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Query: UMLS:C0011570 (
depression
)
172,036
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Digital EEG (DEEG) and quantitative EEG (QEEG) are recently developed tools present in many clinical situations. Besides showing didactic and research utility, they may also have a clinical role. Although a considerable amount of scientific literature has been published related to QEEG, many controversies still subsist regarding its clinical utilization. Clinical applications are: 1. DEEG is already an established substitute for conventional EEG, representing a clear technical advance. 2. Certain QEEG techniques are an established addition to DEEG for: 2a) screening for epileptic spikes or seizures in long-term recordings; 2b) Operation room and intensive care unit EEG monitoring. 3. Certain QEEG techniques are considered possible useful additions to DEEG: 3a) topographic voltage and dipole analysis in epilepsy evaluations; 3b) frequency analysis in cerebrovascular disease and dementia, mostly when other tests have been inconclusive. 4. QEEG remains investigational for clinical use in postconcussion syndrome, learning disability,
attention disorders
, schizophrenia,
depression
, alcoholism and drug abuse. EEG brain mapping and other QEEG techniques should be clinically used only by physicians highly skilled in clinical EEG interpretation and as an adjunct to traditional EEG work.
...
PMID:[Guidelines for recording/analyzing quantitative EEG and evoked potentials. Part II: Clinical aspects]. 1034 40
Multiple sclerosis is an immune-mediated inflammatory demyelinating disease of the central nervous system clinically characterized by relapses and remissions of neurological disturbance. A typical relapse, exemplified by optic neuritis, increases in severity over a week or two and after approximately one month begins to remit. Resolution takes place over the course of two to three months. In the early stages, clinical recovery is virtually complete, though persistent abnormalities of conduction can usually be detected by evoked potential techniques and persistent structural abnormalities can be detected by magnetic resonance imaging (MRI). These techniques, together with cerebrospinal fluid examination for oligoclonal IgG, provide supporting evidence for the diagnosis which, in the absence of a specific test, nevertheless remains primarily clinical. The course of the disease is very variable, but after a number of years neurological deficit begins to accumulate after each relapse. In most patients, the relapsing and remitting phase of the disease is followed by a phase of continuous progression of disability. Cognitive disturbances can be detected in many patients even quite early in the course of the illness. Deficits in attention, memory and executive skills may be prominent and tend to become increasingly prominent as neurological deficit increases, although this is not always the case. There is some correlation between the extent of MRI abnormalities in the cerebral white matter and the severity of
cognitive deficit
.
Depression
and anxiety are commonly experienced but are poorly correlated to the lesion load seen on MRI. In contrast, the much rarer psychotic symptoms, euphoria and emotional lability are closely linked to the severity of white matter disease.
...
PMID:Multiple sclerosis: the disease and its manifestations. 1060 14
Mercury has well-established toxic effects on the central nervous system. This article describes comprehensive neuropsychological and emotional functioning of a group of 13 workers exposed to inorganic mercury vapor compared to that of a normal control group. The exposed group was exposed over a 2- to 4-week period and had elevated blood mercury levels. The evaluations were conducted between 10 and 15 months after exposure was terminated. Observed cognitive deficits included impairment in the following domains: motor coordination, speeded processing with and without a motor component, cognitive flexibility, verbal fluency, verbal memory, and visual problem solving and conceptualization. Emotional problems included increased focus on physical functioning,
depression
, anxiety, and social withdrawal.
Cognitive deficits
were, for the most part, not significantly associated with the degree of
depression
present.
...
PMID:Neurobehavioral effects of acute exposure to inorganic mercury vapor. 1063 33
Weight loss is a very common problem for patients with Alzheimer's Disease (AD), whether they live at home or in long-term care facilities. At any rate it depends on an imbalance between energy expenditure and intake. Though in the initial phases of the illness, the weight loss might be caused by socio-environmental and psychological factors and reduced autonomy, in the following stages it depends on Adversive Feeding Behaviours (AFBs). The AFBs invariably lead to protein, fat and sugar deficits as well as a vitamin deficit which presents a positive correlation with the cognitive performance level and negatively affects the course of the disease. Thus it is important to identify AFBs (Blandford Scale) as soon as possible, especially when they can be treated. Furthermore it is very important to recognise weight loss immediately and identify a possible malnutrition state, using investigative methods which allow for follow-up monitoring (Mini Nutritional Assessment). Pharmacological therapy of
cognitive deficit
and AFBs together with possible contemporary conditions (
depression
) and intervention on the nutrition, will be useful to avoid a deficiency state and the consequent negative repercussion on the disease.
...
PMID:[Nutritional deficiency and Alzheimer's disease: how to identify and prevent]. 1076 45
Two recently described polymorphisms in the promoter region of the apolipoprotein E (APOE), the -491A/T and Th1/E47csT/G polymorphism, have been suggested to be associated with an increased risk for Alzheimer's disease (AD) independent from the APOE epsilon 4 carrier status. We studied the association between the APOE epsilon 4 polymorphism and the -491A/T and Th1E47csT/G polymorphisms in a sample of 118 healthy, non-demented controls and 239 consecutively recruited gerontopsychiatric patients diagnosed as: Alzheimer's disease (N = 89), age mild cognitive impairment (N = 32), memory complainers without any
cognitive deficit
(N = 54) and
depression
/other psychiatric disorders (N = 64), to test whether the investigated polymorphisms have a high enough selectivity and specificity to distinguish between the different gerontopsychiatric disorders or to differentiate AD genetically from other forms of dementia, respectively. Also a possible association with the APOE epsilon 4 polymorphism was examined. We found a statistically significant association between the APOE epsilon 4 allele and Alzheimer's disease (p = 0.0001) and age associated memory impairment (p = 0.006). Our study failed to show an association between the promoter polymorphisms -491A/T and Th1E47csT/G in the APOE gene and gerontopsychiatric disorders either alone or in relationship to the APOE epsilon 4 polymorphism. However, if we combine our results with three previous published positive reports there seems to be an association between the -491A/T polymorphism and AD, though its size is less than found in the original publication.
...
PMID:Polymorphisms in the apolipoprotein E (APOE) gene in gerontopsychiatric patients. 1131 14
Paediatric bipolar disorder (PBD) is an increasingly diagnosed disorder affecting an estimated 1% of children and adolescents. Pharmacological treatment studies in PBD have lagged far behind those in adults. Children are currently treated with pharmacological agents, most of which have proven efficacy in adults. However, PBD is distinct from adult forms of bipolar disorder (BD) and may present unique treatment challenges. PBD often presents with rapid cycling and mixed manic states and a high co-morbidity with behavioural and
attention disorders
. Early onset
depression
may also be an early sign of PBD. Due to developmental considerations, the diagnosis of BD may be difficult to make in children without semi-structured interviews. This report discusses the special issues that should be considered when treating PBD and reviews the current literature regarding pharmacotherapy of this population. Mood stabilisers have been studied mostly in an open, uncontrolled fashion but there is growing evidence that lithium, divalproex and carbamazepine are effective in treating PBD. More recent treatment options include atypical antipsychotics and newer anticonvulsants. Other novel agents are currently being investigated in adult BD and may prove applicable to the paediatric form. Finally, based on the available data, a treatment algorithm for PBD is proposed.
...
PMID:Special issues in the treatment of paediatric bipolar disorder. 1133 11
While a complete understanding of the pathogenesis of Alzheimer's disease (AD) remains elusive, many conclusions can be drawn from the numerous epidemiological studies undertaken to date. Prevalence and incidence estimates show consistency, following a roughly exponential pattern with a doubling of both parameters roughly every five years after age 65. Roughly 7% of the population aged 65 and over has AD. The clinical course of the disease is reasonably well established and mortality rates rise with increasing levels of
cognitive deficit
. Four risk factors for AD are firmly established: increasing age, the presence of the apolipoproteinE-epsilon4 allele, familial aggregation of cases, and Down's syndrome. Numerous other associations have been shown in some studies, but not in others. For example, women generally appear at higher risk than men, as do people with lower levels of education;
depression
is probably prodromal; head injury is an established risk factor, and may interact with the apoE gene; several occupational exposures appear hazardous, and exposure to aluminum in the water supply confers excess risk. Hypertension and other vascular symptoms appear to predispose to AD, which is now seen as nosologically closer to vascular dementia than was previously believed. Several apparently protective factors have been identified, although preventive trials based on these have so far shown minimal effectiveness. The use of non-steroidal anti-inflammatory drugs to treat arthritis is associated with a reduced risk of AD, as is estrogen use by post-menopausal women. Physical activity appears beneficial, as does a diet with high levels of vitamins B6, B12 and folate. while red wine in moderate quantities appears protective. This review concludes with a discussion of the strengths and limitations of current epidemiological methods for studying Alzheimer's disease.
...
PMID:Alzheimer's disease: insights from epidemiology. 1144 98
Plasmalogens are glycerophospholipids of neural membranes containing vinyl ether bonds. Their synthetic pathway is located in peroxisomes and endoplasmic reticulum. The rate-limiting enzymes are in the peroxisomes and are induced by docosahexaenoic acid (DHA). Plasmalogens often contain arachidonic acid (AA) or DHA at the sn-2 position of the glycerol moiety. The receptor-mediated hydrolysis of plasmalogens by cytosolic plasmalogen-selective phospholipase A2 generates AA or DHA and lysoplasmalogens. AA is metabolized to eicosanoids. The mechanism of signaling with DHA is not known. The plasmalogen-selective phospholipase A2 differs from other intracellular phospholipases A2 in molecular mass, kinetic properties, substrate specificity, and response to glycosaminoglycans, gangliosides, and sialoglycoproteins. A major portion of [3H]DHA incorporated into neural membranes is found at the sn-2 position of ethanolamine glycerophospholipids. Studies with a mutant cell line defective in plasmalogen biosynthesis indicate that the incorporation of DHA is reduced in this RAW 264.7 cell line by 50%. In contrast, the incorporation of AA remains unaffected. This is reversed completely when the growth medium is supplemented with sn-1-hexadecylglycerol, suggesting that DHA can be selectively targeted for incorporation into plasmalogens. We suggest that deficiencies of DHA and plasmalogens in peroxisomal disorders, Alzheimer's disease (AD),
depression
, and attention deficit hyperactivity disorders (ADHD) may be responsible for abnormal signal transduction associated with learning disability,
cognitive deficit
, and visual dysfunction. These abnormalities in the signal-transduction process can be partially corrected by supplementation with a diet enriched with DHA.
...
PMID:Plasmalogens, phospholipase A2, and docosahexaenoic acid turnover in brain tissue. 1147 81
Although neurologic Lyme disease is known to cause cognitive dysfunction in adults, little is known about its long-term sequelae in children. Twenty children with a history of new-onset cognitive complaints after Lyme disease were compared with 20 matched healthy control subjects. Each child was assessed with measures of cognition and psychopathology. Children with Lyme disease had significantly more cognitive and psychiatric disturbances.
Cognitive deficits
were still found after controlling for anxiety,
depression
, and fatigue. Lyme disease in children may be accompanied by long-term neuropsychiatric disturbances, resulting in psychosocial and academic impairments. Areas for further study are discussed.
...
PMID:A controlled study of cognitive deficits in children with chronic Lyme disease. 1174 19
Cognitive deficits
have been viewed as being characteristic features of schizophrenia. Neuropsychological impairment has been also identified in
depression
and mania. Recent studies have suggested that patients with bipolar disorder do not make full recovery between episodes of illness and that neuropsychological dysfunction may persist beyond these episodes. Remitted bipolar patients performed worse on Wisconsin Card Sorting Test, Verbal fluency and Stroop Test than healthy controls, the results of the patients with affective disorders with psychotic features were comparable with those of schizophrenics. Some studies suggest an association between the course of illness and the intensity of cognitive deficits, this link was not confirmed in other reports. Imaging studies have shown the presence of white matter lesions and other abnormalities in the brains of bipolar patients. The relative reduction in cerebral tissue may contribute to neuropsychological impairment in subgroup of bipolar patients. Results of studies on the role of white matter lesions are inconsistent. Recent studies point to an association between decreased prefrontal cortex volume and cognitive disturbances. Attention is focused on hippocampus volume as well, since it is associated with cognitive deficits in bipolar disorder. Further studies are needed to elucidate whether a severe course of illness is associated with more pronounced cognitive disorders and whether presence of psychotic symptoms during the acute phase of the illness is a predictor of the occurrence of cognitive deficits in patients with bipolar affective disorder.
...
PMID:[Cognitive deficits in the bipolar affective disorder]. 1176 Apr 65
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