Wernicke’s encephalopathy during pregnancy

A 29-year-old pregnant woman with 16 weeks of gestation was brought in a confused and drowsy state with difficulty in walking, restriction of eye movements, and hyperemesis gravidarum. She was disoriented, had gait ataxia, and ophthalmoplegia. Magnetic resonance imaging (MRI) brain, FLAIR/T2 images showed hyperintense signals in bilateral dorsomedial thalami (Fig. 1), around the third ventricle (Fig. 2), periaqueductal grey matter, and tectal plate (Fig. 3), with mild restriction of diffusion (Figs. 4 and 5) suggestive of Wernicke’s encephalopathy (WE). She was managed with the injection thiamine 500 mg twice a day for 5 days, followed by 100 mg twice a day orally. Her ataxia improved, and her sensorium became normal. However, mild memory and new learning were impaired until discharge.

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FIG 1. Symmetrical areas of FLAIR/T2 hyperintense signal are seen involving bilateral dorsomedial thalami. No blooming and perifocal oedema/mass effect is seen (blue arrow)

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FIG 2. Symmetrical areas of FLAIR/T2 hyperintense signal are seen involving the area around the third ventricle (blue arrow)

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FIG 3. Symmetrical areas of FLAIR/T2 hyperintense signal are seen involving the periaqueductal grey matter (blue arrow)

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FIG 4. Mild restriction of diffusion, symmetrical areas of periaqueductal grey matter (blue arrow)

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FIG 5. Mild restriction of diffusion in symmetrical areas involving bilateral dorsomedial thalami (blue arrow)

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Thiamine (vitamin B1) is a micronutrient that acts as a cofactor for five enzymes involved in the pentose phosphate pathway, glycolysis, and the tricarboxylic acid cycle and is essential to generate adenosine triphosphate (ATP).¹ There is increased thiamine requirement in pregnancy to support the growing foetus and changes in metabolism.² Prolonged vomiting leads to starvation. The increased demand for thiamine, coupled with reduced intake, can lead to a deficiency.³ Thiamine deficiency impairs ATP production and induces oxidative stress by generating reactive oxygen species, which can damage brain cells. There is also disruption in neurotransmitters acetylcholine, gamma-aminobutyric acid, and glutamate, which are essential for normal brain function and affect mood, cognition, and behaviour. Changes in membrane potential affects the nerve cells’ ability to transmit signals. These effects contribute to the development of WE. In a case of hyperemesis gravidarum presenting with abnormal behaviour and neurological findings, an MRI of the brain is indicated to diagnose WE.