MR Imaging Findings in Alcoholic and Nonalcoholic Acute Wernicke’s Encephalopathy: A Review

Abstract

Wernicke's encephalopathy (WE) is a severe neurological syndrome caused by thiamine (vitamin B1) deficiency and clinically characterized by the sudden onset of mental status changes, ocular abnormalities, and ataxia. Apart from chronic alcoholism, the most common cause of WE, a lot of other conditions causing malnutrition and decreasing thiamine absorption such as gastrointestinal surgical procedures and hyperemesis gravidarum must be considered as predisposing factors. Due to its low prevalence and clinical heterogeneity, WE is often misdiagnosed, leading to persistent dysfunctions and, in some cases, to death. Nowadays, MR imaging of the brain, showing T2 and FLAIR hyperintensities in typical (thalami, mammillary bodies, tectal plate, and periaqueductal area) and atypical areas (cerebellum, cranial nerve nuclei, and cerebral cortex), is surely the most important and effective tool in the diagnostic assessment of WE. The aim of this paper is to propose a state of the art of the role of MR imaging in the early diagnosis of this complex disease.

A novel encephalopathy in a thiamine-deficient dog resembling human Wernicke’s disease with atypical MRI pattern

“…7(4): 313-318 ________________________________________________________________________________________________________ 317 the second MRI examination, correlated well with the pathophysiology of TD-induced tissue damage. In the acute phase of the disease the most susceptible brain areas during such energetic unbalance are unable to maintain cellular osmotic gradients, which results in swelling of intra-and extracellular spaces (Zuccoli and Pipitone, 2009) and cytotoxic oedema (Manzo et al, 2014). This was reflected in the T2 and FLAIR hyperintensities and the apparent increased volume (swelling) of the caudate nuclei in our dog (Fig.…”

“…However, we did not rule out the possible inability of the low field MRI to find evidence of involvement of other cerebral areas because of its intrinsic low spatial and contrast resolution in comparison to high field systems or histopathological evaluation. In humans with Wernicke's syndrome, the detection of signal intensity alterations in typical (periaqueductal grey matter, periventricular regions of the third ventricle, mammillary bodies, tectal plate of the midbrain and thalami) (Park et al, 2001) and atypical (cerebellum, dentate nuclei, cranial nerve nuclei, red nuclei, caudate nuclei, the splenium, and cerebral cortex) brain areas on MRI (Zuccoli and Pipitone, 2009), is an essential feature in order to reach the right imaging diagnosis associated with clinical presentation (Manzo et al, 2014). Atypical MRI findings always arise in association with the typical pattern of brain lesions in the same patients (Zuccoli and Pipitone, 2009).…”

“…In humans and dogs affected by TD, MRI findings suggest that both vasogenic and cytotoxic oedema are involved in the pathogenic mechanism of the lesions found in the affected brain areas (Harper and Butterworth, 1997). These pathological alterations are typically seen as bilateral and symmetrical hyperintensities on T2-weighted and FLAIR sequences, both in humans (Manzo et al, 2014) and dogs (Palus et al, 2010;Chisolm-Straker and Cherkas, 2013). Bilateral and symmetrical involvement of specific anatomical areas of the CNS, with anatomical preservation, is typical of metabolic-toxic and degenerative diseases (Gavin and Bagley, 2009;Ricciardi et al, 2014).…”

“…Bilateral and symmetrical involvement of specific anatomical areas of the CNS, with anatomical preservation, is typical of metabolic-toxic and degenerative diseases (Gavin and Bagley, 2009;Ricciardi et al, 2014). Among metabolic disorders, TD has been widely reported as one of the major causes of selective, bilateral gray matter damage detectable during MRI examination in humans (Manzo et al, 2014) and small animals (Garosi et al, 2003;Palus et al, 2010). In dogs, the brain areas typically involved during TD include the red nuclei, caudal colliculi, vestibular nuclei of the brainstem, cerebellar nodulus (Garosi et al, 2003), mesencephalic periventricular grey matter, claustrum, lateral geniculate nuclei, occipital and parietal cortex (Vernau et al, 2013).…”

Lingual Hyperkinesia as An Initial Manifestation of Wernicke’s Encephalopathy: Evidence for Localization of Involuntary Hyperkinetic Movement of the Tongue

“…Typical neuro-radiological findings of magnetic resonance imaging (MRI) in WE include symmetric hyperintensity in the thalami, mammillary bodies, tectal plate, and periaqueductal area [3,4]. Movement disorders and complicated involuntary movement symptoms are very rarely reported as an initial manifestation of WE, and some case reports have described complications of WE presenting as dystonia, choreoathetosis, or dystonic tremor [5,6].…”