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Results for “Wernicke Encephalopathy”

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At least 19 recordsLinked to original sources
PubMed2003

Proton MR spectroscopy in Wernicke encephalopathy.

Wernicke encephalopathy is caused by thiamine deficiency. Although the clinical picture has been well established for some time, clinical diagnosis is attained in only 20% of the cases. MR imaging techniques contribute to early diagnosis of Wernicke encephalopathy. We herein report MR imaging and proton MR spectroscopic findings for a patient with clinical and biochemical features consistent with Wernicke encephalopathy. Increased lactate and typical MR imaging findings are discussed in the context of the known pathophysiology of Wernicke encephalopathy.

Adult↗
PubMed2002

[Value of MRI findings in Gayet-Wernicke encephalopathy].

Wernicke encephalopathy (Wernicke-Korsakoff encephalopathy) is related to thiamine deficiency. We report the MRI findings in four patients with visualization of bilateral and symmetrical hyperintense foci on T2W and FLAIR images involving the periaqueductal gray matter, the mamillary bodies and around the third ventricle. Diffusion weighted images obtained in two patients demonstrated mild hypersignal in the same areas. Contrast enhancement within the mamillary bodies was noted in one patient. Follow-up MRI obtained in three patients showed rapid regression of signal abnormalities without correlation with good clinical outcome.

Adult↗
PubMed2005

MR imaging with diffusion-weighted imaging in acute and chronic Wernicke encephalopathy.

Wernicke encephalopathy is a neurologic disorder that results from thiamine deficiency. It is associated with a classic triad of symptoms consisting of ataxia, ocular motor cranial neuropathies, and changes in consciousness. We report 3 cases of Wernicke encephalopathy in which MR imaging, including diffusion-weighted imaging, was performed at the onset and during follow-up. MR imaging findings were correlated with the clinical status of both the acute and chronic stage of Wernicke encephalopathy.

Acute Disease↗
PubMed2006

Pancreatic encephalopathy and Wernicke encephalopathy in association with acute pancreatitis: a clinical study.

AIM: To investigate clinical characteristics and therapy of pancreatic encephalopathy (PE) and Wernicke encephalopathy (WE). METHODS: In a retrospective study of 596 patients with acute pancreatitis (AP), patients with PE were compared to those with WE in regards to history, clinical manifestation, diagnosis, treatment and outcome. RESULTS: There were 93 patients with severe acute pancreatitis (SAP). Encephalopathies were discovered in 10 patients (1.7%). Six patients with PE all developed in SAP (6.5%), and three of them died (3% of SAP, 50% of PE). Four patients with WE developed in AP (0.7%), and two of them died (0.3% of AP, 50% of WE). Two patients with WE were treated with parenteral thiamine and survived. Global confusions were seen in all patients with encephalopathy. Ocular abnormalities were found. Conjugate gaze palsies were seen in 1 of 6 (16.7%) patients with PE. Of 4 patients with WE, one (25%) had conjugate gaze palsies, two (50%) had horizontal nystagmus, three (75%) had diplopia, and one (25%) had myosis. Ataxia was not seen in all patients. None of patients with WE presented with the classic clinical triad. CSF examinations for 2 patients with WE showed lightly-increased proteins and glucose. CT and MRI of the brain had no evidence of characteristic abnormalities. CONCLUSION: PE occurs in early or reiteration stage of SAP, and WE in restoration stage of SAP/AP. Ocular abnormalities are the hallmarks of WE, and horizontal nystagmus is common. It is difficult to diagnose earlier an encephalopathy as PE or WE, as well as differentiate one from the other. Long fasting, hyperemesis and total parenteral nutrition (TPN) without thiamine are main causes of thiamine deficiency in the course of pancreatitis.

Acute Disease↗
PubMed1998

[MRI findings in Wernicke encephalopathy].

Wernicke's encephalopathy (WE) is a consequence of vitamin B1 (thiamine) deficiency and in the majority of cases due to alcoholism. We report here the case of a 26-year-old male alcoholic who had stayed helplessly at home for 4 days until hospital admission. Clinical diagnosis was difficult due to major disturbance of consciousness. MRI showed an increase in signal intensity (T2-, FLAIR-weighted) around the third ventricle, the quadrigeminal bodies, the fornices, the mamillary bodies, the floor of the fourth ventricle and around the aqueduct. These findings were indicative of WE although of unusual extent. In this case MRI correlated well with clinical symptomatology. Therapy with thiamine was started immediately and symptoms as well as MRI findings resolved partially. The presented case illustrates the diagnostic usefulness of MRI in WE especially if the patient is of reduced consciousness and clinical investigation is limited.

Adult↗
PubMed2002

[Pancreatic encephalopathy and Wernicke encephalopathy].

OBJECTIVE AND METHOD: 3 cases of acute severe pancreatitis with symptoms of central nervous system were presented and 30 Chinese articles of acute pancreatitis (AP) with encephalopathy found in the literature were reviewed in CNKI. RESULTS: There were 185 cases of AP with encephalopathy altogether, 84% of them being severe cases, with male slightly outnumbering female and biliary pancreatitis as the predominating type. Encephalopathy appeared in the early course of AP was a part of multiple organ failure which results from acute systemic inflammatory reaction. This is, in fact, pancreatic encephalopathy (PE). There were altogether 107 cases of PE and 61 of them died (57%). Encephalopathy appeared in the later course of AP (> 2 weeks or in recovery period) was caused by deficiency of Vit B(1). This is Wernicke encephalopathy (WE). There were 78 cases of WE and 26 died (33%). The difference between the two groups was significant (P < 0.01). Supplement of thiamine in time was the reason for lower mortality in WE. Of the 78 cases with WE, 17 having supplement of Vit B(1) all survived. Among those who did not receive Vit B(1), the mortality was 43%; this was not so much different with the mortality of PE (P > 0.05). CONCLUSIONS: This article discussed in detail the pathogenesis, diagnosis and management of PE and WE. Treatment of PE includes early diagnosis and comprehensive intensive therapeutic measures in intensive care unit. Patients who have been in fasting for a long time (more than 10 days) should be given thiamine intramuscularly in case WE occurs. As soon as WE is diagnosed, a large doses of Vit B(1) should be given immediately, is the key to reduce the mortality of encephalopathy complicating AP.

Adult↗
PubMed1988

Jakob-Creutzfeldt disease associated with Wernicke encephalopathy.

Wernicke disease (WD) is a complication of alcoholism and malnutrition and usually presents acutely and is characterized by disturbances of consciousness, paralysis of the external ocular muscles, and ataxia. The disease results from deficiency of vitamin B 1, or thiamine, an essential coenzyme in intermediate carbohydrate metabolism. On the other hand, Jakob-Creutzfeldt disease (J-C) results from infection with an unconventional agent with a long incubation period and is characterized by a rapidly progressive dementia and histologically by a spongiform encephalopathy associated with neuronal destruction and pronounced astrogliosis. Combination of both diseases has not been reported in the literature previously and their relationship is uncertain. We present 3 cases with this interesting association and consider their relationship.

Aged↗
PubMed2002

Wernicke encephalopathy in nonalcoholic patients.

BACKGROUND: Wernicke encephalopathy is associated with patients that have a history of alcohol abuse and other malnourished states. However, clinicians may be less likely to recognize this condition in nonalcoholic patients. This study was undertaken to evaluate the cause, diagnosis, treatment, and outcome of nonalcoholic patients with Wernicke encephalopathy. METHODS: A retrospective review was conducted of all cases of Wernicke disease from 1984 to 1999 evaluated at a rural university hospital. Inclusion criteria consisted of patients diagnosed clinically with this disorder who improved after the administration of thiamin. Patients were also included in the series if they had classic pathologic findings of the disease on autopsy even without a prior clinical diagnosis. RESULTS: Twelve patients were identified. Alcohol abuse was noted in only 50%. The patients without a history of alcohol abuse had other malnourished states, such as end-stage cancer, intractable vomiting after gastric reduction procedure, and prolonged hospital courses on intravenous fluids without other sources of nutrition. The mortality rate was 4 of 12 (33%) but due to multiple causes. Autopsies were performed on all 4 patients. Three of these 4 patients had no history of alcohol abuse. Two of the nonalcoholic patients were not diagnosed until autopsy, whereas all the patients with a history of alcohol abuse were diagnosed clinically. DISCUSSION: Our study reveals that Wernicke encephalopathy continues to be a rare but life-threatening condition often overlooked in the nonalcoholic population, resulting in the further progression of an easily treatable condition.

Adult↗
PubMed1990

Wernicke encephalopathy: MR findings in five patients.

Wernicke encephalopathy is a disease usually related to chronic alcoholism. The clinical diagnosis is often difficult to establish, and CT is unable to provide specific findings. MR follow-up studies in five patients affected by Wernicke encephalopathy were performed with the aim of establishing the sensitivity of MR in depicting the typical diencephalic/mesencephalic lesions. All subjects had MR imaging in the acute phase of the disease and were reexamined 6-12 months later, at which time they were in good health. Three of them also had CT scanning. On MR, hyperintense areas seen surrounding the third ventricle and aqueduct during the acute phase of the disease had disappeared or diminished on follow-up evaluations. The third ventricle and aqueduct were dilated. We suggest that these findings reflect the natural evolution of Wernicke encephalopathy. The MR findings in Wernicke encephalopathy enable early diagnosis of the disease, which has a positive effect on both treatment and prognosis.

Adult↗
PubMedDate not supplied

Wernicke encephalopathy: MR findings in five patients.

Wernicke encephalopathy is a disease usually related to chronic alcoholism. The clinical diagnosis is often difficult to establish, and CT is unable to provide specific findings. MR follow-up studies in five patients affected by Wernicke encephalopathy were performed with the aim of establishing the sensitivity of MR in depicting the typical diencephalic/mesencephalic lesions. All subjects had MR imaging in the acute phase of the disease and were reexamined 6-12 months later, at which time they were in good health. Three of them also had CT scanning. On MR, hyperintense areas seen surrounding the third ventricle and aqueduct during the acute phase of the disease had disappeared or diminished on follow-up evaluations. The third ventricle and aqueduct were dilated. We suggest that these findings reflect the natural evolution of Wernicke encephalopathy. The MR findings in Wernicke encephalopathy enable early diagnosis of the disease, which has a positive effect on both treatment and prognosis.

Acute Disease↗
PubMed1999

Wernicke encephalopathy: MR findings in two patients.

Wernicke encephalopathy is a serious neurologic disorder caused by vitamin-B1 or thiamine deficiency. In the literature the characteristic symmetric paraventricular lesions of Wernicke encephalopathy are hyperintense on T2-weighted sequences spin-echo (SE) and enhance on T1-weighted SE sequences after intravenous gadolinium administration in the acute phase. We present two patients in the acute phase of Wernicke encephalopathy with special reference to the MR imaging. One of our reported cases is special because of the MR demonstration of a hemorrhagic focus in the caput of the right nucleus caudatus. The other case demonstrates no enhancement on SE T1-weighted sequences after intravenous gadolinium administration.

Aged↗
PubMed2001

Magnetic resonance reflects the pathological evolution of Wernicke encephalopathy.

BACKGROUND AND PURPOSE: Wernicke encephalopathy (WE) is an acute phase of Wernicke-Korsakoff syndrome. Pathologic findings change between acute and chronic phases. Only a few magnetic resonance imaging (MRI) studies have been done to date. METHODS: To correlate the MRI findings in acute and chronic stages of WE with the known pathologic information, 15 consecutive patients with WE were examined with MRI: 3 before thiamine treatment, 7 within 24 hours of thiamine treatment, 4 between the second and sixth day after thiamine treatment, and 1 fifty-five days after thiamine treatment. Nine of the patients had follow-up MRI between 2 days and 33 months. T1-weighted, proton, and T2-weighted axial images were obtained with additional 5-mm-thick T1-weighted sagittal and coronal images to better visualize the mammillary bodies. RESULTS: In the acute WE, MRI showed high signal intensityon T2-weighted images in periaqueduct and medial thalamic regions. In a few patients with alcoholism, vermian and mammillary body atrophies and third ventricular enlargements were noted. In the chronic phase of WE, T2 hyperintensity disappeared but mammillary bodies and cerebellar vermis became atrophic and third ventricular enlargements were evident. High signal intensity on T2-weighted images disappeared as early as 2 days, and atrophic changes appeared as early as 1 week. CONCLUSION: MRI is useful for in vivo monitoring and reflects the pathological evolution in acute and chronic phases of WE.

Acute Disease↗
PubMed2002

Diffusion-weighted imaging abnormalities in wernicke encephalopathy: reversible cytotoxic edema?

BACKGROUND: Wernicke encephalopathy (WE) is a metabolic disorder of the central nervous system resulting from vitamin B(1) deficiency. The exact mechanisms underlying the pathogenesis of the lesions in WE are not completely understood. Vitamin B1 deficiency is associated with intracellular and extracellular edema by glutamate(N-methyl-D-aspartate) receptor-mediated excitotoxicity. Conventional magnetic resonance imaging (MRI) cannot differentiate the types of edema. Diffusion-weighted imaging (DWI) has been reported to detect early ischemic damage (cytotoxic edema) as bright areas of high signal intensity (SI) and vasogenic edema as areas of heterogeneous SI. OBJECTIVES: To describe the DWI findings and to characterize the types of edema in WE using DWI. SETTING: Tertiary referral center. DESIGN AND METHODS: Two patients with WE underwent DWI and conventional MRI with gadolinium enhancement. Wernicke encephalopathy was diagnosed with salient conventional MRI findings (high SIs in the paramedian thalamus, periaqueductal gray matter, and mamillary bodies) and typical clinical history and symptoms. Apparent diffusion coefficient (ADC) values were measured in abnormal lesions by visual inspection of DWIs and T2-weighted echo planar images. RESULTS: T2-weighted and fluid-attenuated inversion recovery MRIs showed high SIs in the bilateral paramedian thalamus, mamillary bodies, and periaqueductal gray matter. The DWIs showed bright high SI in the corresponding lesions, and ADC values were decreased (patient 1: 512-545 x 10(-6)mm2/s; patient 2: 576-612 x 10(-6)mm2/s). The ADC decrease and the DWI high SI were normalized in 2 weeks with administration of thiamine hydrochloride. CONCLUSIONS: Abnormalities on DWI and ADC decrease became normalized with adequate therapy. The MRI abnormalities in WE might be owing to the "reversible cytotoxic edema" caused by vitamin B1 deficiency.

Aged↗
PubMed2004

Successful treatment of Wernicke encephalopathy in terminally ill cancer patients: report of 3 cases and review of the literature.

Although Wernicke encephalopathy has been reported in the oncological literature, only one terminally ill cancer patient with Wernicke encephalopathy has been reported. Wernicke encephalopathy, a potentially reversible condition, may be unrecognized in terminally ill cancer patients. In this communication, we report three terminally ill cancer patients who developed Wernicke encephalopathy. Early recognition and subsequent treatment resulted in successful palliation of delirium. Two of the three patients did not show the classical triad of Wernicke encephalopathy. Common clinical symptoms were delirium and poor nutritional status. Intravenous thiamine administration dramatically improved the symptoms of delirium in all three patients. In terminally ill cancer patients, clinicians must remain aware of the possibility of Wernicke encephalopathy when patients with a poor nutritional status present with unexplained delirium. Early intervention may correct the symptoms and prevent irreversible brain damage and the quality of life for the patient may improve.

Aged↗
PubMed1994

Mamillary body enhancement on MR as the only sign of acute Wernicke encephalopathy.

We report a case of Wernicke encephalopathy in which the only sign of acute disease was enhancement of the mamillary bodies. This case demonstrates the utility of gadolinium enhancement at MR imaging as a means of diagnosing or confirming the syndrome of Wernicke encephalopathy even in the absence of atrophy or T2 abnormalities within the diencephalon and mesencephalon.

Acute Disease↗
PubMed2005

MR Imaging of nonalcoholic Wernicke encephalopathy: a follow-up study.

We investigated the correlation of MR imaging features with the pathological evolution and prognosis of nonalcoholic Wernicke encephalopathy. A retrospective review and analysis was conducted of 6 cases of nonalcoholic Wernicke encephalopathy, consisting of MR imaging features, clinical characteristics, and outcomes after thiamine administration. One patient died, 1 patient entered a persistent vegetative state, and the others recovered fully from Wernicke encephalopathy within 2 weeks to 1 year after thiamine administration. Typical MR imaging showed areas of increased T2-weighted and fluid-attenuated inversion recovery (FLAIR) signals symmetrically surrounding the aqueduct and the third ventricle, at the floor of fourth ventricle, in the medial thalami, and in the capita of caudate nuclei. Two patients presenting without coma showed increased T2-weighted and FLAIR signals of the periaqueductal area only. All 4 patients presenting with coma showed increased T2-weighted and FLAIR signals symmetrically in the medial thalami and in the capita of caudate nuclei. Of the 4 patients with coma, 2 patients with deep coma showed increased T2-weighted and FLAIR signals in the medial thalami and caudate nuclei as well as in the frontal and parietal cortices. According to the follow-up results, increased T2-weighted and FLAIR signals in the 4 patients without cortical damage decreased in intensity, consistent with clinical recovery within 2 weeks to 1 year. The patient in a persistent vegetative state exhibited progressive atrophy of the whole brain during the 2 years of the follow-up study. MR imaging is helpful not only to diagnose acute nonalcoholic Wernicke encephalopathy but also to evaluate the pathologic evolution and prognosis of the disorder.

Adolescent↗