7/28/2019 Wernicke JBR BTR

1/2

Nausea and vomiting generallypeak between the 8th and 12thweeks of pregnancy, and they areusually mild and self-limited (1).Hyperemesis gravidarum, however,is a severe condition with vomiting

pernicious enough to cause weightloss, dehydration and alkalosis. Itaffects among 0.3-2% of all pregnantpatients (2). Wernickes encephalo-pathy (WE) is a disorder due to thia-mine deficiency associated withalcoholism and malnutrition but canalso arise during the first trimester ofpregnancy, due to hyperemesis gra-vidarum. We present conventionalmagnetic resonanace imaging (MRI)and diffusion weighted imaging(DWI) findings in this unusual caseof WE.

Case report

A 37-year-old gravida 1 para 0woman in her 5th week of gestationpresented with the diagnosis ofhyperemesis gravidarum afteruncontrolled anorexia, constant nau-sea, vomiting and intermittent diarr-hea had persisted longer than5 days. Her physical examinationwas normal. Laboratory studieswere remarkable only for an eleva-ted alanine aminotransferase (ALT)level of 60 U/L [normal range 10-31 U/L] and ketonuria. Other para-

meters including thyroid functiontests, urine and stool culture for bac-terias, abdominopelvic ultrasound,serological tests for hepatitis andimmunological markers for liverdiseases were normal. On hospitalday 6, ultrasound scan revealed a6 week-old heart beating fetus.Routine hyperemesis gravidarum

revealed loss of border-lines of thediscs and papiledema. Vision acuitydecreased to 15 cm. The patient wasnot able to stand and walk becauseof the truncal ataxia. Total parenteralnutrition and electrolyte replace-ment therapy were started. With thedramatic loss in her vision, sheaccepted MRI. Because of the increa-sed rates of thrombotic events inpregnancy, venous sinus thrombosiswas suggested initially. Magnetic

resonance venography and magne-tic resonance angiography showednormal vessels. T2-weighted andfluid attenuated inversion recovery(FLAIR) images demonstratedsymmetrical hyperintense lesionswithin dorsomedial thalamic region(Fig. 1). DWI showed symmetricalpathologic thalamic hyperintensitiesand the apparent diffusion coeffici-ent (ADC) map images showed sig-nal reductions suggesting restricteddiffusion within these regions(Fig. 2).

As the neurologic signs and MRI

findings pointed to a diagnosis ofWE, the patient was transferred toneurology department. Laboratory

therapy continued to the 10th weekof gestation. At that time the patientbecame more depressive (hadattacks of crying) and less cooperati-ve. She had physchiatric consultati-on but no drugs or other medicati-ons were given. Her complete neuro-logical examination was unremar-kable, however a cranial MRI wasoffered to exclude any intracranialpathologies. The patient refused MRIwith pretending her claustrophobia.

Her general state of nause, vomi-ting and insomnia worsened overthe next 2 weeks with 4 kilogramsloss. During the 12th gestationalweek, she developed signs of confu-sion, depression, muscle weakness,ataxia and a tendancy to fall back-wards, and a sudden decrease invision. Fundoscopic examination

JBRBTR, 2011, 94: 24-25.

WERNICKES ENCEPHALOPATHY: A CASE REPORT AND MRI FINDINGS

S. Yucebilgin1, T. Cirpan1, C.Y. Sanhal1, E. Ozan2, T. Acar2, S. Ozsener1

Wernickes encephalopathy (WE) is a serious, potentially fatal acute or subacute neurological disorder caused bythiamine (Vitamin B1) deficiency. Although it is most frequently observed in patients who are chronic alcoholics, WE

may also be associated with hyperemesis gravidarum. We report magnetic resonance imaging (MRI) and diffusionweighted imaging (DWI) findings in this case of WE in a pregnant patient with hyperemesis gravidarum. We conclu-de that DWI should be included in the imaging protocols of patients suspected to suffer from Wernickes encephalo-pathy.

Key-words: Pregnancy, complications Brain, diseases.

From:1. Department of Obstetrics and Gynecology, 2. Department of Radiology, EgeUniversity, Izmir, Turkey.Address for correspondence: Dr C.Y. Sanhal, M.D., Department of Obstetricsand Gynecology, Ege University, Bornova Asfalt, Izmir, Turkey. E-mail:cemsanhal@yahoo.com

Fig. 1. A. T2-weighted transaxial image demonstrating symmetrical bilateralhyperintense lesions in both dorsomedial thalamic regions. B. FLAIR imagedemonstrating symmetrical hyperintense lesions within dorsomedial thalamic regions.

A B

7/28/2019 Wernicke JBR BTR

2/2

WERNICKES ENCEPHALOPATHY YUCEBILGIN et al 25

estimation of serum thiamine wasnot available before administrationof it. Her vision was back three daysafter the initial rapid intravenousinfusion of 250 mg thiamine and theoral treatment of 250 mg/day withother vitamin B complexes. By thesecond week, her symptoms lost.She could stand and walk withouthelp.

Discussion

WE is a rare but known complica-

tion of hyperemesis gravidarumresulting from the combination ofpoor nutritional intake, frequentvomiting, and increased metabolicdemands of pregnancy (3). WE canalso be precipitated by parenteralnutrition or infusion of glucose-containing solutions without prioradministration of thiamine (4, 5).

The clinical features are non-specific but include the classicaltriad of ocular abnormalities, confu-sion and ataxia. It should be remem-bered that the clinical triad is notobligatory. Symptoms may include

lethargy, fatigue, apathy, impairedawareness, equilibrium loss, dis-orientation, difficulty to concentrate,retrograd amnesia, anorexia, muscu-

In conclusion we presented anunusual case of WE in a pregnantpatient with hyperemesis gravida-rum. This case emphasizes that,while conventional MRI is helpful,DWI should be considered as avaluable additional imagingsequence in patients suspected tosuffer from WE.

References

1. Hill J.B., Yost N.P., Wendel G.D. Jr.:Acute renal failure in association withsevere hyperemesis gravidarum.Obstet Gynecol, 2002, 100: 1119-1121.

2. Eliakim R., Abulafia O., Sherer D.M.:Hyperemesis gravidarum: a currentreview. Am J Perinatol, 2000, 17: 207-218.

3. Chiossi G., Neri I., Cavazzuti M.,Basso G., Facchinetti F.: Hyperemesisgravidarum complicated by Wernickeencephalopathy: background, casereport, and review of the literature.Obstet Gynecol Surv, 2006, 61: 255-268.

4. Reuler J.B., Girard D.E., Cooney T.G:Wernickes encephalopathy. N Engl JMed, 1985, 312: 1035-1039.

5. Togay-Isikay C., Yigit A., Mutluer N.:Wernicke's encephalopathy due tohyperemesis gravidarum: an under-recognised condition. Aust N Z JObstet Gynaecol, 2001, 41: 453-456.

6. Accetta S.G., Abeche A.M.,Buchabqui J.A., et al.: Memory lossand ataxia after hyperemesis gravida-rum: a case of Wernicke-Korsakoff

syndrome. Eur J Obstet GynecolReprod Biol, 2002, 102: 100-101.

7. Halavaara J., Brander A., Lyytinen J.,Setl K., Kallela M.: Wernicke'sencephalopathy: is diffusion-weigh-ted MRI useful?. Neuroradiology,2003, 45: 519-523.

8. Fei G.-q., Zhong C., Jin L., et al.:Clinical characteristics and MRimaging features of nonalcoholicWernicke's encephalopathy. Am JNeuroradiol, 2008, 29: 164-169.

9. Ashikaga R., Araki Y., Ono Y., et al.:FLAIR appearance of Wernicke encep-halopathy. Radiat Med, 1997, 15: 251-253.

10. Lapergue B., Klein I., Olivot J.M.,Amarenco P.: Diffusion weightedimaging of cerebellar lesions inWernicke's encephalopathy. J Neuro-radiol, 2006, 33: 126-128.

lar weakness, peripheral numbness,paresthesia, disorientation, halluci-nations, confabulation, memoryloss, impaired linguistic processing,anterograde amnesia and globalintellectual impairment (6). The diag-nosis of WE is based on the clinicalmanifestations and rapid reversal ofsymptoms with thiamine. Early diag-nosis is essential in WE in order toavoid persistent brain damage (7).Determination of blood trans-ketolase activity and thiamine pyro-phosphate reflects the thiamine sta-tus in the body. But only few centershave this diagnostic tool due to tech-nological complexity and cost (8).Hence, MRI plays an important rolein the diagnosis of WE. CommonMRI findings of WE are symmetri-cally increased signal intensities in

the mesencephalic tegmentum,mamillary body and medial thala-mus on proton-density and T2-weighted images. In addition, due tothe possibility that cerebrospinalfluid may mask high signal lesionson T2-weighted and proton-weightedimages, fluid-attenuated inversion-recovery (FLAIR) sequences werefound to be better in detecting thelesion conspicuously (9). Diffusion-weighted imaging (DWI) is based onan echo-planar MRI technique, and itis highly sensitive to intracellularedema. DWI changes with decreased

signal intensity on ADC (apparentdiffusion coefficient) maps are asso-ciated with restricted diffusion andcytotoxic edema, while increasedADC values represent vasogenicedema. The importance of ADC valu-es in the diagnosis of WE is unclear,since decreased or increased ADCvalues have been reported and bothcytotoxic and vasogenic edema pat-terns are present in lesions seen inWE (7, 10). Our patient showed highsignal intensities within the thalamion DWI images and demonstrateddecreased ADC values. We assume

that the high signals seen on DWIimages were, at least in part, causedby true restricted diffusion represen-ting cytotoxic edema.

Fig. 2. DWI image showing hyper-intensities in both thalami.