Article Figures & Data
Figures
- Fig 1.
Typical MR imaging features of nonalcoholic Wernicke encephalopathy. Axial T1-weighted images (A, F, K) show that no abnormal signal intensity was found. Axial T2-weighted (B, G, L), and FLAIR (C, H, M) images show increased signal intensity symmetric within the medial thalami (B, C), periaqueductal area (G, H), and floor of the fourth ventricle (L, M). DWI (D, I, N) imaging shows only slightly increased signal intensities within the bilateral thalami and periacqueductal area but no abnormal signal intensity in the other brain regions. (The ADC values of sites 1, 2, and 3 in the D image were 620.19 ± 27.39, 513.29 ± 9.60, and 381.92 ± 25.73, respectively; the ADC values of sites 1, 2, and 3 in the I image were 657.00 ± 43.13, 442.23 ± 15.43, and 494.94 ± 12.66, respectively.) Contrasting images (E, J, O) show that enhancement of the mammillary bodies and at the floor of the fourth ventricle by gadolinium contrast medium is found (J). No atrophy of the mammillary bodies (F, G, I, J) and cerebellar vermis (K, L, M, N, O) was found.
- Fig 2.
MR imaging manifestations in patients with drowsiness or without disturbances of consciousness. FLAIR images show that only regional damage surrounding the aqueduct (B, C) and the floor of fourth ventricle (D, enhanced by gadolinium contrast) is observed, and no abnormal signal intensity was found in the bilateral medial thalami (A). Arrowheads indicate cavernous hemangioma in the pons (C, E; E was a CT).
- Fig 3.
MR imaging images demonstrating cortical damage in patients with deep coma.
- Fig 4.
MR imaging follow-up of a patient with mild coma. Axial images show symmetric T2-weighted and FLAIR increased signal intensity in the medial thalami in the acute phase of WE (A, B) and normal signal intensities 1 year after thiamine supplementation (C,D).
- Fig 5.
MR imaging follow-up of a patient with deep coma. The images show progressive atrophy 2 years after the onset of WE.
Tables
Cause Author, Year, and Reference Bariatric surgery Singh S, 2007 7; Nolli M, 2005 8; Loh Y, 2004 9 Gastrectomy and gastrojejunostomy Worden RW, 2006 10; Karapanayiotides T, 2006 11 Therapy with intragastric balloon Chaves LC, 2002 13 Colectomy Pagnan L, 1998 12 Hyperemesis gravidarum Chiossi G, 2006 14; Selitsky T, 2006 15; Spruill SC, 2002 16 Parenteral nutrition, hyperalimentation, prolonged intravenous glucose infusion Zhong C, 2005 6; Attard O, 2006 21; Francini-Pesenti F, 2007 22 Prolonged starvation Basoğlu M, 2006 23; Drenick EJ, 1966 24 Anorexia nervosa Peters TE, 2007 18 Terminal tumor Yae S, 2005 25 AIDS Butterworth RF, 1991 19 Hemodialysis Ihara M, 1999 26 Chemical therapy D’Aprile P, 2000 17 Allogenic stem cell transplantation Baek JH, 2005 27 Wrong formula feeding Fattal-Valevski A, 2005 20 Brain stem disease Fei G, 2007 Early-Stage Manifestations Non-neurologic specific manifestations Fatigue, anorexia, dizziness, nausea, vomiting, weight loss, tachycardia Common neurological manifestations Learning and memory disturbance, confabulation Altered mental state: mental sluggishness, apathy, inattentiveness and inability to concentrate, spatial and personal disorientation, mild or marked confusion Ocular abnormalities: nystagmus, diplopia, upward gaze paresis, abducens palsy, conjugate gaze palsies Incoordination of gait and trunk ataxia Generalized hyporeflexia Disturbances of consciousness: drowsiness, lethargy, and mild coma Uncommon neurologic manifestations Stupor Dysarthria Hemiparesis, flaccid paraplegia, or quadriplegia Choreic dyskinesias Pupillary abnormalities: anisocoria, sluggish reactivity Optic neuropathy: amaurosis, visual disturbance, papilledema, retinal hemorrhage Epileptic seizures Hearing loss Hallucinations and behavioral disturbances Painful paresthesias: burning, prickling, or tingling Late-Stage Manifestations Hypotension Hyperthermia or hypothermia Deep coma
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