Comprehensive review of Wernicke encephalopathy: pathophysiology, clinical symptoms and imaging findings
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INVITED REVIEW
Comprehensive review of Wernicke encephalopathy: pathophysiology, clinical symptoms and imaging findings Yoshiaki Ota1,2 · Aristides A. Capizzano1 · Toshio Moritani1 · Shotaro Naganawa1 · Ryo Kurokawa3 · Ashok Srinivasan1 Received: 9 April 2020 / Accepted: 29 April 2020 © Japan Radiological Society 2020
Abstract Wernicke’s encephalopathy (WE) is a severe and life-threatening illness resulting from vitamin B1 (thiamine) deficiency. The prevalence of WE has been estimated from 0.4 to 2.8%. If not treated properly, severe neurologic disorders such as Korsakoff psychosis and even death may occur. The classical triad of clinical symptoms (abnormal mental state, ataxia, and ophthalmoplegia) is found in only 16–33% of patients on initial examination. The originally described underlying condition of WE is alcoholism, but it accounts for about 50% of causes of WE. Nonalcoholic patients are also affected by WE and likely to present symptoms and radiological imaging findings different from patients with alcoholism, which further complicates the diagnosis of WE. Being familiar with predisposing causes, symptoms and radiological imaging findings of WE is important for radiologists and clinicians when making the diagnosis to start immediate treatment. This review discusses pathophysiologies, underlying causes, clinical symptoms, imaging findings and their mimics. Keywords Wernicke encephalopathy · Thiamine · Cytotoxic and vasogenic edema · MRI · Complications
Introduction Wernicke’s encephalopathy (WE) is known as a severe and life-threatening illness resulting from vitamin B1 (thiamine) deficiency. The prevalence of WE in the general population has been estimated from 0.4 to 2.8% [1–7]. If not treated properly, severe neurologic disorders such as Korsakoff psychosis and even death may ensue. The classical triad of clinical symptoms (mental status change, ataxia, and oculomotor abnormality) are found in only 16–33% of patients on initial examination [1, 5, 7]. The originally described underlying condition of WE is alcoholism, but it accounts for about 50% * Yoshiaki Ota [email protected] 1
The Division of Neuroradiology, Department of Radiology, University of Michigan, 1500 E Medical Center Dr, UH B2, Ann Arbor, MI 48109, USA
2
Department of Radiology, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, 465 Kajii‑cho, Kyoto, Kyoto 602‑8566, Japan
3
Department of Radiology, Graduate School of Medicine, The University of Tokyo, 7‑3‑1 Hongo, Bunkyo‑ku, Tokyo 113‑8655, Japan
of the current causes of WE [4]. Therefore, nonalcoholic patients are also affected by WE and are likely to present with clinical symptoms and imaging findings different from those of patients with alcoholism [7–9]. Pathophysiologically, thiamine deficiency causes dysfunction of the Krebs cycle (tricarboxylic acid, TCA cycle) and the pentose phosphate pathway with consequent development of brain cytotoxic edema and vasogenic edema [5, 10]. Magnetic resonance imaging (MRI) typically shows abnormal intensity alt
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