Stem Cell Therapy and Thiamine Deficiency-Induced Brain Damage.

Wernicke's encephalopathy (WE) is a major central nervous system disorder resulting from thiamine deficiency (TD) in which a number of brain regions can develop serious damage including the thalamus and inferior colliculus. Despite decades of research into the pathophysiology of TD and potential therapeutic interventions, little progress has been made regarding effective treatment following the development of brain lesions and its associated cognitive issues. Recent developments in our understanding of stem cells suggest they are capable of repairing damage and improving function in different maladys. This article puts forward the case for the potential use of stem cell treatment as a therapeutic strategy in WE by first examining the effects of TD on brain functional integrity and its consequences. The second half of the paper will address the future benefits of treating TD with these cells by focusing on their nature and their potential to effectively treat neurodegenerative diseases that share some overlapping pathophysiological features with TD. At the same time, some of the obstacles these cells will have to overcome in order to become a viable therapeutic strategy for treating this potentially life-threatening illness in humans will be highlighted.

Wernicke's Encephalopathy in Acute and Chronic Kidney Disease: A Systematic Review.

Thiamine (vitamin B1) deficiency is relatively common in patients with kidney disease. Wernicke's encephalopathy (WE) is caused by vitamin B1 deficiency. Our aim was to systematically review the signs and symptoms of WE in patients with kidney disease. We conducted a systematic literature review on WE in kidney disease and recorded clinical and radiographic characteristics, treatment and outcome. In total 323 manuscripts were reviewed, which yielded 46 cases diagnosed with acute and chronic kidney disease and WE published in 37 reports. Prodromal characteristics of WE were loss of appetite, vomiting, weight loss, abdominal pain, and diarrhea. Parenteral thiamine 500 mg 3 times per day often led to full recovery, while Korsakoff's syndrome was found in those receiving low doses. To prevent WE in kidney failure, we suggest administering high doses of parenteral thiamine in patients with kidney disease who present with severe malnutrition and (prodromal) signs of thiamine deficiency.

Clinical analysis of Wernicke encephalopathy after liver transplantation.

BACKGROUND: Wernicke encephalopathy (WE) is an acute neurological disease resulting from vitamin B1 deficiency, and there are only very few case reports of WE after liver transplantation. The present study aimed to investigate the clinical characteristics, etiology, magnetic resonance imaging (MRI) features, treatment and prognosis of patients with WE after liver transplantation. METHODS: Twenty-three patients with WE after liver transplantation from the First Affiliated Hospital, Zhejiang University School of Medicine and Jiangxi Provincial People's Hospital between January 2011 and December 2021 were retrospectively analyzed. RESULTS: Among the 23 patients diagnosed with WE after liver transplantation, 6 (26%) had a classic triad of impaired consciousness, oculomotor palsy and ataxia, and 17 (74%) had two features. The misdiagnosis rate was 65%. After treatment with high-dose vitamin B1, 19 (83%) patients showed improvement, whereas 4 (17%) showed no improvement, including 3 with residual short-term memory impairments and 1 with residual spatial and temporal disorientation and ataxia. CONCLUSIONS: The misdiagnosis rate is high in the early stage of WE, and the prognosis is closely associated with whether WE is diagnosed early and treated timely. High-dose glucose or glucocorticoids can trigger WE and cannot be administered before vitamin B1 treatment. Vitamin B1 is suggested to be used as a prophylactic treatment for patients with WE after liver transplantation.

Wernicke encephalopathy and beriberi disease presenting as STEMI-equivalent.

Thiamine deficiency is commonly associated with malnutrition, alcoholism and bariatric surgery. Thiamine deficiency can manifest in different ways, especially in developing countries: as peripheric neuropathy, as Wernicke encephalopathy or as beriberi disease. The authors present the case of a 72-year-old male, with a hiatal hernia that led to thiamine deficiency due to malnutrition. The initial clinical manifestation was an ST-elevation myocardial infarct equivalent, an ECG with a shark-fin pattern that evolved to a Wellens type B pattern. The patient evolved with severe altered mental status. A Wernicke encephalopathy diagnosis was confirmed by MRI; the patient was medicated with high-dose thiamine, with quick recovery, both neurologic and cardiac. The clinical history and response to treatment confirm the diagnosis of Wernicke encephalopathy and beriberi disease.

Alcohol and the central nervous system.

Ethanol use is common to most cultures but with varying doses and to varying extents. While research has focused on the effects on the liver, alcohol exerts a range of actions on the function and structure of the nervous system. In the central nervous system (CNS) it can provoke or exacerbate neurological and psychiatric disease; its effects on the peripheral nervous system are not included in this review. Sustained alcohol intake can predispose to acute neurochemical changes which, with continued ingestion and incomplete treatment, can lead to chronic structural changes in the CNS: these include generalised cortical and cerebellar atrophy, amnesic syndromes such as Korsakoff's syndrome, and specific white matter disorders such as central pontine myelinolysis and Marchiafava-Bignami syndrome. Alcohol in pregnancy commonly and significantly affects fetal health, though this receives less medical and political attention than other causes of fetal harm. This review looks at the range of disorders that can follow acute or chronic alcohol use, and how these should be managed, and we provide a practical overview on how neurologists might diagnose and manage alcohol addiction.

SARS-COVID-19 TRIGGERED WERNICKE'S ENCEPHALOPATHY (CLINICAL CASE).

Patient P., born in 1956, was found by relatives in a state of confused consciousness, an act of involuntary urination and defecation, numbness and weakening of the strength of both lower limbs were recorded. He was taken by ambulance to the reception room of the Regional Clinical Center of Neurosurgery and Neurology. The following concomitant diseases are known from the life anamnesis: Atrial fibrillation, gout, hypertension and type II non-insulin-dependent diabetes mellitus. Objective status: general condition of medium severity, tophuses of small joints of hands and feet, knee and elbow joints. Pronounced deformity of hands and feet due to gouty lesions. Heart tones are weakened. Breath sounds are weakened. The abdomen is soft, not painful on palpation. Glasgow coma scale 14-15 points. Consciousness is confused, disoriented in time, space and own person. To clarify the diagnosis, clinical and laboratory and instrumental diagnostic methods were used. Neurological complications, in particular, acute encephalopathy, on the background of coronavirus infection, may develop in patients with the presence of such risk factors as advanced age, cardiovascular diseases, hypertension, diabetes, gout. Most of the neurological complications in COVID-19 are probably not related to the direct penetration of the virus into the CNS, but are a trigger for the development of the pathology. Neuroimaging in such cases does not reveal pathological changes or reflects non-specific disorders.

Bromisoval-induced bromism with status epilepticus mimicking Wernicke's encephalopathy: report of two cases.

BACKGROUND: Bromine compounds are used in several drugs, including over-the-counter drugs. They sometimes cause intoxication known as bromism. Although the acute neurological symptoms and sequelae of bromism vary, few reports have mentioned acute encephalopathy. CASE PRESENTATION: We report two cases of bromisoval-induced bromism with status epilepticus. Presence of pseudohyperchloremia and history of over-the-counter medication use guided the diagnosis. In the acute phase, our patients showed bilateral medial thalamic lesions on magnetic resonance imaging. The imaging findings were similar to those of Wernicke's encephalopathy. Although these findings improved in the chronic phase, neuropsychiatric sequelae, such as confabulation and amnesia, occurred. CONCLUSION: Bromism can cause acute encephalopathy, and it is important to differentiate it from Wernicke-Korsakoff syndrome.

A case of new cognitive changes in a patient with seronegative paraneoplastic limbic encephalitis: encephalitis relapse or Wernicke's encephalopathy?

Wernicke's encephalopathy (WE) and paraneoplastic limbic encephalitis (PLE) can both present with acute-to-subacute memory impairment and cognitive dysfunction. Both can lead to significant morbidity and mortality without rapid identification and treatment. Often patients with WE may not have the typical clinical triad of ophthalmoplegia, gait ataxia, and altered mental status. Furthermore, both WE and PLE may share similar MRI findings. Here, we present a case of a patient with a history of seronegative PLE presenting with acute-to-subacute cognitive changes and gait imbalance. Initially, it was felt to be a relapse of PLE but upon further history and testing may potentially have represented WE in the setting of a recent dietary change.

Atypical neurological manifestations in Wernicke's encephalopathy due to hyperemesis gravidarum.

OBJECTIVES: Hyperemesis gravidarum is known to induce nutritional, water and electrolyte deficiencies which can be fatal if not treated urgently. Thiamine deficiency may lead to a constellation of neurological symptoms that include Wernicke encephalopathy. Moreover, Wernicke encephalopathy is typically manifested as ocular paresis, ataxia and confusion. METHODS: Retrospective review of 6 women who developed neurological abnormalities following hyperemesis gravidarum and were treated with varying dosage of parenteral thiamine. RESULTS: Five women developed atypical neurological symptoms, namely, slurred speech, visual loss, seizure and aggressive behaviour while one woman developed typical clinical triad of Wernicke encephalopathy after hyperemesis gravidarum. Magnetic Resonance Imaging (MRI) scans revealed abnormalities suggestive of Wernicke encephalopathy in three women only. All women improved after parenteral thiamine administration during hospital stay and had a complete neurological recovery during 2 months follow up. DISCUSSION: Wernicke encephalopathy may not be necessarily associated with the typical neurological triad and may not have noticeable hyperintensity signal in dorsomedial thalami, mammillary bodies, hippocampus and periaqueductal region during magnetic resonance imaging. Atypical neurological signs and symptoms following hyperemesis gravidarum would invariably respond immediately to appropriate dosage of parenteral thiamine. A lower loading dosage of thiamine (100 mg thrice daily) appeared adequate for management in women with normal MRI scans.

Wernicke's encephalopathy secondary to hyperemesis gravidarum: A clinical challenge.

Wernicke's encephalopathy (WE) is an acute neurological condition characterized by a triad of ophthalmoplegia, ataxia and altered mental status. The underlying cause is thiamine deficiency, which may be due to multiple aetiologies. Thiamine is essential for carbohydrate and amino acid metabolism. Its deficiency shunts glucose to anaerobic pathways producing metabolic abnormalities. Diagnosing WE relies heavily on clinical suspicion. Magnetic Resonance Imaging can show some specific findings. We report this case of a 35 year old pregnant woman with gestational diabetes who was admitted in hospital for high blood sugar levels and electrolyte abnormalities. She had a history of ten miscarriages. From undergoing laparoscopic cholecystectomy for intractable vomiting to spontaneous expulsion of the foetus to being intubated for acidosis, her hospital stay was prolonged and eventful. Although the cause of her repeated miscarriages could not be established despite extensive workup, thiamine deficiency leading to Wernicke's encephalopathy was the most probable cause.

Wernicke Encephalopathy Mimicking MELAS.

OBJECTIVES: a stroke-like lesion, the morphological equivalent of a stroke-like episode and the hallmark of mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome, have not been reported as manifestations of thiamine deficiency. CASE REPORT: a 62-year-old man with a history of chronic alcoholism was admitted after a series of epileptic seizures. Upon waking up from the coma, he presented with disorientation, confusion, confabulation, psychomotor agitation, aggressiveness, right hemianopsia, aphasia, and right hemineglect over weeks. Electroencephalography showed a questionable focal status epilepticus over the left hemisphere, responsive to lorazepam and oxcarbazepine. Follow-up electroencephalographies no longer recorded epileptiform discharges. Cerebral magnetic resonance imaging (MRI) revealed T2-/diffusion weighted imaging (DWI) hyperintensity in the left occipito-temporal region that was not congruent to a vascular territory which persisted for at least nine weeks. Since a lactate-peak could be seen in this lesion by magnetic resonance-spectroscopy, this was interpreted as a stroke-like lesion. Since thiamine was reduced, the stroke-like lesion was attributed to thiamine deficiency after the exclusion of differential diseases, including MELAS and status epilepticus. The patient's behavioural and cognitive dysfunctions largely resolved upon vitamin-B1 substitution. CONCLUSIONS: the case suggests that thiamine deficiency presumably causes mitochondrial dysfunction with cerebrospinal fluid lactic acidosis and a stroke-like lesion mimicking MELAS syndrome. It should be further studied whether nutritional deficits, such as thiamine deficiency, could give rise to secondary stroke-like lesions.

[A Case of Wernicke Encephalopathy with Ileus by Small Intestinal Cancer].

The patient was a 74 year-old woman. She came to the hospital with the chief complaint of vomiting, difficulty walking, and disorientation. The MRI study showed increased FLAIR and DWI signals in the bilateral medial thalamus. Abdominal enhanced CT scan showed a 2.4 cm tumor in the jejunum. And ileus due to small intestinal tumor was observed. She diagnosed Wernicke's encephalopathy associated with gastrointestinal transit disorder. Vitamin B1 300 mg/day for 3 days was started, and eye movements and disorientation improved on the day following the start of administration. On the 10th day after admission, partial resection of the small intestine was performed for a small intestinal tumor. She was diagnosed as small intestinal cancer. She was transferred to the hospital on the 20th postoperative day.

Restrictive diet in a patient with irritable bowel syndrome leading to Wernicke encephalopathy.

BACKGROUND: We present a case of a woman with a past medical history of irritable bowel syndrome (IBS) and anxiety, who presents with ophthalmoplegia, ataxia and memory loss, characteristic of Wernicke encephalopathy. CASE PRESENTATION: A 64-year-old woman presented with double vision, unsteady gait and memory loss. These symptoms began after 3 months on an unfortified restricted diet, which she initiated to alleviate IBS symptoms. Magnetic resonance imaging of the brain demonstrated hyperintense T2-weighted signal in the dorsomedial aspect of bilateral thalami, periaqueductal grey matter and around the third ventricle. The patient's visual symptoms improved significantly after thiamine supplementation, although her memory deficits persisted. CONCLUSION: Although WE is often associated with chronic alcohol abuse, this case demonstrates the importance of recognizing WE in any patient with a restricted diet and subsequent timely initiation of thiamine.

Wernicke encephalopathy following advanced caecum cancer.

A 26-year-old lactating mother presented with a 3-week history of abdominal pain, constipation, and vomiting. She denied any history of alcohol abuse or other gastrointestinal problems. Contrast-enhanced CT identified a small-bowel obstruction caused by a cecum cancer (Fig. 1A). Therefore, she underwent right hemicolectomy and ileocolic anastomosis. Post-operatively, she gradually developed drowsiness, fainting, and a rapid heart rate at 130 bpm. However, blood tests were all normal.

Non-alcoholic beriberi, Wernicke encephalopathy and long-term eating disorder: case report and a mini-review.

INTRODUCTION: Nowadays, reports of beriberi are rare in developed countries. Wernicke encephalopathy may be present in about 25% of patients with beriberi. CASE REPORT: We report the case of a woman with history of depression and chronic eating disorder, who complained Wernicke encephalopathy and beriberi. Sural nerve and muscular biopsy were performed, showing severe axonal neuropathy. Thiamine supplementation was started with rapid improvement of the pulmonary and cardiac affections; improvement of peripheral neuropathy was incomplete. CONCLUSIONS: Thiamine deficiency can be misdiagnosed. Beriberi is an important cause of acute flaccid paralysis; hence, clinicians should consider this diagnosis and prompt start thiamine treatment to avoid permanent neurological sequelae.

Visual Disturbances in a Grave's Disease Patient After Sleeve Gastrectomy.

Wernicke encephalopathy (WE) is a neuropsychiatric disorder that results from untreated severe thiamine deficiency, frequently described as a triad of ophthalmoplegia, ataxia, and confusion. While this triad is commonly used to describe WE, all three symptoms are observed in less than 20 percent of individuals with this diagnosis. Most commonly, WE is observed in individuals with significant alcohol use and associated malnutrition resulting in thiamine deficiency. However, this condition can also be diagnosed in patients with other sources of malnutrition, and less frequently in hypermetabolic states such as those with hyperthyroidism. Due to its broad clinical presentation and numerous causes, Wernicke encephalopathy can be difficult to diagnose. Diagnosis of WE guides management, as glucose before IV thiamine administration can be detrimental. Therefore, it is essential to understand the complexities of WE. In this paper, we discuss a patient who presented to the emergency department complaining of central vision loss, change in color perception, tinnitus, and difficulty walking two months post gastric sleeve and a recently diagnosed and, possibly inadequately treated, hyperthyroidism. The combination of recent sleeve gastrectomy and hyperthyroidism likely led to thiamine malabsorption and hypermetabolism, resulting in WE.

From psychosis to Wernicke encephalopathy: a case of hunger strike in prison.

Wernicke encephalopathy (WE) is a neuropsychiatric condition associated with  thiamine deficiency that includes a triad of mental status changes, ophthalmoplegia, and ataxia. Worsening WE may lead to Korsakoff syndrome(KS), in which cognitive impairments such as confabulation and memory deficits and also psychiatric symptoms may occur. Diagnosis of Wernicke-Korsakoff syndrome can be complicated in many cases. We present the case of a prisoner who commenced a hunger strike and developed WE. The preceding factors were associated with his oral intake refusal, which originated from his mental disorder with psychotic content. We discuss the clinical and treatment concerns for this complicated condition.

Missing the early signs of thiamine deficiency. A case associated with a liquid-only diet.

BACKGROUND: Wernicke encephalopathy (WE) predominantly occurs in alcoholic patients. Few case reports have described this diagnosis as a result of dieting. The diagnosis is often missed or delayed resulting in permanent and severe neurologic sequelae and even death. The typical neurological signs may be absent or missed during the early stages of thiamine deficiency. CASE REPORT: A 23-year-old female presented to the hospital with confusion, bilateral lateral rectus palsy, and ataxia. Based on the typical neurological triad, WE was suspected. The brain MRI was also typical for WE. Prompt clinical improvement was seen within days after intravenous thiamine supplementation. A detailed medical history revealed that during the past 3 months she had been following a liquid-only diet and had lost about 30 kg. During that time, she had visited the emergency department on multiple occasions due to fatigue, nausea, and vomiting. CONCLUSION: A high level of suspicion is required by physicians to recognize that fatigue, nausea, and vomiting may represent early signs of thiamine deficiency in patients at risk for nutritional deficiencies. Empirical thiamine supplementation may be reasonable in such cases.

Wernicke encephalopathy associated with hyperemesis gravidarum.

Emergency physicians frequently treat hyperemesis gravidarum and should be aware of possible complications. Wernicke encephalopathy secondary to thiamine deficiency should be considered in the differential diagnosis of acute encephalopathy in pregnant women. A seventeen-week pregnant 27-year-old woman presented to the Emergency Department with nausea, emesis, and right upper quadrant abdominal pain. Ultrasound diagnosed gallbladder sludge. Surgical consultant offered cholecystectomy versus expectant management. She improved with IV hydration, ondansetron, and was discharged on hospital day 3 with a diagnosis of hyperemesis gravidarum and gallbladder sludge. Three days later she presented with continued emesis and altered mental status. She and family members denied alcohol or illicit drug use. Vital signs were pulse 99/min, blood pressure 115/70, temperature 36.4 °C, respiratory rate 18, and oxygen saturation 99%. Neurological examination was delirium, variable mentation, and inability to follow commands. She had internuclear opthalmoplegia with bilateral nystagmus. CT scan of brain was negative. MRI found abnormal T2-weighted signal in the central pons and medial thalami. Radiographic differential included central pontine myelinolysis, dysmyelinating conditions from malnutrition, toxic encephalopathy, and Wernicke encephalopathy. Thiamine level was below the limits of detection. Alcohol and urine drug screen were negative. Diagnosis was thiamine deficiency secondary to hyperemesis gravidarum with Wernicke encephalopathy. Emergency physicians frequently treat hyperemesis gravidarum. Nutritional status should be evaluated in patients who are unable to take neonatal vitamins. Awareness should exist of possible complications, including Wernicke encephalopathy secondary to thiamine deficiency.

Wernicke's encephalopathy in a patient with late-onset enterocolic fistula after bariatric surgery.

Wernicke´s encephalopathy (WE) is an acute neurologic disorder secondary to thiamine deficiency. We report the case of a patient with history of bariatric surgery who develops a late-onset enterocolic fistula, with alcohol consumption associated.