Non-alcoholic Wernicke's Encephalopathy Research Articles

Editorial introductions

Editorial introductions

Non-Alcoholic Wernicke's Encephalopathy in a Post Bariatric Surgery Patient

Non-Alcoholic Wernicke's Encephalopathy in a Post Bariatric Surgery Patient

A Case of Non-alcoholic Wernicke Encephalopathy with Papillitis

A Case of Non-alcoholic Wernicke Encephalopathy with Papillitis

Wernicke's encephalopathy after total parenteral nutrition in patients with Crohn's disease.

Micronutrient deficiencies in Crohn's disease (CD) patients are not uncommon and usually result in a combination of reduced dietary intake, disease-related malabsorption, and a catabolic state. Decreased serum thiamine levels are often reported in patients with CD. Wernicke's encephalopathy (WE) is a severe form of thiamine deficiency that can cause serious neurologic complications. Although WE is known to occur frequently in alcoholics, a number of non-alcoholic causes have also been reported. Here, we report two cases of non-alcoholic WE that developed in two severely malnourished CD patients who were supported by prolonged total parenteral nutrition without thiamine supplementation. These patients complained of sudden-onset ophthalmopathy, cerebellar dysfunction, and confusion. Magnetic resonance imaging allowed definitive diagnosis for WE despite poor sensitivity. The intravenous administration of thiamine alleviated the symptoms of WE dramatically. We emphasize the importance of thiamine supplementation for malnourished patients even if they are not alcoholics, especially in those with CD.

Association between malignancy and non-alcoholic Wernicke's encephalopathy: a case report and literature review.

Wernicke's encephalopathy is a serious medical condition associated with high morbidity and mortality caused by deficiency of thiamine. This disease is classically associated with alcoholism, but is underappreciated in the nonalcoholic population. There is growing acknowledgement of the development of Wernicke's encephalopathy in patients with malignancies. We conducted a literature review in PubMed for cases of Wernicke's encephalopathy occurring in patients with malignancy. We also present the case of a 47-year-old woman with recurrent laryngeal cancer and multiple hospital admissions for malnutrition. Neurological examination was notable for pendular nystagmus, severe gait ataxia, confusion, and poor memory consolidation. MRI of the brain was significant for T2-weighted fluid-attenuated inversion recovery hyperintensities in periaqueductal regions, medial thalami, and the tectal plate, typical for Wernicke's encephalopathy. She was treated with thiamine repletion, and had marked improvement in her mental status and some improvement in her vision problems and ataxia, although some nystagmus and significant short-term memory impairment persisted. The literature review yielded dozens of case reports of Wernicke's encephalopathy in patients with malignancy, dominated by cases of patients with malignancies of the gastrointestinal system, followed by those with hematologic malignancies. Malignancy is an important risk factor for the development of Wernicke's encephalopathy. This diagnosis is underappreciated and difficult for the clinician to discern from multifactorial delirium. Clinicians should be aware to treat at-risk patients with thiamine immediately, especially if multiple risk factors are present.

Case: Wernicke Encephalopathy after Bariatric Surgery

Background: Wernicke encephalopathy after bariatric surgery is rare and difficult to recognize. The severity of the disease and the preventable but irreversible long-term implications lead us to emphasize the importance of timely and correct diagnosis and treatment. Nonalcoholic Wernicke encephalopathy often manifests atypical clinical presentation and disease progression that makes it prone to be underestimated. Clinical case: We report the medical history of a 48-year old lady after bariatric surgery. It is a case of possible Wernicke encephalopathy. The patient presents with a constellation of physical features that may represent a complex clinical situation due to longer existing vision problems or an as yet uncharacterized Wernicke encephalopathy. We discuss diagnosis, underlying pathology, metabolic mechanism and common therapeutic approach. Conclusion: With the ongoing global epidemic of obesity the need for obesity surgery will increase, thus leading to increased occurrence of Wernicke encephalopathy. This emphasizes the importance of awareness of this clinical entity and the need for early detection and prevention.

Nonalcoholic Wernicke Encephalopathy in a Pediatric Patient with a History of Medulloblastoma

Nonalcoholic Wernicke Encephalopathy in a Pediatric Patient with a History of Medulloblastoma

Usefulness of Magnetic Resonance Imaging in the Diagnosis of Non-Alcoholic Wernicke's Encephalopathy.

A 38-year-old normotensive, non-diabetic, non-alcoholic male patient presented with altered sensorium and three episodes of generalized tonic clonic seizures in the past 3 days. Patient had undergone a right hemicolectomy and chemotherapy for cecal carcinoma 3 years ago, followed by excision of recurrent ileo-colic mass 2 years ago. Patient had received repeat chemotherapy 4 months ago for peritoneal metastatic disease, which had induced severe vomiting and diarrhea. He was on parenteral nutrition since then. On examination, the patient was obtunded, afebrile, pale, anicteric with stable vitals. He had bilateral decerebrate posture, was unresponsive to verbal commands and opened eyes only to a painful stimulus. Bilateral extensor plantar response and ankle clonus were elicited.

About pathognomonic images: an infrequent case of acute encephalopathy

BACKGROUND The occurrence of acute encephalopathy is a dramatic clinical dilemma when usual diagnostic techniques (blood tests, cerebral CT and cerebrospinal fluid analysis) show no abnormalities. CLINICAL CASE We describe a case of a 73 years old man admitted in our Internal Medicine Unit for acute diarrhoea with vomiting and fever who developed a prolonged gastrointestinal dysmotility syndrome with poor nutritional intake. Although a parenteral support was provided, he developed acute encephalopathy followed by hypotension and lactic acidosis without evidence of renal and hepatic disease or glycemic alterations. Likewise, no cerebral CT and cerebrospinal fluid alterations were found. Conversely, cerebral MRI showed marked and diffuse DP-2 and FLAIR hyperintensity of the mesencephalic tectal plate, of the periaqueductal area, and of the periventricular region of the third ventricle including the median thalamic area. These MRI descriptions were considered pathognomonic of Wernicke encephalopathy. Thus, the immediate use of ev thiamine was followed by a prompt and complete recovery of neurological, hemodinamic and metabolic conditions. CONCLUSIONS Non-alcoholic Wernicke encephalopathy is a rare and dramatic clinical event with high mortality. In this context, brain MRI is the best diagnostic tool providing a typical picture.

Wernicke encephalopathy with atypical magnetic resonance imaging

Wernicke encephalopathy (WE) is a medical emergency caused by thiamine (vitamin B1) deficiency. Typical clinical manifestations are mental change, ataxia, and ocular abnormalities. Wernicke encephalopathy is an important differential diagnosis in all patients with acute mental change. However, the disorder is greatly underdiagnosed. Clinical suspicion, detailed history taking, and neurologic evaluations are important for early diagnosis. Magnetic resonance imaging (MRI) is currently considered the diagnostic method of choice. Typical MRI findings of WE are symmetrical involvement of medial thalamus, mammillary body, and periaqueductal gray matter. Prompt thiamine supplement is important in avoiding unfavorable outcomes. Here, we report a case of alcoholic WE with typical clinical presentation but with atypical MRI. Axial fluid-attenuated inversion recovery images showing symmetrical hyperintensity lesions in dentate nuclei of cerebellum, olivary bodies, and dorsal pons. Although atypical MRI findings are more common in nonalcoholic WE, it can also occur in alcoholic WE. This article is aimed to highlight the potential pitfalls in diagnosing acute mental change, the importance of clinical suspicion, and early treatment in WE.

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

We describe a non-alcoholic diabetic patient with central pontine myelinolysis (CPM) and Wernicke encephalopathy (WE). A 69-year-old man developed consciousness disturbance after parenteral hyperalimentation for liver abscess and sepsis. Neurological examination revealed drowsiness and no articulation. MRI disclosed T2-hyperintense lesions in the dorsal medulla oblongata and dentate nuclei, and symmetric enhancement in the inferior colliculus. Thiamine treatment (1,000 mg/day, div) attenuated neurological deficits. Seven days later, WE-related lesions were markedly regressed and a central pontine T2-hyperintensity lesion appeared. Serum sodium levels were normal. Physicians should pay more attention to rapid development of normonatremic CPM under thiamine supplementation in non-alcoholic WE patients.

Wernicke's encephalopathy in non-alcoholic patients: A series of 8 cases

Introduction Wernicke's encephalopathy (WE) is an underdiagnosed condition, usually associated with alcoholism, and has a worse prognosis if there is a delay in diagnosis. A series of 8 non-alcoholic patients with WE is presented and an assessment is made on whether a delay in diagnosis leads to a worse prognosis. Patients and methods The clinical records of patients admitted to 2 university hospitals between 2004 and 2009 with the diagnosis of WE, excluding those with a history of alcoholism, were retrospectively reviewed. Results The study included 4 men and 4 women aged 35–82 of whom 7 had a history of gastrointestinal pathology, and persistent vomiting was the precipitating factor in 7. Encephalopathy was the most frequent onset symptom (4). The classical triad was present in seven patients. Thiamine levels were low in 3/6 and normal in 3/6 cases. MRI was abnormal in seven patients, with high signal intensity in the diencephalon and mammillary bodies (7), periaqueductal grey matter (6), cortex (3) and cerebellum (1). Seven improved with thiamine. Sequelae were mild in 6, and severe in 2 after 6–12 months of follow-up. All patients with a diagnostic delay less than 18 days had mild sequelae. Conclusions Non-alcoholic WE frequently occurs after gastrointestinal disturbances that could result in lower thiamine absorption. Whereas thiamine levels can be normal in many cases, in almost all cases the MRI shows signal alterations in typical locations. A delay in the diagnosis, and therefore, in treatment leads to a worse prognosis.

Encefalopatía de Wernicke en pacientes no alcohólicos: una serie de 8 casos

Introduction Wernicke's encephalopathy (WE) is an underdiagnosed condition, usually associated with alcoholism, and has a worse prognosis if there is a delay in diagnosis. A series of 8 non-alcoholic patients with WE is presented and an assessment is made on whether a delay in diagnosis leads to a worse prognosis. Patients and methods The clinical records of patients admitted to 2 university hospitals between 2004 and 2009 with the diagnosis of WE, excluding those with a history of alcoholism, were retrospectively reviewed. Results The study included 4 men and 4 women aged 35-82 of whom 7 had a history of gastrointestinal pathology, and persistent vomiting was the precipitating factor in 7. Encephalopathy was the most frequent onset symptom (4). The classical triad was present in seven patients. Thiamine levels were low in 3/6 and normal in 3/6 cases. MRI was abnormal in seven patients, with high signal intensity in the diencephalon and mammillary bodies (7), periaqueductal grey matter (6), cortex (3) and cerebellum (1). Seven improved with thiamine. Sequelae were mild in 6, and severe in 2 after 6-12 months of follow-up. All patients with a diagnostic delay less than 18 days had mild sequelae. Conclusions Non-alcoholic WE frequently occurs after gastrointestinal disturbances that could result in lower thiamine absorption. Whereas thiamine levels can be normal in many cases, in almost all cases the MRI shows signal alterations in typical locations. A delay in the diagnosis, and therefore, in treatment leads to a worse prognosis.

Nonalcoholic Wernicke Encephalopathy with Extensive Cortical Involvement: Cortical Laminar Necrosis and Hemorrhage Demonstrated with Susceptibility-Weighted MR Phase Images: Fig 1.

Wernicke encephalopathy (WE) is an acute neuropsychiatric condition due to an initially reversible brain lesion caused by depleted intracellular thiamine levels in neurons.[1][1] Most of the affected patients are malnourished alcoholics; however, WE has also been associated with other conditions.

MRI Findings in Nonalcoholic Wernicke's Encephalopathy

MRI Findings in Nonalcoholic Wernicke's Encephalopathy

Non-Alcoholic Wernicke Encephalopathy: MR Imaging and Review of the Literature

We describe a patient with non-alcoholic Wernicke's encephalopathy caused by long-term parenteral nutrition. The diagnosis is based on clinical and magnetic resonance findings. We also reviewed the literature review in typical and atypical findings at MR examination.

Non-alcoholic Wernicke's encephalopathy: broadening the clinicoradiological spectrum

Wernicke's encephalopathy (WE) is a serious neurological disorder secondary to thiamine deficiency. Improved recognition by radiologists and allied health providers of the different clinical settings and imaging findings associated with this emergency can optimise the management of this condition and help prevent its severe consequences. The aim of this study is to illustrate the broad clinicoradiological spectrum of non-alcoholic WE, while emphasising atypical MRI findings.

Neuroimaging findings in pediatric Wernicke encephalopathy: a review

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 Can Predict the Development of Nonalcoholic Wernicke Encephalopathy: Fig 1.

We read with great interest the article by Fei et al[1][1] in which symmetric paraventricular regions in MR imaging were shown to be useful in the diagnosis of nonalcoholic Wernicke encephalopathy (WE). Among clinical studies, MR imaging is currently considered the most valuable method for

Clinical Characteristics and MR Imaging Features of Nonalcoholic Wernicke Encephalopathy

Nonalcoholic Wernicke encephalopathy (WE) is prone to be underestimated in clinical practice. The purpose of this study was to improve its awareness and early accurate diagnosis. We conducted a retrospective review of the cases of 12 patients with nonalcoholic WE, consisting of clinical characteristics and MR imaging features as well as follow-up after administration of thiamine. Patients with mild coma or lethargy (7/12) exhibited typical MR features of symmetric brain paraventricular damage. Patients without disturbances of consciousness or who only had drowsiness (3/12) exhibited a lesion of the periaqueductal area only. In addition to typical MR manifestations, symmetric cortical involvement was observed in 2 of 12 patients with deep coma. Gadolinium enhancement of the mammillary bodies was observed in 2 of 3 patients. No atrophy of the mammillary bodies and cerebellar vermis was found in any patients. Of 10 patients without deep coma and cortical damage, 2 missed the follow-up and 8, who recovered clinically, also showed accordant resolution of abnormal hyperintense signal intensity on T2-weighted and fluid-attenuated inversion recovery images within 2 weeks to 1 year after thiamine supplementation. Two patients with deep coma and cortical damage showed a poor prognosis:1 patient died 15 days after being diagnosed with WE, and the other entered a persistent vegetative state during a follow-up of 2 years. Typical symmetric damage of the mammillary bodies and brain paraventricular regions may permit a specific diagnosis of nonalcoholic WE. In all patients, no atrophy of the mammillary bodies and cerebellar vermis was found. Cortical involvement in patients with nonalcoholic WE may be indicative of irreversible lesions and a poor prognosis.