Thiamine Replacement Research Articles

Thiamine deficiency in diabetes, obesity and bariatric surgery: Recipes for diabetic ketoacidosis.

Diabetic ketoacidosis (DKA) is a life-threatening condition affecting individuals with diabetes characterised by hyperglycaemia, metabolic acidosis and ketonemia. The incidence and financial burden of DKA is still high. Thiamine deficiency is well documented in patients with DKA and could be associated with cardiac dysfunction in those patients. Thiamine deficiency leads to cardiac dysfunction, neuronal death and worsens the prognosis of DKA. There is an existing metabolic relationship between thiamine deficiency in diabetes, obesity and bariatric surgery. Careful monitoring of thiamine, along with other vitamins, is essential for diabetic patients, obese individuals and postbariatric surgery. Further research and clinical studies are urgently needed to assess the following: (1) Whether diabetes, obesity and bariatric surgery make individuals more prone to have DKA related to thiamine deficiency and (2) Whether supplementation of thiamine can protect diabetic patients, obese subjects and individuals undergoing bariatric surgery from DKA. This review summarises the biochemistry of thiamine and the existing metabolic relationships between thiamine deficiency in DKA, diabetes, obesity and bariatric surgery. Primary and family physicians have an important role in ensuring adequate replacement of thiamine in individuals with diabetes, obesity and bariatric surgery.

Wernicke Syndrome: Case Report and Literature Review of Contributing Factors—Can Malpractice Dynamics Be Identified?

Wernicke Encephalopathy (WE) is a neurological acute syndrome related to vitamin B1 deficiency and is relatively common in patients with chronic alcoholism. In the case of Hyperemesis Gravidarum, thiamine body stores become unable to meet the increased demand, resulting in acute deficiency. WE is associated with typical clinical and radiological findings. Treatment pathways rely on thiamine replacement. The case herein reported is centered around a 33-year-old diabetic patient at 12 weeks of gestation, with WE due to hyperemesis gravidarum. The disease manifested itself with weakness, mental confusion, headache, and impaired vision. The diagnosis was established after the detection of typical findings by MRI. Thirty days after therapy was started, most of the patient’s neurological disorders were resolved. The patient was discharged 40 days later with instructions to continue daily thiamine supplementation. The pregnancy outcome was good. Unfortunately, mild ataxia persisted in 2-year follow-up as a long-term consequence. When diagnosed and treated, WE has a favorable prognosis. However, roughly 80% of patients experience memory loss, which may continue for a long time, while gait disorders reportedly affect about 35% of patients. Mild ataxia and dysmetria may persist, too. We reviewed the scientific literature on WE in women with HG until February 2023. Hardly any authors report data on long-term sequelae. Our report emphasizes how important it is to take into consideration this complication in clinical practice, referring to published guidelines and recommendations. Neurological maternal sequelae can demonstrably persist despite early diagnosis and appropriate management. For this reason, a long-term follow-up is recommended. Wernicke syndrome management cannot yet rely on well-established conclusive guidelines; hence, a cautionary approach ought to be prioritized in order to ensure medicolegal soundness.

Síndrome de realimentação no desnutrido grave: os desafios nutricionais

INTRODUCTION: Refeeding Syndrome (RS) is a set of signs and symptoms that occur in a situation of abrupt nutrient supply in malnourished or starving children and adults. Its incidence in pediatrics is unknown and is underreported due to underdiagnosis or insufficient monitoring. Hypophosphatemia is the most characteristic analytical finding of SR, although it is not always present. Hydro-electrolyte disturbances such as hypokalemia and hypomagnesemia can produce cardiac, muscular, and neurological changes with a risk of serious complications. OBJECTIVE: To warn of the severity of this syndrome and to identify patients at risk. CASE REPORT: A 3-year and 5-month-old patient with chronic nonprogressive encephalopathy (CPE), BMI: 10.9 (Z-score -4.76) sought emergency care due to irresponsiveness and pallor. He was hypotheremic, hypoglycemic, and had isochoric and punctiform pupils. After initial management, the patient evolved with eye movement and limb mobility. Laboratory tests were ordered with mild anemia, hospital admission was requested, and a polymeric diet was started via gastrostomy 180ml every 3/3 hours. The patient evolved with hypokalemia, hypomagnesemia, and severe hypophosphatemia. A diagnosis of SR was made and thiamine replacement, correction of hydroelectrolytic disturbances and reduction of the diet was initiated with slow progression. CONCLUSION: The main tool to avoid SR is to perform an adequate prevention. To do this, one should initially identify patients at risk, perform a biochemical evaluation, and progress the diet carefully and slowly. Vitamin supplementation is necessary, especially thiamine.

ЭНЦЕФАЛОПАТИЯ ВЕРНИКЕ ПОСЛЕ БАРИАТРИЧЕСКОЙ ОПЕРАЦИИ: СЛУЧАЙ ИЗ ПРАКТИКИ

Objective: To review the signs and symptoms of Wernicke encephalopathy (WE) after bariatric surgery based on 2 case reports and a literature data analysis. Methods: We present two case reports of WE. In these patients, thiamine deficiency developed due to bariatric gastric surgery, which was performed to treat class III obesity, formerly known as morbid obesity. The patients underwent comprehensive physical and neurological examinations; clinical, laboratory, and instrumental data were collected from medical records and analyzed. The researchers also performed a computerized search using the keywords "Wernicke encephalopathy after bariatric surgery" to find relevant publications in the PubMed/Medline, Scopus, and Web of Science databases. Results: The presented acute neurological condition related to vitamin B1 deficiency in two patients after undergoing a weight loss surgery, specifically a mini-gastric bypass. The clinical picture in one patient was dominated by memory impairment, ataxic, and polyneuritic syndrome, while in the other, it was only polyneuritic syndrome. Conclusion: The initial symptoms of WE are often overlooked, leading to the progression of the disease with the development of severe neurological deficits. To prevent the progression of encephalopathy, it is necessary to begin treatment with high doses of parenteral thiamine replacement therapy as early as possible. Keywords: Obesity, bariatric surgery, Wernicke encephalopathy, thiamine, case report

Celiac disease in a teenager revealed with Wernicke Encephalopathy

Background: Wernicke encephalopathy is an acute neurological condition defined by a clinical triad of ophthalmoplegia, ataxia, and confusion. This disease is due to thiamine deficiency. Case presentation: After persistent diarrhea and vomiting, a 15-year-old boy presented up-beating nystagmus, with binocular vertical diplopia and unstable gait. An etiological workup revealed a celiac disease. Magnetic resonance imaging showed bilateral periaqueductal region lesions. Treatment and discussion: Because of suspected Wernicke’s encephalopathy, the patient was treated with thiamine replacement and significant improvement of symptoms took place. Wernicke encephalopathy is a serious medical disorder with enormous morbidity and mortality. Evaluation should include patient history with a physical and ophthalmologic examination and laboratory workup with appropriate imaging. Conclusion: Undiagnosed celiac disease can lead to malabsorption of vitamin B1 causing acute symptoms of Wernicke encephalopathy.

Alcoholic ketoacidosis evaluated with a point-of-care capillary beta-hydroxybutyrate measurement device.

The diagnosis of alcoholic ketoacidosis (AKA) has traditionally been made based only on clinical history and the presence of severe metabolic acidosis with a high anion gap (AG); however, the concentration of beta-hydroxybutyrate (BOHB), a pivotal ketone body in AKA, is not evaluated in most cases. The aim of this study was to clarify the clinical spectrum of AKA in terms of the severity of ketoacidosis by using a point-of-care capillary BOHB measurement device. This retrospective case series was conducted at a Japanese private teaching hospital. Patients with suspected AKA, based on their clinical history, who underwent BOHB measurement using a point-of-care capillary measurement device in the emergency department, were included. Data on their clinical presentations, blood tests, and treatments were collected, described, and compared between patients with a BOHB concentration higher than 3.0mmol/L (H-BOHB) and those with a concentration less than 3.0mmol/L (L-BOHB). A total of 83 patients were included in this study. Sixty-eight patients were categorized as having H-BOHB and 15 as having L-BOHB. Nausea (71%), vomiting (71%), tachycardia (76%), and tachypnea (46%) were commonly observed at presentation. Hyponatremia (46%), hypokalemia (34%), hypomagnesemia (42%), and hyperphosphatemia (41%) were frequent electrolyte abnormalities upon presentation. Rehydration with balanced crystalloids and glucose-containing intravenous fluids, electrolyte supplementation, and thiamine replacement were the major treatments. The mean length of stay in the ICU and hospital were 4.4 and 7.0 days, respectively, with low overall mortality (1%). The H-BOHB and L-BOHB groups did not differ in terms of clinical data. Seventy percent of patients with L-BOHB had severe metabolic acidosis with a high AG due to hyperlactatemia (mean lactate concentration: 8.5mmol/L). We described the clinical features of AKA measured by using a point-of-care capillary BOHB measurement device. Although certain patients diagnosed with AKA based only on their clinical history had predominant lactic acidosis with minor elevations in BOHB concentration, the BOHB concentration had no effect on the clinical spectrum of AKA in this study.

Wernicke-Korsakoff Syndrome associated with hyperemesis gravidarum and fetal death: Case report and literature review

We describe a clinical case of a pregnant patient with hyperemesis gravidarum who progressed to abortion, Wernicke's encephalopathy, and Korsakoff's psychosis, all related to thiamine deficiency. The patient presented symptoms of disorientation, nonspecific limb movements, and fever, initially treated with metronidazole and ceftriaxone for suspected infected abortion. Subsequently, the patient was diagnosed with retained and infected abortion, and thiamine replacement therapy was initiated with an intravenous loading dose of 900 mg/day. During hospitalization, the patient presented with tetraparesis, nystagmus, decreased level of consciousness, anterograde and retrograde amnesia, confabulation, and aphasia. Magnetic resonance imaging showed lesions in the pons, typical of Wernicke's encephalopathy. The patient was empirically treated with acyclovir and ampicillin and showed clinical improvement. The text also provides a brief narrative review of the literature on the topic.

Wernicke encephalopathy in a malnourished, depressed 16-year-old male

BackgroundWernicke encephalopathy (WE) is an acute neurological disorder characterized by a triad of confusion, ophthalmoplegia, and ataxia secondary to thiamine deficiency most commonly seen in adults with severe alcoholism. In the pediatric population, WE is rare though has been reported in patients with anorexia nervosa, malignancy, intensive care unit stays, and parenteral nutrition.[1] PurposeTo describe a case of WE in a 16-year-old male patient with severe malnutrition in the setting of depression MethodsThe patient and guardian/family were interviewed. Literature relevant to the case was reviewed prior to and after the diagnosis. PatientIn this report we present a 16-year-old male with depression in the setting of a 17-kilogram weight loss over a 2-month period. He reports not eating much after moving out of his guardian's home because he did “not want the other people he was living with to not have food.” He presented clinically with confusion, dysarthria, ophthalmoplegia, nystagmus, memory impairment and gait instability. Magnetic resonance imaging (MRI) demonstrated hyperintense signals along the margins of the third ventricle and cerebral aqueduct. Laboratory work confirmed low thiamine levels. This overall presentation was consistent with Wernicke's encephalopathy. Intravenous thiamine followed by parenteral thiamine replacement and nutritional support contributed to the recovery of his ataxia, nystagmus, confusion, dysarthria, and improvement of memory impairment over a 1 week hospitalization. ConclusionThe reported case of WE was likely secondary to severe depression and decreased food intake. WE should be considered in pediatric patients with depression. Initiation of thiamine therapy should be considered in cases of significant confusion after following a negative stroke protocol.

Acute Thiamine Deficiency Detected by Video Head Impulse Test in a Patient with Gastric Mucosa-Associated Lymphoid Tissue (MALT) Lymphoma

Thiamine deficiency may cause Wernicke encephalopathy (WE) characterized by ataxia, ophthalmoplegia, and confusion. Aside from the triad of cardinal symptoms, selective or predominant impairments of bilateral horizontal canals may be observed in WE. Here, we report a patient with gastric mucosa-associated lymphoid tissue (MALT)-lymphoma complicated by an early stage of WE due to thiamine deficiency manifesting bilateral vestibular dysfunctions. A 78-year-old man recently diagnosed gastric MALT-lymphoma presented with dizziness and disequilibrium for several weeks. He showed mild imbalance while tandem walking and abnormal catch-up saccades bilaterally during bedside head impulse test (HIT). Video HIT revealed decreased vestibulo-ocular reflex gains with catch-up saccades for the bilateral horizontal and several vertical canals. Diagnostic work-up demonstrated decreased serum thiamine and lesions in the mammillary body and periaqueductal gray matter on brain magnetic resonance images. Furthermore, with thiamine replacement, his clinical symptoms were markedly improved. Also, vestibular symptoms and signs may be an early manifestation of WE, and video HIT could be a useful diagnostic tool to aid early detections.

Abstract #1404234: Hypoglycemia & Lactic Acidosis Due to Warburg Effect

Warburg effect (Aerobic Glycolysis) is a form of cellular adaptation by cancer cells to support its biosynthetic requirement, when in the presence of abundant oxygen and mitochondria, cell utilizes anaerobic pathway to convert glucose to lactate producing only 2 ATP’s. This phenomenon has been studied extensively and clinically can results in high glucose uptake by the tumor cells causing hypoglycemia and type B lactic acidosis. 41-year-old male with no PMHx admitted with weakness, instability, vision changes and unintentional 30 lbs weight loss x 3 months. In the ER he was found to be have BP 90/60, HR 113 and afebrile with Glucose of 20, lab showed AKI with lactic acidosis (Cr. 2.17 and lactic acid >10) and CT Abd/Plv showed multiple liver metastatic disease and entrocolitis. Started on IV fluids with dextrose, Pressor support, Antibiotics and admitted to ICU for care. Workup showed HIV positive and antibiotics coverage was broadened. Kidney function continued to worsen and started on CRRT. Patient’s hypoglycemia persisted despite dextrose infusion and endocrine team was consulted. Work up showed appropriately low insulin & c-peptide with negative sulfonylurea screen. Biopsy of liver confirmed Large B-Cell Lymphoma, but not a candidate for therapy due to acute illness. Patient lactic acidosis persisted >10 despite therapy suggestive of Type B lactic acidosis. Family changed goals of care & patient passed away within 48 hours of comfort care measures. Presence of hypoglycemia and lactic acidosis is a medical emergency suggesting hyper metabolic state with poor tissue oxygenation, mostly caused by severe inflammatory resulting in Type A Lactic Acidosis. Rarely this is seen in normoxic condition called Type B Lactic acidosis and one of the potential causes is Warburg effects, in patients with solid and hematological malignancy. This is triggered by oncogenic lesions such as expression of hypoxia-inducible factor-1α (HIF1α) causing up regulation of major glycolytic enzymes like hexokinase and Tumor M2 Pyruvate Kinase. This provides cancer cell with metabolic intermediates required for synthesis of cellular components for cell proliferation and also produces less amounts of free radicals. Proliferating cancer cells also outpace the vascular supply and warburg effect ensures survival in the hypoxic environment. Patients with type B lactic acidosis and hypoglycemia poses grim prognosis with mortality around 75% (7 out of 29 patient survivals, in chart review of cases). Therapeutic measure includes: tumor directed therapies, IV Bicarb Infusion, IV Dextrose, Renal Replacement Therapy and Thiamine replacement. Purpose of this case presentation is to further enhance clinical evidence of Warburg effect.

Nystagmus Response to Thiamine Replacement, a Predictor of Wernicke-Korsakoff (WE) Syndrome Outcome. A 21-patient Cohort Study (S12.002)

<h3>Objective:</h3> To identify an easily recognizable clinical marker of thiamine deficiency to procure timely diagnosis <h3>Background:</h3> Wernicke’s Encephalopathy (WE) treatment outcome depends on genetic factors, duration of insufficient thiamine, metabolic demand and comorbidities. Nystagmus is by far the most frequent ocular motor finding abnormality in thiamine deficiency. Its response to treatment predicts outcome. <h3>Design/Methods:</h3> This is a retrospective series of 21-patient cohort, 16 acute patients, studied as on-going acute vestibular syndrome/ataxia cohort (two telemedicine), and 5 outpatients. All underwent neurological and neurophthalmologic examination and nystagmus recordings, they had at least one abnormal ancillary test; low serum pre-treatment thiamine, or abnormal head MRI. <h3>Results:</h3> Nine patients had horizontal (h) nystagmus (two types: vestibular and gaze holding nystagmus); thiamine replacement led to rapid nystagmus resolution, and prevented encephalopathy in all (including one, who had also upbeat nystagmus/truncal ataxia (UBN/TA), one patient has chronic UBN/TA for one year with improving WE at a slower pace. Six patients had conversion from UBN to permanent downbeat nystagmus/truncal ataxia (DBN/TA), and slower WE recovery; one patient had improved UBN/TA. Three outpatients with permanent DBN/TA had a previous history and labs compatible with thiamine deficiency. One patient did not have nystagmus. None of the study-cohort patients developed Korsakoff’s syndrome (KS). <h3>Conclusions:</h3> In patients at WE risk, h-nystagmus was the earliest sign of thiamine deficiency in this cohort, had the fastest response to thiamine, which also prevented WE. Vertical nystagmus had longer WE recovery, and six patients had enduring DBN/TA. Interestingly, none of the 21 patients developed KS. This series highlight the key role of nystagmus analysis in thiamine deficiency. Adding nystagmus to Caine’s diagnostic criteria may enhance the early features of thiamine deficiency. <b>Disclosure:</b> Dr. Kattah has received personal compensation in the range of $500-$4,999 for serving as an Expert Witness for Bonezzi, Switzer , Poilitto and Hupp Legal Firm.

Wernicke-Korsakoff Syndrome in a Young Adult on Dialysis Who Showed Bilateral Ganglia Lesions: A Case Report.

A 30-year-old man admitted with renal dysfunction (serum creatinine, 8.19 mg/dL) was diagnosed with immunoglobulin A nephritis through a renal biopsy. He was treated with intravenous methylprednisolone pulse therapy and urgent hemodialysis, and eventually, he underwent maintenance hemodialysis. On day 108, he developed amnesia. Magnetic resonance imaging revealed bilateral basal ganglia lesions. Wernicke encephalopathy (WE) was diagnosed based on decreased serum thiamine concentration (12.8 μg/dL; reference range, 24-66 μg/dL). Thiamine replacement therapy was initiated, but the Wernicke-Korsakoff syndrome persisted. Careful monitoring of thiamine is required in patients undergoing dialysis. In addition, patients with WE may exhibit bilateral basal ganglia lesions.

Cerebellar restricted diffusion in Wernicke's encephalopathy.

A 50-year-old woman presented to an outside hospital for acute onset bilateral lower limb pain. She was diagnosed with aortoiliac stenosis and underwent stent placement. Post-procedure, she was noted to have altered mental status, truncal ataxia, neck titubation, and incomplete external ophthalmoplegia. She rapidly declined to a stuporous state. She had a history of uterine cancer treated with chemoradiation which was complicated by chronic radiation enteritis. She was also reported to have poor oral intake, recurrent emesis, and weight loss for a month before her presentation. After an extensive work up, she arrived at our facility where an MRI of the brain showed restricted diffusion and T2-FLAIR sequence showed hyperintensities of bilateral cerebellum. T2-FLAIR hyperintensities of bilateral dorsomedial thalami, fornix, and post-contrast-enhancement of mammillary bodies were also noted. The clinical picture with imaging findings was concerning for possible thiamine deficiency. In Wernicke's encephalopathy, restricted diffusion, T2-FLAIR hyperintensities, and contrast enhancement may be seen in mammillary bodies, dorsomedial thalami, tectal plate, periaqueductal grey matter, and rarely in the cerebellum as well. Her thiamine level was 70 nmol/l (reference range: 70-180 nmol/l). Thiamine levels can be falsely elevated in patients who are on enteral feeds, which was the case in our patient. She was started on high dose thiamine replacement. At time of discharge, repeat MRI brain revealed resolution of cerebellar changes with mild atrophy and patient had subtle neurological improvement including consistent eye opening, tracking, and attending to examiner, as well as mumbling words.

Is there a time window for MRI in Wernicke encephalopathy - a decade of experience from a tertiary hospital.

Wernicke encephalopathy (WE) is a neuropsychiatric syndrome caused by thiamine deficiency. Despite its low sensitivity, brain magnetic resonance imaging (MRI) is the most useful diagnostic technique. Our aim was to investigate whether the timing of the imaging study, and thiamine replacement can influence brain MRI findings in these patients. Retrospective observational study of hospitalized patients between January/2008 and December/2020 with a clinical diagnosis of WE. Data from clinical presentation, diagnostic features, therapeutic approach, and outcomes were collected. We identified 41 patients (55 ± 13.3years) with WE. Brain MRI was performed in 36 patients, and one third had T2/FLAIR hyperintensities suggestive of WE. We found an association between a history of poor diet and periventricular hyperintensities (p = 0.023), especially on the ventral surface of the thalamus and the periaqueductal region. It was found that the odds of having a typical imaging of WE decreased by 5.3% for each additional unit (100mg) of thiamine administered (p = 0.046)(95% CI [0.89, 0.99]). On the other hand, the number of days from clinical presentation was not found to be a viable predictor (p = 0.254) (95% CI [0.88, 1.03]) Recovery was positively correlated with the total dose of thiamine received until discharge (p = 0.020). MRI hyperintensities seem to be dependent on the timing of thiamine correction and, particularly, on the thiamine dosage prescribed at admission. Nevertheless, thiamine replacement should not be delayed, as its timely prescription is associated with a better prognosis at discharge.

Wernicke encephalopathy with epileptic seizures during pregnancy

ABSTRACT A 22-year-old woman was admitted to the emergency department with headache, dizziness, and numbness on the left side of the body. Neurologic examination revealed gaze-evoked nystagmus. Cranial magnetic resonance imaging, venous and arterial magnetic resonance angiography were normal. Generalized epileptogenic activity was observed in the electroencephalography. The erythrocyte thiamine transketolase levels were found to be 13 u/L. She received intravenous thiamine. On discharge, she had no neurologic sequelae. The diagnosis of Wernicke encephalopathy in our patient is based on increased thiamine requirement due to pregnancy, nystagmus, low transketolase level, and reversal of symptoms after thiamine replacement. .

Recurrent Diabetic Ketoacidosis following Bariatric Surgery: The Role of Micronutrients

We report a case of a 29-year-old woman admitted twice to our hospital with diabetic ketoacidosis (DKA) within 45 days following her bariatric surgery. The first admission required intensive care during her postoperative days after bariatric surgery. Subsequently, she continued to report high level of ketones on a daily basis. At her second admission, she presented with all three criteria of DKA. She was treated with a standard protocol for DKA, but ketones plasma level remained high despite significant improvement in pH and glycemic control. The administration of thiamine replacement was associated with normalization of the hyperketonemia. Thiamine deficiency can be associated with bariatric surgery and can lead to high ketone level in individuals with type 1 diabetes.

Teaching NeuroImage: Nonalcoholic Wernicke Encephalopathy.

A 40-year-old woman with chronic gastritis who did not have alcoholism had lost 50 pounds in the past 45 days and presented with dyscoordination and diplopia. Examination showed confabulation, ophthalmoplegia, nystagmus, and appendicular ataxia. Brain MRI (Figure) showed diffusion-weighted imaging and fluid-attenuated inversion recovery abnormalities suggestive of Wernicke encephalopathy (WE). With classic triad of WE and MRI findings, IV thiamine 500 mg TID was administered for 3 days, followed by maintenance oral thiamine. The patient showed substantial improvement. Thiamine replacement therapy should be considered in patients with malnutrition or malabsorption as it is important in maintaining cellular osmotic gradients. Thiamine deficiency may lead to cytotoxic edema, especially in high metabolic demand regions such as thalami and mammillary bodies.1

Efficacy of Thiamine in Patients with Clinically Suspected Dry Beriberi: An Open Labeled Hospital Based Study

Background: Thiamine deficiency-related disorders are increasingly being reported in countries where polished rice is the main dietary constituent and diet is not balanced in calorie, protein, and micronutrient contents. Thiamine deficiency often associated with sensory-motor neuropathy (dry beriberi) without Wernicke’s encephalopathy and cardiac dysfunction. Objectives: The objective of our study is to evaluate the efficacy of thiamine in patients with suspected dry beriberi. Methods: This study was a prospective, open-labeled, self-controlled clinical trial (quasi-experimental study) carried out in the Neurology and Medicine Ward of Chittagong Medical College Hospital from May 2018 to April 2019. Fifty-five (55) patients of suspected dry beriberi were recruited as per inclusion and exclusion criteria. All patients were given 200mg IV Thiamine HCl per day for 1 week, then oral Tab. Thiamine 100mg twice daily for the remaining 11week. They were evaluated clinically before treatment and followed up at the end of 1 week, 6 weeks, and 12 weeks after treatment. Results: There is a significant improvement of leg swelling (p&lt;0.001), muscle cramp (p&lt;0.001), muscle power (p&lt;0.001), the total score of the Overall Neuropathy Limitation Scale (ONLS) (p&lt;0.001) within 1 week of thiamine replacement. The treatment also successfully reduced individual components of sensory impairment (i.e., pain, touch, position, vibration) from baseline to 12 weeks (p&lt;0.001). Only deep tendon reflexes did not return to normal in all patients within 12 weeks. Long-time follow-up is needed for this. Conclusion: Thiamine deficiency should be actively considered as a possible cause of peripheral neuropathy and variability of its clinical features should be taken into consideration. Thiamine is highly effective in reversing most of the clinical features of its deficiency-related peripheral neuropathy. Creating public health awareness about this disease in the community will lead to early diagnosis and treatment.

Wernicke encephalopathy complicating catatonic schizophrenia

IntroductionWernicke’s encephalopathy is a potentially fatal neurological emergency caused by thiamine deficiency. Although it is often associated with chronic alcoholism, it can also occur in all situations that lead to a thiamine deficiency such as undernutrition and exclusive artificial feeding.ObjectivesIn this work, we propose to study the clinical and treatment concerns of Wernicke’s encephalopathy complicating catatonic schizophrenia.MethodsWe retrospectively report the case of a patient who developed a Wernicke’s encephalopathy in the aftermath of catatonic schizophrenia.ResultsMr H.L, a 47-year-old-male has been followed in psychiatric hospital since the age of 27 for catatonic schizophrenia. He has been hospitalized in July 2020 because of oral intake refusal, social isolation and lack of self-care with a poor compliance to treatment. Examination of the patient revealed catalepsy, mutism and negativism. He was treated with antipsychotics drugs, benzodiazepines and parenteral nutrition. About six weeks after his hospitalization, the patient developed horizontal nystagmus and ataxic gait. Magnetic resonance imaging was consistent with Wernicke encephalopathy. Vitamin B1 dosage was 32nmol/l. Parenteral thiamine replacement therapy was initiated with clinical improvementConclusionsCatatonic schizophrenia can be associated with severe malnutrition and thus with thiamine deficiency and Wernicke’s encephalopathy. An early intervention by supplying prophylactic thiamine given parenterally in high-risk patients is crucial to avoid Korsakoff syndrome, as well as cardiovascular and neuropsychiatric complications associated with thiamine deficiency.

High-dose thiamine strategy in Wernicke-Korsakoff syndrome and related thiamine deficiency conditions associated with alcohol use disorder.

Thiamine is essential for the activity of several enzymes associated with energy metabolism in humans. Chronic alcohol use is associated with deficiency of thiamine along with other vitamins through several mechanisms. Several neuropsychiatric syndromes have been associated with thiamine deficiency in the context of alcohol use disorder including Wernicke–Korsakoff syndrome, alcoholic cerebellar syndrome, alcoholic peripheral neuropathy, and possibly, Marchiafava–Bignami syndrome. High-dose thiamine replacement is suggested for these neuropsychiatric syndromes.