Acute Wernicke's Encephalopathy: Comparison of Magnetic Resonance Images and Autopsy Findings.

Abstract

This is the first report of acute Wernicke's encephalopathy in which characteristic magnetic resonance (MR) findings have been verified by postmortem histopathological examination. The high-signal areas surrounding the third and the fourth ventricles and the aqueduct on the T2-weighted images reflected the spongy disintegration of the neuropil, which is the typical pathological finding in Wernicke's encephalopathy. Weconfirmed that MRimaging is essential to the early diagnosis of Wernicke's encephalopathy. (Internal Medicine 35: 831-834, 1996)

Wernicke's Encephalopathy following Hyperemesis Gravidarum

“…Diffusion-weighted imaging (DWI) reveals diffusion restriction and has been recommended to enhance the sensitivity of MRI in making a diagnosis 16,17 . The signal change corresponds to spongy degeneration of neuropil 2,18 . Restricted diffusion may be due to a breakdown of cell membranes as thiamine plays an important role in maintaining osmotic balance across cell membranes.…”

MR Imaging Findings in 56 Patients with Wernicke Encephalopathy: Nonalcoholics May Differ from Alcoholics

“…3 Signal-intensity alterations in the cerebellum, cerebellar vermis, cranial nerve nuclei (CNN), red nuclei, dentate nuclei, caudate nuclei, splenium, and cerebral cortex represent atypical MR imaging findings. 3,[4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19] The prognosis of patients with WE depends on the time of onset of thiamine supplementation. When WE is unrecognized, Korsakoff psychosis and even death may ensue; therefore, neuroimaging plays a central role in the early stage of the disease.…”

Rapid Development of Central Pontine Myelinolysis after Recovery from Wernicke Encephalopathy: A Non-alcoholic Case without Hyponatremia

“…In healthy adults, thiamine requirement is influenced by the carbohydrate intake and the daily necessary dose is approximately 1-2 mg. Because the body's store of thiamine is only 30-50 mg, the reserve would be completely depleted at 4-6 weeks after the lack of thiamine intake. Various clinical diseases or conditions disrupt the adequate absorption of thiamine, including chronic alcoholism, gastrointestinal surgery, hyperemesis gravidarum (HG), chemotherapy, systemic infectious diseases and malnutrition (3,5,(9)(10)(11)(12)(13)(14)(15)(16)(17). More specifically, low rates of thiamine absorption at the mucosal level, hepatic dysfunction and alcohol-induced hypermetabolism of thiamine may trigger chronic thiamine deficiency (13).…”

“…Thiamine-deficient cell membranes are unable to maintain osmotic gradients and result in the swelling of intra-and extracellular spaces. Pathological features have revealed edema, spongy degeneration of the neuropil, neuron sparing, swelling of capillary endothelial cells and extravasation of erythrocytes (17). In WE, the blood-brain barrier is damaged in the periventricular regions where thiamine-related glucose and oxidative metabolism are increased (4).…”