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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To date, positron emission tomography (PET) has been the only technology for the quantitative imaging of the changes of regional cerebral glucose (rCMRGl) or oxygen metabolism and blood flow (rCBF) associated with psychophysical stimulation and with the performance of mental tasks. So far, the majority of studies performed in healthy subjects demonstrated activation patterns involving not only certain limbic structures, most of all hippocampus, amygdala, parahippocampus, and cingulate, but also temporal, parietal, and occipital association cortex, depending on the applied paradigm. Indeed, the closest correlation between regional metabolism and memory test scores was found in mesiotemporal structures during the performance of memory tasks. Metabolic or CBF studies also seem to indicate that memorizing strategies may differ among individuals. PET was repeatedly used to investigate metabolic and/or blood flow abnormalities in patients with various amnestic syndromes. In cases with uni- or bilateral lesions of mesiotemporal structures, caused by surgery, herpes simplex encephalitis, or permanent ischemic, anoxic, or toxic damage, disturbances of metabolism and blood flow typically extended far beyond the morphological defects detected by computed tomography or magnetic resonance. In acute transient global amnesia, CBF and metabolism were decreased bilaterally in the mesiotemporal lobes, where hypometabolism persisted for some time, while higher values were observed in thalamus and some cortical areas. Diencephalic lesions causing Korsakoff's syndrome were associated with decreased rCMRGl in the hippocampal formation, upper brainstem, cingulate, and thalamus. Discrete thalamic infarcts caused amnesia and metabolic depression in the morphologically intact ipsilateral thalamus and in various projection areas of the infarcted nuclei. In ischemic forebrain lesions, amnestic deficits could be related to involvement of the anterior cingulate and of basal cholinergic nuclei. A large number of pathologies are diffusely spread out in the brain and affect partially or predominantly structures in memory processing. This holds true especially in the various dementias where memory disturbances are a consistent and often leading feature. Notably, Alzheimer's disease can be distinguished from other dementias by its characteristic pattern of metabolic dysfunction, with the most prominent changes occurring in parietotemporal and frontal association cortex whose residual metabolism is related to the severity of the disease. Therefore, activation studies using paradigms involving memory functions enhance that typical pattern. Only in the activated state is metabolism of mesiotemporal structures significantly correlated with the performance in memory tests. Other dementias also affect some of the distributed memory networks, with Huntington's disease suggesting a role of the striatum in memory processing.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:PET correlates of normal and impaired memory functions. 156 50

Limited information is available regarding the relationship between elderly individuals and depression; but the clinician can anticipate problems in those who have had depression in the past, in those who are bereaved, in caretakers, and in patients with a number of other illnesses, including Alzheimer's disease, Parkinson's disease, Huntington's disease, stroke, alcoholism, and severe medical illness. Treatment may shorten the duration of the depression, limit long-term sequelae, and reduce the likelihood of suicide. More research with careful methodology would be helpful in clarifying directions for primary, secondary, and tertiary prevention.
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PMID:The prevention of major depression in the elderly. 157 73

A role of the caudate nucleus in depression has been suggested from relevant clinical conditions, such as patients with Huntington's disease or caudate infarcts, as well as animal studies. Correlations of caudate nucleus disease with depressive symptoms have been limited to autopsy studies and cases of gross pathological disorder, such as large infarcts. We used serial axial high-field magnetic resonance images and an unbiased stereological technique to estimate the volumes of the caudate nuclei in 50 patients who met DSM-III criteria for major depression (23 men, 48.3 +/- 17 years old) in comparison with 50 age- and gender-matched normal controls free of major neurological and psychiatric disorders. Depressed patients had smaller caudate nucleus volumes (5.2 +/- 1.6 cm3) compared with controls (6.2 +/- 1.7 cm3). Right and left caudate nucleus volumes were smaller in depressed patients compared with controls. Age was negatively correlated with caudate nucleus volumes in depressed patients as well as in controls. Caudate nucleus volumes in depressed patients were inversely correlated with the bicaudate and bifrontal indices. These results may be the first demonstration of diminished caudate nucleus volumes in depression and suggest a role for the caudate nucleus in the pathogenesis of major depression.
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PMID:Magnetic resonance imaging of the caudate nuclei in depression. Preliminary observations. 162 46

The predictive test for Huntington disease (HD) has allowed those at risk to determine gene status prior to symptoms. The purpose of this research was to understand the motivation and the anticipated reactions of those requesting the test. Forty persons at 50% risk for HD and 31 companions participated in a structured personal interview as part of the predictive test protocol. Reasons for taking the test centered on the reduction of anxiety and uncertainty associated with being at risk and enhanced planning and decision making. Participants also believed that taking the test would produce more positive than negative outcomes. With a favorable result, most anticipated a reduction of anxiety, a more normal future, and relief knowing their children would be at a very low risk. Most also cited benefits as more likely than consequences with an unfavorable result. Making the most of life, easier planning, and reduced uncertainty were rated as more likely than any of the adverse impacts, including short-term depression and becoming frightened. Almost all participants (95%) said they would rather learn that they have the HD gene than remain at 50% risk. The uncertainty, anxiety, and chronic stress associated with being at risk appears to underlie the motivation of many seeking the predictive test for HD.
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PMID:Understanding the decision to take the predictive test for Huntington disease. 167 28

At present, PET is the only technology affording the quantitative, three-dimensional imaging of various aspects of brain function. Since function and metabolism are coupled, and 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 parieto-occipito-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.
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PMID:Positron emission tomography in the differential diagnosis of organic dementias. 175 42

All cases (86) of Huntington's Disease presenting between 1970 and 1987 in the Grampian Health Board region were identified and a case note analysis of neurological and psychiatric syndromes carried out--the latter using the PSE syndrome check-list. The commonest syndromes were organic impairment, irritability, loss of interest and concentration and simple depression and these were often the presenting psychiatric syndromes. General anxiety, worrying and social unease occurred early, commonly before movement disorder and were associated with longer survival.
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PMID:The clinical manifestation of mental disorder in Huntington's disease: a retrospective case record study of disease progression. 182 3

The rate of disease progression was assessed for 42 persons affected by Huntington's disease who had been neurologically examined at least six times and followed up for at least 3 years. Disease progression was assessed by a disability rating scale administered at each examination. Slow progression was associated with older age at onset of disease and with heavier weight (body mass index) at the first examination. Men tended to have a slower disease progression than did women, and this was particularly evident among men inheriting Huntington's disease from affected mothers. Neither the butyrophenone haloperidol nor the tricyclic antidepressant imipramine were related to rate of progression. Assessments of depression, hostility, and tobacco use were also unrelated to rate of progression. Clinical trials in Huntington's disease should consider these factors when designing therapeutic studies.
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PMID:Factors associated with slow progression in Huntington's disease. 153 11

Twenty patients with Huntington's disease (HD) and a comparison group were studied by a depression scale (MADRS) and a neuropsychological test-battery assessing central areas of cognitive function. The main purpose was to analyze the consistency of findings across patients and focus on the role of specific factors in the impairments. The HD-patients are impaired relative to norms and the comparison-group in all areas but verbal conceptual function. We further divided the HD-patients into subgroups according to severity of neuropsychological impairment. The groups generally show a pattern of increasing deficits. Early changes are found in tests of cognitive efficiency, memory and sensomotor function, but the pattern of impairment is variable. The more severely affected subgroups show an increased decline in performance and progressive involvement of a broader range of functions. The pattern of depressive symptoms in HD-patients indicates that cognitive symptoms of concentration difficulties and lassitude are prominent in all subgroups.
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PMID:Neuropsychological findings and depressive symptoms in patients with Huntington's disease. 183 96

Neuronal loss in the cerebral cortex in Huntington's disease (HD) has not been well documented, nor has its laminar pattern been definitively established. We therefore counted neurons in individual cortical laminae in the dorsal frontal cortex of 5 HD and 5 control autopsy brains. Significant neuronal loss (to 57% of control, P = 0.002) was found in layer VI of HD brains. These cells project principally to the thalamus, the claustrum and other regions of cerebral cortex; thus their loss is unlikely to be the result of retrograde degeneration secondary to striatal pathology. Layer V neurons were also decreased (to 71% of control, P = 0.034). Degeneration of cerebral cortical neurons may be at least partly responsible for some of the non-choreic symptoms of HD, such as dementia, irritability, apathy, and depression.
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PMID:Neuronal loss in layers V and VI of cerebral cortex in Huntington's disease. 184 78

The excitatory amino acid glutamate plays an important role in the mammalian CNS. Studies conducted from 1940 to 1950 suggested that oral administration of glutamate could have a beneficial effect on normal and retardate intelligence. The neurotoxic nature of glutamate resulting in excitotoxic lesions (neuronal death) is thought possibly to underlie several neurological diseases including Huntington's disease, status epilepticus. Alzheimer's dementia and olivopontocerebellar atrophy. This neurodegenerative effect of glutamate also appears to regulate the formation, modulation and degeneration of brain cytoarchitecture during normal development and adult plasticity, by altering neuronal outgrowth and synaptogenesis. In addition to its function as a neurotransmitter in several regions of the CNS, glutamate seems to be specifically implicated in the memory process. Long-term potentiation (LTP) and long-term depression (LTD), two forms of synaptic plasticity associated with learning and memory, both involve glutamate receptors. Studies with antagonists of glutamate receptors reveal a highly selective dependency of LTP and LTD on the N-methyl-D-aspartate and quisqualate receptors respectively. The therapeutic value of glutamate receptor antagonists is being actively investigated. The most promising results have been obtained in epilepsy and to some extent in ischaemia and stroke. The major drawback remains the inability of antagonists to permeate the blood-brain barrier when administered systemically. Efforts should be directed towards finding antagonists that are lipid soluble and able to cross the blood-brain barrier and to find precursors that would yield the antagonist intracerebrally.
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PMID:Glutamate in the mammalian CNS. 198 Nov 50


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