A 17-year-old primiparous female in the 13th week of gestation was admitted with a 4-day history of acute flaccid paralysis and confusion. The patient did not consume alcohol and had no pre-existing medical conditions. Her relatives reported that she had been suffering from severe vomiting and loss of appetite for 2 months. The patient was confused, pale and weak, but did not have fever. Physical examination revealed bilateral nystagmus, finger-to-nose ataxia, areflexia, and lower extremity weakness (muscle strength grade 2/5). Abnormal laboratory findings included anemia, mild hyponatremia (130 mmol/L), and hypokalemia. Cerebral MRI showed bilaterally high symmetrical signal intensity in the mammillary body and periaqueductal gray (Figure a), as well as bilaterally slightly increased signal intensity in the dorsomedial thalamus on the FLAIR sequence (Figure b). Furthermore, the patient was thiamine-deficient at a level of 49 nmol/L. The diagnosis was Wernicke encephalopathy with beriberi secondary to hyperemesis gravidarum. Treatment consisted of intravenous thiamine supplementation, antiemetics, and electrolyte replacement. After 1 week of this treatment, the patient’s confusion resolved.
Figure.
a) Transverse brain MRI: the FLAIR sequence shows bilaterally high symmetrical signal intensity in the mammillary body (white arrow) and periaqueductal gray (red arrow); b) transverse brain MRI, FLAIR sequence: bilaterally slightly increased signal intensity in the dorsomedial thalamus (white arrow).
Translated from the original German by Christine Rye.
Cite this as: Saghir K, Louhab N, Kissani, N: Wernicke encephalopathy.
Footnotes
Conflict of interest statement:
The authors state that no conflict of interest exists.