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

**Authors:** Kavitha B Chittaragi, Timothy Chelliah, Sudha Kiran Das, Sidharthan S, Shashank Sharma

PMC · DOI: 10.7759/cureus.86954 · Cureus · 2025-06-29

## TL;DR

This study reports cases of Wernicke’s encephalopathy in non-alcoholic patients in South India, emphasizing the importance of early diagnosis and treatment to prevent neurological damage.

## Contribution

The study expands the understanding of Wernicke’s encephalopathy beyond alcoholism by presenting a case series with diverse nonalcoholic causes.

## Key findings

- Ten out of 14 WE cases were nonalcoholic, with causes like hyperemesis gravidarum and nutritional deficiency.
- MRI findings confirmed WE in all cases, with typical and atypical imaging patterns observed.
- Thiamine therapy led to improvement in 12 patients, highlighting the importance of early treatment.

## 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.

## Linked entities

- **Chemicals:** thiamine (PubChem CID 1130)
- **Diseases:** Wernicke’s encephalopathy (MONDO:0007020), hyperemesis gravidarum (MONDO:0006791)

## Full-text entities

- **Genes:** TKT (transketolase) [NCBI Gene 7086] {aka HEL-S-48, HEL107, SDDHD, TK, TKT1}
- **Diseases:** Marchiafava-Bignami disease (MESH:D054319), refeeding syndrome (MESH:D055677), confusion (MESH:D003221), ophthalmoplegia (MESH:D009886), diplopia (MESH:D004172), Malnutrition (MESH:D044342), abdominal distension (MESH:D000007), portal hypertension (MESH:D006975), dural arteriovenous fistula (MESH:D020785), hypertension (MESH:D006973), Deficiency (MESH:D007153), gastrointestinal diseases (MESH:D005767), neuronal death (MESH:D009410), ataxia (MESH:D001259), cognitive impairment (MESH:D003072), jaundice (MESH:D007565), lactic acidosis (MESH:D000140), Diabetes mellitus (MESH:D003920), intracranial hemorrhage (MESH:D020300), cerebellar dysfunction (MESH:D002526), blurred vision (MESH:D014786), tubercular meningitis (MESH:D014390), substance misuse (MESH:D009293), mitochondrial dysfunction (MESH:D028361), chronic kidney disease (MESH:D051436), Thiamine deficiency (MESH:D013832), heart failure (MESH:D006333), neurological condition (MESH:D019636), neurological damage (MESH:D020196), encephalopathy (MESH:D001927), malabsorption (MESH:D008286), CKD (MESH:D012080), polioencephalitis hemorrhagica superioris (MESH:D011695), sepsis (MESH:D018805), pulmonary tuberculosis (MESH:D014397), Alcoholism (MESH:D000437), hyperemesis gravidarum (MESH:D006939), gait instability (MESH:D043171), chronic alcoholism (MESH:D006519), hyperglycemia (MESH:D006943), ischemic heart disease (MESH:D017202), nonalcoholic (MESH:D065626), liver disease (MESH:D008107), cirrhosis of the liver (MESH:D008103), anorexia nervosa (MESH:D000856), uremic encephalopathy (MESH:D006463), oculomotor abnormalities (MESH:D015840), hepatocerebral degeneration (MESH:D006527), neurological deficits (MESH:D009461), dysmetabolic encephalopathy (MESH:D024821), Korsakoff's psychosis (MESH:D020915), Vomiting (MESH:D014839), end-stage chronic kidney disease (MESH:D007676), malignancy (MESH:D009369), inflammatory (MESH:D007249), gait disturbances (MESH:D020233), thiamine metabolism disorders (MESH:C537658), paucity of movements (MESH:D016738), WE (MESH:D014899), limb weakness (MESH:D018908)
- **Chemicals:** Thiamine (MESH:D013831), pentose phosphate (MESH:D010428), alcohol (MESH:D000438)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

24 references — full list in the complete paper: https://tomesphere.com/paper/PMC12306145/full.md

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Source: https://tomesphere.com/paper/PMC12306145