Journals / Ege Tıp Dergisi / 2019 / Cilt: 58 - Sayı: 2

Magnetic resonance imaging findings of Wernicke’s encephalopathy in non-alcoholic patients

Non-alkolik nedenlere bağlı gelişen Wernicke ensefalopatisinde manyetik rezonans görüntüleme bulguları

Pages
115–120
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusion: According to the results of the presented study, cranial MRI has similar findings in alcoholic and nonalcoholic WE patients.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Aim: Wernicke encephalopathy (WE) is a neuropsychiatric disease that develops due to the deficiency of thiamine (vitamin B1).
📊
Key Findings & Data:Results: Typical involvement areas in cranial MRI were determined as bilateral medial thalamus in 10 patients, bilateral mammillary bodies in 8 patients, periaqueductal area/tectal plate in 7 patients.
💡
Conclusion & Impact:Conclusion: According to the results of the presented study, cranial MRI has similar findings in alcoholic and nonalcoholic WE patients.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Aim: Wernicke encephalopathy (WE) is a neuropsychiatric disease that develops due to the deficiency of thiamine (vitamin B1). It is often observed due to chronic alcoholism; however it can arise in any condition that causes deficiency in the intake or absorption of thiamine. The aim of this study is to emphasize the importance of magnetic resonance imaging (MRI) in the diagnosis and follow-up of this disease which can even lead to death when it is not treated. Materials and Methods: Ten patients, who had been hospitalized in our institution and diagnosed as WE due to non-alcoholic reasons, were included in our study. In the MRI examinations of the patients, typical and atypical findings were evaluated according to the localization of involvement areas. The existence of accompanying diffusion restriction was evaluated. Results: Typical involvement areas in cranial MRI were determined as bilateral medial thalamus in 10 patients, bilateral mammillary bodies in 8 patients, periaqueductal area/tectal plate in 7 patients. Atypical involvement areas were determined as fornix in 5 patients, cerebral cortex in 4 patients, putamen in 2 patients and cerebellum involvement in 1 patient. These findings were accompanied by diffusion restriction in 8 patients. Conclusion: According to the results of the presented study, cranial MRI has similar findings in alcoholic and nonalcoholic WE patients. We conclude that, the utilization of cranial MRI in these patients has an important role to prevent the latency of the diagnosis and treatment.

Özet

Amaç: Wernicke ensefalopatisi (WE) tiamin (vitamin B1) eksikliğine bağlı olarak gelişen nöropsikiyatrik bir hastalıktır. Sıklıkla kronik alkolizme bağlı olarak görülmekle birlikte tiamin alım veya emilim eksikliğine neden olan her türlü durumda ortaya çıkabilir. Bu çalışmanın amacı tedavi edilmediği takdirde ölüme kadar giden ciddi sonuçlar doğurabilen bu hastalığın tanı ve izleminde manyetik rezonans görüntülemenin (MRG) önemini vurgulamaktır. Gereç ve Yöntem: Çalışmamıza kurumumuzda hospitalize edilen ve non-alkolik nedenlerle WE tanısı alan 10 hasta dahil edildi. Hastaların MRG tetkiklerinde tutulum yerlerinin lokalizasyonuna göre tipik ve atipik bulguların varlığı değerlendirildi. Ayrıca eşlik eden difüzyon kısıtlılığı varlığı araştırıldı. Bulgular: Kraniyal MRG’de tipik tutulum alanları 10 hastada bilateral talamus mediali, 8 hastada bilateral mamiller cisim, 7 hastada periakuaduktal alan/tektal plak olarak tespit edildi. Atipik tutulum alanları ise 5 hastada forniks, 4 hastada serebral korteks, 2 hastada putamen, 1 hastada ise serebellum tutulumu şeklinde idi. 8 hastada bu bulgulara difüzyon kısıtlılığı eşlik etmekteydi. Sonuç: Sunulan çalışmanın sonuçlarına göre, non-alkolik WE tanılı olgularda MRG’de, alkolik WE tanılı olgularla benzer bulgular gözlenmektedir. Bu hastaların tanı ve tedavilerinin gecikmemesi amacıyla MR görüntülemenin kullanımının önemli rol oynadığı sonucuna varılmıştır.

🔖

Cite This Article

ERASLAN, C., GÜLER, A., KURT, E., ÇALLI, C., KİTİŞ, Ö. (2019). Magnetic resonance imaging findings of Wernicke’s encephalopathy in non-alcoholic patients. Ege Tıp Dergisi, Cilt: 58 - Sayı: 2, 115–120. https://ajindex.com/articles/222685

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (15)

  1. Saad L, Silva LF, Banzato CE, Dantas C, Garcia C. Anorexia nervosa and Wernicke-Korsakoff syndrome: A case report. J Med Case Rep 2010;4:217
  2. Chiossi G, Neri I, Cavazzuti M, Basso G, Facchinetti F. Hyperemesis gravidarum complicated by Wernicke encephalopathy: background, case report, and review of the literature. Obstet Gynecol Surv 2006;61(4):255-68
  3. Loh Y, Watson WD, Verma A, Chang ST, Stocker DJ, Labutta RJ. Acute Wernicke’s encephalopathy following bariatric surgery: Clinical course and MRI correlation. Obes Surg 2004;14(1):129-32
  4. Sequeira Lopes da Silva JT, Almaraz Velarde R, Olgado Ferrero F, et al. Wernicke’s encephalopathy induced by total parental nutrition. Nutr Hosp 2010;25(6):1034-6
  5. Azim W, Walker R. Wernicke’s encephalopathy: A frequently missed problem. Hosp Med 2003;64(6):326-7
  6. Harper CG, Giles M, Finlay-Jones R. Clinical signs in the Wernicke-Korsakoff complex: A retrospective analysis of 131 cases diagnosed at necropsy. J Neurol. Neurosurg Psychiatry 1986;49(4):341-45
  7. Zuccoli G, Gallucci M, Capellades J, et al. Wernicke encephalopathy: MR findings at clinical presentation in twenty-six alcoholic and nonalcoholic patients. AJNR Am J Neuororadiol 2007;28(7):1328-31
  8. Harper C. The incidence of Wernicke’s encephalopathy in Australia-a neuropathological study of 131 cases. J Neurol Neurosurg Psychiatry 1983;46(7):593-8
  9. Harper C, Butterworth R. Nutritional and metabolic disorders. In: Graham DI, Lantos PL (eds). Greenfield’s Neuropathology. Vol. 1, 6th ed. London: Hodder Arnold;1997:601-52
  10. Zhong C, Jin L, Fei G. MR Imaging of nonalcoholic Wernicke encephalopathy: A follow-up study. AJNR Am J Neuroradiol 2005;26(9):2301-5
  11. Thomson AD. Mechanisms of vitamin deficiency in chronicalcohol misusers and the development of the Wernicke Korsakoff syndrome. Alcohol Alcohol Suppl 2000;35(1):2-7
  12. Park SH, Kim M, Na DL, Jeon BS. Magnetic resonance reflects the pathological evolution of Wernicke encephalopathy. J Neuroimaging 2001;11(4):406-11
  13. Gui QP, Zhao WQ, Wang LN. Wernicke’s encephalopathy in nonalcoholic patients: Clincal and pathologic features of three cases and literature reviewed. Neuropathology 2006;26(3):231-5
  14. Zuccoli G, Santa Cruz D, Bertolini M, et al. MR imaging findings in 56 patients with Wernicke encephalopathy: nonalcoholics may differ from alcoholics. AJNR Am J Neuororadiol. 2009;30(1):171-6
  15. Manzo G, De Gennaro A, Cozzolino A, Serino A, Fenza G, Manto A. MR imaging findings in al