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

Acquired immune deficiency syndrome (AIDS) has become a major public health problem with over 12,000 cases and 6,000 deaths reported to date. Although there has been an explosion of knowledge in the virology, immunology and pathology of AIDS, relatively little has been written on the neuropsychiatric aspects. This report reviews the existing literature on the neuropsychiatric complications of AIDS. As many as 40 percent of patients with AIDS have neurologic complications at some point in their illness. These complications include either focal deficits attributable to opportunistic organisms infecting the CNS or diffuse encephalopathy caused by viral infection or lymphoma infiltration. Psychiatric complications include major depression, adjustment disorder with depressed mood, and organic brain syndrome with affective, delusional or demented features. Inpatient and consulting psychiatrists must be alert to these complications of AIDS so as to make accurate diagnoses and deliver appropriate therapy. Further studies, integrating both psychiatric and neurologic perspectives, are needed to better elucidate the neuropsychiatric complications of AIDS and help plan appropriate therapeutic interventions.
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PMID:Neuropsychiatric complications of AIDS: a literature review. 352 60

A case of major depressive disorder complicated by carbon monoxide (CO)-induced Parkinson's syndrome is reported. Computerized axial tomography (CAT) revealed bilateral globus pallidus necrosis. Clinical, CAT, and neuropathological findings in other cases of CO encephalopathy with and without parkinsonism are reviewed. The utility of CAT in the diagnostic workup and in following clinical course is discussed, as are the difficulties of making a diagnosis of an antecedent primary psychiatric disorder in the presence of neurological and psychiatric sequelae of CO intoxication. There was no clinical response to a tricyclic antidepressant, but both the mood and movement disorders responded fully to L-dopa. The implications of these findings with regard to the central neurochemical pathophysiology in this patient and in major depressive disorder in general are discussed.
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PMID:Major depression and carbon monoxide-induced parkinsonism: diagnosis, computerized axial tomography, and response to L-dopa. 402 Mar 69

We report a case of FIRDA in the EEG of a patient diagnosed as major depression with pituitary adenoma and hyponatremic encephalopathy. The pituitary adenoma appeared to be a major factor responsible for FIRDA in this case. Although other factors associated with this case, i.e., diffuse encephalopathy and administration of antipsychotic drugs, have been reported to be causative, FIRDA remained in the EEG after these other factors diminished. Although size of the pituitary adenoma that might be associated with FIRDA in the EEG recording was not identified in this study, FIRDA may be associated with a small pituitary adenoma less than 10 mm in diameter. We think a diligent search for additional pathology is recommended if FIRDA is seen in the EEG of an otherwise normal patient.
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PMID:Frontal intermittent rhythmic delta activity (FIRDA) in pituitary adenoma. 755 5

The eosinophilia-myalgia syndrome (EMS), a multisystem disorder associated with ingestion of L-tryptophan-containing products, causes sclerodermatous skin changes, cardiopulmonary disease, and a range of peripheral neurologic complications. Many EMS patients also report cognitive difficulty in association with the disease. To determine the frequency of objective neurocognitive impairment in EMS patients with subjective complaints of cognitive difficulty and to assess the relationship of neurocognitive loss with demographic features, degree of peripheral eosinophilia, and psychiatric diagnosis, we compared 24 EMS patients with 32 age- and education-matched healthy controls, using a comprehensive neuropsychological test battery. EMS patients additionally underwent a psychiatric interview and rheumatologic evaluation. Sixty-two percent (15 of 24) of the EMS patients demonstrated neurocognitive deficits. Compared with healthy controls, EMS patients demonstrated significant impairment on tests of verbal memory, visual memory, conceptual reasoning, and motor speed. Cognitively impaired EMS patients did not differ from those without cognitive impairment on demographic markers, degree of peripheral eosinophilia, presence of peripheral neuropathy, or frequency of concurrent psychiatric disorder, including major depression. These data support the hypothesis that EMS is associated with an encephalopathy in addition to its previously recognized peripheral neuropathy and other rheumatologic manifestations.
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PMID:Neurocognitive dysfunction in the eosinophilia-myalgia syndrome. 849 48

The paper gives a brief review of human molybdenum metabolism and toxicity and presents the first known case of acute clinical poisoning with molybdenum from the dietary molybdenum (Mo) supplement in a male patient in late thirties. In over 18 days, the patient had consumed a cumulative dose of 13.5 mg Mo (300-800 micrograms Mo/day). Followed the development of acute psychosis with visual and auditory hallucinations, a series of petit mal seizures, and one life threatening grand mal attack. The symptoms remitted several hours after the start of chelation therapy with calcium ethylene diamine tetraacetic acid (CaEDTA). A battery of neuropsychological tests and Spectral Emission Computer Tomography demonstrated evident frontal cortical damage of the brain. One year after the Mo poisoning, the patient was diagnosed toxic encephalopathy with executive deficiencies, learning disability, major depression, and post-traumatic stress disorder. The paper strongly advocates issuance of and strict adherence to written warnings on the instruction labels not to mix potentially harmful neurotoxic substances, such as molybdenum, with other nutriceuticals and to instructions stating maximal single and cumulative doses. Molybdenum is a new and unwelcome member of the "metal madness" family.
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PMID:A case report of acute human molybdenum toxicity from a dietary molybdenum supplement--a new member of the "Lucor metallicum" family. 1064 45

This retrospective study characterized the P300 component of the auditory event related potential (ERP) and assessed its diagnostic value in occupational chronic solvent encephalopathy (CSE). The P300 was recorded on 86 CSE patients by the classical oddball paradigm. In addition to the laboratory's reference values, we used an age and education matched control group that consisted of 104 blue-collar workers with no known occupational solvent exposure. The association of P300 values with solvent exposure indices, major depression, alcohol consumption, and neuropsychological parameters was studied. The P300 amplitude was lower in CSE patients (mean 7.5 microV; S.D. 3.6) compared to laboratory controls (mean 11.8 microV; S.D. 4.1; F(1,167)=24.4; p<0.001, 95% CI -4.4 to -1.8) and to matched controls (mean 9.0 microV; S.D. 4.0; p=0.007, 95% CI -2.6 to -0.4). The P300 latency was longer in the CSE patients (mean 358 ms; S.D. 28) compared to laboratory controls (mean 339 ms; S.D. 19, F(1,167)=7.6, p=0.006, 95% CI 3.12-18.7) but did not differ from matched controls (mean 358 ms; S.D. 22; p=0.947, 95% CI -7.4 to 6.9). The solvent exposure indices, major depression, or alcohol consumption did not associate with the P300 values. The P300 amplitude correlated positively with the Digit Symbol test. All the amplitude values in the patient group and in the matched control group were classified as normal (i.e. age corrected mean+/-2.5S.D.) against the laboratory's reference values. Thirty percent of the latencies in the CSE patient group and 26% in the matched control group were classified as abnormal. At group level, the decreased P300 amplitudes in CSE patients may reflect solvent-related pathophysiology. However, the P300 measured with the classical oddball paradigm does not seem to be sensitive at individual level or useful in clinical practice.
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PMID:P300 of auditory event related potentials in occupational chronic solvent encephalopathy. 1786 44

Thyroid dysfunctions may be accompanied by numerous neurological and psychiatric disorders. The most known is cognitive impairment and depression in hypothyroid patients, as well as an increased risk of cerebrovascular accidents. A separate, although a rare entity, is Hashimoto's encephalopathy. In hyperthyroidism there is an increased incidence of psychiatric disorders, including apathetic hyperthyroidism and hyperthyroid dementia. Functional imaging of cerebral blood flow and metabolism helped establish both global and/or regional decrease of both cerebral blood flow and metabolism in hypothyroidism, particularly in regions mediating attention, motor speed and visuospatial processing. Hypothyroid dementia may be mediated by neurocircuitry different from that in major depression. Less is known on flow/metabolism changes in hyperthyroidism. Global blood flow may be slightly increased, with regional deficits of blood flow, particular in hyperthyroid dementia. As presented above radionuclide functional imaging showed some metabolic patterns in thyroid dysfunctions, but still many issues remain unresolved. In particular little is known about the underlying pathology of cognitive impairment and depression in hypothyroidism, which may differ from ones in euthyroid patients. Also little is known about the reversibility of changes in cerebral blood flow following thyroid replacement therapy. In hyperthyroid patients functional imaging might contribute to elucidate the background of apathetic hyperthyroidism and potential different background of psychiatric complications.
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PMID:Neurological and psychiatric disorders in thyroid dysfunctions. The role of nuclear medicine: SPECT and PET imaging. 1838 53

Central nervous system (CNS) concentrates almost 10% of total zinc in the human body. Imbalances in zinc concentration are associated with numerous CNS diseases. Zinc deficiency is associated with nervous anorexia, major depression, cognitive impairment, and uncontrolled behavior. Our data reveal that plasma zinc concentration is decreased in major depression and it significantly increases following sertraline or amitriptyline treatment. Also, we found that ZnCl2 administration while inducing morphine-dependence in rats significantly decreases the symptoms of opioid-withdrawal syndrome. Recent data incriminate zinc deficit in the development of encephalopathy following severe impairment of hepatic function. On the other hand, zinc content of certain brain areas in Alzheimer disease is twice that in controls. Parkinson disease is also associated with higher zinc concentrations in the brain than normal. The ratio plasma zinc- other bivalent cations is also important for normal brain function.
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PMID:[Zinc involvements in the brain]. 1838 91

Encephalopathy associated with septic shock as well as psychiatric disorders can be caused by the central nervous formation of reactive oxygen species (ROS) associated with inflammation. The systemic application of lipopolysaccharide (LPS, 100 mug/kg i.p.) also serves as a model for major depression and results in enhanced inflammatory processes. which are characterized by the stimulation of microglia or macrophages that then impair normal brain function. The aim of the present study was to analyze the effect of peripherally applied LPS on the central nervous formation of ROS and IL-6 in wild-type mice and in mice lacking the NADPH oxidase Nox2 subunit gp91phox. Microdialysis was performed in the striatum of the mice. Central nervous ROS were detected by electron spin resonance spectroscopy using 1-hydroxy-3-methoxycarbonyl-2,2,5,5-tetramethylpyrrolidine (CMH) as reactant, which was infused via a microdialysis probe. IL-6 was measured in microdialysis samples by an immunoassay. Finally, blood samples were taken by heart puncture to detect IL-6 in plasma. In the wild-type mice, LPS significantly increased the ROS formation in the striatum of wild-type mice and resulted in a significantly enhanced IL-6 production. In the mice lacking the NADPH oxidase Nox2 subunit gp91phox, LPS did not enhance ROS formation, while central IL-6 was significantly increased. IL-6 plasma values were enhanced in both types of mice. In conclusion, the gp91phox-containing NADPH oxidase complex is involved in the central nervous ROS formation after peripheral LPS stimulation and might be a pharmacological target in patients with septic shock.
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PMID:Lipopolysaccharide-induced radical formation in the striatum is abolished in Nox2 gp91phox-deficient mice. 1986 38

Mitochondrial respiratory chain disorders are a group of genetically and clinically heterogeneous disorders caused by the biochemical complexity of mitochondrial respiration and the fact that two genomes, one mitochondrial and one nuclear, encode the components of the respiratory chain. These disorders can manifest at birth or present later in life. They result, at least in part, in defective production of ATP. Typically, mitochondrial disorders affect tissues with high energetic demands such as skeletal muscle, cardiac muscle, and the central nervous system. Neurological dysfunction is the most frequent clinical presentation of these disorders. The central nervous system is highly dependent on oxidative metabolism, and particular mitochondrial disorders are accompanied by focal brain necrosis (Leigh disease), dementia, or static encephalopathy. Furthermore, many children with mitochondrial encephalomyopathies present with more subtle and indolent signs including focal cognitive deficits of memory, perception, and language. Some subjects with mitochondrial disorders may also exhibit nonverbal cognitive impairment, compromised visuospatial abilities, and short-term memory deficits associated with working memory that likely reflect defects in synaptic plasticity. Psychiatric features are found within the clinical spectrum of mitochondrial syndromes. It is increasingly recognized that mitochondrial dysfunction may be associated with neuropsychiatric abnormalities such as dementia, major depression, and bipolar disorder. Furthermore, several lines of evidence suggest that there is involvement of mitochondrial dysfunction in schizophrenia, including documented alterations in brain energy metabolism, electron transport chain activity, and expression of genes involved in mitochondrial function. The purpose of this review article is to summarize the psychiatric features observed in mitochondrial cytopathies and discuss possible mechanisms of dysfunctional cellular energy metabolism that underlie the pathophysiology of major subsets of psychiatric disorders.
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PMID:The role of mitochondrial dysfunction in psychiatric disease. 2081 28


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