Gene/Protein Disease Symptom Drug Enzyme Compound
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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dementia, delirium and depression are the 3 most prevalent mental disorders in the elderly. While dementia and depression are prevalent in the community, hospitals and nursing homes, delirium is seen most often in acute care hospitals. Much of the management of these syndromes is undertaken by primary care physicians rather than psychiatrists. Therefore, it is imperative that generalist physicians be adept at recognising, evaluating and managing patients with these syndromes. Because no diagnostic tests are pathognomonic of these syndromes, the differential diagnosis hinges on a careful clinical evaluation. The first step is to recognise which of the syndromes is present. Dementia is defined by a chronic loss of intellectual or cognitive function of sufficient severity to interfere with social or occupational function. Delirium is an acute disturbance of consciousness marked by an attention deficit and a change in cognitive function. Depression is an affective disorder evidenced by a dysphoric mood, but the most pervasive symptom is a loss of ability to enjoy usual activities. It is important to recognise that these syndromes are not mutually exclusive, as dementia frequently coexists with delirium and depression. Furthermore, physical diagnoses, such as chronic obstructive lung disease, congestive heart failure, stroke and endocrine disorders, are frequently associated with depressive symptoms. Given this, a comprehensive evaluation is mandatory. Laboratory tests are necessary to exclude concurrent metabolic, endocrine and infectious disorders, and drug effects. Imaging studies should be obtained selectively in patients with signs and symptoms, such as focal neurological findings and gait disturbances, which are suggestive of structural lesions: stroke, subdural haematoma, normal pressure hydrocephalus and brain tumours. Appropriate management involving pharmacological and nonpharmacological measures will result in significant improvement in most patients with these syndromes. Potentially offending drugs should be discontinued. In delirious patients the underlying illness must be treated concomitantly with the use of psychotropics, if necessary. Although no current medications have been shown to have a significant effect on the functional status of patients with the 2 most common causes of dementia, Alzheimer's disease and multi-infarct dementia, the management of concomitant illness in these patients may result in improved function for as long as a year. Tacrine, an anticholinesterase inhibitor, improves cognitive function slightly in selected patients with Alzheimer's disease over short periods. Finally, the treatment of depression with medications or electroconvulsive therapy (ECT) results in significant reductions in mortality and morbidity.
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PMID:Differential diagnosis of dementia, delirium and depression. Implications for drug therapy. 785 69

A 39-year-old man was admitted because of an abrupt onset of right-side weakness and dysarthria. During the 2 years before admission, he had suffered from insomnia, depressed mood and progressive memory disturbance. Neurological and psychiatric examination revealed severe intellectual impairment in addition to the neurological deficits. Neuroradiological examinations revealed multiple brain infarcts. He had no risk factor for stroke except for lupus anticoagulant. He was diagnosed as having multi-infarct dementia associated with antiphospholipid antibodies. This case suggests that it is necessary to investigate antiphospholipid antibodies in addition to neuroradiological examination when relatively young patients present with unexplained cognitive or behavioral symptoms.
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PMID:A young case with multi-infarct dementia associated with lupus anticoagulant. 791 28

In recent years, interest in vascular causes of dementia has increased and it has been proposed that vascular dementia (VAD) may be more common than previously supposed. This may have important implications, because VAD at present may be more amenable to prevention and treatment than Alzheimer's disease (AD). Several vascular factors have been related to cognitive decline and dementia in the elderly, including stroke and white matter disease. However, while numerous case-control studies have been concerned with the risk factors for AD, studies on risk factors for VADs are rare. The problems inherent in the diagnostic criteria make it difficult to interpret the results from the few studies that have been performed. Generally, risk factors for multi-infarct dementia are supposed to be the same as those for stroke, and include hypertension, diabetes mellitus, advanced age, male sex, smoking and cardiac diseases. White matter dementia has mainly been related to hypertension. Recent research suggests that vascular factors may also be important in AD, especially in the late-onset type. In stroke patients, dementia has been associated with higher age, less formal education, cerebral atrophy, left-sided or bilateral infarcts, volume of macroscopic infarcts, bilateral symptoms, previous stroke and white matter lesions. The pathogenetic mechanism through which these factors cause dementia is still not clear. Furthermore, it is not known if risk factors for VAD differ from those found in stroke patients. There is now an urgent need for further research on risk factors for VAD and on factors related to dementia in subjects with cerebrovascular disorders.
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PMID:Risk factors for vascular dementia: a review. 808 68

Cerebrospinal fluid (CSF) levels of corticotropin-releasing hormone (CRH) and ACTH, plasma levels of ACTH and cortisol, and serum levels of phospholipid and its fractions were determined in samples taken simultaneously from patients with senile dementia of the Alzheimer type (SDAT), multi-infarct dementia (MID) or dementia following a cerebrovascular accident (CVD), and the borderline-to-normal control subjects. CRH levels in CSF were significantly reduced in patients with SDAT and CVD but not with MID compared to the borderline-to-normal controls. ACTH levels in CSF were significantly reduced in SDAT compared to MID. The levels of circulating lecithin (phosphatidyl-choline) were depressed in a similar fashion to the levels of CRH in CSF in the SDAT patients and the group of severe dementia. Dementia and its severity did not affect the morning plasma levels of ACTH and cortisol. CSF CRH was positively correlated with CSF ACTH, while CSF ACTH was negatively correlated with plasma cortisol. No significant correlations were found between serum lecithin and CSF CRH or ACTH. These findings suggest that: 1) abnormalities in the extrahypothalamic CRH system play a role in the pathophysiology of senile dementia, which may not be specific to SDAT; 2) the CRH system and the ACTH system correlate with each other within the brain; 3) CSF ACTH is subject to the feedback inhibition by circulating cortisol; and 4) in the SDAT patients and the severe dementia group CSF CRH and serum lecithin are reduced probably via independent mechanisms.
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PMID:Cerebrospinal fluid corticotropin-releasing hormone and ACTH, and peripherally circulating choline-containing phospholipid in senile dementia. 839 71

Twenty-five patients with various types of gait disorders of multi-infarct dementia (MID) were reported. The types of gait disorders consisted of lower body parkinsonism (LBP) plus ataxia (6 patients), LBP plus apraxia (5 patients), and a combination of LBP plus ataxia and apraxia (14 patients). Hypertension occurred in 23 (92%) of the 25 patients. Nevertheless, individual stroke risk factors and the locations of infarcts were not significantly different between the subgroups. Ventriculomegaly and "leuko-araiosis" as demonstrated by computed tomography occurred in more than 80% of patients in each subgroup. Atrophy of the superior vermis was seen in 16 (80%) of 20 patients with ataxia as compared to 2 (40%) of the 5 patients without ataxia (p < 0.005). These data suggest that LBP and apraxia of MID were probably determined by the presence of ventriculomegaly or leuko-araiosis or both, and the presence of ataxic component of gait disorder most probably indicates the presence of vermian atrophy.
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PMID:Gait disorders of multi-infarct dementia. CT and clinical correlation. 847 97

Apolipoprotein E type 4 allele (apoE epsilon4) is associated with Alzheimer's disease (AD) in the late-onset familial form and in sporadic cases, but the age-associated risk in a randomly sampled elderly population is not established. We examined the association of apoE epsilon4 with AD and other dementias (mainly multi-infarct or dementia following stroke) in 1,030 persons aged 71 to 100 years in the population-based Framingham Study cohort. Kaplan-Meier survival analysis revealed that 55% of the apoE epsilon4/epsilon4 homozygotes developed AD by age 80, whereas 27% of apoE epsilon3/epsilon4 heterozygotes developed AD by age 85, and 9% of those without a 4 allele developed AD by age 85 years. In comparison with persons without a 4 allele, the risk ration for AD was 3.7 (95% CI = 1.9 to 7.5) for apoE epsilon3/epsilon4 heterozygotes and 30.1 (95% CI = 10.7 to 84.4) for apoE epsilon4 homozygotes. ApoE epsilon2 (2/2, 2/3, or 2/4 genotypes) was associated with an absence of AD. One-half (n=21) of the 43 AD patients were either homozygous or heterozygous for apoE epsilon4. We found evidence for an association of apoE epsilon4 with other dementia, primarily multi-infarct dementia and stroke. The risk ratio was 2.3 (95% CI = 0.9 to 6.1) for non-AD dementias among persons with apoE epsilon3/epsilon4. Although the apoE epsilon4 allele is a potent risk factor for AD and may be associated with other forms of dementia, most apoE epsilon4 carriers do not develop dementia, and about one-half of AD is not apoE epsilon4 associated. The low positive predictive value of this marker (0.10) suggest that use of apoE genotyping as a screening test for AD is not supported.
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PMID:Apolipoprotein E epsilon4 association with dementia in a population-based study: The Framingham study. 861 65

Vascular dementia (VD) and Alzheimer's type dementia are two main causes of dementia in the aged. Considering historical backgrounds and ethnic differences, a simplified classification of VD is suggested. First, poststroke dementia of acute onset associated with an infarct that is large enough to impair general cognitive functions, or strategically located. Second, multi-infarct dementia that develops incrementally with increasing numbers of infarcts, and which should be classified as multiple cortical infarct dementia and multiple small infarctor lacunar dementia. Third, vascular dementia of the Binswanger type (VDBT). We compared two types of white matter lesions, periventricular hyperintensity (PVH) and confluent centrum semiovale hyperintensity (CCSH) in lacunar stroke patients with regard to the cerebral blood flow (CBF). In patients with PVH, there was a significant positive correlation between the dementia scores and the CBF in the parietal and temporal areas but not in the frontal area. In CCSH patients, there was a significant positive correlation in the frontal area but not in the parieto-temporal areas. Therefore, dementia in most patients with PVH may not be primarily related to the PVH, but may possibly be due to coexisting Alzheimer's type dementia, and dementia in most CCSH patients may be related to cerebrovascular disease. VDBT is unique clinically in its slowly progressive intellectual deterioration and pathologically in diffuse, confluent, and almost symmetrical white matter lesions. For the pathogenesis of VDBT, our studies suggest that hypertension, short-term variations in blood pressure, and a sustained nighttime elevation of blood pressure promote small vessel disease and cause ischemia of the cerebral white matter that is located in the end-fields of penetrating arteries; this leads to an imparied integrity of the blood-brain barrier and free radical generation, both of which may have important roles in producing diffuse white matter degeneration.
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PMID:[Problems in vascular dementia]. 864 89

Functional, ambulatory, community-dwelling subjects (n = 423, aged 75 to 85 years) underwent baseline 24-hour ambulatory electrocardiography (ECG) examinations as part of the Bronx Aging Study, a 10-year prospective cohort study designed to identify risk factors and disease markers for cardiovascular, cerebrovascular, and dementia illnesses in old people. Premature ventricular contractions were the most commonly observed arrhythmia noted (93% of subjects), with a low prevalence of nonsustained ventricular tachycardia (5%), paroxysmal atrial tachycardia (13%), atrial fibrillation (4%), and atrioventricular blocks (4%). A 24-hour sinus rate of < 60 beats/min was noted in 13% of subjects, and 11% of subjects were noted to have transient episodes of severe bradycardia (< 40 beats/min). In a multivariate analysis, nonsustained ventricular tachycardia was an independent predictor of death (p = 0.015; relative risk [RR] 2.8; 95% confidence interval [CI] 1.4 to 5.8) and myocardial infarction (p = 0.031; RR 3.2; CI 1.2 to 9.4). Transient atrioventricular block was an independent predictor of stroke (p - 0.0006; RR 9.7; CI 3.3 to 28.9), as was sinus bradycardia over a 24-hour period (p = 0.033; RR 2.7; CI 1.2 to 6.4). Ventricular tachycardia approached significance as an independent predictor of multiinfarct dementia (p = 0.052; RR 6.3; CI 1.4 to 28.7). Episodes of paroxysmal atrial fibrillation, a trial tachycardia, and severe bradycardia were not associated with adverse outcomes. Some arrhythmias found on the ambulatory ECG in very old subjects can predict an increased risk for subsequent death, myocardial infarction, stroke, and multiinfarct dementia.
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PMID:Twenty-four-hour ambulatory electrocardiography in elderly subjects: prevalence of various arrhythmias and prognostic implications (report from the Bronx Longitudinal Aging Study). 870 90

Patients with multi-infarct dementia often have periventricular low density lesions on computed tomography and periventricular hyper-intensity lesions on computed tomography and periventricular hyper-intensity lesions on magnetic resonance imaging. Hachinski called this condition leukoaraiosis and results of previous studies that in multi-infarct dementia leukoaraiosis correlates with cerebral hypoperfusion. Periventricular low-density lesions in the white matter also occur, but their origin and clinical significance insuch patients is unknown. We studied when these lesions develop in patients with Alzheimer's dementia, and whether their presence correlates with clinical findings and cerebral blood flow. The subjects were 37 patients with a probable diagnosis of Alzheimer's dementia, as based on the Neuroepidermilogy Branch of the National Institute of Neurological Disorders and Stroke and the Alzheimer's disease and Related Disorders Association system. Autopsy findings were also available for 2 patients. Patients at higher Functional Assessment Staging of Senile Dementia of Alzheimer Type stages had more extensive periventricular low-density lesions. Patients with the lesions were more likely to have grasp reflex and sucking relex. Blood flow to the frontal and parietal cortices was significantly less in patients with the lesions than in those without the lesions. Neither of the 2 autopsies cases yielded evidence of arteriolosclerosis. Periventricular low-density lesions in Alzheimer's dementia may be closely associated with a degenerative process different from that seen in multi-infarct dementia.
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PMID:[Clinico-pathological evaluation of leukoaraisosis in Alzheimer's disease]. 895 37

To clarify the neuropathologic criteria for the diagnosis of vascular dementia principally caused by large-vessel cerebral infarction, we solicited autopsy cases of vascular dementia from 10 university neuropathology laboratories. We included only those cases with progressive dementia clinically diagnosed as Alzheimer's disease (AD) or multi-infarct dementia, in whom autopsy revealed only cerebral infarction, without significant neuropathologic features of AD or other neurodegenerative disorders. Only six cases, all men, met these criteria. Each of them had, for a year or longer, gradually increasing cognitive impairment sufficient to interfere with daily activities, without clear evidence of "stepwise" progression. The age of onset of dementia was 66 years or less in five of the six patients. The duration of dementia ranged from 2 to 14 years. Five of the six cases had a history of either cerebral ischemia or acute stroke with residual focal neurologic deficits. Only two were known to have hypertension. At autopsy severe atherosclerosis of the cerebral arteries was present in three cases; two of these had a thrombotic occlusion of one internal carotid artery and one had partial obstruction of other cerebral arteries. In five of six brains, gross infarctions were present involving the thalamus, caudate, putamen, or large portions of the frontal, parietal, and temporal lobes of one or both hemispheres. Vascular amyloid was absent in all but one of these five brains. In four cases, the dementia was clinically indistinguishable from AD except for a history of focal neurologic deficits. The difficulty encountered in finding large numbers of cases of VaD without coexisting neuropathologic evidence of AD suggests that "pure" vascular dementia is very uncommon.
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PMID:Clinical-neuropathologic findings in multi-infarct dementia: a report of six autopsied cases. 940 94


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