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Query: UMLS:C0085584 (encephalopathy)
18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A remarkable, intermittent sudden-onset vigilance and movement disorder in an exclusively breast-fed infant is reported, which was caused by cobalamin depletion due to maternal vitamin B12 malabsorption. The lack of cobalamin caused a severe encephalopathy in the infant, whose brain displayed a striking loss of volume and a delay of myelination. Proton magnetic resonance spectroscopy revealed an accumulation of lactate in the gray and white matter of the brain and a sustained depletion of choline-containing compounds in the white matter, reflecting a reversible disturbance of oxidative energy metabolism in brain cells and a long-lasting hypomyelination disorder. The clinical picture in conjunction with MRI and spectroscopic data of this case study yields more insight into the functions of cobalamin in the cerebral metabolism.
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PMID:Infantile cobalamin deficiency with cerebral lactate accumulation and sustained choline depletion. 1459 32

A male patient with portal hypertension, portal vein thrombosis, spontaneous splenorenal shunt formation, and encephalopathy, thought to have post-hepatitis B cirrhosis, is described. His condition deteriorated and necessitated liver transplantation. In the explant liver, nodular regenerative hyperplasia with pronounced vascular lesions both in portal venules and in arterioles was found instead of classical cirrhosis. Two years post-transplant he developed bilateral ischaemic femur head necrosis. The three disorders (portal vein thrombosis, nodular regenerative hyperplasia, and ischaemic hip necrosis) seemed to be due to a common vasculopathy induced by hyperhomocyteinaemia. Genetic studies showed that he carried a mutation in the gene encoding for formation of methylenetetrahydrofolate reductase. Treatment with folic acid combined with pyridoxine (vitamin B6) and cyanocobalamin (vitamin B12) normalised his serum homocysteine levels.
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PMID:Nodular regenerative hyperplasia, portal vein thrombosis, and avascular hip necrosis due to hyperhomocysteinaemia. 1669 59

A 57-year-old man was admitted to our hospital with a diagnosis of psychiatric emergency. His symptoms were similar to encephalitis, metabolic encephalopathy or acute depressive psychosis because of poor focal neurological signs. Laboratory examinations, including routine hematological and biochemical investigations, serum vitamin B1 B12 levels, and cerebrospinal fluid obtained by lumbar puncture, were normal. Brain CT was also normal, therefore it was difficult to make a diagnosis. But, we could clinically diagnose him as having pulmonary adenocarcinoma with numerous metastatic nodules of the brain. Because miliary lesions in the cerebral hemispheres, brainstem and cerebellum were disclosed on brain MRI. Furthermore, chest CT revealed the lung tumor in the left S8 area. In addition, laboratory examination showed a rise of tumor marker and cytologic examination of sputum revealed class V. Fluid-attenuated inversion recovery and contrast-enhanced MR images demonstrated more prominently miliary metastases, in particular lesions in the cerebral cortex, than T1- and T2-weighted images. There was neither edema in the surrounding region of metastatic nodules nor mass effect on all MR images. Spinal MRI showed no metastatic lesions. The patient died of respiratory failure at the age of 58, about eight months after the disease onset. The brain weighed 1,575 g. Neuropathological findings revealed diffuse miliary brain metastases located in all parts of the brain, except for the medulla oblongata. Histological examination disclosed multiple metastases from a well-differentiated adenocarcinoma with a predominant tubular pattern. There was neither edema nor glial reaction in the surrounding area of metastatic lesions. Many pseudorosettes were recognized and carcinoma cells, extending through perivascular spaces into the subarachnoid space, were noticed.
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PMID:[An autopsy case of miliary brain metastases]. 1651 14

During the last decade, scientific evidence is mounting that elevated plasma levels of homocysteine are associated with an increased risk of atherosclerosis and cardiovascular ischemic events. Despite this evidence, however, there are still concerns about the mechanisms(s) by which homocysteine exerts its pro-atherogenic effect, and it is unclear whether the decreased plasma levels of homocysteine through diet or drugs may be paralleled by a reduction in cardiovascular risk. Experimental studies have shown that many possible mechanisms are implicated in the pro-atherogenic effect of homocysteine. Endothelial function is altered in subjects with hyperhomocysteinemia, and endothelial dysfunction is correlated with plasma levels of homocysteine. Exercise training reduces plasma levels of homocysteine and improves endothelial function, however without evidence of a better outcome. Larger studies are needed in order to demonstrate that the reduction of plasma levels of homocysteine by oral supplementation with folates and vitamins B6 and B12 translates into a decreased incidence of ischemic events, in particular in patients with documented coronary artery disease and ischemic encephalopathy.
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PMID:[Hyperhomocysteinemia in pediatric age and nutritional aspects of folates: an early cardiovascular risk factor]. 1731 47

A 65-year-old woman was admitted to our hospital because of subacute deterioration of cognitive function. On admission, she presented with marked disorientation of time and place and inability to carry out commands. Mini-Mental State Examination score was 5/30. Although routine laboratory examinations including thyroid function, vitamin B1 and B12, serum syphilitic reaction, sIL-2 receptor level, titers of herpes simplex and zoster viruses, and HIV antibody were normal, titers of anti-thyroglobulin (TG) antibodies and thyroid peroxidase (TPO) antibodies were elevated. Cerebrospinal fluid showed normal findings. Brain MRI revealed diffuse high intensity in the white matter on diffusion- and T2-weighted images, mimicking leukoencephalopathy. We made a diagnosis of Hashimoto's encephalopathy, based on clinical features and high titers of anti-thyroid antibodies. Following administration of steroid hormone, her cognitive impairment gradually improved, associated with decrease of the white matter abnormality on MRI. Hashimoto's encephalopathy should be kept in mind in the differential diagnosis of subacute leukoencephalopathy with cognitive decline.
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PMID:[Case of Hashimoto's encephalopathy with diffuse white matter lesions on diffusion-weighted MRI]. 1751 Dec 80

We describe an unusual case of a 25-year-old human immunodeficiency virus (HIV)-positive male with a pre-treatment CD4 count of 144 cells/microL, who had received highly active antiretroviral therapy (HAART) consisting of lamivudine, stavudine and nevirapine for three months, developing immune reconstitution inflammatory syndrome (IRIS) manifesting as disseminated tuberculosis (TB), myelopathy, encephalopathy and deep venous thrombosis (DVT). In addition to HAART and antituberculosis treatment (ATT), the patient was given non-steroidal anti-inflammatory drugs, oral vitamin B12 and heparin, which was later switched to oral warfarin.
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PMID:Immune reconstitution inflammatory syndrome manifesting as disseminated tuberculosis, deep venous thrombosis, encephalopathy and myelopathy. 1903 57

A 52-year-old woman was admitted to the hospital because of appetite loss, unsteadiness, psychogenic symptoms, ataxia, and consciousness disturbance as a result of the ingestion of a diet restricted to only carbohydrates for a long term. Laboratory examination indicated the presence of pancytopenia with macrocytic anemia; further, decreased vitamin B1 and B12 levels were detected in her serum. Magnetic resonance imaging fluid attenuated inversion recovery (FLAIR), revealed high-signal intensity in the bilateral corpus striatum, third ventricle circumference, and cerebellar cortex. Thereafter, she received drip infusion that did not include vitamin B1 or B12 and subsequently suffered a cardiac arrest due to the aggravation of cardiac insufficiency; consequently, she was transferred to our hospital. Upon admission the patient was diagnosed to have obvious cardiomegaly with pleural effusion; further, a negative T-wave was obtained on the electrocardiogram. A diagnosis of beriberi heart disease was made because of thiamine deficiency. She was treated by thiamine administration, following which the cardiac symptoms improved immediately. Various neurological symptoms caused by encephalopathy, peripheral neuropathy and subacute combined spinal cord degeneration improved by treatment with thiamine and cyanocobalamine administration; however, some of these symptoms still remained. General awareness of the fact that neurological symptoms can be caused by vitamin deficiency is essential.
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PMID:[Case of Wernicke's encephalopathy and subacute combined degeneration of the spinal cord due to vitamin deficiency showing changes in the bilateral corpus striatum and cardiac arrest due to beriberi heart disease]. 1980 6

This review is an update of the long-term follow-up of nutritional and metabolic issues following bariatric surgery, and also discusses the most recent guidelines for the three most common procedures: adjustable gastric bands (AGB); sleeve gastrectomy (SG); and roux-en-Y gastric bypass (GBP). The risk of nutritional deficiencies depends on the percentage of weight loss and the type of surgical procedure performed. Purely restrictive procedures (AGB, SG), for example, can induce digestive symptoms, food intolerance or maladaptative eating behaviours due to pre- or postsurgical eating disorders. GBP also has a minor malabsorptive component. Iron deficiency is common with the three types of bariatric surgery, especially in menstruating women, and GBP is also associated with an increased risk of calcium, vitamin D and vitamin B12 deficiencies. Rare deficiencies can lead to serious complications such as encephalopathy or protein-energy malnutrition. Long-term problems such as changes in bone metabolism or neurological complications need to be carefully monitored. In addition, routine nutritional screening, recommendations for appropriate supplements and monitoring compliance are imperative, whatever the bariatric procedure. Key points are: (1) virtually routine mineral and multivitamin supplementation; (2) prevention of gallstone formation with the use of ursodeoxycholic acid during the first 6 months; and (3) regular, life-long, follow-up of all patients. Pre- and postoperative therapeutic patient education (TPE) programmes, involving a new multidisciplinary approach based on patient-centred education, may be useful for increasing patients'long-term compliance, which is often poor. The role of the general practitioner has also to be emphasized: clinical visits and follow-ups should be monitored and coordinated with the bariatric team, including the surgeon, the obesity specialist, the dietitian and mental health professionals.
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PMID:Medical follow up after bariatric surgery: nutritional and drug issues. General recommendations for the prevention and treatment of nutritional deficiencies. 2015 42

Background. Vitamin B12 is vital for optimal functioning of various organ systems but more importantly the central nervous system and the hematological system. Deficiency of vitamin B12 clinically manifests as excessive daytime fatigue, memory difficulties, encephalopathy, myelopathy, peripheral neuropathy, and optic neuropathy. In occupational medicine, vitamin B12 deficiency has been reported with exposure to nitrous oxide in health care workers. However, not much is known about exposure to Freons in other industries and vitamin B12 deficiency. Aim. We are reporting a case of vitamin B12 deficiency in the setting of exposure to chlorofluorocarbon (CFC) gases. Case Report. A 55-year-old male refrigerator mechanic experienced recurrent visual symptoms, which included diplopia and blurring. A complete workup was done and was significant of vitamin B12 deficiency. However, his B12 levels were refractory to supplementation. Appropriate precautions at workplace improved patient's symptoms and were associated with significant improvement in B12 levels. Conclusion. To the best of our knowledge, this is the first reported case of vitamin B12 deficiency (that remains refractory to supplementation) in the setting of exposure to Freon gases.
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PMID:Vitamin B12 Deficiency due to Chlorofluorocarbon: A Case Report. 2146 74

Approximately one in three Americans is obese. Current society guidelines recommend bariatric surgery after conservative measures at weight loss have failed. The frequency of bariatric surgeries has increased significantly over the past decade. While considered both safe and effective, bariatric surgery presents a distinct set of risks. This review focuses on the neurological complications of bariatric surgery. Injuries have been reported at all levels of the nervous system, including the central, peripheral, and enteric nervous system. Injury can be classified according to time of presentation and location. The two main mechanisms of nerve injury are from mechanical injury or as a consequence of malnutrition. Encephalopathy, peripheral neuropathies, myelopathies, and radiculoneuropathies have all been reported. Mechanical injuries likely occur from mechanical compression. Malnutrition injuries result from multi-micronutrient deficiencies. The most likely candidates are vitamin B12, folate, zinc, thiamin, copper, vitamin A, and vitamin E deficiencies.
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PMID:Neurologic complications of bariatric surgery: involvement of central, peripheral, and enteric nervous systems. 2266 Dec 92


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