Magnetic resonance imaging in a case of Wernicke's encephalopathy (original) (raw)
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Wernicke’s encephalopathy in pregnancy
International Journal of Reproduction, Contraception, Obstetrics and Gynecology, 2022
Wernicke's encephalopathy (WE) is a reversible neurological emergency which is a rare but known complication of hyperemesis gravidarum due to thiamine deficiency. Prolonged vomiting in pregnancy results in thiamine depletion. Most frequently Wernicke's encephalopathy is found among persons suffering from excessive drinking. Unusually it can also be seen in women presenting with hyperemesis gravidarum with pre-existing malnutrition, as avitaminosis can result from the acute malnutrition associated with prolonged pregnancy-related hyperemesis. The early recognition of its clinical signs and symptoms is essential to establish the suspected diagnosis and can be confirmed by MRI. Most patients present with the triad of ocular signs, ataxia, and confusion. It can be associated with life-threatening complication like central pontine myelinolysis. Here we stress upon the importance of early diagnosis and prompt treatment of WE. The aim of this report is to present cases of Wernicke&...
Wernicke’s Encephalopathy : Similar and Different Aspects of Three Cases
Archives of Neuropsychiatry, 2018
Wernicke encephalopathy is a neurological disorder, clasically characterized by altered consciousness, ophtalmoparesis, and ataxia results from tiamin deficiency. It is frequently associated with chronic alcohol abuse; however, many conditions which lead to thiamine deficiency such as gastric surgery, hyperemesis, parenteral nutrition, malnutrition may also be the cause. WE is a life-threatening condition that requires early diagnosis and rapid initiation of intravenous thiamin therapy. In patients, findings of characteristic examinations may not always be seen; therefore, imaging methods are of great importance. In this article, we aimed to emphasize the similar and different aspects of three WE cases with typical and atypical imaging findings.
Japanese Journal of Radiology
Wernicke's encephalopathy (WE) is a severe and life-threatening illness resulting from vitamin B1 (thiamine) deficiency. The prevalence of WE has been estimated from 0.4 to 2.8%. If not treated properly, severe neurologic disorders such as Korsakoff psychosis and even death may occur. The classical triad of clinical symptoms (abnormal mental state, ataxia, and ophthalmoplegia) is found in only 16-33% of patients on initial examination. The originally described underlying condition of WE is alcoholism, but it accounts for about 50% of causes of WE. Nonalcoholic patients are also affected by WE and likely to present symptoms and radiological imaging findings different from patients with alcoholism, which further complicates the diagnosis of WE. Being familiar with predisposing causes, symptoms and radiological imaging findings of WE is important for radiologists and clinicians when making the diagnosis to start immediate treatment. This review discusses pathophysiologies, underlying causes, clinical symptoms, imaging findings and their mimics.
CT and MRI of Wernicke's encephalopathy
La Radiologia medica, 2011
The purpose of this pictorial essay is to present the computed tomography (CT) and magnetic resonance imaging (MRI) findings of Wernicke's encephalopathy, a rare, severe, acute neurological syndrome due to thiamine (vitamin B1) deficiency, associated with high morbidity and mortality. The classical clinical triad, which includes ocular signs, altered consciousness and ataxia, can be found in only one-third of patients. Although chronic alcoholic patients are the most commonly affected, Wernicke's encephalopathy may complicate malnutrition conditions in nonalcoholic patients, in whom it is greatly underestimated. CT and above all MRI of the brain play a fundamental role in diagnosing the condition and ruling out other diseases. MRI is the most sensitive technique and is required in all patients with a clinical suspicion of Wernicke's encephalopathy. Medial thalami, mamillary bodies, tegmentum, periaqueductal region, and tectal plate are typical sites of abnormal MRI signa...
Wernicke encephalopathy: MR findings and clinical presentation
European radiology, 2003
Wernicke encephalopathy (WE) is a severe neurological disorder caused by vitamin B1 deficiency. The aim of the study was to analyse MRI findings typical for this disease and to evaluate the significance of their correlations with clinical symptoms. Magnetic resonance images and clinical features of 12 patients with WE were analysed. The patients underwent MR imaging within 3-14 days after onset of clinical symptoms. In 7 of 12 patients MR imaging showed symmetrical diencephalic and midbrain lesions. Postcontrast T1-weighted images from 5 of 9 patients examined during the initial 6 days of acute WE showed a subtle enhancement of the mamillary bodies, the tectal plate, the periaqueductal area and the periventricular region of the third ventricle including the paramedian thalamic nuclei. In addition, T2-weighted and fluid-attenuated inversion recovery (FLAIR) images revealed hyperintense signals in these regions (except for 2 patients where the mamillary bodies were normal). Hyperinten...
Wernicke Encephalopathy: A Case Report I. Case Study
Wernicke encephalopathy is a medical emergency cause by thiamine or B1 deficiency that results life-threatening brain disruption, confusion, staggering and stumbling, lack of coordination, and abnormal involuntary eye movements. Chronic alcohol intake is the most common reason but it is also common in prolonged intravenous feeding, fasting, refeeding after starvation, prolonged vomiting such as hyperemesis gravidarum, anorexia nervosa, patients receiving dialysis , thyrotoxicosis, congestive heart failure with long term diuretic treatment. In non-alcoholic patients Wernicke Encephalopathy might develop due to the exclusion of upper portions of the gastrointestinal tract (e.g. after gastrectomy, gastrojejunostomy, gastric bypass surgery) or malabsorption. Other described conditions in which Wernicke Encephalopathy may develop include HIV/AIDS and several types of malignancy (inoperable gastric cancer, leukaemia and lymphoma). Wernicke encephalopathy, if not recognized and treated, can become irreversible.-A 50-year-old man was admitted in our Hospital with the chief complaint of acute confusion, visual hallucination, persecutory idea, restlessness and disorientation and gait ataxia for 6 days. He had multiple episodes of vomiting 5 days back. He had weakness in lower limbs, inability to walk, ataxic gait and forgetfulness for last four months. He had been an alcoholic for 23 years and was still drinking alcohol at the time of this illness. During admission, vitals were stable with normal systemic examination. Physical examination showed a drowsy and disorientated man with a body temperature of 38.C He showed mild intentional tremor, symmetrical mild weakness, diminished deep tendon reflexes in all limbs, horizontal nystagmus, impaired finger-nose and heel-shin test, and dysdiadokinesia. Concentration was impaired. Disorientation to time and place was present. Memory was impaired. He also had positive signs of chronic liver disease. Other findings were unremarkable. The complete blood count, serum glucose, BUN, creatinine, electrolytes, urinary analysis and chest X-ray were within normal limits. Liver function test revealed an elevated Liver enzyme level. The MRI of the brain showed multiple, scattered, small non-enhanced low signal intensity on T1WI, high signal intensity on T2WI involving at bilateral basal ganglias, thalami, midbrain, pons, and periventricular regions with evidence of brain atrophy. The mamillary bodies could not be identified. A cerebrospinal fluid analysis was within normal limits. He was treated with parentral thiamine intravenously 500 mg in 0.9% normal saline thrice daily for two consecutive days followed by 500 mg intravenously once daily for an additional 5 days. The nystagmus, double-vision, incordination, weakness of lower limbs, ataxia improved but memory problems, and loss of insight remained. II. Discussion Wernicke Encephalopathy is a medical emergency caused by thiamine or B1 deficiency. This micronutrient, a water-soluble vitamin, is absorbed primarily in the duodenum, acts as a co-factor in carbohydrate metabolism, and is important in neuron cell function. The human body cannot synthesize thiamin and regular dietary intake of thiamin is essential. The most common cause is found in alcoholism but it is also common in prolonged intravenous feeding, fasting, refeeding after star vation, prolonged vomiting such as hyperemesis gravidarum, anorexia nervosa, patients receiving dialysis, thyrotoxicosis, congestive heart failure with long term diuretic treatment. However, it is also caused by a genetic abnormality resulting from a defection in tr an sket ol a se st r uct ur e th a t di m ini sh ed bi n din g with coenzyme thiamine pyrophosphate. Thiamin is a cofactor for transketolase, alpha-ketoglutarate dehydrogenase, pyruvate dehydrogenase, and branch-chain alpha-keto acid dehydrogenase that are
Wernicke’s Encephalopathy with Normal Neuroimaging - Suspect and Treat - A Case Report
Journal of Evolution of Medical and Dental Sciences, 2021
Wernicke’s encephalopathy (WE) is an unrecognized nutritional deficiency which often goes unnoticed. WE is clinically often composed of a triad including nystagmus, ophthalmoplegia and altered mental status. Although this triad practically is present only in a handful of cases1 it is also described as an acute neuropsychiatric presentation of thiamine deficiency. Early diagnosis and prompt treatment are of utmost importance here as it can prevent chronic brain damage which is often the end effect of thiamine deficiency. Wernicke’s encephalopathy is most commonly found in patients with chronic alcoholism, less frequent in non-alcoholic patients. In non-alcoholic patients, Wernicke’s encephalopathy might develop due to erosion of upper portion of gastrointestinal tract or secondary to intractable vomiting, inadequate dietary intake or malabsorption. Other causes include malignancies (gastric cancer, leukaemia, lymphoma), hyperemesis, anorexia, thyroid conditions.1,2 Wernicke’s encepha...
Mild symptomatic Wernicke’s Encephalopathy: a case report
Journal of Health Sciences
Wernicke’s encephalopathy (WE) is an acute, neuropsychiatric syndrome which results from a deficiency in vitamin B1 (thiamine), which in its biologically active form, thiamine pyrophosphate, is an essential coenzyme in several biochemical pathways in the brain, often due to alcohol abuse (alcoholic WE). Non-alcoholic WE variant manifests in many different clinical settings, such as gastrointestinal tumors, hyperemesis gravidarum, chemotherapy, acquired immunodeficiency syndrome, prolonged therapeutic fasting, protracted parenteral nutrition and bariatric surgery, anorexia nervosa and can even be secondary to socioeconomic factors. The classic triad of encephalopathy, oculomotor dysfunction, and gait ataxia is only seen in approximately one-third of patients and is more common in alcoholics; only some of these symptoms are usually present. Here we describe a case of an occasional neuroradiological finding of Wernicke Encephalopathy not related to symptoms or signs.
15 Wernicke ’ s Encephalopathy
2017
Wernicke’s Encephalopathy (WE) is an underdiagnosed, potentially fatal, acute or subacute neurologic disorder caused by the impairment of thiamine (vitamin B1) -dependent enzymatic activity in susceptible brain cells. The biologically active form of thiamine (TH), thiamine diphosphate (THDP), serves as a cofactor for several apoenzymes involved mainly in the carbohydrate metabolism. Except for very rare cases, WE occurs in the presence of TH deficiency, which is directly related to at least two other clinical entities: neurological beriberi and cardiovascular beriberi. The preferential expression of one (or more) of these entities may be the consequence of genetic polymorphism of genes encoding TH transporters. The topography of WE brain lesions is highly specific, typically the periventricular and periaqueductal grey areas being symmetrically involved. In the majority of cases the early so-called ‘biochemical lesions’ are completely reversed if TH is promptly supplied. However, if ...