Wernicke's Encephalopathy Beyond Alcoholism: A Radio-Clinical Case Series From a Tertiary Care Center in South India

Abstract

Introduction Wernicke's encephalopathy (WE) is a serious yet potentially reversible neurological condition resulting from thiamine (vitamin B1) deficiency. Although traditionally linked to chronic alcohol consumption, an increasing number of cases are now being recognized in nonalcoholic individuals, where atypical clinical presentations often lead to diagnostic challenges and delays in treatment. This case series highlights a spectrum of WE cases with varied underlying etiologies, along with their clinical manifestations and characteristic neuroimaging findings. By emphasizing the importance of early recognition and imaging, this study aims to increase clinical awareness and promote timely, appropriate management, thereby reducing morbidity and improving outcomes. Materials and methods This retrospective case series analyzed 14 patients diagnosed with WE between January 2020 and January 2025 at a tertiary care center in South India. The inclusion criteria were clinical suspicion of WE, with supportive MRI findings showing bilateral symmetrical T2/FLAIR hyperintensities in typical regions (thalami, mammillary bodies, and periaqueductal gray). Patients with alternative diagnoses were excluded. Clinical details, comorbidities, etiological factors, imaging findings, treatment response, and outcomes were reviewed. All patients received thiamine therapy. Descriptive statistics were used to summarize the data. Results Among the 14 patients, four were chronic alcoholics, while 10 had nonalcoholic causes such as hyperemesis gravidarum (3), nutritional deficiency (4), parenteral nutrition (2), and CKD on dialysis (1). Most patients presented with altered sensorium and incomplete classical triad symptoms. MRI consistently showed typical WE findings, with additional atypical sites in some nonalcoholic cases. Twelve patients improved with thiamine supplementation, while two were lost to follow-up. All pregnant patients had favorable obstetric outcomes. Conclusions WE is often underdiagnosed, especially in nonalcoholic patients, due to atypical presentations. Clinicians and radiologists should maintain a high index of suspicion for WE in patients with risk factors beyond alcohol use. Early diagnosis and treatment are critical to prevent irreversible neurological damage.

Keywords: chronic alcoholism; hyperemesis gravidarum; mri; nonalcoholic we; periaqueductal grey matter; thiamine deficiency; wernicke’s encephalopathy.

Figure 1. Visual overview of the multifactorial causes of WE (n=14)

WE: Wernicke’s encephalopathy, CKD: chronic kidney disease, HD: hemodialysis

Figure 2. MRI brain of a 58-year-old male who presented with altered sensorium, ataxia, and vomiting following percutaneous transluminal coronary angioplasty for ischemic heart disease. (A & B) Axial T2-weighted, FLAIR, DWI, and ADC images demonstrate symmetrical hyperintensities (orange arrows and circled areas) in the mammillary bodies, dorsomedial thalami, periaqueductal gray matter, and around the third ventricle with diffusion restriction, findings characteristic of acute WE secondary to prolonged parenteral nutrition. (C) Following thiamine supplementation, the patient clinically improved, and follow-up imaging showed resolution of previous abnormalities with normalized signal intensity, indicating radiological recovery (red arrows)

MRI: magnetic resonance imaging, FLAIR: fluid attenuated inversion recovery, DWI: diffusion weighted image, ADC: apparent diffusion coefficient, WE: Wernicke’s encephalopathy

Figure 3. Imaging findings in a 28-year-old male with chronic alcoholism presenting with altered sensorium and paucity of movements. (A) Initial non-contrast CT of the brain shows subtle hypodensity in the splenium of the corpus callosum (blue arrow). (B, C) Further evaluation with MRI, including axial FLAIR sequences, demonstrates symmetric hyperintensities in the dorsomedial thalami and periaqueductal gray matter (red arrows), typical of WE. (D) Coronal T2-weighted image reveals hyperintensities in the bilateral centrum semiovale and corona radiata (yellow arrowheads). (E–G) DWI and (H–J) ADC images show areas of diffusion restriction involving the bilateral centrum semiovale (yellow arrowheads), splenium of the corpus callosum (green arrow), and posterior limb of the internal capsule (white arrows), with corresponding signal drop-out on ADC maps confirming restricted diffusion. These imaging findings are suggestive of a possible overlap between WE and Marchiafava-Bignami disease. The patient was treated with intravenous thiamine and showed symptomatic improvement

CT: computed tomography, MRI: magnetic resonance imaging, FLAIR: fluid attenuated inversion recovery, DWI: diffusion weighted image, ADC: apparent diffusion coefficient, WE: Wernicke’s encephalopathy

Figure 4. Imaging findings in a 38-year-old male who presented with easy fatigability, abdominal distension, jaundice, slurred speech, and blurred vision. (A–D) MRI and axial FLAIR sequences demonstrate symmetrical hyperintensities around the third ventricle, dorsomedial thalami, and periaqueductal gray matter (orange arrows), consistent with thiamine deficiency-related WE. (E) Axial T1-weighted sequence shows bilateral symmetric hyperintensities in the globus pallidus and subthalamic regions (blue arrows), suggestive of AHCD. (F) To further investigate the underlying etiology, contrast-enhanced CT of the abdomen was performed, which revealed cirrhosis of the liver with portal hypertension (blue arrowhead), confirming alcohol-related liver disease as the likely precipitating factor for the neurological findings

CT: computed tomography, MRI: magnetic resonance imaging, FLAIR: fluid attenuated inversion recovery, AHCD: acquired hepatocerebral degeneration, WE: Wernicke’s encephalopathy

Figure 5. MRI findings in a 76-year-old male with altered sensorium and a history of hypertension, diabetes mellitus, and chronic kidney disease on long-term hemodialysis. (A) Axial DWI sequences show symmetrical hyperintensities around the third ventricle, dorsomedial thalami, and periaqueductal gray matter (orange arrows), suggestive of WE. (B) Axial and coronal FLAIR images reveal bilateral parieto-occipital cortical and subcortical hyperintensities (blue arrows). (C) Follow-up imaging shows resolution of parieto-occipital lobe signal changes on FLAIR sequence, correlating with clinical improvement (blue arrowhead). The imaging features are consistent with dysmetabolic encephalopathy due to a combination of WE and dialysis-related metabolic stress

MRI: magnetic resonance imaging, DWI: diffusion-weighted imaging, WE: Wernicke’s encephalopathy, FLAIR: fluid attenuated inversion recovery

Figure 6. MRI findings in a 25-year-old female with a history of pulmonary tuberculosis and tubercular meningitis on antitubercular therapy, who presented with altered sensorium and blurring of vision. (A) Axial FLAIR image shows symmetrical hyperintensities in the bilateral medial thalami and periaqueductal region (orange arrows), consistent with WE secondary to nutritional deficiency and antitubercular therapy-related malabsorption. (B) Follow-up imaging performed one month later during a subsequent episode of ataxia shows resolution of the previously observed thalamic and periaqueductal hyperintensities (blue arrowhead), indicating radiological improvement of WE. However, new hyperintense signal changes are noted on both FLAIR and DWI sequences in the cerebellum (blue arrows), suggestive of cerebellitis (C&D)

MRI: magnetic resonance imaging, FLAIR: fluid attenuated inversion recovery, WE: Wernicke’s encephalopathy, DWI: diffusion-weighted imaging

Figure 7. MRI of the brain of a 24-year-old pregnant woman (G3A2, 14 weeks gestation) with a history of persistent vomiting for 15 days presented with limb weakness and slurred speech. (A-D) Axial FLAIR images demonstrate symmetrical hyperintensities (orange arrows) in the dorsomedial thalami, around the third ventricle, periaqueductal gray matter, and tectal plate, typical of acute WE secondary to thiamine depletion resulting from hyperemesis gravidarum. (E) Additional DWI showing corresponding diffusion restriction. (F) Follow-up MRI after thiamine supplementation shows resolution of signal changes, indicating radiological recovery (blue arrowhead). She delivered a healthy baby via elective cesarean at 39 weeks

MRI: magnetic resonance imaging, FLAIR: fluid attenuated inversion recovery, WE: Wernicke’s encephalopathy, DWI: diffusion-weighted imaging