Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0751295 (memory loss)
 3,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution and severity of the brain lesions were studied in 45 cases (age range: 26-84 years) of Wernicke's encephalopathy. The process was acute or subacute (active) in 24 cases and chronic (inactive) in 21. Cases with acute and subacute disease had more extensive and severe lesions than the chronic ones. The majority of the acute cases had lesions involving the mammillary bodies and thalamus and the subependymal structures along the third and fourth ventricles and the aqueduct. Only three acute cases had lesions restricted to the mammillary bodies. Among the chronic cases, the majority of the lesions were restricted to the mammillary bodies and the thalamus. Only two lesions extended as far down as the inferior collicles. Eleven out of 21 chronic cases has isolated lesions of the mammillary bodies. The affection of the mammillary bodies in chronic cases varied from barely visible to subtotal destruction of the tissue. Similarly, the lesions in the thalamus varied from slight gliosis in the dorsomedial nucleus to extensive nerve cell loss in several nuclei. There were similar variations in the severity of the clinical picture. Memory loss was recorded in three cases with isolated lesions of the mammillary bodies.
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PMID:Topographic distribution and severity of brain lesions in Wernicke's encephalopathy. 310 41

A case of Wernicke's encephalopathy with ataxia, confusion, memory loss, partial seizures of complex behavior and hypothermia, subsequent to thiamine depletion due to chronic malnourishment and triggered by an episode of acute vomiting and diarrhea, is reported, Computerized tomography (CT-scan) depicted small bilateral lesions in areas adjacent to the walls of the third ventricle, common location of the lesions seen in autopsy material of Wernicke's encephalopathy. Early diagnosis and treatment with vitamin B complex supplemented with intensive mnemonic and cognitive therapy led to complete recovery in a ten day period.
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PMID:Wernicke's encephalopathy. A case report with neurophysiologic and CT-scan studies. 686 52

Wernicke's encephalopathy and Korsakoff's psychosis represent a continuum of the same pathologic process. The etiology is an absolute deficiency of thiamine rather than a direct toxic effect of alcohol. The triad of Wernicke's encephalopathy--global confusional state, ophthalmoplegia and nystagmus, and ataxia--is occasionally seen in chronic alcoholics and is often attenuated by immediate thiamine treatment. The triad of Korsakoff's psychosis--memory loss, learning deficits and confabulation--may be seen in either the acute or the long-term care setting.
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PMID:The Wernicke-Korsakoff syndrome. 742 67

We present here 2 cases of Wernicke's encephalopathy developed several years after total gastrectomy. Case 1. A 48-year-old male developed impaired recent memory and unsteady gait. He had undergone total gastrectomy for advanced gastric cancer 5 years previously; he had been on tegafur regimen for 4 and a half years. He had had 630 ml of beer every day for 6 months until admission. On admission, there were bilateral abducens palsy, horizontal nystagmus, gait ataxia, and areflexia. Cranial MR imaging was unremarkable. After intravenous infusion of vitamin B1, the patient improved. Case 2. A 56-year-old male developed exertional dyspnea, memory loss, and unsteady gait. He had undergone total gastrectomy for a large submucosal tumor 4 years previously; he had had 300-500 ml of sake almost every day thereafter. Examination revealed bilateral abducens palsy, severe gait ataxia, and areflexia. Chest CT scans demonstrated moderate amount of pericardial effusion. Blood vitamin B1 level was abnormally low. After administration of vitamin B1, he improved. Both patients had had alcoholic drinks; laboratory findings demonstrated no liver dysfunction. Drinking alcohol, even in relatively small quantities, could precipitate the development of Wernicke's encephalopathy in gastrectomized individuals. Our 2 cases stress the importance of supplementary vitamin B1 administration after total gastrectomy.
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PMID:[Wernicke's encephalopathy developed several years after total gastrectomy. Report of 2 cases]. 950 77

A case of Creutzfeldt-Jakob disease (CJD) with presenting Wernicke encephalopathy (WE)-like symptoms and severe insomnia is presented. An 80-year-old alcoholic man with a 6 month history of tremors, ataxia, memory loss and confabulation, developed profound insomnia, confusion, and delirium with vivid hallucinations. Polysomnography revealed a marked reduction of sleep time, with central-type sleep apnea. Neither myoclonus nor periodic synchronous discharge (PSD) was observed. An autopsy revealed diffuse spongiform changes and astrocytosis throughout the cerebral gray matter, with severe involvement of the mammillary bodies and thalamus. Prion protein (PrP) immunostaining was positive in kuru plaques in the cerebellum, PrP polymorphism at codon 129 was heterozygous Met/Val, and proteinase K resistant PrP (PrP(res)) was demonstrated by Western blotting. The lack of necrotizing lesions in the mammillary bodies, thalamus, and periaqueductal gray matter could rule out WE. The data suggest that the present case of CJD is consistent with PrP(res) type 2 (CJD M/V 2), but was unique in the lack of some typical CJD signs and the presence of signs of WE and sleep abnormalities.
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PMID:Wernicke encephalopathy-like symptoms as an early manifestation of Creutzfeldt-Jakob disease in a chronic alcoholic. 1037 Oct 84

Postoperative complications resulting from bariatric surgery can lead to severe vitamin-deficiency states, such as Wernicke's encephalopathy (WE). We present a 29-year-old woman with BMI 41.7 with no history of alcoholism who developed acute WE after a gastric bypass for morbid obesity. After persistent vomiting for 2 weeks postoperatively, symptoms began with headache, vertigo, diplopia, nystagmus, tingling and weakness in both upper and lower extremities, urinary incontinence, and memory loss to recent events. All investigations, including upper GI endoscopy, Gastrografin meal and even MRI, were normal. A dramatic improvement occurred in 24 hrs after starting 100 mg thiamine infusion daily. We recommend that patients undergoing bariatric surgery should be started on thiamine supplementation once oral intake begins, because this case showed that postoperative acute WE can develop before 6 weeks, unlike other reports.
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PMID:Very early onset of Wernicke's encephalopathy after gastric bypass. 1668 41

It is generally assumed that neuronal cell death is minimal in liver failure and is insufficient to account for the neuropsychiatric symptoms characteristic of hepatic encephalopathy. However, contrary to this assumption, neuronal cell damage and death are well documented in liver failure patients, taking the form of several distinct clinical entities namely acquired (non-Wilsonian) hepatocerebral degeneration, cirrhosis-related Parkinsonism, post-shunt myelopathy and cerebellar degeneration. In addition, there is evidence to suggest that liver failure contributes to the severity of neuronal loss in Wernicke's encephalopathy. The long-standing nature of the thalamic and cerebellar lesions, over 80% of which are missed by routine clinical evaluation, together with the probability that they are nutritional in origin, underscores the need for careful nutritional management (adequate dietary protein, Vitamin B(1)) in liver failure patients. Mechanisms identified with the potential to cause neuronal cell death in liver failure include NMDA receptor-mediated excitotoxicity, lactic acidosis, oxidative/nitrosative stress and the presence of pro-inflammatory cytokines. The extent of neuronal damage in liver failure may be attenuated by compensatory mechanisms that include down-regulation of NMDA receptors, hypothermia and the presence of neuroprotective steroids such as allopregnanolone. These findings suggest that some of the purported "sequelae" of liver transplantation (gait ataxia, memory loss, confusion) could reflect preexisting neuropathology.
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PMID:Neuronal cell death in hepatic encephalopathy. 1785 42

A young woman who underwent gastric bypass surgery for morbid obesity had intractable nausea and vomiting for several weeks postoperatively, leading to poor intake and excessive weight loss. In the ninth postoperative week, she became confused and off balance and reported blurred and double vision. Examination disclosed slow saccades, nystagmus, and impaired abduction of both eyes as well as memory loss and ataxia. Visual acuity was slightly subnormal, and ophthalmoscopy disclosed a thickened and telangiectatic peripapillary nerve fiber layer with retinal hemorrhages. MRI showed high T2 and FLAIR signal in the dorsomedial thalamus and mamillary bodies bilaterally, substantiating a clinical diagnosis of Wernicke encephalopathy (WE). After thiamine treatment, visual acuity returned to normal and eye movements and alignment almost completely normalized. Fundus abnormalities eventually regressed. Although the ocular motor findings of WE have been well documented, the ophthalmoscopic findings have not. Resembling the findings in Leber hereditary and toxic optic neuropathies, they may represent manifestations of impaired mitochondrial function in retinal ganglion cells and capillaries. Recognition that these ophthalmoscopic findings may occur in WE is important to avoid procedures such as lumbar puncture that may delay urgent treatment with thiamine.
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PMID:Peripapillary nerve fiber layer thickening, telangiectasia, and retinal hemorrhages in wernicke encephalopathy. 2018 9

Wernicke's syndrome, caused by thiamine deficiency, is most commonly associated with alcoholism but can also occur in patients who are malnourished or have malabsorption of nutrients for other reasons. Since the classic triad of encephalopathy, nystagmus and ataxia occurs simultaneously in only 10-33% of cases, a high index of suspicion is needed in any patient with confusion and memory loss. In this case report, we present a 56-year-old female patient with metastatic colon cancer complicated with enterocutaneous fistula. She developed Wernicke's encephalopathy precipitated by 5-fluorouracil infusion. Replacement with thiamine rapidly reversed her neurologic symptoms and signs.
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PMID:Wernicke's Encephalopathy in Colon Cancer. 2153 79

Thiamin is a water-soluble vitamin also known as vitamin B1. Its biologically active form, thiamin pyrophosphate (TPP), is a cofactor in macronutrient metabolism. In addition to its coenzyme roles, TPP plays a role in nerve structure and function as well as brain metabolism. Signs and symptoms of thiamin deficiency (TD) include lactic acidosis, peripheral neuropathy, ataxia, and ocular changes (eg, nystagmus). More advanced symptoms include confabulation and memory loss and/or psychosis, resulting in Wernicke's encephalopathy and/or Wernicke's Korsakoff syndrome, respectively. The nutrition support clinician should be aware of patients who may be at risk for TD. Risk factors include those patients with malnutrition due to 1 or more nutrition-related etiologies: decreased nutrient intake, increased nutrient losses, or impaired nutrient absorption. Clinical scenarios such as unexplained heart failure or lactic acidosis, renal failure with dialysis, alcoholism, starvation, hyperemesis gravidarum, or bariatric surgery may increase the risk for TD. Patients who are critically ill and require nutrition support may also be at risk for TD, especially those who are given intravenous dextrose void of thiamin repletion. Furthermore, understanding thiamin's role as a potential therapeutic agent for diabetes, some inborn errors of metabolism, and neurodegenerative diseases warrants further research. This tutorial describes the absorption, digestion, and metabolism of thiamin. Issues pertaining to thiamin in clinical practice will be described, and evidence-based practice suggestions for the prevention and treatment of TD will be discussed.
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PMID:Thiamin in Clinical Practice. 2556 26


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