CASE 11799 Published on 11.05.2014

A rare case of Wernicke’s encephalopathy and central pontine myelinolysis induced by hyperemesis gravidarum

Section

Neuroradiology

Case Type

Clinical Cases

Authors

Sekhar K S, Saravana Kumar S, Malathi V, Parveen Sulthana M

Billroth Hospitals,
Department of Radiology;
Lakshmi Talkies Road,
Shenoy Nagar
600 030 Chennai, India;
Email:drspjkmc@gmail.com
Patient

19 years, female

Categories
Area of Interest Neuroradiology brain ; Imaging Technique MR, MR-Diffusion/Perfusion
Clinical History
A 19-year-old young pregnant woman of 5 months gestation with history of excessive vomiting (hyperemesis) was brought to the emergency in a confused state with complaints of being restless and drowsy for 3 days. She was referred for MRI brain.
Imaging Findings
MRI brain revealed bilateral symmetric T2W and FLAIR hyperintense signal along the posteromedial thalami. Subtle FLAIR hyperintense signal was also noted in the periaqueductal grey matter and mammillary bodies with no abnormal areas of restricted diffusion. The above features and clinical history were consistent with Wernicke’s encephalopathy. Immediate treatment with intramuscular thiamine was initiated which resulted in significant improvement in patient’s orientation and general condition. Nearly a week after admission, the patient developed pain and mild weakness of both lower limbs with sluggish deep tendon reflexes and a power of 3/5. During the course of the patient’s stay in hospital, the serum electrolytes levels were within normal limits. Follow-up MRI done 10 days after the initial MRI showed a new onset of T2W and FLAIR hyperintense signal in the central pons, relatively sparing the periphery with patchy areas of restricted diffusion. These findings were more in favour of central pontine myelinolysis.
Discussion
Wernicke’s encephalopathy (WE), described by Carl Wernicke in 1881 is an acute neurological emergency manifested by a triad of confusion, opthalmoplegia and ataxia. It occurs due to thiamine deficiency and is more common in alcoholics [1]. It is one of rare complications in patients with hyperemesis gravidarum with an approximate incidence of about 12.2% [2]. Typical findings on MRI include symmetric T2W and FLAIR hyperintense signal in the thalami, mamillary bodies, tectal plate, and periaqueductal grey matter [1].
Central pontine myelinolysis (CPM) or osmotic demyelination syndrome mostly occurs due to rapid correction of hyponatraemia. It has also been reported in patients with chronic alcoholism, malnutrition, liver disease and hypokalaemia [3]. The classical MRI finding is T2W hyperintense signal in the central pons [4]. Recently, decreased ADC values have been reported in patients with CPM, presumably due to swelling of oligodendrocytes caused by shift of water from the extracellular compartment to the intracellular compartment in a hypernatraemic state [5].
The cause for both these conditions in our patient could be due to nutritional deficiency of essential nutrients.
Many cases of WE as a result of hyperemesis gravidarum and isolated cases of CPM in hyperemesis gravidarum have been reported in the literature. However, there are very few case reports describing both CPM and WE subsequent to hyperemesis gravidarum [6, 7, 8, 9]. In any pregnant woman presenting with hyperemesis and altered mental status, possibility of WE should be excluded. Prompt treatment with thiamine will prevent the associated morbidity and mortality and poor fetal outcome [10].
Differential Diagnosis List
Wernicke’s encephalopathy and central pontine myelinolysis induced by hyperemesis gravidarum
Creutzfeldt-Jakob disease
Venous infarction
Final Diagnosis
Wernicke’s encephalopathy and central pontine myelinolysis induced by hyperemesis gravidarum
Case information
URL: https://www.eurorad.org/case/11799
DOI: 10.1594/EURORAD/CASE.11799
ISSN: 1563-4086