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

In this study, we present the clinical manifestations, brain magnetic resonance imaging (MRI) and concurrent polyneuropathies in two patients with non-alcoholic Wernicke's encephalopathy (WE) after gastrojejunostomy (Billroth II) anastomosis procedures. These patients developed sub-acute onset of disorientation and disturbance of consciousness following several weeks of poor intake. Peripheral neuropathy of varying severity was noted before and after the onset of WE. Brain MRI of the patients showed cerebellar vermis and symmetric cortical abnormalities in addition to typical WE changes. Electrophysiological studies demonstrated axonal sensorimotor polyneuropathy. Prompt thiamine supplement therapy was initiated and both patients gradually recovered, however mild amnesia was still noted 6 months later. We reviewed non- alcoholic WE with atypical cortical abnormalities in English language literatures and identified 29 more cases. Eight out of 31 (25.8%) patients died during follow-up. Nine patients with gait disturbance or motor paresis had showed hyporeflexia in neurological examinations. In addition to classic triad, seizure was recorded in seven patients. Dietary deprivation is a risk factor for non-alcoholic WE among elderly patients receiving gastrointestinal surgery. The prognosis is good after thiamine supplement therapy. Recognizing the MRI features and predisposing factors in patients who have undergone gastrectomy can aid in the diagnosis and management.

Wernicke Encephalopathy Associated With Semaglutide Use.

A patient presenting to the emergency room with neurological symptoms is more commonly found to have manifestations of stroke, transient ischemic attack, or nervous system injury. Alcoholic Wernicke encephalopathy (WE) is also another common manifestation of neurological dysfunction; however, the prevalence of non-alcoholic WE is relatively uncommon. We discuss a 37-year-old male who presented to the ED with dysphagia, slurred speech, word-finding difficulty, and restricted extraocular movements from non-alcoholic WE in the setting of semaglutide use.

Silent Echoes: A Case Report of Wernicke Encephalopathy's Unheard Voice.

Wernicke encephalopathy (WE) is an acute neuropsychiatric emergency that is caused by a deficiency in vitamin B1 (thiamine). This condition is most commonly seen in patients with alcohol use disorder; however, patients with other disorders of severe malnourishment are also at increased risk. In severe cases, this disease may be followed by Korsakoff's psychosis and even death.  We present a case of a 64-year-old African American female with a history of alcohol use disorder who presented to the emergency department on account of an acute confusional state. Neurological examination revealed right beating nystagmus on the left gaze and a wide-based gait. Initial laboratory work-up was unrevealing; however, magnetic resonance imaging (MRI) of the brain demonstrated an abnormal T2 fluid-attenuated inversion recovery (FLAIR) signal involving the bilateral mammillary bodies and surrounding lateral ventricles that extended into the periaqueductal parenchyma. The patient was admitted to the neurology unit, and high-dose intravenous thiamine was commenced. During hospitalization, the patient's confusion improved and they were subsequently discharged with oral thiamine. The spectrum of severity of WE is wide, ranging from fatal disease and can lead to permanent brain damage or even Korsakoff syndrome, characterized by severe memory loss and confabulation. The diagnosis is mainly clinical and based on the presence of symptoms in the classic triad of mental status change, oculomotor abnormality, and ataxia. This triad is only present in about 10% of cases, making the diagnosis very challenging. Laboratory testing can assist in making the diagnosis, but it is not always reliable or available. In situations of clinical uncertainty, imaging may also be used to support diagnosis or rule out other differentials. The mainstay of treatment is with high-dose parenteral thiamine.

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.

Non-alcoholic Wernicke's Encephalopathy Masquerading As CNS Relapse of Acute Myeloid Leukemia.

While Wernicke's encephalopathy (WE) is mostly caused by thiamine deficiency secondary to chronic alcohol use, other conditions that may affect one's nutritional status, such as bariatric surgery, hyperemesis gravidarum, chronic gastrointestinal disease, HIV/AIDS, and certain malignancies, may also lead to this outcome. We are discussing one such case, WE, in a young man with acute myeloid leukemia (AML) who underwent chemotherapy. The patient presented with blurred vision, paresthesia, weakness, and vomiting. Although he denied alcohol abuse, his symptoms, physical exam findings, and MRI results were consistent with WE. Treatment with thiamine resulted in a significant improvement in his visual disturbances and mental status. The authors highlight the importance of recognizing WE in non-alcoholic patients, particularly those undergoing prolonged hospitalization and chemotherapy, as nutritional deficiencies can develop. They recommend thiamine supplementation for patients receiving chemotherapy and those with poor oral intake. The case underscores the need for high clinical suspicion and early intervention in atypical cases of WE.

Thiamine Deficiency in a Patient With Schizophrenia: Precautions and Countermeasures for Subclinical Thiamine Deficiency.

Patients with schizophrenia often experience problems associated with ordinary exercises of life due to their mental symptoms. Those experiencing problems related to feeding behavior, in particular, are considered to be susceptible to developing Wernicke encephalopathy due to a deficiency in thiamine, the physiological stores of which are limited; however, there are few reported cases, and most of them were accompanied by the classical triad of signs. We report our experience with asymptomatic thiamine deficiency (TD) in a schizophrenia patient. A 73-year-old female was receiving medication for schizophrenia as an outpatient. No symptoms such as hallucinations or delusions were observed, the patient had a sociable personality and was able to function at a level where she could live alone. Although there were no active complaints about eating by the patient, we investigated the situation due to reports of TD in schizophrenia patients. As results revealed a significant decrease in whole blood thiamine to 19 ng/mL (reference range: 24-66 ng/mL), we administered a large dose of thiamine. No changes were observed in psychosomatic symptoms before and after administration. Patients with schizophrenia experience problems that may lead to TD, such as dietary imbalances and disturbed feeding habits. Therefore, even if patients with schizophrenia do not actively complain about their feeding behavior, it may be necessary to take medical measures such as blood sampling in consideration of the potential for developing TD.

Wernicke Encephalopathy in a Patient With Bipolar Disorder: A Case Report.

Wernicke encephalopathy (WE) is a combination of neurological findings including confusion, ataxia, and ophthalmoplegia. It is most commonly associated with patients who have a history of alcohol abuse. This aspect leads to the majority of cases going undiagnosed in non-alcoholic patients who have other potential thiamine deficiency-causing conditions such as malignancy, chronic kidney disease (CKD) on hemodialysis, hyperemesis gravidarum, and psychiatric disorders leading to starvation and malnourishment. Here we present the case of a 59-year-old female patient with decompensated bipolar disorder who came in with altered mental status and multiple syncopal episodes. On examination, she was completely confused and had a fixed gaze. She was worked up for broad differential diagnoses including stroke, arrhythmias, seizures, drug intoxication, and infections. But due to her severely malnourished appearance, Wernicke's encephalopathy was suspected early on, and she was started on thiamine therapy, to which she responded well. It was also confirmed by an MRI of the brain showing flair in the bilateral medial thalamic region. Therefore, to suspect the presence of WE in non-alcoholic patients with psychiatric disorders and to differentiate behavioral symptoms from delirium and encephalopathy is difficult and requires a high degree of clinical suspicion.

A Case of Wernicke's Encephalopathy Due to Idiopathic Gastroparesis: A Rare Cause of Encephalopathy in a Young Woman.

Wernicke's encephalopathy (WE) is a rare, life-threatening neurological disease due to thiamine deficiency. It is most commonly associated with chronic alcoholism but is also associated with disorders of malabsorption and malnutrition. We present a case of a young female with idiopathic gastroparesis who developed Wernicke's encephalopathy due to poor oral intake and malnutrition as a result of gastroparesis. This case exemplifies that Wernicke's encephalopathy should be on the differential in patients who present with encephalopathy with a history of gastroparesis.

An Unusual Case of Wernicke's Encephalopathy in a Child.

Wernicke's encephalopathy (WE) is a manifestation of thiamine deficiency. The majority of affected patients are alcoholics and are adults. Often, clinicians fail to recognize that WE can also be found in non-alcoholic patients at risk for thiamine deficiency. Sometimes patients may not present with all the classic features, or the individual clinical signs may be treated as single problems and not a constellation of signs that form a diagnosis of WE. We present a unique case of a four-year-old male with a past medical history of food aversion who presented with intractable vomiting and weakness. The patient's clinical features showed signs of severe dehydration and weight loss. His clinical state subsequently progressed to having ophthalmoplegia and gait ataxia. Brain MRI demonstrated mamillary body changes, and serum thiamine level was significantly below the normal limit. Based on the patient's clinical assessment, deficient serum thiamine, and MRI findings, WE was diagnosed. The patient was evaluated by Pediatric Neurology and started on treatment with high dose IV thiamine. He showed an excellent response to thiamine treatment and had a significant resolution in his symptoms before discharge.

Wernicke Encephalopathy in an Elderly Patient Due to Chronic Malnutrition From an Atypical Diet.

Wernicke encephalopathy has traditionally been associated with chronic alcohol abuse leading to thiamine deficiency. Clinical symptoms include mentation change, gait ataxia, and oculomotor abnormalities. However, it is often an underdiagnosed condition in patients suffering from chronic malnutrition, especially in the West. We examine a unique case of non-alcoholic Wernicke encephalopathy in an elderly patient. The patient had a long history of chronic malnutrition due to her atypical diet, consuming an unbalanced diet deprived of thiamine, unbeknownst to her. She presented with symptoms of encephalopathy, recurrent falls, and pupillary changes. After exhausting all other therapeutic interventions, she received a thiamine infusion; her mentation and other symptoms improved dramatically.  Thiamine deficiency can lead to severe complications, including Wernicke encephalopathy and cardiomyopathy. Wernicke encephalopathy can progress to Korsakoff syndrome, which is characterized by amnesia and confabulation. Case reports, such as ours, may remind clinicians to keep thiamine deficiency as a viable differential while evaluating acute encephalopathy, especially in the malnourished geriatric population.

An Unusual Presentation of Catatonia in Non-alcoholic Wernicke Encephalopathy.

Wernicke encephalopathy (WE) is an acute reaction to thiamine deficiency, which presents with the classic triad of ocular findings, cerebellar dysfunction, and confusion. However, thiamine deficiency can also present with several neuropsychiatric signs and symptoms other than the classical triad. We report a patient who presented with catatonia as a presenting feature of WE. The objective of this report is to recognize the presentation of catatonia in WE. Some cases of WE are missed by physicians; therefore, a high index of suspicion and appropriate investigations depending on presentation and clinical condition can result in prompt diagnosis and early management.