Nonalcoholic Wernicke Research Articles

Treatment of nasopharyngeal carcinoma and prevention of non-alcoholic Wernicke’s disease: A case report and review of literature

BACKGROUND Wernicke encephalopathy is a neurological disorder caused by thiamine deficiency, commonly seen in alcoholic populations but also involving other circumstances that may lead to thiamine deficiency. The recognition of Wernicke encephalopathy often depends on clinicians’ keen ability to detect its typical triad of features; however, most cases do not present with the full constellation of signs, which complicates the timely identification of Wernicke encephalopathy. CASE SUMMARY This case report describes a patient with nasopharyngeal carcinoma who developed abnormal ocular function and ataxia following concurrent chemoradiotherapy, without a history of alcohol abuse. With the aid of radiological examinations, he received a timely diagnosis and treatment; however, his symptoms did not fully resolve during follow-up. CONCLUSION For patients with malignant tumors exhibiting neurological symptoms, clinicians should consider the possibility of Wernicke encephalopathy and provide prophylactic thiamine therapy.

When It Rains It Pours...: Wernicke Encephalopathy with Sudden Blindness after Bariatric Surgery in a Patient with Congenital Deafness.

Malabsorption syndromes are known chronic complications of bariatric surgery. Therefore, it is recommended to take oral supplementation with multivitamins. Wernicke's encephalopathy represents an acute neuropsychiatric syndrome associated with alcoholism or severe malnutrition; sporadic cases of this potential complication related to bariatric surgery are described in the literature. We present a case of Wernicke's encephalopathy due to severe vitamin B1 deficiency after bariatric surgery. A 31-year-old woman with deaf-mutism from the age of 3 years old, operated 3 months before with a mini-gastric bypass for severe obesity, was transferred to our unit after accessing the emergency room. In the immediate medical history, there was the sudden and rapid decline in vision, leading to complete loss of vision, marked asthenia, and paresthesia in the four limbs. Considering the previous bariatric surgery, the diagnosis of non-alcoholic Wernicke's syndrome was suspected, for which IV therapy with Vitamin B1 was started at a dosage of 5 vials of 200 mg in 100 cc of saline solution (three times a day for the first 72 hours, subsequently 1 once/day). After 12 hours, there was an improvement in visual acuity, and the symptoms completely resolved within 48 hours. She was discharged with complete resolution of all symptoms after 1 month. Initial vision loss without confusion or encephalopathy is one atypical presentation of Wernicke syndrome. Clinical suspicion must be high in case of alcoholism or post-bariatric surgery. Early recognition of atypical symptoms, including vision loss, and timely administration of therapy improves the prognosis of this potentially reversible but time-dependent neurological emergency.

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.

Non-alcoholic Wernicke’s encephalopathy in a kidney transplant recipient

Background. Non-alcoholic Wernicke’s encephalopathy occurs in various somatic conditions with thiamine deficiency, excessive excretion of thiamine, or impaired thiamine metabolism. Very few cases of this pathology have been described in chronic kidney disease (CKD). We present a unique case of non-alcoholic Wernicke’s encephalopathy in a patient with a kidney transplant is presented.Past medical history. The patient underwent kidney transplantation in 2008. Outpatient follow-up by a nephrologist was irregular. Renal graft function remained relatively stable: blood creatinine 200–240 μmol/L, estimated glomerular filtration rate 40–30 mL/min, tacrolimus plasma concentrations tended to increase (5.7–7.6–8.4–10.4 ng/mL); repeated graft biopsy (in 2015 and in 2017) determined the chronic toxicity of calcineurin inhibitors. The patient’s condition worsened in late January 2020: body temperature increased to 38°C, nausea, vomiting, loose, watery stools for up to 5 times per day, 8 kg weight loss, decreased diuresis. A few days later, double vision, shaky gait and then immobility appeared. Biochemical examination results: potassium 3.8 mmol/L, sodium 139 mmol/L, alpha-amylase 159 units/L (norm 0–100 units/L), creatinine 242 mmol/L, urea 13.2 mmol/L; ultrasound signs of pancreatitis. Magnetic resonance imaging (MRI) of the brain: bilateral diffuse lesions of the midbrain, thalamus, and cerebellum. Based on the clinical picture and on brain MRI results, Wernicke’s encephalopathy was diagnosed. Parenteral administration of thiamine had a good effect.Conclusion. Possible mechanisms of the development of Wernicke’s encephalopathy in a patient were discussed. Vigilance is required regarding this disease when metabolic disorders occur in patients with CKD.

Good Response to Thiamine in Bilateral Thalamic Infarction Simulating a Wernicke Syndrome: Does it Has a Role in Acute Stroke?

The classic clinical triad of Bilateral Thalamic Infarction is consciousness compromise, ocular motility disturbances, and cognitive deterioration; and would be an obligatory differential diagnosis of Wernicke´s Syndrome, which usually has, as clinical findings, altered mental status, ataxic gait and ophtalmoplegia. While Wernicke´s Syndrome is frequently associated with alcohol intake, it is known that there are some cases not related to alcohol consumption, these subtypes are called atypical non-alcoholic Wernicke´s Syndrome and are provoked by malnutrition as their most important etiology.

Psychogenic anorexia and non-alcoholic Wernicke's encephalopathy

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.

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.

Non-Alcoholic Wernicke’s Encephalopathy in a Middle-aged Male Presenting with Psychosis (4060)

Non-Alcoholic Wernicke’s Encephalopathy in a Middle-aged Male Presenting with Psychosis (4060)

A Case of Non-alcoholic Wernicke’s Encephalopathy and Dry Beri-beri with GI Involvement Following a Period of Prolonged Gastrointestinal Illness (1266)

A Case of Non-alcoholic Wernicke’s Encephalopathy and Dry Beri-beri with GI Involvement Following a Period of Prolonged Gastrointestinal Illness (1266)

Editorial introductions

Editorial introductions

A case of nonalcoholic Wernicke’s encephalopathy due to an extreme diet based on magnetic resonance imaging features

Wernicke’s encephalopathy is a rare occurrence in Indonesia because alcohol consumption is very low. However, in Indonesia, Wernicke’s encephalopathy could be triggered by an inadequate intake of thiamine (vitamin B1) due to an extreme diet for several months. It is a case of a 31-year-old male, who presented to the emergency room with a decreased level of consciousness. According to the family, for the last few weeks, he has become less responsive and less attentive. Fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging (MRI) revealed a unique picture with symmetrical lesions in the bilateral medial thalamus, mammillary bodies, periaqueductal gray matter, and the dorsal surface of the medulla oblongata. Clinically, there is no neck stiffness and no fever. The laboratory results from the blood and cerebrospinal fluid have ruled out meningitis. Treatment with thiamine 200 mg t.i.d. has shown an excellent response and significant clinical improvement. The earlier thiamine substitution treatment is started, the better the outcome because thiamine will prevent further injury to the brain and enhance recovery.

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.

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.