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David W Desmond

Publications and source records attributed to David W Desmond.

5 recordsLinked to original sources

The neuropsychology of vascular cognitive impairment: is there a specific cognitive deficit?

The concept of Vascular Cognitive Impairment (VCI) encompasses patients across the entire continuum of cognitive impairment resulting from cerebrovascular disease (CVD), ranging from high-risk patients with no frank cognitive deficit (the "brain-at-risk" stage) through vascular dementia (VaD). There are accepted differences in the neuropsychological profile of patients with Alzheimer's disease (AD) and VaD. In patients with VaD, executive functions that tend to be disproportionately impaired include planning and sequencing, speed of mental processing, performance on unstructured tasks, and attention. Language production may be impaired in patients with VaD but primary language functions otherwise tend to be preserved. Patients with VaD also exhibit significantly more perseverations than patients with AD. Memory impairment is typically evident in patients with AD+CVD but memory impairment may also occur as a primary consequence of stroke in the posterior cerebral artery territory with involvement of the medial temporal lobe, or as a secondary consequence of a cognitive syndrome involving inattention due to primary executive dysfunction. Compared to VaD, patients with AD may exhibit greater deficits in functions (including memory) mediated by posterior cortical structures, such as the temporal and parietal lobes. AD patients exhibit a faster rate of information decay, reduced ability to benefit from cues to facilitate retrieval, and higher frequency of intrusion errors; in addition, certain aspects of language function, such as naming, may exacerbate deficits on verbal memory tasks. AD tends to affect lexicon while VaD tends to affect syntax. When patients with AD exhibit perseverations, they tend to be elicited by tests of semantic knowledge.

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Ischemic stroke and depression.

Previous studies of depression after stroke have reported widely variable findings, possibly due to differences between studies in patient characteristics and methods for the assessment of depression, small sample sizes, and the failure to examine stroke-free reference groups to determine the base rate of depression in the general population. In an effort to address certain of those methodologic issues and further investigate the frequency and clinical determinants of depression after stroke, we administered the Structured Interview Guide for the Hamilton Depression Rating Scale (SIGH-D) and neurological, neuropsychological, and functional assessments to 421 patients (age = 71.5 +/- 8.0 years) 3 months after ischemic stroke and 249 stroke-free control subjects (age = 70.8 +/- 6.7 years). We required a SIGH-D total score > 11 for the identification of depression. We found that depression was less frequent (47/421 patients, or 11.2%, and 13/249 control subjects, or 5.2%), less severe, and less persistent in our stroke cohort than previously reported, possibly due to the underrepresentation of patients with a premorbid history of affective illness. Depression was associated with more severe stroke, particularly in vascular territories that supply limbic structures; dementia; and female sex. SIGH-D item analyses suggested that a reliance on nonsomatic rather than somatic symptoms would result in the most accurate diagnoses of depression after ischemic stroke.

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Mortality in patients with dementia after ischemic stroke.

OBJECTIVE: Although dementia is typically considered to be a consequence of a variety of neurologic diseases, it can also serve as a risk factor for other adverse outcomes. The authors investigated dementia as a predictor of long-term survival among patients with ischemic stroke. METHODS: Neurologic, neuropsychological, and functional assessments were administered to 453 patients (mean age +/- SD, 72.0 +/- 8.3 years) 3 months after ischemic stroke. The authors diagnosed dementia in 119 (26.3%) of the patients using modified Diagnostic and Statistical Manual of Mental Disorders, Revised 3rd Edition, criteria requiring deficits in memory and two or more additional cognitive domains as well as functional impairment. Dementia as a predictor of long-term survival during up to 10 years of follow-up was then investigated. RESULTS: The mortality rate was 15.90 deaths per 100 person-years among patients with dementia and 5.37 deaths per 100 person-years among nondemented patients. A Cox proportional hazards analysis found that the relative risk (RR) of death was increased in association with dementia (RR = 2.4; 95% CI = 1.6 to 3.4), adjusting for the following: a major hemispheral stroke syndrome (RR = 1.4); a middle cerebral artery territory index stroke (RR = 1.7); a Stroke Severity Scale score of > or = 4, representing more severe stroke (RR = 1.8); atrial fibrillation (RR = 1.8); congestive heart failure (RR = 2.2); recurrent stroke occurring during follow-up (RR = 3.9); and demographic variables. The risk of death increased in association with the severity of dementia, but it did not differ by dementia subtype. CONCLUSIONS: Dementia is a significant independent risk factor for reduced survival after ischemic stroke, adjusting for other recognized predictors of mortality. The authors hypothesize that patients with dementia are at an elevated risk of mortality because of their increased burden of cerebrovascular disease, a tendency toward undertreatment for stroke prophylaxis among clinicians, or patient noncompliance with treatment regimens.

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Cognition and white matter lesions.

Although it is recognized that ischemic stroke is a potent risk factor for vascular dementia, the influence of white matter lesions (WML) on cognitive function is less clear. In community-based MRI studies that have administered mental status tests to subjects who were free of clinically evident neurologic disease, a weak relationship between WML and generalized cognitive function has been reported. In studies that have administered neuropsychological test batteries, a stronger and more specific association has been recognized between WML and deficits in executive function, most likely due to the involvement of frontal-subcortical pathways. Cognitive deficits may be related to the total volume of the WML, with a threshold perhaps needing to be surpassed before such deficits are evident, but it is likely that the location of the WML also plays a role, with that threshold varying in association with the distribution of the lesions. Potential confounders of the results of previous studies include small, strategically located subcortical infarctions that may be masked by more extensive WML and other comorbid neurologic disorders, particularly Alzheimer's disease. Future studies should be prospective, utilize standardized methods for structural and functional brain imaging, and administer comprehensive neuropsychological assessments in order to more rigorously investigate the relationship between evolving WML and declining cognitive functions.

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Incidence of dementia after ischemic stroke: results of a longitudinal study.

BACKGROUND AND PURPOSE: A number of cross-sectional epidemiological studies have reported that one fourth of elderly patients meet criteria for dementia 3 months after ischemic stroke, but few longitudinal studies of the incidence of dementia after stroke have been performed. We conducted the present study to investigate the incidence and clinical predictors of dementia after ischemic stroke. METHODS: We administered neurological, neuropsychological, and functional assessments annually to 334 ischemic stroke patients (age, 70.4+/-7.5 years) and 241 stroke-free control subjects (age, 70.6+/-6.5 years), all of whom were nondemented in baseline examinations. We diagnosed incident dementia using modified Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition criteria requiring deficits in memory and > or =2 additional cognitive domains, as well as functional impairment. RESULTS: The crude incidence rate of dementia was 8.49 cases per 100 person-years in the stroke cohort and 1.37 cases per 100 person-years in the control cohort. A Cox proportional-hazards analysis found that the relative risk (RR) of incident dementia associated with stroke was 3.83 (95% CI, 2.14 to 6.84), adjusting for demographic variables and baseline Mini-Mental State Examination score. Within the stroke cohort, intercurrent medical illnesses associated with cerebral hypoxia or ischemia were independently related to incident dementia (RR, 4.40; 95% CI, 2.20 to 8.85), adjusting for recurrent stroke, demographic variables, and baseline Mini-Mental State Examination score. CONCLUSIONS: The risk of incident dementia is high among patients with ischemic stroke, particularly in association with intercurrent medical illnesses that might cause cerebral hypoxia or ischemia, suggesting that cerebral hypoperfusion may serve as a basis for some cases of dementia after stroke.

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