 13-year-old boy who developed acute cerebellar findings while receiving total parenteral nutrition after gastroduodenostomy for duodenal stenosis. RESULTS: The diagnosis of Wernicke encephalopathy was based on his clinical history, neurological examination, and imaging results. We immediately started intravenous thiamine replacement therapy. Two weeks later, the patient’s clinical signs had resolved except for mild clumsiness, which was observed during his tandem gait examination. CONCLUSION: Our report emphasizes the importance of clinical and magnetic resonance imaging pattern recognition in timely diagnosis, as well as the importance of prompt thiamine replacement therapy. We also demonstrate the importance of thiamine supplementation during total parenteral nutrition after gastrointestinal surgery. Keywords: Wernicke encephalopathy, MRI, children, gastroenterological surgery, thiamine deficiency, magnetic resonance imaging, ophthalmoplegia
Pediatr Neurol 2014; 51: 840-842 Ó 2014 Elsevier Inc. All rights reserved.
Introduction
Wernicke encephalopathy is a potentially life-threatening reversible neurological disease caused by thiamine deficiency. The disease is characterized by the typical triad of ophthalmoplegia, ataxia, and confusion. Autopsy studies report that both adults and children may not be accurately diagnosed.1 Diagnosis is based on clinical findings and This paper was presented as a poster in the 15th Turkish Pediatric Society Scientific Congress 22-25 May, 2013, Sivas, Turkey.
Article History: Received July 11, 2014; Accepted in final form August 30, 2014 * Communications should be addressed to: Dr. Acar Arslan; Department of Pediatric Neurology; Hacettepe University Children’s Hospital; PC 06100; Sıhhıye, Ankara, Turkey. E-mail address: [email protected] 0887-8994/$ - see front matter Ó 2014 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.pediatrneurol.2014.08.034
probable etiologic factors.2 It is most often observed in alcoholics and in malnourished adults. The disease may also occur in association with hyperemesis gravidarum,3 gastric by-pass surgery,4,5 pancreatitis,6,7 cancer treatment in pediatric patients,8 nephrotic syndrome,9 and as a complication of gastrointestinal surgery.10,11 A frequent cause is the inadequate supply of vitamin B1 in total parenteral nutrition (TPN) solutions during treatment for chronic diseases. Patients usually respond well to acute thiamine replacement therapy. However, some patients may exhibit only one or two components of the disease, and B1 deficiency may not accompany the clinical picture.1 Parenteral thiamine is preferred to oral supplementation.12 Increased T2-weighted signal intensity in the periaqueductal area of the midbrain and the periventricular area of the thalamus confirms the diagnosis.13 Recognition of the clinical and magnetic resonance imaging
E. Acar Arslan et al. / Pediatric Neurology 51 (2014) 840e842
(MRI) patterns of the disease is extremely important for effective treatment and patients’ long-term prognoses. Patient Description A 13-year-old boy was referred by the Pediatric Surgery Department for acute titubation, nystagmus, and ataxia. He had undergone surgical resection of duodenal ulcerations at age 6 years, and an anastomosis between the antrum and the jejunum was performed 18 months before presentation, for duodenal stenosis. He had since been receiving nasogastric decompression and TPN treatment. He developed drowsiness, headache, head titubation, and ataxia within 2 days. His neurological examination was significant for drowsiness, bilateral isocoric pupils, bilateral gaze-evoked horizontal nystagmus, upward gaze palsy, dysmetria and dysdiadokinesis, truncal and gait ataxia, and absent deep tendon reflexes. There was no upbeating nystagmus. His Glasgow coma score was 14. His tongue was erythematous and smooth. His cranial MRI revealed T2 signal hyperintense areas in the periaqueductal area and both medial thalami, particularly in the pulvinar area (Figure). The diagnosis of Wernicke encephalopathy was considered based on the boy’s medical history, neurological examination, and radiological findings. He had not been receiving vitamin supplementation with his TPN formula during the 18 months following period after surgery. We immediately started intravenous thiamine at a dose of 100 mg/day and continued maintenance treatment for 1 week. After the first week of therapy, he converted to oral thiamine at a dose of 50 mg/kg. His signs improved within 1-2 days. When examined two weeks later his clinical signs had disappeared with the exception of mild clumsiness observed on his tandem gait examination. A cranial MRI obtained during follow-up revealed that the previous abnormalities had returned to normal.
841
Discussion
Wernicke encephalopathy is rarely observed in children. Wernicke first described the disease as a distinctive entity in 1881.14-16 Thirty-one pediatric patients (age <20 years) with Wernicke encephalopathy were reviewed by Vasconcelos et al.14 The most common preceding event observed by their study was malignancy (11 of 31 patients). The high rate of diagnosis of Wernicke encephalopathy during autopsy examinations suggests that the diagnosis is often overlooked in clinical settings.14 More than 20 pediatric reports have since been published based on searches of PubMed and MED-LINE using key words such as Wernicke encephalopathy, pediatric, and children, although only two describe cases resulting from gastrointestinal disease.17,18 Wernicke encephalopathy most often occurs two to eight months after surgery and primarily affects individuals with weight loss greater than 7 kg per month.1,19-21 Approximately 58% of affected individuals may be missed on routine clinical examinations.1,14 Thiamine is absorbed in the duodenum by an active, carrier-mediated, and rate-limited process and is transported across the blood-brain barrier by both active and passive mechanisms. Thiamine is subsequently converted to thiamine pyrophosphate by neurons and glial cells; the latter are responsible for several biochemical pathways in the brain, including intermediate carbohydrate metabolism,
FIGURE. (A) An axial T2-weighted image at the level of the basal ganglia demonstrates alterations of the medial thalamic nuclei. (B) An axial T2-weighted image demonstrates marked hyperintensity of the tectal plate. (C) Increased signal intensity with respect to the hypothalamus is observed on an axial fluid attenuated inversion recovery image. The lesions are consistent with reversible cytotoxic edema. One month after thiamine replacement, a partial regression of the lesions involving the medial thalamic nuclei (D) and hypothalamus is observed (E). Signal alterations at the tectal plate have completely resolved (F).
842
E. Acar Arslan et al. / Pediatric Neurology 51 (2014) 840e842
lipid metabolism, and production of amino acids and glucose-derived neurotransmitters such as glutamic acid and gamma-aminobutyric acid.1 Moreover, thiamine also appears to have a role in acetylcholinergic and serotoninergic synaptic transmission.1,22-24 Clinical signs of thiamine deficiency vary depending on the degree of deficiency and on the age and genetic predisposition of the patient. Although short-term severe thiamine deficiency often induces Wernicke encephalopathy, mild-to-moderate and prolonged thiamine deficiency generally result in peripheral nerve damage. Subclinical thiamine deficiency is difficult to diagnose. Thiamine deficiency persisting for 2-3 weeks causes damage to selective regions of the brainstem and the diencephalon, resulting in Wernicke encephalopathy.1 The disease is diagnosed on the basis of typical MRI findings and is characterized by a distinct pattern of alterations, including symmetrical alterations in the thalami, mammillary bodies, tectal plate, and periaqueductal area.25 Although Wernicke encephalopathy is rare after gastrointestinal surgery, thiamine supplementation must be part of any total parenteral nutrition treatment administered to patients. The diagnosis of Wernicke encephalopathy is challenging in some cases because of the inability of clinicians to recognize data and nonspecific clinical signs or neurological signs of the disease. The most sensitive diagnostic test is an MRI. Conclusion
Wernicke encephalopathy should be considered in children with risk factors for the disease. Recognition of characteristic clinical and MRI patterns is crucial for both the timely treatment and prevention of this life-threatening disease and its neurological complications. References 1. Sechi G, Serra A. Wernicke’s encephalopathy: new clinical settings and recent advances in diagnosis and management. Lancet Neurol. 2007;6:442-455. 2. Christopoulos P, Katsanoulas C, Timplalexi G, Lathyris D, Vasiliaqkou S, Anroniadou E. Wernicke’s encephalopathy and anabolic steroid drug abuse. Is there any possible relation? Hippokratia. 2012;16:371-372. 3. Leitner G, Kvistad KA, Aasly J. Pregnant woman with hyperemesis, confusion, ataxia and nystagmus. Tidsskr Nor Laegeforen. 2006;126: 1069-1071. 4. Morel L, Fontana E, Michel JM, Ruffieux A, Ottiger M, Regamey C. New treatment: bariatric surgery; a new complication: WernickeKorsakoff encephalopathy. Presse Med. 2008;37:49-53. 5. Bohnsack BL, Patel SS. Peripapillary nerve fiber layer thickening, telangiectasia, and retinal hemorrhages in Wernicke encephalopathy. J Neuroophthalmol. 2010;30:54-58.
6. Basit S, Elsås T, Kvistad KA, Høsøien LS. Wernicke’s encephalopathy because of pancreatitis in a young boy. Acta Ophthalmol. 2011;89: 656-657. 7. Muwakkit S, Al-Aridi C, Saab R, Hourani R, Yazbeck N, Abboud M. Wernicke’s encephalopathy during total parenteral nutrition in a child with acute lymphoblastic leukemia and acute pancreatitis. Neuropediatrics. 2009;40:249-251. 8. La Spina M, Catania R, Lo Nigro L, De Grandi C, Palmucci S, Di Cataldo A. Neurological complications during treatment of childhood cancer: mind Wernicke encephalopathy. Pediatr Hematol Oncol. 2010;27:320-323. 9. Nishida M, Sato H, Kobayashi N, Morimoto M, Hamaoka. Wernicke’s encephalopathy in a patient with nephrotic syndrome. Eur J Pediatr. 2009;168:731-734. 10. Saab RO, El Khoury MI, Jabbour RA. Wernicke encephalopathy after Roux-en-Y gastric bypass and hyperemesis gravidarum. Surg Obes Relat Dis. 2013;9:e105-e107. 11. Xu Y, Shao QS, Wang YX, Yang J, Xu J. Clinical analysis of 10 patients with Wernicke encephalopathy after major abdominal surgery. Zhonghua Wei Chang Wai Ke Za Zhi. 2013;16:471-473. 12. Thomson AD, Cook CC. Parenteral thiamine and Wernicke’s encephalopathy: the balance of risks and perception of concern. Alcohol Alcohol. 1999;32:207-209. 13. Antunez E, Estruch R, Cardenal C, Nicolas JM, Fernandez-Sola J, Urbano-Marquez A. Usefulness of CT and MR imaging in the diagnosis of acute Wernicke’s encephalopathy. AJR Am J Roentgenol. 1998;171:1131-1137. 14. Vasconcelos MM, Silva KP, Vidal G, Silva AF, Domingues RC, Berditchevsky CR. Early diagnosis of pediatric Wernicke’s encephalopathy. Pediatr Neurol. 1999;20:289-294. 15. Thomson AD, Cook CC, GuerriniSheedy D, Harper C, Marshall EJ. Wernicke’s encephalopathy revisited. Translation of the case history section of the original manuscript by Carl Wernicke ’Lehrbuch der Gehirnkrankheiten fur Aerzte and Studirende’ (1881) with a commentary. Alcohol Alcohol. 2008;43:174-179. 16. Wernicke C. Lehrbuch der gehirnkrank heiten für aerzte and studirende. Kassel Theodor Fischer. 1881;2:229-242. 17. Sparacia G, Banco A, Lagalla R. Reversible MRI abnormalities in an unusual paediatric presentation of Wernicke’s encephalopathy. Pediatr Radiol. 1999;29:581-584. 18. Rodan LH, Mishra N, Tein I. MR spectroscopy in pediatric Wernicke encephalopathy. Neurology. 2013;80:969. 19. Thomson AD, Cook CC, Touquet R, Henry JA. Royal College of Physicians report on alcohol: guidelines for managing Wernicke’s encephalopathy in the accident and Emergency Department. Alcohol Alcohol. 2002;37:513-521. 20. Worden RW, Allen HM. Wernicke’s encephalopathy after gastric bypass that masqueraded as acute psychosis: a case report. Curr Surg. 2006;63:114-116. 21. Shuster MH, Vazquez JA. Nutritional concerns related to Roux-en-Y gastric bypass: what every clinician needs to know. Crit Care Nurs Q. 2005;28:227-260. 22. Al-Fahad T, Ismael A, Soliman MO, Khoursheed M. Very early onset Wernicke’s encephalopathy after gastric bypass. Obes Surg. 2006; 16:671-672. 23. Lockman PR, McAfee JH, Geldenhuys WJ, Allen DD. Cation transport specificity at the blood-brain barrier. Neurochem Res. 2004;29: 2245-2250. 24. Manzo L, Locatelli C, Candura SM, Costa LG. Nutrition and alcohol neurotoxicity. Neurotoxicology. 1994;15:555-565. 25. Zuccoli G, Pipitone N. Neuroimaging findings in acute Wernicke’s encephalopathy: review of the literature. AJR Am J Roentgenol. 2009; 192:501-508.
Contents lists available at ScienceDirect
Pediatric Neurology journal homepage: www.elsevier.com/locate/pnu
Clinical Observations
Wernicke Encephalopathy Due to Thiamine Deficiency After Surgery on a Child With Duodenal Stenosis Elif Acar Arslan MD a, *, Saniye Ekinci MD b, Pınar Zengin Akkus¸ MD a, lu MD a Rahs¸an Göçmen MD c, Göknur Halilog a
Department of Pediatric Neurology, Hacettepe University Children’s Hospital, Ankara, Turkey Department of Pediatric Surgery, Hacettepe University Children’s Hospital, Ankara, Turkey c Department of Radiology, Hacettepe University, Ankara, Turkey b
abstract BACKGROUND: Wernicke encephalopathy is rare in children and is caused by thiamine deficiency. It is characterized
by acute or subacute ataxia, altered consciousness, and ophthalmoparesis. Gastroenterological surgery, total parenteral nutrition for short bowel syndrome, and alcoholism are common risk factors for Wernicke encephalopathy. Typical magnetic resonance imaging features include selective symmetrical signal changes in the mammillary bodies, medial thalamus, tectum, periaqueductal region, cranial nerves, cerebellum, red nucleus, dentate nucleus, fornix, splenium, cerebral cortex, and putamen. If left undiagnosed and untreated, the disease may be fatal. PATIENT DESCRIPTION: We describe a 13-year-old boy who developed acute cerebellar findings while receiving total parenteral nutrition after gastroduodenostomy for duodenal stenosis. RESULTS: The diagnosis of Wernicke encephalopathy was based on his clinical history, neurological examination, and imaging results. We immediately started intravenous thiamine replacement therapy. Two weeks later, the patient’s clinical signs had resolved except for mild clumsiness, which was observed during his tandem gait examination. CONCLUSION: Our report emphasizes the importance of clinical and magnetic resonance imaging pattern recognition in timely diagnosis, as well as the importance of prompt thiamine replacement therapy. We also demonstrate the importance of thiamine supplementation during total parenteral nutrition after gastrointestinal surgery. Keywords: Wernicke encephalopathy, MRI, children, gastroenterological surgery, thiamine deficiency, magnetic resonance imaging, ophthalmoplegia
Pediatr Neurol 2014; 51: 840-842 Ó 2014 Elsevier Inc. All rights reserved.
Introduction
Wernicke encephalopathy is a potentially life-threatening reversible neurological disease caused by thiamine deficiency. The disease is characterized by the typical triad of ophthalmoplegia, ataxia, and confusion. Autopsy studies report that both adults and children may not be accurately diagnosed.1 Diagnosis is based on clinical findings and This paper was presented as a poster in the 15th Turkish Pediatric Society Scientific Congress 22-25 May, 2013, Sivas, Turkey.
Article History: Received July 11, 2014; Accepted in final form August 30, 2014 * Communications should be addressed to: Dr. Acar Arslan; Department of Pediatric Neurology; Hacettepe University Children’s Hospital; PC 06100; Sıhhıye, Ankara, Turkey. E-mail address: [email protected] 0887-8994/$ - see front matter Ó 2014 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.pediatrneurol.2014.08.034
probable etiologic factors.2 It is most often observed in alcoholics and in malnourished adults. The disease may also occur in association with hyperemesis gravidarum,3 gastric by-pass surgery,4,5 pancreatitis,6,7 cancer treatment in pediatric patients,8 nephrotic syndrome,9 and as a complication of gastrointestinal surgery.10,11 A frequent cause is the inadequate supply of vitamin B1 in total parenteral nutrition (TPN) solutions during treatment for chronic diseases. Patients usually respond well to acute thiamine replacement therapy. However, some patients may exhibit only one or two components of the disease, and B1 deficiency may not accompany the clinical picture.1 Parenteral thiamine is preferred to oral supplementation.12 Increased T2-weighted signal intensity in the periaqueductal area of the midbrain and the periventricular area of the thalamus confirms the diagnosis.13 Recognition of the clinical and magnetic resonance imaging
E. Acar Arslan et al. / Pediatric Neurology 51 (2014) 840e842
(MRI) patterns of the disease is extremely important for effective treatment and patients’ long-term prognoses. Patient Description A 13-year-old boy was referred by the Pediatric Surgery Department for acute titubation, nystagmus, and ataxia. He had undergone surgical resection of duodenal ulcerations at age 6 years, and an anastomosis between the antrum and the jejunum was performed 18 months before presentation, for duodenal stenosis. He had since been receiving nasogastric decompression and TPN treatment. He developed drowsiness, headache, head titubation, and ataxia within 2 days. His neurological examination was significant for drowsiness, bilateral isocoric pupils, bilateral gaze-evoked horizontal nystagmus, upward gaze palsy, dysmetria and dysdiadokinesis, truncal and gait ataxia, and absent deep tendon reflexes. There was no upbeating nystagmus. His Glasgow coma score was 14. His tongue was erythematous and smooth. His cranial MRI revealed T2 signal hyperintense areas in the periaqueductal area and both medial thalami, particularly in the pulvinar area (Figure). The diagnosis of Wernicke encephalopathy was considered based on the boy’s medical history, neurological examination, and radiological findings. He had not been receiving vitamin supplementation with his TPN formula during the 18 months following period after surgery. We immediately started intravenous thiamine at a dose of 100 mg/day and continued maintenance treatment for 1 week. After the first week of therapy, he converted to oral thiamine at a dose of 50 mg/kg. His signs improved within 1-2 days. When examined two weeks later his clinical signs had disappeared with the exception of mild clumsiness observed on his tandem gait examination. A cranial MRI obtained during follow-up revealed that the previous abnormalities had returned to normal.
841
Discussion
Wernicke encephalopathy is rarely observed in children. Wernicke first described the disease as a distinctive entity in 1881.14-16 Thirty-one pediatric patients (age <20 years) with Wernicke encephalopathy were reviewed by Vasconcelos et al.14 The most common preceding event observed by their study was malignancy (11 of 31 patients). The high rate of diagnosis of Wernicke encephalopathy during autopsy examinations suggests that the diagnosis is often overlooked in clinical settings.14 More than 20 pediatric reports have since been published based on searches of PubMed and MED-LINE using key words such as Wernicke encephalopathy, pediatric, and children, although only two describe cases resulting from gastrointestinal disease.17,18 Wernicke encephalopathy most often occurs two to eight months after surgery and primarily affects individuals with weight loss greater than 7 kg per month.1,19-21 Approximately 58% of affected individuals may be missed on routine clinical examinations.1,14 Thiamine is absorbed in the duodenum by an active, carrier-mediated, and rate-limited process and is transported across the blood-brain barrier by both active and passive mechanisms. Thiamine is subsequently converted to thiamine pyrophosphate by neurons and glial cells; the latter are responsible for several biochemical pathways in the brain, including intermediate carbohydrate metabolism,
FIGURE. (A) An axial T2-weighted image at the level of the basal ganglia demonstrates alterations of the medial thalamic nuclei. (B) An axial T2-weighted image demonstrates marked hyperintensity of the tectal plate. (C) Increased signal intensity with respect to the hypothalamus is observed on an axial fluid attenuated inversion recovery image. The lesions are consistent with reversible cytotoxic edema. One month after thiamine replacement, a partial regression of the lesions involving the medial thalamic nuclei (D) and hypothalamus is observed (E). Signal alterations at the tectal plate have completely resolved (F).
842
E. Acar Arslan et al. / Pediatric Neurology 51 (2014) 840e842
lipid metabolism, and production of amino acids and glucose-derived neurotransmitters such as glutamic acid and gamma-aminobutyric acid.1 Moreover, thiamine also appears to have a role in acetylcholinergic and serotoninergic synaptic transmission.1,22-24 Clinical signs of thiamine deficiency vary depending on the degree of deficiency and on the age and genetic predisposition of the patient. Although short-term severe thiamine deficiency often induces Wernicke encephalopathy, mild-to-moderate and prolonged thiamine deficiency generally result in peripheral nerve damage. Subclinical thiamine deficiency is difficult to diagnose. Thiamine deficiency persisting for 2-3 weeks causes damage to selective regions of the brainstem and the diencephalon, resulting in Wernicke encephalopathy.1 The disease is diagnosed on the basis of typical MRI findings and is characterized by a distinct pattern of alterations, including symmetrical alterations in the thalami, mammillary bodies, tectal plate, and periaqueductal area.25 Although Wernicke encephalopathy is rare after gastrointestinal surgery, thiamine supplementation must be part of any total parenteral nutrition treatment administered to patients. The diagnosis of Wernicke encephalopathy is challenging in some cases because of the inability of clinicians to recognize data and nonspecific clinical signs or neurological signs of the disease. The most sensitive diagnostic test is an MRI. Conclusion
Wernicke encephalopathy should be considered in children with risk factors for the disease. Recognition of characteristic clinical and MRI patterns is crucial for both the timely treatment and prevention of this life-threatening disease and its neurological complications. References 1. Sechi G, Serra A. Wernicke’s encephalopathy: new clinical settings and recent advances in diagnosis and management. Lancet Neurol. 2007;6:442-455. 2. Christopoulos P, Katsanoulas C, Timplalexi G, Lathyris D, Vasiliaqkou S, Anroniadou E. Wernicke’s encephalopathy and anabolic steroid drug abuse. Is there any possible relation? Hippokratia. 2012;16:371-372. 3. Leitner G, Kvistad KA, Aasly J. Pregnant woman with hyperemesis, confusion, ataxia and nystagmus. Tidsskr Nor Laegeforen. 2006;126: 1069-1071. 4. Morel L, Fontana E, Michel JM, Ruffieux A, Ottiger M, Regamey C. New treatment: bariatric surgery; a new complication: WernickeKorsakoff encephalopathy. Presse Med. 2008;37:49-53. 5. Bohnsack BL, Patel SS. Peripapillary nerve fiber layer thickening, telangiectasia, and retinal hemorrhages in Wernicke encephalopathy. J Neuroophthalmol. 2010;30:54-58.
6. Basit S, Elsås T, Kvistad KA, Høsøien LS. Wernicke’s encephalopathy because of pancreatitis in a young boy. Acta Ophthalmol. 2011;89: 656-657. 7. Muwakkit S, Al-Aridi C, Saab R, Hourani R, Yazbeck N, Abboud M. Wernicke’s encephalopathy during total parenteral nutrition in a child with acute lymphoblastic leukemia and acute pancreatitis. Neuropediatrics. 2009;40:249-251. 8. La Spina M, Catania R, Lo Nigro L, De Grandi C, Palmucci S, Di Cataldo A. Neurological complications during treatment of childhood cancer: mind Wernicke encephalopathy. Pediatr Hematol Oncol. 2010;27:320-323. 9. Nishida M, Sato H, Kobayashi N, Morimoto M, Hamaoka. Wernicke’s encephalopathy in a patient with nephrotic syndrome. Eur J Pediatr. 2009;168:731-734. 10. Saab RO, El Khoury MI, Jabbour RA. Wernicke encephalopathy after Roux-en-Y gastric bypass and hyperemesis gravidarum. Surg Obes Relat Dis. 2013;9:e105-e107. 11. Xu Y, Shao QS, Wang YX, Yang J, Xu J. Clinical analysis of 10 patients with Wernicke encephalopathy after major abdominal surgery. Zhonghua Wei Chang Wai Ke Za Zhi. 2013;16:471-473. 12. Thomson AD, Cook CC. Parenteral thiamine and Wernicke’s encephalopathy: the balance of risks and perception of concern. Alcohol Alcohol. 1999;32:207-209. 13. Antunez E, Estruch R, Cardenal C, Nicolas JM, Fernandez-Sola J, Urbano-Marquez A. Usefulness of CT and MR imaging in the diagnosis of acute Wernicke’s encephalopathy. AJR Am J Roentgenol. 1998;171:1131-1137. 14. Vasconcelos MM, Silva KP, Vidal G, Silva AF, Domingues RC, Berditchevsky CR. Early diagnosis of pediatric Wernicke’s encephalopathy. Pediatr Neurol. 1999;20:289-294. 15. Thomson AD, Cook CC, GuerriniSheedy D, Harper C, Marshall EJ. Wernicke’s encephalopathy revisited. Translation of the case history section of the original manuscript by Carl Wernicke ’Lehrbuch der Gehirnkrankheiten fur Aerzte and Studirende’ (1881) with a commentary. Alcohol Alcohol. 2008;43:174-179. 16. Wernicke C. Lehrbuch der gehirnkrank heiten für aerzte and studirende. Kassel Theodor Fischer. 1881;2:229-242. 17. Sparacia G, Banco A, Lagalla R. Reversible MRI abnormalities in an unusual paediatric presentation of Wernicke’s encephalopathy. Pediatr Radiol. 1999;29:581-584. 18. Rodan LH, Mishra N, Tein I. MR spectroscopy in pediatric Wernicke encephalopathy. Neurology. 2013;80:969. 19. Thomson AD, Cook CC, Touquet R, Henry JA. Royal College of Physicians report on alcohol: guidelines for managing Wernicke’s encephalopathy in the accident and Emergency Department. Alcohol Alcohol. 2002;37:513-521. 20. Worden RW, Allen HM. Wernicke’s encephalopathy after gastric bypass that masqueraded as acute psychosis: a case report. Curr Surg. 2006;63:114-116. 21. Shuster MH, Vazquez JA. Nutritional concerns related to Roux-en-Y gastric bypass: what every clinician needs to know. Crit Care Nurs Q. 2005;28:227-260. 22. Al-Fahad T, Ismael A, Soliman MO, Khoursheed M. Very early onset Wernicke’s encephalopathy after gastric bypass. Obes Surg. 2006; 16:671-672. 23. Lockman PR, McAfee JH, Geldenhuys WJ, Allen DD. Cation transport specificity at the blood-brain barrier. Neurochem Res. 2004;29: 2245-2250. 24. Manzo L, Locatelli C, Candura SM, Costa LG. Nutrition and alcohol neurotoxicity. Neurotoxicology. 1994;15:555-565. 25. Zuccoli G, Pipitone N. Neuroimaging findings in acute Wernicke’s encephalopathy: review of the literature. AJR Am J Roentgenol. 2009; 192:501-508.