# Silent Echoes: A Case Report of Wernicke Encephalopathy's Unheard Voice

**Authors:** Stefan Gafoor, Raheem Robertson

PMC · DOI: 10.7759/cureus.52151 · Cureus · 2024-01-12

## TL;DR

This case report describes a 64-year-old woman diagnosed with Wernicke encephalopathy, a thiamine deficiency disorder, and highlights the importance of early diagnosis and treatment to prevent severe neurological damage.

## Contribution

The paper presents a rare clinical case of Wernicke encephalopathy with detailed MRI findings and treatment outcomes.

## Key findings

- MRI showed abnormal T2 FLAIR signals in the bilateral mammillary bodies and surrounding areas.
- High-dose intravenous thiamine improved the patient's confusion during hospitalization.
- The case emphasizes the challenges in diagnosing Wernicke encephalopathy due to its non-specific symptoms.

## Abstract

Wernicke encephalopathy (WE) is an acute neuropsychiatric emergency that is caused by a deficiency in vitamin B1 (thiamine). This condition is most commonly seen in patients with alcohol use disorder; however, patients with other disorders of severe malnourishment are also at increased risk. In severe cases, this disease may be followed by Korsakoff's psychosis and even death.

We present a case of a 64-year-old African American female with a history of alcohol use disorder who presented to the emergency department on account of an acute confusional state. Neurological examination revealed right beating nystagmus on the left gaze and a wide-based gait. Initial laboratory work-up was unrevealing; however, magnetic resonance imaging (MRI) of the brain demonstrated an abnormal T2 fluid-attenuated inversion recovery (FLAIR) signal involving the bilateral mammillary bodies and surrounding lateral ventricles that extended into the periaqueductal parenchyma. The patient was admitted to the neurology unit, and high-dose intravenous thiamine was commenced. During hospitalization, the patient's confusion improved and they were subsequently discharged with oral thiamine.

The spectrum of severity of WE is wide, ranging from fatal disease and can lead to permanent brain damage or even Korsakoff syndrome, characterized by severe memory loss and confabulation. The diagnosis is mainly clinical and based on the presence of symptoms in the classic triad of mental status change, oculomotor abnormality, and ataxia. This triad is only present in about 10% of cases, making the diagnosis very challenging. Laboratory testing can assist in making the diagnosis, but it is not always reliable or available. In situations of clinical uncertainty, imaging may also be used to support diagnosis or rule out other differentials. The mainstay of treatment is with high-dose parenteral thiamine.

## Linked entities

- **Chemicals:** thiamine (PubChem CID 1130)
- **Diseases:** Wernicke encephalopathy (MONDO:0007020)

## Full-text entities

- **Diseases:** confusional state (MESH:D003221), death (MESH:D003643), Korsakoff syndrome (MESH:D020915), mental status change (MESH:D013226), brain damage (MESH:D001925), ataxia (MESH:D001259), neurology (MESH:D009461), vitamin B1 (MESH:C566196), emergency department (MESH:D004630), deficiency (MESH:D007153), memory loss (MESH:D008569), beating nystagmus (MESH:D009759), alcohol use disorder (MESH:D000437), oculomotor abnormality (MESH:D015840), WE (MESH:D014899), Voice (MESH:D014832), malnourishment (MESH:D044342)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

18 references — full list in the complete paper: https://tomesphere.com/paper/PMC10859680/full.md

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Source: https://tomesphere.com/paper/PMC10859680