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

Vascular dementia results from ischemic injury to the brain. Depression is a frequent complication of cerebrovascular dementia (CVD) occurring in 25 to 80% of patients during the course of their illness. Depression is unrelated to the severity of intellectual compromise or to the co-existence of delusions. The symptom profile of depression in CVD is indistinguishable from that of late-onset idiopathic major depressive episodes. The frequency of depression differs with the subtype of CVD and is most common in disorders with lesions of the frontal lobes, either cortical or subcortical. In addition to lesion site, other contributors to depression in CVD include vascular disease of other organs, drug therapy of co-existing medical conditions, and psychological reactions to disability. The depression of CVD responds to treatment with antidepressant agents.
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PMID:Depression in vascular dementia. 322 47

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

Vascular dementia (VAD) is currently considered to be the second most common cause of dementia in Europe and the USA, second to dementia of the Alzheimer's type (DAT). However, in Asia and many developing countries the incidence of VAD exceeds that of DAT. The positive clinical diagnostic workup for VAD requires six steps: (1) clear-cut quantitative assessment of cognitive deficits utilizing standard neuropsychological tests to establish and quantify the dementia syndrome and rule out pseudo-dementia OF depression; (2) ascertaining the presence of risk factors for stroke; (3) identifying cerebral vascular lesions by neuroimaging (MRI, Iodine or Xenon contrasted CT, PET and SPECT); (4) exclusion of other causes of dementia; (5) differential diagnosis of possible, probable or definite VAD versus DAT and ascertaining when there are mixtures of the two; and (6) temporal identification of causality between onset and progression of the dementia with identified cerebral vascular lesions. There are eight subtypes of VAD: (1) multi-infarct dementias. These are due to large cerebral emboli, and are usually readily identifiable; (2) strategically placed infarctions causing dementia; (3) multiple subcortical lacunar lesions. Patients with these develop VAD at least five to twenty-five times more frequently than those in age-matched general population samples; (4) Binswanger's disease (arteriosclerotic subcortical leuko-encephalopathy). This form is rare. Neuroimaging confirms the diagnosis during life but the diagnosis can not be made by neuroimaging alone; (5) mixtures of two or more of above VAD subtypes; (6) hemorrhagic lesions causing dementia; (7) subcortical dementias due to cerebral autosomally dominant arteriolopathy with subcortical infarcts and leuko-encephalopathy (CADASIL), or to familial amyloid angiopathies and coagulopathies all of which present with multiple subcortical lacunar lesions similar to Binswanger's disease; (8) mixtures of DAT and VAD. The clinical significance of leukoaraiosis and its suspected relationships to VAD remains to be better established. The presence of ischemic infarctions, single or multiple large or multiple small (lacunar) by neuroimaging are necessary for the diagnosis of VAD, but identifying their presence, by neuroimaging alone, does not permit the diagnosis of dementia which can only be established by neuropsychological assessments. VAD is a clinical entity, identifiable in at least 30-70% of patients after strokes but mechanisms responsible for the cognitive impairments are complex. Some of these mechanisms are incompletely understood but provide subjects for important future research.
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PMID:Vascular dementia: still a debatable entity? 898 Dec 95

Vascular dementia is one of the most frequently occurring dementia syndromes. Its prevalence is about 5% among subjects above 85 years of age. Elevated blood pressure and atherosclerosis are the most important risk factors. According to international criteria, vascular dementia usually occurs within three months after having a stroke. However, the diagnosis can be difficult as some strokes are clinically 'silent' and may go unnoticed. Other factors may also contribute to the dementia syndrome, and concomitant depression may mask its clinical picture. In population studies, treatment of vascular risk factors is associated with a relatively low incidence of vascular dementia, but this effect has not been investigated in a randomized clinical trial. The value of acetylsalicylic acid in attenuating cognitive deterioration in patients with vascular dementia is uncertain. Acetylcholinesterase inhibitors may slow down cognitive decline not only in some patients with Alzheimer's disease but also in patients with vascular dementia.
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PMID:[Vascular dementia]. 1522 29

We examined the pattern of neuropsychological deficits in Vascular Cognitive Impairment-No Dementia (Vascular CIND) by comparing the cognitive and behavioral performance of 41 post-stroke Vascular CIND patients to that of 62 post-stroke patients with no cognitive impairment (NCI). Neuropsychological test scores were grouped into seven cognitive and four behavioral domains, then converted to standardized, weighted principle component scores (PCS) for each domain. Multivariate logistic regression models built on cognitive domains found the immediate recall and psychomotor domains to best predict diagnostic group membership. In a separate model limited to behavioral data, the depressed mood domain best predicted group membership. The combination of immediate memory deficits, psychomotor slowness and depression have also been found in Vascular Dementia (VaD), suggesting that the pattern of deficits in Vascular CIND and VaD neuropsychological deficits are similar. This cognitive and behavioral pattern similarity supports the hypothesis that Vascular CIND lies on a continuum between NCI and VaD.
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PMID:The pattern of neuropsychological deficits in Vascular Cognitive Impairment-No Dementia (Vascular CIND). 1559 57

Vascular dementia is the second most prevalent type of dementia in the United States today. This article includes a review of its pathophysiology, which involves the damage of small vessels in the brain, an abundance of which are in the subcortical region, thus creating a subcategory called subcortical vascular dementia (SVD). Various diseases, such as diabetes and high blood pressure, predispose the individual to damage to these small vessels. The symptoms of SVD are included as a review and helpful outline to differentiate SVD from Alzheimer's dementia and depression. Additionally, evidence-based interventions are reviewed. Nurses play a unique role in preventing and minimizing this dementia, which afflicts such a large percentage of our elderly population.
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PMID:Subcortical vascular dementia. 1582 27

The current research sought to test the hypothesis that psychotic symptoms in patients with dementia might be due to relatively greater executive control and visuoperceptual deficits. Twenty-four dementia patients with psychosis and 24 outpatients without psychosis diagnosed with either probable Alzheimer's disease (AD) or possible/probable Ischemic Vascular Dementia (IVD) were studied. Groups did not differ with respect to age, education, severity of dementia, or depression. Presence and severity of psychosis was measured with a modification of the Neuropsychiatric Inventory (NPI; Cummings, J. L., Mega, M., Gray, K., Rosenberg-Thompson, S., Carusi, D. A., & Gorbein, J. (1994). The neuropsychiatric inventory: Comprehensive assessment of psychopathology in dementia. Neurology, 44, 2308-2314). Between-group and regression analyses found a consistent relationship such that patients with psychosis obtained low scores on the Boston Revision Wechsler Memory Scale-Mental Control subtest (WMS-MC subtest), a test of executive control. On some analyses patients with psychosis also made more perceptual errors on tests of naming and obtained higher scores on tests of delayed recognition memory. However, the relationship between severity of psychosis and performance on visuoperceptual and memory measures was considerably less robust. These data suggest a strong relationship between severity of psychosis and poor performance on executive control. Less evidence was obtained to support our contention that psychotic symptoms in dementia may arise from an interaction of neuropsychological deficits involving greater impairment in executive and visuoperceptual functioning.
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PMID:Neuropsychological functioning of dementia patients with psychosis. 1593 21

Vascular dementia (VaD) is the second most common cause of dementia, accounting for about 20% of all cases. Psychiatric and behavioral problems are at least as common in VaD as in Alzheimer's disease but are very different qualitatively. Patients with VaD, and especially those with small vessel disease, typically manifest symptoms related to damage to the frontal-subcortical system of the brain, including loss of executive function (which is not generally detected with most conventional tests of cognitive function), loss of drive, and disinhibited behaviors. Patients with VaD also commonly develop treatable mood disorders, most commonly depression. Once the symptoms are recognized, the clinician is in an ideal position to manage them and to educate caregivers about their nature.
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PMID:Psychiatric and behavioral manifestations of vascular dementia. 1748 68

Alzheimer's disease (AD) and Vascular dementia represent the most common forms of dementia. If left unabated, the economic cost of caring for patients with these maladies would consume the entire gross national product of the industrialized world by the middle of this century. Until recently, the only available drugs for this condition were cholinergic treatments, which symptomatically enhance cognitive state to some degree, but they were not neuroprotective. Many potential neuroprotective drugs tested in clinical trials failed because of intolerable side effects. However, after our discovery of its clinically-tolerated mechanism of action, one putatively neuroprotective drug, memantine, was recently approved by the European Union and the U.S. Food and Drug Administration (FDA) for the treatment of dementia. Recent phase 3 clinical trials have shown that memantine is effective in the treatment of both mild and moderate-to-severe Alzheimer's disease and possibly Vascular dementia (multi-infarct dementia). Here we review the molecular mechanism of memantine's action and also the basis for the drug's use in these neurological diseases, which are mediated at least in part by excitotoxicity. Excitotoxicity is defined as excessive exposure to the neurotransmitter glutamate or overstimulation of its membrane receptors, leading to neuronal injury or death. Excitotoxic neuronal cell damage is mediated in part by overactivation of N-methyl-D-aspartate (NMDA)-type glutamate receptors, which results in excessive Ca(2+) influx through the receptor associated ion channel and subsequent free radical formation. Physiological NMDA receptor activity, however, is also essential for normal neuronal function. This means that potential neuroprotective agents that block virtually all NMDA receptor activity will very likely have unacceptable clinical side effects. For this reason many previous NMDA receptor antagonists have disappointingly failed advanced clinical trials for a number of neurodegenerative disorders. In contrast, studies in our laboratory have shown that the adamantane derivative, memantine, preferentially blocks excessive NMDA receptor activity without disrupting normal activity. Memantine does this through its action as an uncompetitive, low-affinity, open-channel blocker; it enters the receptor-associated ion channel preferentially when it is excessively open, and, most importantly, its off-rate is relatively fast so that it does not substantially accumulate in the channel to interfere with subsequent normal synaptic transmission. Clinical use has corroborated the prediction that memantine is well tolerated. Besides Alzheimer's disease, memantine is currently in trials for additional neurological disorders, including HIV-associated dementia, depression, glaucoma, and severe neuropathic pain. A series of second-generation memantine derivatives are currently in development and may prove to have even greater neuroprotective properties than memantine. These second-generation drugs take advantage of the fact that the NMDA receptor has other modulatory sites in addition to its ion channel that potentially could also be used for safe but effective clinical intervention.
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PMID:Pathologically-activated therapeutics for neuroprotection: mechanism of NMDA receptor block by memantine and S-nitrosylation. 1750 5

Deficits in cognitive function may impact one's ability to attend to stimuli, think clearly, reason, and remember. Impaired cognitive function is a common complaint among older women presenting for treatment in both mental health and medical care settings, and differential diagnosis of type and extent of cognitive impairment is important for appropriate treatment planning and prognosis. Although overall gender differences in prevalence of cognitive dysfunction are minimal, it is important when treating older women to take into account unique challenges they face in the aging process that impact the cause, type and extent of cognitive complaints with which they present in clinical settings. The current paper provides an overview to guide accurate diagnosis, particularly in women, of different types of cognitive impairment under the broad category of dementias, including Alzheimer's, Lewy Body Disease, Vascular Dementia, and due to general medical conditions such as coronary artery bypass surgery, head injury, menopause, hypothyroidism, breast cancer treatment, Fibromyalgia, and chronic fatigue. In addition, emotional factors such as depression in older female patients complicate differential diagnosis of cognitive impairment and must be addressed. Given the multiplicity of causes of cognitive difficulties for women across the life span, careful assessment is crucial; the current paper reviews assessment strategies to prepare an integrated, biopsychosocial strategy for identifying particular cognitive deficits and related psychological and medical problems. In addition, prognostic indicators and treatment planning are discussed to help the practitioner organize an empathic, reasoned and multifaceted treatment approach to maximize recovery, minimize deterioration, and manage symptoms for older women in the context of their social support system and living environment.
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PMID:Cognitive functioning and aging in women. 1758 77


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