Wernicke Encephalopathy

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Giulio Zuccoli - One of the best experts on this subject based on the ideXlab platform.

  • Neuroimaging findings in pediatric Wernicke Encephalopathy: a review
    Neuroradiology, 2010
    Co-Authors: Giulio Zuccoli, Nasir Siddiqui, Ariel Bailey, Stefano C. Bartoletti
    Abstract:

    Wernicke Encephalopathy (WE) is an acute neurological disease resulting from dietary thiamine (vitamin B1) deficiency. WE is characterized by changes in consciousness, ocular dysfunction, and ataxia. Neuroradiologic findings usually show symmetric signal intensity alterations in the mammillary bodies, medial thalami, tectal plate, and periaqueductal area. Selective involvement of the cranial nerve nuclei, cerebellum, red nuclei, dentate nuclei, fornix, splenium, cerebral cortex, and basal ganglia characterize nonalcoholic WE patients. Furthermore, symmetric basal ganglia alterations with involvement of the putamen have only been observed in children. The incidence of WE is underestimated in both adult and pediatric patients. Interestingly, the frequency of WE in children appears to be similar to that observed in adults. The prognosis of the disease largely depends on the time from diagnosis to thiamine supplementation. The aim of this pediatric literature review is to provide an update on neuroradiologic findings in children affected by WE in an effort to determine pertinent clinical and imaging findings that can improve the detection and early identification of the disease. A thorough knowledge of the MRI findings of WE will assist in arriving at an early diagnosis, thereby reducing the morbidity and mortality associated with this disease in children.

  • mr imaging findings in 56 patients with Wernicke Encephalopathy nonalcoholics may differ from alcoholics
    American Journal of Neuroradiology, 2008
    Co-Authors: Giulio Zuccoli, M Gallucci, Marco Bertolini, Santa D Cruz, Alex Rovira, C Carollo, Nicolo Pipitone
    Abstract:

    BACKGROUND AND PURPOSE: Wernicke Encephalopathy (WE) is a severe neurologic disorder resulting from dietary vitamin B 1 deficiency. This study was undertaken to analyze and compare MR imaging findings and neurologic manifestations at clinical presentations of patients with WE with and without a history of alcohol abuse. MATERIALS AND METHODS: WE patients were identified using diagnostic neurologic data bases. Fifty-six patients (29 females, 27 males) diagnosed between 1999 and 2008 with WE who improved within 1 month from the onset of thiamine administration were included in the analysis. Patients’ records were reviewed for clinical manifestations and imaging studies’ findings. MR imaging was performed in the acute phase of the disease at a field strength of 1T (16 patients) and 1.5T (40 patients). All MR images were of acceptable to good quality and were retrospectively reviewed. We compared imaging findings and clinical presentation in the alcoholic (AL) group versus the non-alcoholic (NA) group using the 2-tailed Fisher exact test and the Phi coefficient as appropriate. RESULTS: Forty-three percent of the patients were in the AL group, whereas 57% were in the NA group. Eighty-nine percent showed changes in consciousness, 75% had ocular manifestations, and 54% had ataxia. On MR imaging, 80% of the patients had evidence of symmetric lesions in the medial thalami and in the periventricular region of the third ventricle; 59%, in the periaqueductal area; 45%, in the mamillary bodies; 36%, in the tectal plate; and 7%, in the periventricular gray matter located anteriorly to the fourth ventricle. Signal-intensity alterations in areas considered atypical for the disease were noted only in the NA group and always in association with the typical findings. Contrast enhancement of the thalamus and mamillary bodies was significantly associated with alcohol abuse. CONCLUSIONS: Contrast enhancement in the mamillary bodies and thalamus is a typical finding of the disease in AL patients. Atypical MR imaging findings characterize NA patients.

  • metronidazole induced and Wernicke Encephalopathy two different entities sharing the same metabolic pathway
    American Journal of Neuroradiology, 2008
    Co-Authors: Giulio Zuccoli, Nicolo Pipitone, Santa D Cruz
    Abstract:

    We read with interest the recent article by Kim et al[1][1] on MR imaging features of metronidazole-induced Encephalopathy (MIE). They described MR findings from 7 patients treated with metronidazole, 5 of whom suffered from gastrointestinal tract disease. All of the patients showed symmetric signal

  • Wernicke Encephalopathy mr findings at clinical presentation in twenty six alcoholic and nonalcoholic patients
    American Journal of Neuroradiology, 2007
    Co-Authors: Giulio Zuccoli, M Gallucci, Jaume Capellades, L Regnicolo, B Tumiati, Cabada T Giadas, W Bottari, Jessica Mandrioli, Marco Bertolini
    Abstract:

    BACKGROUND AND PURPOSE: Wernicke Encephalopathy is a severe neurologic disorder that results from a dietary vitamin B1 deficiency. It is characterized by changes in consciousness, ocular abnormalities, and ataxia. This study was undertaken to analyze and compare findings on MR imaging and neurologic symptoms at clinical presentations of patients with Wernicke Encephalopathy with and without a history of alcohol abuse. MATERIALS AND METHODS: A multicenter study group retrospectively reviewed MR brain imaging findings, clinical histories, and presentations of 26 patients (14 female, 12 male) diagnosed between 1999 and 2006 with Wernicke Encephalopathy. The age range was 6–81 years (mean age, 46 .6 ± 19 years). RESULTS: Fifty percent of the patients had a history of alcohol abuse, and 50% had no history of alcohol abuse. Eighty percent showed changes in consciousness, 77% had ocular symptoms, and 54% had ataxia. Only 38% of the patients showed the classic triad of the disease at clinical presentation. At MR examination, 85% of the patients showed symmetric lesions in the medial thalami and the periventricular region of the third ventricle, 65% in the periaqueductal area, 58% in the mamillary bodies, 38% in the tectal plate, and 8% in the dorsal medulla. Contrast enhancement of the mamillary bodies was statistically positively correlated with the alcohol abuse group. CONCLUSIONS: Our study confirms the usefulness of MR in reaching a prompt diagnosis of Wernicke Encephalopathy to avoid irreversible damage to brain tissue. Contrast enhancement in the mamillary bodies is a typical finding of the disease in the alcoholic population.

Marco Bertolini - One of the best experts on this subject based on the ideXlab platform.

  • mr imaging findings in 56 patients with Wernicke Encephalopathy nonalcoholics may differ from alcoholics
    American Journal of Neuroradiology, 2008
    Co-Authors: Giulio Zuccoli, M Gallucci, Marco Bertolini, Santa D Cruz, Alex Rovira, C Carollo, Nicolo Pipitone
    Abstract:

    BACKGROUND AND PURPOSE: Wernicke Encephalopathy (WE) is a severe neurologic disorder resulting from dietary vitamin B 1 deficiency. This study was undertaken to analyze and compare MR imaging findings and neurologic manifestations at clinical presentations of patients with WE with and without a history of alcohol abuse. MATERIALS AND METHODS: WE patients were identified using diagnostic neurologic data bases. Fifty-six patients (29 females, 27 males) diagnosed between 1999 and 2008 with WE who improved within 1 month from the onset of thiamine administration were included in the analysis. Patients’ records were reviewed for clinical manifestations and imaging studies’ findings. MR imaging was performed in the acute phase of the disease at a field strength of 1T (16 patients) and 1.5T (40 patients). All MR images were of acceptable to good quality and were retrospectively reviewed. We compared imaging findings and clinical presentation in the alcoholic (AL) group versus the non-alcoholic (NA) group using the 2-tailed Fisher exact test and the Phi coefficient as appropriate. RESULTS: Forty-three percent of the patients were in the AL group, whereas 57% were in the NA group. Eighty-nine percent showed changes in consciousness, 75% had ocular manifestations, and 54% had ataxia. On MR imaging, 80% of the patients had evidence of symmetric lesions in the medial thalami and in the periventricular region of the third ventricle; 59%, in the periaqueductal area; 45%, in the mamillary bodies; 36%, in the tectal plate; and 7%, in the periventricular gray matter located anteriorly to the fourth ventricle. Signal-intensity alterations in areas considered atypical for the disease were noted only in the NA group and always in association with the typical findings. Contrast enhancement of the thalamus and mamillary bodies was significantly associated with alcohol abuse. CONCLUSIONS: Contrast enhancement in the mamillary bodies and thalamus is a typical finding of the disease in AL patients. Atypical MR imaging findings characterize NA patients.

  • Wernicke Encephalopathy mr findings at clinical presentation in twenty six alcoholic and nonalcoholic patients
    American Journal of Neuroradiology, 2007
    Co-Authors: Giulio Zuccoli, M Gallucci, Jaume Capellades, L Regnicolo, B Tumiati, Cabada T Giadas, W Bottari, Jessica Mandrioli, Marco Bertolini
    Abstract:

    BACKGROUND AND PURPOSE: Wernicke Encephalopathy is a severe neurologic disorder that results from a dietary vitamin B1 deficiency. It is characterized by changes in consciousness, ocular abnormalities, and ataxia. This study was undertaken to analyze and compare findings on MR imaging and neurologic symptoms at clinical presentations of patients with Wernicke Encephalopathy with and without a history of alcohol abuse. MATERIALS AND METHODS: A multicenter study group retrospectively reviewed MR brain imaging findings, clinical histories, and presentations of 26 patients (14 female, 12 male) diagnosed between 1999 and 2006 with Wernicke Encephalopathy. The age range was 6–81 years (mean age, 46 .6 ± 19 years). RESULTS: Fifty percent of the patients had a history of alcohol abuse, and 50% had no history of alcohol abuse. Eighty percent showed changes in consciousness, 77% had ocular symptoms, and 54% had ataxia. Only 38% of the patients showed the classic triad of the disease at clinical presentation. At MR examination, 85% of the patients showed symmetric lesions in the medial thalami and the periventricular region of the third ventricle, 65% in the periaqueductal area, 58% in the mamillary bodies, 38% in the tectal plate, and 8% in the dorsal medulla. Contrast enhancement of the mamillary bodies was statistically positively correlated with the alcohol abuse group. CONCLUSIONS: Our study confirms the usefulness of MR in reaching a prompt diagnosis of Wernicke Encephalopathy to avoid irreversible damage to brain tissue. Contrast enhancement in the mamillary bodies is a typical finding of the disease in the alcoholic population.

Seong-ho Park - One of the best experts on this subject based on the ideXlab platform.

  • Upbeat Nystagmus: Clinicoanatomical Correlations in 15 Patients
    Journal of Clinical Neurology, 2006
    Co-Authors: Bora Yoon, Sun Young Oh, Kwang-dong Choi, Seong-ho Park
    Abstract:

    BACKGROUND AND PURPOSE: The mechanism of upbeat nystagmus is unknown and clinicoanatomical correlative studies in series of patients with upbeat nystagmus are limited. METHODS: Fifteen patients with upbeat nystagmus received full neuro-ophthalmological evaluation by the senior author. Nystagmus was observed using video Frenzel goggles and recorded with video-oculography. Brain lesions were documented with MRI. RESULTS: LESIONS RESPONSIBLE FOR NYSTAGMUS WERE FOUND THROUGHOUT THE BRAINSTEM, MAINLY IN THE PARAMEDIAN AREA: in the medulla (n=8), pons (n=3), pons and midbrain with or without cerebellar lesions (n=3), and midbrain and thalamus (n=1). Underlying diseases comprised cerebral infarction (n=10), multiple sclerosis (n=2), cerebral hemorrhage (n=1), Wernicke Encephalopathy (n=1), and hydrocephalus (n=1). Upbeat nystagmus was mostly transient and showed occasional evolution during the acute phase. In one patient with a bilateral medial medullary infarction, the upbeat nystagmus changed into a hemiseesaw pattern with near complete resolution of the unilateral lesion. Gaze and positional changes usually affected both the intensity and direction of the nystagmus. A patient with a cervicomedullary lesion showed a reversal of upbeat into downbeat nystagmus by straight-head hanging and leftward head turning while in the supine position. Gaze-evoked nystagmus (n=7), ocular tilt reaction (n=7), and internuclear ophthalmoplegia (n=4) were also commonly associated with upbeat nystagmus. CONCLUSIONS: In view of the responsible lesions and associated neuro-ophthalmological findings, upbeat nystagmus may be ascribed to damage to the pathways mediating the upward vestibulo-ocular reflex or the neural integrators involved in vertical gaze holding.

  • diffusion weighted imaging abnormalities in Wernicke Encephalopathy reversible cytotoxic edema
    JAMA Neurology, 2002
    Co-Authors: Kon Chu, Dongwha Kang, Han Joon Kim, Yongseok Lee, Seong-ho Park
    Abstract:

    Background Wernicke Encephalopathy (WE) is a metabolic disorder of the central nervous system resulting from vitamin B 1 deficiency. The exact mechanisms underlying the pathogenesis of the lesions in WE are not completely understood. Vitamin B 1 deficiency is associated with intracellular and extracellular edema by glutamate N-methyl-D-aspartate receptor–mediated excitotoxicity. Conventional magnetic resonance imaging (MRI) cannot differentiate the types of edema. Diffusion-weighted imaging (DWI) has been reported to detect early ischemic damage (cytotoxic edema) as bright areas of high signal intensity (SI) and vasogenic edema as areas of heterogeneous SI. Objectives To describe the DWI findings and to characterize the types of edema in WE using DWI. Setting Tertiary referral center. Design and Methods Two patients with WE underwent DWI and conventional MRI with gadolinium enhancement. Wernicke Encephalopathy was diagnosed with salient conventional MRI findings (high SIs in the paramedian thalamus, periaqueductal gray matter, and mamillary bodies) and typical clinical history and symptoms. Apparent diffusion coefficient (ADC) values were measured in abnormal lesions by visual inspection of DWIs and T2-weighted echo planar images. Results T2-weighted and fluid-attenuated inversion recovery MRIs showed high SIs in the bilateral paramedian thalamus, mamillary bodies, and periaqueductal gray matter. The DWIs showed bright high SI in the corresponding lesions, and ADC values were decreased (patient 1: 512-545 × 10 −6 mm 2 /s; patient 2: 576-612 × 10 −6 mm 2 /s). The ADC decrease and the DWI high SI were normalized in 2 weeks with administration of thiamine hydrochloride. Conclusions Abnormalities on DWI and ADC decrease became normalized with adequate therapy. The MRI abnormalities in WE might be owing to the "reversible cytotoxic edema" caused by vitamin B 1 deficiency.

  • magnetic resonance reflects the pathological evolution of Wernicke Encephalopathy
    Journal of Neuroimaging, 2001
    Co-Authors: Seong-ho Park, Manho Kim, Beom S Jeon
    Abstract:

    Background and Purpose. Wernicke Encephalopathy (WE) is an acute phase of Wernicke-Korsakoff syndrome. Pathologic findings change between acute and chronic phases. Only a few magnetic resonance imaging (MRI) studies have been done to date. Methods. To correlate the MRI findings in acute and chronic stages of WE with the known pathologic information, 15 consecutive patients with WE were examined with MRI: 3 before thiamine treatment, 7 within 24 hours of thiamine treatment, 4 between the second and sixth day after thiamine treatment, and 1 fifty-five days after thiamine treatment. Nine of the patients had follow-up MRI between 2 days and 33 months. T1-weighted, proton, and T2-weighted axial images were obtained with additional 5-mm-thick T1-weighted sagittal and coronal images to better visualize the mammillary bodies. Results. In the acute WE, MRI showed high signal intensity on T2-weighted images in periaqueduct and medial thalamic regions. In a few patients with alcoholism, vermian and mammillary body atrophies and third ventricular enlargements were noted. In the chronic phase of WE, T2 hyperintensity disappeared but mammillary bodies and cerebellar vermis became atrophic and third ventricular enlargements were evident. High signal intensity on T2-weighted images disappeared as early as 2 days, and atrophic changes appeared as early as 1 week. Conclusion. MRI is useful for in vivo monitoring and reflects the pathological evolution in acute and chronic phases of WE.

Josep Vidal - One of the best experts on this subject based on the ideXlab platform.

  • nystagmus an uncommon neurological manifestation of thiamine deficiency as a serious complication of sleeve gastrectomy
    Nutrition in Clinical Practice, 2012
    Co-Authors: Violeta Moize, Ainitze Ibarzabal, Bernardo Sanchez Dalmau, Lilliam Flores, Alba Andreu, Antonio M Lacy, Josep Vidal
    Abstract:

    Wernicke Encephalopathy—a debilitating acute or subacute neurological disorder—is caused by a deficiency in thiamine (vitamin B1). It is characterized by a classical clinical triad of symptoms: ocular impairment, cerebellar dysfunction, and confusion. Although bariatric surgery can certainly improve the overall health of an obese individual, it can also make him or her more susceptible to serious nutrition deficiencies. Following surgery, inadequate caloric intake, rapid and excessive weight loss, food intolerance, lack of adherence to nutrition supplementation, and/or the onset of prolonged vomiting can lead to severe nutrition deficiencies. It is generally believed that the more malabsorptive the surgery proves, the more likely is it that such a deficiency will occur. The case presented here shows that after sleeve gastrectomy (SG), a patient may also develop dangerous nutrition deficits that can negatively affect his or her life. In this particular case, a patient presented with a severe vitamin B1 def...

Friedhelm E Zanella - One of the best experts on this subject based on the ideXlab platform.

  • Wernicke Encephalopathy mr findings and clinical presentation
    European Radiology, 2003
    Co-Authors: Stefan Weidauer, Michael Nichtweiss, Heinrich Lanfermann, Friedhelm E Zanella
    Abstract:

    Wernicke Encephalopathy (WE) is a severe neurological disorder caused by vitamin B1 deficiency. The aim of the study was to analyse MRI findings typical for this disease and to evaluate the significance of their correlations with clinical symptoms. Magnetic resonance images and clinical features of 12 patients with WE were analysed. The patients underwent MR imaging within 3–14 days after onset of clinical symptoms. In 7 of 12 patients MR imaging showed symmetrical diencephalic and midbrain lesions. Postcontrast T1-weighted images from 5 of 9 patients examined during the initial 6 days of acute WE showed a subtle enhancement of the mamillary bodies, the tectal plate, the periaqueductal area and the periventricular region of the third ventricle including the paramedian thalamic nuclei. In addition, T2-weighted and fluid-attenuated inversion recovery (FLAIR) images revealed hyperintense signals in these regions (except for 2 patients where the mamillary bodies were normal). Hyperintense lesions on T2-weighted images without any enhancement on postcontrast T1-weighted images were detected in 2 patients by MR imaging performed 11 or 14 days after onset of WE. Patients with hyperintensities on T2-weighted images of the periventricular region of the third ventricle and the paramedian thalamic nuclei had poor recovery from their mental dysfunction. The MR examination in case of WE shows a typical pattern of lesions in 58% of cases. Enhancement of the mamillary bodies, the periventricular region of the third ventricle including the paramedian thalamic nuclei, and the periaqueductal area on postcontrast T1-weighted images can be observed in the initial period after clinical onset of symptoms and are characteristic signs of the acute stage of WE. Hyperintense lesions in the periventricular region and the paramedian thalamic nuclei on T2-weighted and FLAIR images in the subacute stage of WE and enhancement on postcontrast T1-weighted images of the mamillary bodies and the paramedian thalamic nuclei are indicators of poor prognosis despite vitamin B1 substitution.