Non-alcoholic Wernicke's Encephalopathy Research Articles

Nonalcoholic Wernicke encephalopathy with petechial hemorrhage in the tectal region.

Nonalcoholic Wernicke encephalopathy with petechial hemorrhage in the tectal region.

Gayet-Wernicke Encephalopathy Complicating a Pregnancy of 17 Weeks of Amenorrhea: A Case Report

Gayet-Wernicke encephalopathy is a neuropsychiatric emergency due to thiamine (vitamin B1) deficiency, secondary to several factors, it is a disorder characterized by confusion of acute onset, nystagmus, partial ophthalmoplegia and ataxia. The diagnosis is mainly clinical. The disorder may resolve with treatment, persist, or degenerate into Korsakoff's psychosis. We report a case of Gayet-Wernicke encephalopathy in a 39 year old non-ethylic patient, pregnant at 17 weeks of age who presented with consciousness disorders with paresthesia of the 4 limbs and dyspnea. Clinical and magnetic resonance imaging (MRI) have an important place, especially in the diagnosis of non-alcoholic Wernicke's encephalopathy.

Non-alcoholic Wernicke's encephalopathy with atypical brain MRI in setting of severe subacute malnutrition

Wernicke encephalopathy (WE) classically presents as encephalopathy, oculomotor dysfunction, and gait ataxia. WE usually occurs in the setting of chronic alcohol use and thiamine insufficiency. MRI imaging generally demonstrates edema of the periaqueductal region of the midbrain, mammillary bodies, and thalamus. Basal ganglia (BG) involvement, more commonly seen in pediatric WE, is classically thought to differentiate pediatric versus adult WE. However, we report a case of adult non-alcoholic WE with both thalamic and BG involvement.

Editorial introductions.

Editorial introductions.

A Case of Wernicke Encephalopathy Secondary to Anorexia Nervosa Complicated by Refeeding Syndrome and Takotsubo Cardiomyopathy

Patient: Female, 20-year-oldFinal Diagnosis: Anorexia nervosa • refeeding syndrome • takotsubo cardiomyopathy • Wernicke encephalopathySymptoms: Altered mental status • lethargy • weight lossMedication: —Clinical Procedure: —Specialty: Critical Care MedicineObjective:Unusual clinical courseBackground:Wernicke encephalopathy (WE) is a neurological condition commonly associated with sustained alcohol abuse. However, it should be noted that disorders resulting in severe malnutrition, such as anorexia nervosa (AN), can precipitate nonalcoholic WE. AN is a life threatening psychological and eating disorder defined by inappropriate weight loss from food restriction due to the fear of gaining weight and immoderate desire to be thin. Treatment of those suffering with AN can often be complicated by severe electrolyte derangements after caloric intake termed refeeding syndrome. Although extremely rare, severe cardiomyopathy and ultimately death may occur in patients from AN.Case Report:Herein describes the case of a 20-year-old female with AN induced WE complicated by refeeding syndrome and hemodynamic compromise in the setting of findings consistent with takotsubo cardiomyopathy. She required ventilatory and hemodynamic support with aggressive intravenous thiamine and phosphorus repletion. Nutritional supplementation was imperative and carefully administered throughout her hospitalization. Her symptoms improved over the course of a few weeks with an ultimate reversal of her cardiomyopathy.Conclusions:Given the morbidity surrounding AN, practitioners should exhibit caution when caring for those with severe nutritional deficiencies. Clinicians must monitor for severe electrolyte abnormalities and offer aggressive repletion. In addition to electrolyte derangements, severe cardiomyopathy may result as a rare sequela of the aforementioned complications associated with AN. Moreover, it is imperative to understand that patients with AN have the highest mortality of any psychiatric disorder and early intervention is necessary for survival in this vulnerable patient population.

Ambiguous Presentations of Pyruvate Dehydrogenase Deficiency: Combined Case Studies

Background: The pyruvate dehydrogenase (PDH) complex is essential in the glycolytic conversion of pyruvate to acetyl-CoA. This reaction helps yield adenosine triphosphate (ATP) – a source for energy. Hence, PDH deficiency will lead to metabolic dysfunction. Case: The case report at hand unearths the perplexing presentation of two genetically predisposed Emirati siblings that were found to be thiamine responsive. Both patients complained of a variety of symptoms at the same age following an episode of gastritis. They undergo extensive laboratory tests and imaging and are initially diagnosed with non-alcoholic Wernicke encephalopathy (WE). Objective: It has come to our attention that this rapidly debilitating condition demonstrates a constellation of seemingly incongruent gastrointestinal and neuropsychiatric manifestations. It is imperative that the peculiarities of this disease be recognized. Because PDH deficiency does not conform to defined diagnostic criteria outlined in evidence-based guidelines, treatment is likely to be delayed. Method: A careful retrospective scrutiny of the patients’ initial presentation and peculiar hospital course encourages identification of our limitations in providing efficacious quality care and in hopes of devising a systematic approach for future encounters. Conclusion: Any patient presenting to the emergency department with prolonged vomiting or diarrhea, for example, should be given thiamine as it is safe, inexpensive and may be lifesaving. We herein report two patients with indistinct, yet similar, signs and symptoms.

Psychogenic anorexia and non-alcoholic Wernicke's encephalopathy: Complete clinicoradiological recovery with thiamine

Rationale: Prolonged undernutrition may arise out of depression and lead to Wernicke's encephalopathy if timely diagnosis and intervention are missed. Wernicke's encephalopathy is potentially treatable, and appropriate treatment may revert clinical depression and cognitive dysfunction to some extent.Patient's concern: A 69-year-old female who had been taking escitalopram for one year developed tremor, ophthalmoplegia, ataxia, progressive cognitive decline, and convulsions. Diagnosis: Non-alcoholic Wernicke's encephalopathy and hypomagnesemia due to psychogenic anorexia.Interventions: High dose intravenous thiamine and magnesium were supplemented.Outcomes: The patient showed remarkable improvement in neurological complications and even in depressive features. Lessons: Wernicke's encephalopathy should not be ignored in the treatment of depression.

Editorial introductions

Editorial introductions

Nonalcoholic Wernicke's encephalopathy: a retrospective study of 17 cases.

ObjectiveNonalcoholic Wernicke’s encephalopathy (WE) is a devastating neuropsychiatric syndrome caused by thiamine deficiency. Although many case reports on WE have been published, more studies are required to guide the diagnosis and treatment of nonalcoholic WE.MethodsWe retrospectively studied patients who were diagnosed with WE in our hospital. Data on demographics, possible causes, phenomenology, and diagnostic and treatment delays were abstracted from medical records by chart reviews.ResultsSeventeen patients were diagnosed with nonalcoholic WE. Nonalcoholic WE had many causes, such as gastrointestinal surgery, gastrointestinal tract diseases, vomiting, and psychiatric diseases. Most patients presented with abnormal mental symptoms, including those in a coma.ConclusionIn summary, we recommend using operational criteria to diagnose and treat nonalcoholic WE as early as possible to avoid misdiagnosis and treatment delays. Nonalcoholic WE remains a clinical diagnosis, and certain examinations are helpful for this diagnosis, such as measuring serum thiamine concentrations. We should focus on patients who present with abnormal mental symptoms, even those in a coma, and administer parenteral thiamine before any carbohydrate to reduce the high frequency of residual morbidity.

Clinical characteristics and magnetic resonance imaging findings in nine patients with nonalcoholic Wernicke's encephalopathy: a retrospective study.

PurposeWernicke’s encephalopathy (WE) is a severe neurological disorder caused by thiamine deficiency. The most common cause of WE is alcoholism. However, there is a significant paucity of information in the existing literature relating to nonalcoholic WE. In this study, we investigated the clinical characteristics and neuroimaging findings of nine patients with nonalcoholic WE.Patients and methodsWe retrospectively collated clinical data from nine patients who had been diagnosed with WE in accordance with established criteria including age, gender, risk factors and clinical manifestations. We also collated initial hematological and neuroimaging findings.ResultsThe mean age of the nine patients was 54.0±17.1 years; four of these patients (44.4%) were male. All nine patients had a history of fasting (range, 5–47 days) prior to WE. Four of the nine patients (44.4%) exhibited the classical triad, and eight (88.9%) showed alterations in mental status. Magnetic resonance imaging (MRI) scans showed that all nine patients had symmetric lesions of the medial thalamus. MRI also revealed other WE-related lesions in mammillary bodies (22.2%), the periaqueductal region (55.6%), the tectal plate of the midbrain (77.8%), cranial nerve nuclei (77.8%) and in the symmetric subcortical white matter (11.1%).ConclusionOur analysis showed that fasting is a common cause of WE in nonalcoholic patients and that MRI is a useful tool for the diagnosis of WE. The most common MRI findings were symmetrical lesions of the medial thalamus lesions, followed by the tectal plate of the midbrain and cranial nerve nuclei.

Refeeding Syndrome and Non-Alcoholic Wernicke’s Encephalopathy in a Middle-aged Male Initially Presenting with Gallstone Pancreatitis: A Clinical Challenge

Wernicke’s Encephalopathy (WE) is a neurological condition characterized by ophthalmoplegia, ataxic gait, and altered mental status. It is an underdiagnosed yet severely limiting disease process precipitated by thiamine deficiency. Often times, it can occur in conjunction with other disease states like refeeding syndrome in which the underlying etiology is prolonged periods of malnutrition. We present a unique case of non-alcoholic WE in a middle-aged male who initially presented with gallstone pancreatitis complicated with severe metabolic derangements. This ultimately resulted in the development of non-alcoholic WE. Prevention of this condition is a clinical challenge for most physicians as the classic features associated with thiamine deficiency lack diagnostic sensitivity and specificity in critically ill patients. As a result, early recognition and prompt management of this can dramatically decrease morbidity and mortality. Our case highlights and emphasizes the importance of maintaining a high index of suspicion for WE and refeeding syndrome in the setting of altered sensorium and metabolic derangements.

Cognitive and Motor Impairment Severity Related to Signs of Subclinical Wernicke's Encephalopathy in HIV Infection.

Wernicke's encephalopathy (WE) is a neurological condition resulting from thiamine deficiency. Although commonly associated with alcoholism, nonalcoholic WE has been described in individuals with HIV infection, but subclinical WE may be underdiagnosed. The current study questioned whether the presence of subclinical WE signs underlies cognitive and motor deficits in HIV individuals as observed in alcoholism. Fifty-six HIV-positive individuals (HIV+) and 53 HIV-negative controls (HIV-) were assessed on 6 cognitive and motor domains: attention/working memory, production, immediate and delayed episodic memory, visuospatial abilities, and upper-limb motor function. Based on a rating scheme by Caine et al, HIV+ individuals were categorized by subclinical WE risk factors (dietary deficiency, oculomotor abnormality, cerebellar dysfunction, and altered mental state). Performance was expressed as age- and education-corrected Z-scores standardized on controls. Sorting by Caine criteria yielded 20 HIV+ as Caine 0 (ie, meeting no criteria), 22 as Caine 1 (ie, meeting one criterion), and 14 as Caine 2 (ie, meeting 2 criteria). Comparison among HIV+ Caine subgroups revealed a graded effect: Caine 0 performed at control levels, Caine 1 showed mild to moderate deficits on some domains, and Caine 2 showed the most severe deficits on each domain. This graded severity pattern of performance among Caine subgroups suggests that signs of subclinical WE can partly explain the heterogeneity in HIV-related cognitive and motor impairment. This study highlights the utility of Caine criteria in identifying potential causes of HIV-related neurocognitive disorders and has implications for disease management.

Editorial introductions

Editorial introductions

Non-alcoholic Wernicke's encephalopathy: from MRI findings of a case to differential diagnosis checklist

Non-alcoholic Wernicke's encephalopathy: from MRI findings of a case to differential diagnosis checklist

Korsakoff Syndrome in Non-alcoholic Psychiatric Patients. Variable Cognitive Presentation and Impaired Frontotemporal Connectivity.

Background: Non-alcoholic Wernicke's encephalopathy and Korsakoff syndrome are greatly underdiagnosed. There are very few reported cases of neuropsychologically documented non-alcoholic Korsakoff syndrome, and diffusion tensor imaging (DTI) data are scarce.Methods: We report clinical characteristics and neuropsychological as well as radiological findings from three psychiatric patients (one woman and two men) with a history of probable undiagnosed non-alcoholic Wernicke's encephalopathy and subsequent chronic memory problems.Results: All patients had abnormal neuropsychological test results, predominantly in memory. Thus, the neuropsychological findings were compatible with Korsakoff syndrome. However, the neuropsychological findings were not uniform. The impairment of delayed verbal memory of the first patient was evident only when the results of the memory tests were compared to her general cognitive level. In addition, the logical memory test and the verbal working memory test were abnormal, but the word list memory test was normal. The second patient had impaired attention and psychomotor speed in addition to impaired memory. In the third patient, the word list memory test was abnormal, but the logical memory test was normal. All patients had intrusions in the neuropsychological examination. Executive functions were preserved, except for planning and foresight, which were impaired in two patients. Conventional MRI examination was normal. DTI showed reduced fractional anisotropy values in the uncinate fasciculus in two patients, and in the corpus callosum and in the subgenual cingulum in one patient.Conclusions: Non-alcoholic Korsakoff syndrome can have diverse neuropsychological findings. This may partly explain its marked underdiagnosis. Therefore, a strong index of suspicion is needed. The presence of intrusions in the neuropsychological examination supports the diagnosis. Damage in frontotemporal white matter tracts, particularly in the uncinate fasciculus, may be a feature of non-alcoholic Korsakoff syndrome in psychiatric patients.

Editorial introductions

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Correction to: Non-alcoholic Wernicke's encephalopathy with cortical involvement and polyneuropathy following gastrectomy.

In the original publication of the article, author name Hong-Shiu Chang was incorrectly written as Hong-Chiu Chang.

Hypomagnesaemia as a trigger of relapsing non-alcoholic Wernicke encephalopathy: a case report

Hypomagnesaemia as a trigger of relapsing non-alcoholic Wernicke encephalopathy: a case report

Nonalcoholic Wernicke's Encephalopathy: A Retrospective Study from a Tertiary Care Center in Northern India.

Objective:The objective of this study was to describe the demographic features, clinical presentation, and management and outcome of fifty cases of nonalcoholic Wernicke's encephalopathy from a tertiary care hospital of a region with reported incidence of thiamine deficiency disorders.Materials and Methods:In a retrospective study, fifty adult cases of Wernicke's encephalopathy were analyzed. The diagnosis of Wernicke's encephalopathy was made according to the European federation of neurological societies guidelines 2010. Response to thiamine replacement and associated brain magnetic resonance imaging (MRI) findings were also considered as supportive evidence.Results:The mean age of patients was 50.38 years with 20 males and 30 females. The most common clinical manifestations were alteration in sensorium in 30 (60%), ataxia in 18 (36%), memory impairment in 15 (30%), nystagmus in 35 (70%), ophthalmoparesis in 11 (22%), and seizures in 4 (8%). A total of 42 patients had a history of recurrent vomiting. All patients had polished rice as their staple diet. Thirty-five patients had associated polyneuropathy and 15 had a gastrointestinal disorder. Twenty patients underwent MRI which showed both typical and atypical lesions. Majority of patients showed partial or complete response to intravenous thiamine. On discharge, the most common residual symptoms were lower limb weakness, ataxia, and memory impairment.Conclusion:The study shows high incidence of nonalcoholic Wernicke's encephalopathy in the region with predominant causative factor being a thiamine deficient diet. Recurrent vomiting can be a prominent early symptom of thiamine deficiency and its recognition can help in the early diagnosis of Wernicke's encephalopathy and related thiamine deficiency disorders. Thiamine fortification of food should be done in areas with reported incidence of thiamine deficiency disorders.

It’s Easy to Spot When You Know What to Look for: 18 Cases of Nonalcoholic Wernicke Encephalopathy

Renal transplant recipients are at an increased risk of developing verrucae due to chronic immunosuppression, and certain therapies may confer a greater risk. Herein, we describe a 51-year-old woman with a 10-year-old unrelated kidney transplant who developed numerous therapy-resistant verrucae while on mycophenolate mofetil and tacrolimus maintenance immunosuppression. Over several years of immunosuppressant therapy, she declined the approach of reducing her mycophenolate mofetil dose to potentially improve her verrucae. Unfortunately, she later developed graft rejection requiring reversion to peritoneal dialysis. Within months of reducing her mycophenolate mofetil dose (her tacrolimus dose remained unchanged), she experienced dramatic resolution of many of her verrucae. In the current case, the observed clinical improvement may have resulted from either the total reduction of immunosuppression or the specific reduction of mycophenolate mofetil. Consequently, mycophenolate mofetil may contribute to the refractory nature of verrucae within renal transplant recipients, and further research should determine the relationship between verrucae development and both specific immunosuppressant therapies and the degree of immunosuppression.