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)

A random sample of patients aged 70 and over from a general practice were interviewed in their own homes. Information was sought on their hearing difficulty and mental state: standardised measures of anxiety, depression, and memory loss were used. Of the 657 subjects interviewed, 33% reported having difficulty hearing normal conversations and 6% reported experiencing "much difficulty." Hearing difficulty was associated with both depression and anxiety, but the associations weakened when adjustment was made for physical disability. The association with memory loss disappeared when adjusted for physical disability. There was a close relationship both with age and physical disability.
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PMID:Hearing difficulty and its psychological implications for the elderly. 623 51

Primary hyperparathyroidism is a not uncommon disease in the elderly. A prevalence of 3% for women and 1% for men is reported in subjects aged 65 years and over. Routine serum calcium determination and parathyroid hormone radioimmuno-assay allow to make an early diagnosis in still asymptomatic subjects. In the elderly the clinical features of the disease are often aspecific presenting with psychiatric and/or neuromuscular and/or cardiovascular disorders. This report refers to a 75 year-old woman admitted to our Department with a suspicion of senile dementia. She was affected by loss of memory, hallucinations, nausea, loss of appetite, mild polydipsia and polyuria. The patient was dependent in one activity of daily living (Index of Independence in Activities of Daily Living, ADL) and partially dependent in instrumental activities of daily living (Instrumental Activities of Daily Living Scale, IADL). The Short Portable Mental Status Questionnaire (SPMSQ) and the Geriatric Depression Scale (GDS) showed mild mental impairment and mild depression. Routine biochemical screening revealed a significant hypercalcemia. Parathormon assay and parathyroid scintigram were performed to confirm the diagnosis of primary hyperparathyroidism. After treatment of dehydratation and hypercalcemia, parathyroidectomy was performed: a single parathyroid adenoma was found and removed. On discharge the patient was lucid and able to carry out all ADLs and IADLs.
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PMID:[Neuropsychologic symptoms of primary hyperparathyroidism in the elderly. Report of a clinical case]. 773 70

Memory loss and other cognitive dysfunctions, although common in elderly persons, are not universal features of old age. Instead they herald the presence of various neuropsychiatric diseases, which are first recognized as syndromes. The two most common neuropsychiatric syndromes, dementia and delirium, produce global changes in cognition and other capacities. They are differentiated by the patient's level of consciousness, which is impaired in delirium but intact in dementia. Delirium is generally reversible and often indicates serious physical illness. Although dementia is occasionally reversible, the mainstays of its management and treatment are palliative. Comorbid psychiatric symptoms are common in patients with both delirium or dementia, and their recognition and treatment constitute an important task for the geropsychiatrist. The differential diagnosis of primary dementing illness and other psychiatric illnesses such as depression is complex, because symptoms of the two kinds of disorders often coexist and common pathogenetic mechanisms may underlie both syndromes.
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PMID:Diagnosis and management of memory loss and cognitive disorders among elderly persons. 789 18

Altered noradrenergic function is associated with alcoholism. Reduced brain norepinephrine (NE) concentrations and beta-adrenergic receptor supersensitivity following chronic alcohol consumption suggest a reduced level of noradrenergic neurotransmission. To further elucidate the reason for changes in noradrenergic function, we determined the number of melanin-containing noradrenergic neurons in the locus coeruleus (LC) postmortem from 11 controls and 7 alcoholics. Controls did not have a known history of psychiatric or neurologic disorders and were drug-free by toxicological screen. The diagnosis of alcohol-dependence was based on DSM-III-R criteria. Alcoholics differed from controls in having 23% fewer LC neurons (control: 43,472 +/- 1,021; alcoholic: 33,398 +/- 2184; P < 0.0005) and 46% lower density of neurons (control: 1,227 +/- 89 cells per mm3; alcoholic: 663 +/- 94 cells per mm3; P = 0.001). The reduction in neurons was bilateral and throughout the middle third of the LC. The two groups did not differ with respect to LC length (control: 16.1 +/- 0.6 mm; alcoholic 15.3 +/- 0.9 mm; P = 0.47) or total LC volume (control: 37.3 +/- 2.8 mm3; alcoholic: 46.5 +/- 4.2 mm3; P = 0.09). Changes in noradrenergic neurotransmission in alcoholics may be due to fewer noradrenergic neurons in the locus coeruleus and may contribute to memory loss and depression, common consequences of alcoholism.
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PMID:Fewer pigmented neurons in the locus coeruleus of uncomplicated alcoholics. 795 60

Vascular dementia (VAD) is common, and small vessel disease is one of the most frequent etiologies of the disorder. Lacunar state and Binswanger's disease are the two types of VAD associated with small vessel disease. Lacunar state and Binswanger's disease produce a dementia syndrome with characteristics of subcortical dementia including slowing of information processing, impaired memory, and poor sustained attention. Executive dysfunction includes poor word list generation and verbal fluency (design generation), impaired motor programming with perseveration and impersistence, and difficulty with set shifting. Memory loss in subcortical VAD is characterized by poor retrieval and intact recognition. Apathy is ubiquitous in VAD and depression and psychosis are common. Parkinsonism with prominent gait disturbances in conjunction with pyramidal tract signs, dysarthria, pseudobulbar affect, and incontinence are frequent motor manifestations of VAD with small vessel disease. The lesions of subcortical VAD affect the structures--caudate nucleus, globus pallidus, thalamus-and connecting fibers of frontal--subcortical circuits and produce a clinical syndrome similar to that seen in other subcortical diseases.
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PMID:Vascular subcortical dementias: clinical aspects. 808 75

Brief perfusion of salines containing elevated (10.5-50 mM) [K+] plus glutamate (2.5 or 5 mM) could erase long-term potentiation (LTP) in rat hippocampal slices. Prolonged perfusion with high-[K+]/glutamate could cause persistent neuronal depression lasting > 1 h. LTP erasure occurred in the absence of generalized depression of axonal responsiveness, while persistent neuronal depression was associated with a failure of antidromic invasion of cells. The protocols used may contribute to the development of a model for the cellular study of memory loss following neurological dysfunction.
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PMID:Perfusion with high potassium plus glutamate can cause LTP erasure or persistent loss of neuronal responsiveness in the CA1 region of the hippocampal slice. 809 26

Age-related memory impairments may be due to dysfunction of the septohippocampal system. The medial septal area (MSA) provides the major cholinergic projection to the hippocampus and is critical for memory. Knowledge of the neurobiological mechanisms by which the cholinergic system can attenuate age-related memory loss can facilitate the development of effective cognitive enhancers. At present, one of the best neurobiological models of memory formation is long-term potentiation/long-term depression (LTP/LTD). In previous studies, intraseptal infusion of the muscarinic agonist oxotremorine, which excites MSA neurons, improved memory in aged rats. The present study examined LTP and LTD in aged Fisher 344 rats following intraseptal infusion of oxotremorine. LTP and LTD were assessed using the slope of the EPSP recorded from the hilar region of the dentate gyrus. Induction of LTP was blocked in the lateral perforant path, but not in the medial perforant path, following intraseptal infusions of oxotremorine. The generation and amplitude of heterosynaptic LTD was enhanced in the medial perforant path, but not in the lateral perforant path. The results provide evidence that pharmacological activation of the MSA can modulate LTP and LTD in the hippocampus of aged rats. The implications of these results with respect to memory and synaptic plasticity in the hippocampus are discussed.
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PMID:Activation of the medial septal area attenuates LTP of the lateral perforant path and enhances heterosynaptic LTD of the medial perforant path in aged rats. 814 24

We investigated memory self-report in Alzheimer's disease (AD) and age-associated memory impairment (AAMI). AD and AAMI patients and healthy elderly subjects were administered a self-report memory questionnaire, memory tests, a family-rated memory questionnaire, and a depression scale. The AD group reported worse memory than the control group, but many individual AD subjects reported normal memory. This finding confirms clinical observations that unawareness of memory loss is common in AD but variable across patients. Multiple regression analysis revealed that worse memory self-ratings were associated with greater dementia severity and higher depression scores. In the AAMI group, memory self-ratings were predicted by family ratings of memory ability but not by memory test scores. There was a nonsignificant trend for depression scores to predict memory self-ratings. Finally, level of self-reported memory ability did not differ for AD and AAMI, contradicting clinical lore that memory complaint is a useful diagnostic indicator.
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PMID:Memory self-report in Alzheimer's disease and in age-associated memory impairment. 819 32

Carbon disulfide-induced neurobehavioral effects are well known and do not need further evidence. Carbon disulfide vasculopathy and the syndromic complex resulting in depression, loss of memory and concentration, and behavior disturbances have been widely demonstrated. Less known is the evolution of the symptomatology when the environmental conditions are consistently improved, that is, the reversibility or the progression of the dysfunctions observed. This paper reports on a neurobehavioral follow-up in a viscose rayon factory carried out, in intervals, from 1974 to 1990. Several successive improvements were implemented in the plant through the years, until finally, the most radical changes were made at the end of the Seventies and these resulted in exposure levels far below the current Threshold Limit Values. A total of 493 subjects were examined and some of them were reexamined up to six times. The last examination was completed in September, 1990. In this paper, studies by our group over the 15 years of monitoring are discussed. The results show that the general mental state, as measured by neurobehavioral methods, reflects past and current exposure. This point was explored by dividing the subjects into six groups on the basis of their length of exposure and year of examination and by comparing their performances. The results show that even exposure to levels of carbon disulfide not exceeding 8 mg/m3 may induce absentmindedness and difficulties in perceptive abilities.
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PMID:Carbon disulfide and the central nervous system: a 15-year neurobehavioral surveillance of an exposed population. 824 19

Transient global amnesia (TGA) is a transient, benign neurological syndrome, characterized by global loss of memory, preserved consciousness and self-awareness, associated with some behavioral changes (in particular, repetitive questioning). It generally resolves within 24 h. Mild brain stem symptoms can often be demonstrated during the attack, but major neurological abnormalities never occur. The only sequel is a permanent amnesic gap for the duration of the episode. The episode is often preceded by typical precipitating events, such as physical activity, emotional stress, acute pain, comprising haemodynamic changes of the body. The diagnosis is easy provided one is acquainted with the syndrome. The prevalence of vascular risk factors is low and the risk for stroke is not increased. Although much evidence indicates the possibility of a causative ischaemia in the inferomedial parts of the temporal lobes, an atherothrombo-embolic TIA is not the cause of TGA, and TGA is unrelated to cerebrovascular disease in general. In the author's view, the cause of TGA is a transient ischemic attack (TIA) but a haemodynamic one of the vertebrobasilar system, producing a transient dysfunction of inferomedial parts of the temporal lobes, regions that are particularly sensitive to impaired blood supply. For a full pathogenetic explanation of TGA, clarification of the underlying mechanisms is a prerequisite. This touches on the genesis of migraine and Leao's spreading depression phenomenon. The term 'amnesic TIA' would reflect the pathogenesis more appropriately.
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PMID:Transient global amnesia. 829 84


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