Wernicke encephalopathy is caused by thiamine (vitamin B1) deficiency and is commonly seen in alcoholics. On MRI, it shows symmetrical increased signal in the mammillary bodies, dorsomedial thalami, tectal plate, periaqueductal area, and around the third ventricle. The document discusses the clinical presentation and risk factors of Wernicke encephalopathy and provides examples of MRI and CT images demonstrating its characteristic radiological findings. It concludes that knowledge of the neuroimaging patterns can help make an early diagnosis to reduce morbidity and mortality.
2. Wernicke encephalopathy, also referred as Wernicke-Korsakoff
syndrome, is due to thiamine (vitamin B1) deficiency, and is typically
seen in alcoholics.
On imaging, it is commonly seen on MRI as areas of symmetrical
increased T2/FLAIR signal involving the mammillary bodies,
dorsomedial thalami, tectal plate, periaqueductal area, and around
the third ventricle.
Clinical presentation
It was originally described as characterised by the triad of:
Acute confusion.
Ataxia.
Ophthalmoplegia.
Wernicke encephalopathy can evolve into the chronic form of thiamine
deficiency known as Korsakoff psychosis, characterised by:
Memory loss (global amnesia).
Confabulation.
The two terms are often concatenated to form Wernicke-Korsakoff
syndrome.
3. Aetiology
Thiamine deficiency results from malnutrition or
malabsorption, which can occur for a number of
reasons:
Alcohol abuse (up to 90% in industrialized countries)
Starvation/fasting.
Prolonged total parental nutrition without
supplementation.
Post bariatric surgery.
Hyperemesis gravidum.
Gastrointestinal malignancy.
Chronic dialysis.
4. Radiographic features
CT
usually normal
MRI
T2/FLAIR: symmetrically increased signal intensity in the:
mammillary bodies
dorsomedial thalami
tectal plate
periaqueductal area
around the third ventricle
T1 C+ (Gd): contrast enhancement can also be seen in the same
regions, most commonly of the mamillary bodies
DWI/ADC: restricted diffusion can also be seen in the same
regions
MR spectroscopy: may show decreased or normal NAA with the
notable presence of lactate
5. Midsagittal T2-weighted MR image with gray-scale inversion in healthy 37-
year-old man shows schematic representation of anatomic regions typically
(circles) and infrequently (asterisks) affected by Wernicke's encephalopathy.
Note that caudate capita and dentate nuclei are not seen in this view.
7. A 54-year-old woman with leukemia, changes in consciousness, and ataxia. FLAIR axial images (11,000/140/2
[TR/TE/NEX]). A, The prepositus hypoglossal nuclei show symmetric high-signal-intensity alterations (arrows). B,
The medial vestibular nuclei show symmetric hyperintense lesions (arrows). C, Symmetric high-signal-intensity
alterations in the facial nuclei (arrows) are detected. Subtle signal-intensity alterations in the abducens nuclei are
seen (arrowheads). D, The tectum of the midbrain and the periaqueductal gray matter shows signal-intensity
alterations (arrow). E, The mamillary bodies (arrows) show signal-intensity alterations. F, Note signal-intensity
alterations (arrows) of the medial thalami and periventricular region of the third ventricle.
8. A 54-year-old woman with a history of food refusal had changes in consciousness. FLAIR coronal
images (11,000/140/2 [TR/TE/NEX]). A, Signal-intensity alterations with different intensity
patterns are seen in the thalami (arrows). Diffuse signal-intensity alterations of the frontal cortex
(arrowheads) are present. B, Note signal-intensity alterations in the mamillary bodies (arrows),
periventricular region of the third ventricle (empty arrows), and brain cortex (arrowheads).
14. A, The prepositus hypoglossi nuclei regions show symmetric high signal-intensity alterations (arrows). B, The
abducens nuclei regions show symmetric hyperintense alterations (black arrows). Symmetric high signal-intensity
alterations in the facial nuclei (white arrows) are seen. C, The tectum of the midbrain and the periaqueductal gray
matter demonstrates signal-intensity alterations (black arrows). Focal lesions in the medial lemniscus are seen
bilaterally (white arrows). D, The inferior quadrigeminal plate, the periaqueductal gray matter (black arrows), and
the corticospinal tracts (white arrows) show contrast enhancement. E, Signal-intensity alterations of the mamillary
bodies are detected (white arrows). F and G, Symmetric alterations of the posterior putamen (white arrows) and
periventricular region of the third ventricle (black arrows) are seen on fluid-attenuated inversion recovery and
diffusion-weighted images, respectively. H, Signal-intensity alterations are seen in the motor strip (arrows).
15. T2-weighted images show
the high signal intensities in
the bilateral paramedian
thalami with mamillary
bodies (A) and in the
periaqueductal gray matter
(B). Diffusion-weighted
images show the bright high
signal intensities in the
corresponding lesions (C and
D). The corresponding
apparent diffusion
coefficient values of the
lesions range from 512 to
545 × 10−6mm2/s.
17. Magnetic resonance images in a patient affected by alcoholic Wernicke’s encephalopathy. A-D: MR images
before intravenous administration of thiamine therapy; E-H: MR images after intravenous administration of
thiamine therapy. Axial FLAIR images (A,B) and DWI images (C,D) show signal abnormalities in the
periaqueductal area and in the medial thalami. Axial FLAIR (E,F) and DWI (G,H) follow-up MR images, after
intravenous administration of thiamine therapy, show resolution of the signal abnormalities previously
observed. MR: Magnetic resonance; FLAIR: Fluid-attenuated inversion recovery; DWI: Diffusion weighted image.
18. Wernicke-Korsakoff syndrome in a nonalcoholic patient: (A) Gadolinium-enhanced T1-weighted axial
MRI shows symmetric enhancement of the mamillary bodies (paired arrowheads). (B) Enlarged axial
view of the region of the hypothalamus showing mamillary body enhancement (paired arrowheads).
(C) Enlarged coronal view of the mamillary body enhancement (paired arrowheads). (D) FLAIR
hyperintensity of the hypothalamus is seen in an axial view (arrows). (E) FLAIR hyperintensity of the
periaqueductal gray (arrows). (F) FLAIR hyperintensity of the dorsomedian thalamus (arrows). (G)
FLAIR hyperintensity of the floor of the fourth ventricle (arrows). (H) FLAIR hyperintensity is seen
throughout the low medulla (arrows).
19.
20. Alcoholic 65 years-old patient with Wernicke’s encephalopathy. There are symmetrical
hyperintense lesions on these axial T2-WIs in the paraventricular regions of the thalamus
and hypothalamus, periaqueductal regions of the midbrain, and floor of the fourth ventricle
21. Symmetrical
hyperintense lesions
on these axial FLAIR
images in the
paraventricular
regions of the
thalamus and
hypothalamus and
periaqueductal
regions of the
midbrain.
22. 33-year-old woman, primipara, in her 16th week of gestation: coronal FLAIR (a) and
sagittal T2-weighted (b) MR images showing bilateral and symmetric hyperintense signal
alteration at the level of the medial portion of the thalami and of the tectal plate.
23. Wernicke encephalopathy in a 29-year-old woman who had severe hyperemesis
gravidarum throughout pregnancy. Axial fluid-attenuated inversion-recovery and Diffusion
weighted MR image shows bilateral symmetrical FLAIR hyperintensity with some diffusion
restriction in dorsomedial thalami, mammillary bodies and periaqueductal grey (arrows)
24. CONCLUSION.
Wernicke's encephalopathy is characterized
by a quite distinct pattern of MR alterations,
which include symmetrical alterations in the
thalami, mamillary bodies, tectal plate, and
periaqueductal area, but atypical alterations
may also been seen. A thorough knowledge
of the neuroimaging findings of Wernicke's
encephalopathy will assist in arriving at an
early diagnosis, thus reducing the morbidity
and mortality associated with this disease.