Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diagnostic evaluation of dementia is directed toward the identification of treatable causes. It can be facilitated by classification of the dementia into one of four categories: attentional, amnestic, cognitive, and intentional. Intentional dementia reflects dysfunction of frontal lobe systems, components of which include the frontal cortex, basal ganglia, thalamus, limbic structures, and subcortical white matter. Disorders that affect one or more of these components and produce intentional dementia include Binswanger's disease, Parkinson's disease, Huntington's disease, HIV infection, closed head injury, normal pressure hydrocephalus, neoplasms, syphilis, vitamin B12 deficiency, multiple sclerosis, and a number of uncommon degenerative and acquired syndromes. Depression may resemble intentional dementia. Guidelines for diagnosis and management are discussed.
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PMID:Multi-infarct dementia, subcortical dementia, and hydrocephalus. 203 8

Huntington's disease (HD) is an inherited neuropsychiatric degenerative process characterized by movement disorder, dementia, and, often, affective disorder (AfD) (seen in 38% of patients). Depression in HD is not just an understandable reaction to fatal illness: 10% of HD patients develop mania; AfD can occur 20 yr before neurological signs; and mood disorders are not randomly distributed, but occur in a subset of HD families. This evidence suggests that AfD in HD relates to brain pathophysiology. With its clear neuropathology, HD is proposed as one model for biological underpinnings of idiopathic AfD. There is striking atrophy and neuronal loss in HD neostriatum, particularly caudate. Caudate has rich connections to the limbic system. It is hypothesized that AfD in HD relates to dysfunction of the part of the neostriatum damaged earliest, dorsal medial caudate. Preliminary studies on neuropathological differences between HD patients with and without AfD are discussed. HD neurochemistry is reviewed, emphasizing the excitotoxin hypothesis, which involves dysfunction of the glutamate neurotransmitter system in HD (especially the NMDA receptor, which contains a channel with a phencyclidine (PCP) binding site). Based on the HD model, it is suggested that the glutamate system (particularly NMDA receptors) be examined in idiopathic AfD.
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PMID:Huntington's disease as a model for mood disorders. Clues from neuropathology and neurochemistry. 214 28

The problem of multiple diagnoses in the same patient is a very real one in psychiatry. Theoretical causes of disease associations are reviewed and illustrated with examples from a variety of psychiatric conditions. These include Huntington's disease and depression, mitroprolapse and panic attacks, anxiety disorder and depression, and others.
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PMID:The application of genetic methods to the study of disease associations in psychiatry. 228 Oct 7

Event-related potentials (ERPs) were studied in patients with Huntington's disease (HD) and their offspring at risk in a simple auditory oddball paradigm requiring the counting of the rarer of two stimulus categories. Group statistical analysis revealed prolongation of latencies of components P2, N2 and especially P3 in HD patients and to a lesser extent in at-risks. In a large population of normals the age-latency relationship for component P3 showed a non-linear shape with increasing slope and scatter in the older age groups. A bipartate linear regression analysis splitting the normal population at age 50 was used for detection of abnormalities of P3 latency in individual cases. Abnormal P3 latencies were present in the majority of HD patients and also in 25% of clinically normal at-risks. Correlation analysis of ERP components with detailed psychometry revealed a particularly high association of P3 latencies with measurements requiring speeded information processing in non-verbal tasks. P3 amplitude did not covary with performance scores but unlike P3 latency showed association with depression and psychosis scores. From the results it appears that analysis of ERPs is a useful electrophysiological tool for an objective assessment of cognition both in clinically definite and subclinical stages.
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PMID:Event-related potentials in patients with Huntington's disease and relatives at risk in relation to detailed psychometry. 242 5

Patients with Huntington's disease (HD) commonly have concomitant depressive disorders. Prompted by reports of elevated corticotropin releasing factor (CRF) and reduced 5-hydroxyindoleacetic acid (5-HIAA) concentrations in lumbar cerebrospinal fluid (CSF) of patients with major depression, these CSF constituents were examined in 56 nonmedicated patients who were in the early stages of HD. Elevated CRF concentrations were found in patients with HD in comparison with a control group of 21 subjects without neurologic illness. The CSF 5-HIAA concentrations in patients with HD did not differ from that in four normal volunteers. Patients with HD who had depressive disorders (major depression or dysthymia) did not differ from those without depression with respect to CSF 5-HIAA or CRF concentration. However, a positive correlation was observed between severity of major depression and CRF concentration. These findings suggest that the depression associated with HD may differ neurochemically from that seen in other major depressive disorders, and support the notion that clinically significant depressive symptoms reflect heterogeneous pathophysiologic conditions with different neurochemical correlates.
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PMID:Cerebrospinal fluid correlates of depression in Huntington's disease. 245 53

Motor (postural tremor of the outstretched hands, most rapid voluntary alternating index finger movements and rise times of most rapid voluntary isometric index finger extensions) and psychometric tests (multiple choice vocabulary test - form b, syndrome short test, the German version of the standard progressive matrices - Raven, and the psychic and somatic findings according to the AMDP-system) as well as MRI-Scans were analysed in 100 HIV-infected patients of all stages according to the actual CDC-classification, but without any central-nervous or psychic deficit. Patients with drug, alcohol or tranquilizer abuse, opportunistic, cerebral infections or fever were excluded from the study. Tremor-peak-frequencies and reaction times did not show any significant difference to an age- and sex-matched control group; the other motor parameters revealed significant slowing in the patient group and a worsening with the CDC-stages. MRI-scans of all the patients were normal. The psychometric tests did not show significant alterations on a group statistical level, especially not in the depression scales. Morphologically, the motor performances of the HIV-infected patients resembled those of patients with basal ganglia diseases (M. Huntington, M. Wilson, M. Parkinson). Correspondingly, in some cases of clinically demented HIV-positive patients, MRI-scans showed lesions in the basal ganglia. It can be concluded, that there is an early subclinical central-nervous system affection in HIV-infected patients, especially of the basal ganglia, detectable with appropriate motor function tests sometimes considerably preceeding structural deficits seen later in the course of the disease in MRI-scans.
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PMID:[New electrophysiological findings on the incidence of brain involvement in clinically and neurologically asymptomatic HIV infections]. 251 87

Huntington's Chorea is a rare hereditary disease characterized by chronic progressive chorea and dementia, the exact cause of which is still under study, although many hypotheses are present. The patient has abnormality in gait, choreic movements of the limbs, face, slow mental deterioration and ill sustained depression. At later stages the patient becomes emaciated and succumbs. It is yet untreatable and diagnosed by CT Scans, bio-chemical analysis, family history and classic clinic picture. This disease poses a challenge for effective nursing care. There are studies conducted about the nursing aspects--effects of individualized care, effect of musical therapy. It has been shown that diversional therapies, short walks and giving the patient freedom in activities of daily living would help. The prevention at the present day seems to be voluntary sterilization of those at risk after proper counselling.
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PMID:Huntington's chorea: implications for nursing in India. 252 59

At present, positron emission tomography (PET) is the only technology affording the quantitative three-dimensional imaging of various aspects of brain function. Since glucose is the dominant substrate of the brain's energy metabolism, studies of glucose metabolism by PET of 2(18F)-fluoro-2-deoxy-D-glucose (FDG) are widely applied for investigating the participation of various brain systems in simple or complex stimulations and tasks. In focal or diffuse disorders of the brain, functional impairment of affected or inactivated brain regions is a reproducible finding. While glucose metabolism is decreased slightly with age in a regionally different degree, in most types of dementia severe changes of glucose metabolism are observed. Degenerative dementia of the Alzheimer type is characterized by a metabolic disturbance most prominent in the parietooccipito-temporal association cortex and later in the frontal lobe, while primary cortical areas, basal ganglia, thalamus, and cerebellum are not affected. By this typical pattern Alzheimer disease can be differentiated from other dementia syndromes, as e.g. Pick's disease (with the metabolic depression most prominent in the frontal and temporal lobe), multi infarct dementia (with multiple focal metabolic defects), and Huntington's chorea (with metabolic disturbance in the neostriatum). In demented patients PET studies can also be applied to the quantification of treatment effects on disturbed metabolism. Such studies demonstrated an equalization of metabolic heterogeneities in patients responding to muscarinergic cholinagonists and diffuse increase of metabolism during treatment with piracetam. The therapeutic relevance of such metabolic effects, however, must be proved in controlled clinical trials.
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PMID:Positron emission tomography findings in dementia disorders: contributions to differential diagnosis and objectivizing of therapeutic effects. 267 13

The probability of carrying the gene for Huntington's disease can in many cases be estimated in the children of affected persons by identifying a specific DNA marker that is genetically linked to the gene. We studied 47 persons at 50 percent risk of inheriting Huntington's disease who requested a presymptomatic or prenatal genetic-linkage test between September 1986 and January 1988. The participants were given pre-test counseling and psychological and neurologic evaluations. Nineteen persons later voluntarily withdrew from the protocol, including one who would have been excluded anyway, and one person was from a family that was too small to allow testing. Three D4S10 restriction-fragment-length polymorphisms produced by the HindIII, EcoRI, and Bg/I enzymes were used for all tests, and the probability that a subject was a Huntington's disease carrier was calculated. The accuracy of the test was compromised by a 4 percent recombination frequency between D4S10 and the Huntington's disease gene. Fifteen presymptomatic tests and one prenatal test were completed. Four yielded positive results, seven yielded negative results, and five were uninformative; seven persons are awaiting test results. All participants with positive tests experienced intermittent depression, but none required hospitalization, and no suicide threats were reported. Five participants received a diagnosis of Huntington's disease on the basis of the neurologic assessment. We conclude that some persons in the early stages of Huntington's disease may seek presymptomatic testing rather than neurologic evaluations.
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PMID:Predictive testing for Huntington's disease with use of a linked DNA marker. 289 60

The neurochemical effect of tetrabenazine was assessed by determining the levels of dopamine, noradrenaline and 5-hydroxytryptamine and their metabolites in post-mortem brain from Huntington's disease patients with or without a history of tetrabenazine treatment. The tetrabenazine-treated group showed a general description of monoamines in all regions studied, the greatest reduction being dopamine in the caudate. This provides the basis for the effect of tetrabenzine on chorea, while monoamine losses in limbic regions may mediate the production of side effects, such as depression.
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PMID:Depletion of monoamine transmitters by tetrabenazine in brain tissue in Huntington's disease. 290 81


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