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            : Diverse MRI signal intensities with Wernicke encephalopathy

Roh, Jee Hoon; Kim, J. H.; Koo, Yong Seo; Seo, Woo‐Keun; Lee, J.-M; Lee, Y. H.; Park, Moon Ho

doi:10.1212/01.wnl.0000308951.21103.49

Cited by 6 publications

(4 citation statements)

References 2 publications

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“…4 e 7), ma lo studio DWI-ADC può essere negativo [15,23,24]. Proprio per la natura dinamica della fi siopatologia dell'encefalopatia di Wernicke, peraltro, è possibile la presenza contemporanea di aree di restrizione della diffusione e aree con diffusione normale o aumentata [29]. Le aree di restrizione della diffusione sono compatibili con edema citotossico di astrociti e neuroni da danno eccitotossico, mentre le lesioni con valori di ADC normali o aumentati corrispondono alla presenza di edema vasogenico.…”

Section: Paramagnetic Contrast Materialsunclassified

“…4 and 7) ADC values, but the DWI-ADC study may be negative [15,23,24]. Because of the dynamic nature of Wernicke's encephalopathy pathophysiology, areas of reduced diffusion and areas with normal or increased diffusion may be present simultaneously [29]. Areas of reduced diffusion are compatible with cytotoxic oedema of astrocytes and neurons due to excitotoxicity, whereas lesions with normal or increased ADC values indicate the presence of vasogenic oedema.…”

Section: Diffusion-weighted Mri With Apparent Diffusion Coeffi Cient mentioning

confidence: 99%

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CT and MRI of Wernicke’s encephalopathy

et al. 2011

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The purpose of this pictorial essay is to present the computed tomography (CT) and magnetic resonance imaging (MRI) findings of Wernicke's encephalopathy, a rare, severe, acute neurological syndrome due to thiamine (vitamin B1) deficiency, associated with high morbidity and mortality. The classical clinical triad, which includes ocular signs, altered consciousness and ataxia, can be found in only one-third of patients. Although chronic alcoholic patients are the most commonly affected, Wernicke's encephalopathy may complicate malnutrition conditions in nonalcoholic patients, in whom it is greatly underestimated. CT and above all MRI of the brain play a fundamental role in diagnosing the condition and ruling out other diseases. MRI is the most sensitive technique and is required in all patients with a clinical suspicion of Wernicke's encephalopathy. Medial thalami, mamillary bodies, tegmentum, periaqueductal region, and tectal plate are typical sites of abnormal MRI signal. The dorsal medulla, red nuclei, cranial nerve nuclei, cerebellum, corpus callosum, frontal and parietal cerebral cortex are less common sites of involvement although they are more frequently affected in nonalcoholic patients. Paramagnetic contrast material may help to identify lesions not otherwise visible.

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Section: Paramagnetic Contrast Materialsunclassified

Section: Diffusion-weighted Mri With Apparent Diffusion Coeffi Cient mentioning

confidence: 99%

CT and MRI of Wernicke’s encephalopathy

et al. 2011

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“…The role of diffusion-weighted sequences (DWI) and apparent diffusion coefficient (ADC) is unclear [26] due to the simultaneous presence of areas of restricted, normal, or increased diffusion [26] ; in particular, the areas of diffusion restriction reflect the presence of cytotoxic edema of neurons or astrocytes and those with normal or increased ADC values represent areas of vasogenic edema; in a retrospective study [27] restricted diffusion was seen in 100% of non-alcoholic and 66% alcoholic WE patients although the sample examined in this study was not large.…”

Section: Discussionmentioning

confidence: 99%

Beyond the bowel: Wernicke's encephalopathy as a neurological complication of Crohn's disease: A case report

Failla,

Tiralongo,

Crimi

et al. 2024

Radiology Case Reports

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“…The involvement of the vermis, the paravermis together with the medial aspects of both thalami, has been described by some researchers as specific for nonalcoholic WE. [11,12] The involvement of the cerebellar hemispheres, albeit atypical, has been described in WE. [13] Gastrointestinal manifestations are described as being common in SLE, with nausea and vomiting occurring in >50% of cases in some series.…”

Section: Discussionmentioning

confidence: 99%

Systemic lupus erythematosus: A possible cause of non-alcoholic Wernicke’s encephalopathy

2017

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Systemic lupus erythematosus (SLE) is a multisystemic auto immune disorder, with neurological manifestations being common. Attribution of neurological features to SLE is often a challenging process that requires a thorough clinical evaluation, relevant laboratory investigations and imaging studies. Acute cerebellar ataxia has been described in SLE, although little has been published in this regard. Wernicke's encephalopathy (WE) is a neurological complication of thiamine deficiency. Poor eating habits and vomiting are well-described causes of non-alcoholic WE. Gastrointestinal manifestations commonly occur, with nausea and vomiting reported in >50% of cases in some series. It is important that WE is considered in patients with SLE and ataxia, as it is treatable and carries a significant morbidity and mortality without appropriate treatment. Case reportA 24-year-old black female patient was referred to the rheumatology clinic at Dr George Mukhari Academic Hospital, a tertiary hospital in Pretoria, South Africa, with suspected SLE. Dermatologists had been treating her for a biopsy-proven bullous lupus for a few months. The initial consultation at the rheumatology clinic confirmed the diagnosis of SLE, based on the presence of acute cutaneous lupus, non-scarring generalised alopecia, haemolytic anaemia, positive antinuclear antibody, positive anti-Smith antibody, a weakly positive lupus anticoagulant test, and a low level of serum complement 3 (C3), unequivocally fulfilling the Systemic Lupus International Collaborating Clinics classification criteria for SLE.[1] Although her bullous lesions had healed, she had an active interarticular rash on her fingers and haemolytic anaemia, with a haemoglobin of 6.4 g/dL, confirming the presence of active disease. She received 2 U of blood and was treated with oral prednisone and oral azathioprine.Five weeks later, she presented again, complaining of intermittent vomiting and nausea of ~3 weeks' duration. She also reported weight loss and vertigo. A physical examination revealed sinus tachycardia, drowsiness, mild confusion, nystagmus, dysarthria, truncal and limb ataxia and bilateral partial 6th cranial nerve palsies. Her haemoglobin was 11.4 g/dL. All other laboratory tests for detecting active SLE in various organ systems were normal, except for hypoalbuminaemia, with a serum albumin of 26 g/L. Her renal function test was normal and there was no proteinuria. Hypoalbuminaemia seemed to reflect the severity of vomiting and possibly the negative acute-phase response. Typical features of SLE-related protein-losing enteropathy, such as diarrhoea, profound pitting oedema and effusions in serous cavities, were absent. Barium studies and gastroscopy did not show any abnormalities to explain the reasons for her vomiting, suggesting that SLE itself was the likely cause. SLE activity was thought to be the cause of sinus tachycardia, as other causes such as thyrotoxicosis, lung diseases, pulmonary embolism and myocarditis were excluded. With regard to her neurological symptoms and sign...

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Teaching Neuro Image : Diverse MRI signal intensities with Wernicke encephalopathy

Cited by 6 publications

References 2 publications

CT and MRI of Wernicke’s encephalopathy

CT and MRI of Wernicke’s encephalopathy

Beyond the bowel: Wernicke's encephalopathy as a neurological complication of Crohn's disease: A case report

Systemic lupus erythematosus: A possible cause of non-alcoholic Wernicke’s encephalopathy

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