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D W Desmond

Publications and source records attributed to D W Desmond.

At least 19 recordsLinked to original sources
PubMed1998

The effect of patient attrition on estimates of the frequency of dementia following stroke.

BACKGROUND: Given that prevalence surveys may underestimate the magnitude of the association between an exposure and a disease with high morbidity or mortality, we investigated the effects of patient attrition on estimates of the frequency of dementia following ischemic stroke. PATIENTS AND METHODS: We examined 251 patients 3 months after stroke and diagnosed dementia in 66 (26.3%) based on the results of neuropsychological and functional assessments and modified criteria from the Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised. Those 251 patients were drawn from a larger cohort of 297 patients, with the majority of the remaining 46 patients being unavailable for assessment due to death, severe stroke, or comorbid medical disorders. Using the coefficients in a logistic model of the clinical determinants of dementia based on the 251 patients who were examined, we calculated the probability of dementia for each of the 46 patients who were not examined. We considered a patient to have dementia when that probability was higher than the mean of the median probabilities of dementia in the groups of patients with and without dementia who completed the examinations. RESULTS: The sensitivity and specificity of our diagnostic method were 75.8% and 72.4%, respectively. We recognized dementia in 21 (45.7%) of the 46 unavailable patients, a significantly higher frequency than among examined patients. Additional analyses determined that the factors that increased the risk of becoming unavailable for follow-up, which included more severe stroke, left and right hemisphere infarct locations, and a history of prior stroke, are similar to the factors that increase the risk of dementia after stroke. CONCLUSION: Our findings suggest that dementia is differentially associated with early patient attrition, potentially resulting in the underestimation of its frequency and underrecognition of its importance as an outcome of ischemic stroke.

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PubMed1998

Dementia as a predictor of adverse outcomes following stroke: an evaluation of diagnostic methods.

BACKGROUND AND PURPOSE: Although it is understood that dementia is a risk factor for adverse outcomes, little is known about the predictive validity of the numerous methods that have been proposed for its diagnosis. Thus, we performed the present study to assess the utility of a variety of diagnostic methods in the prediction of adverse outcomes following stroke. METHODS: We administered neuropsychological, neurological, and functional examinations to 244 patients (age, 71.7+/-8.5 years) 3 months after ischemic stroke. We diagnosed dementia using each of the following methods: (1) neuropsychological testing, requiring deficits in increasing numbers of cognitive domains, both with and without memory impairment, as well as functional impairment; (2) Mini-Mental State Examination (MMSE) score of <24; and (3) neurologists' clinical judgment. We then used survival analyses to investigate the ability of diagnoses based on those methods to predict death and recurrent stroke during long-term follow-up. RESULTS: Log-rank tests and Cox proportional hazards analyses, with recurrent stroke entered as a time dependent covariate, determined that all of the paradigms were significant predictors of mortality, but the performance of paradigms based on neuropsychological testing was superior to the use of the MMSE and clinical judgment, particularly when memory impairment was required. Log-rank tests determined that paradigms based on neuropsychological testing were the only significant predictors of recurrent stroke and performed best when memory impairment was required. CONCLUSIONS: Our results suggest that dementia diagnosis based on neuropsychological assessment and an operationalized paradigm requiring deficits in memory and other cognitive domains is superior to other conventional methods in its ability to identify patients at elevated risk of adverse outcomes following stroke.

Activities of Daily Living↗
PubMed1997

Dementia after stroke increases the risk of long-term stroke recurrence.

BACKGROUND: Although risk factors for first stroke have been identified, the predictors of long-term stroke recurrence are less well understood. We performed the present study to determine whether dementia diagnosed three months after stroke onset is an independent risk factor for long-term stroke recurrence. METHODS: We examined 242 patients (age = 72.0 +/- 8.7 years) hospitalized with acute ischemic stroke who had survived the first three months without recurrence and followed them to identify predictors of long-term stroke recurrence. We diagnosed dementia three months after stroke using modified DSM-III-R criteria based on neuropsychological and functional assessments. The effects of conventional stroke risk factors and dementia status on survival free of recurrence were estimated using Kaplan-Meier analyses, and the relative risks (RR) of recurrence were calculated using Cox proportional hazards models. RESULTS: Dementia (RR = 2.71, 95% CI = 1.36 to 5.42); cardiac disease (RR = 2.18, CI = 1.15 to 4.12); and sex, with women at higher risk (RR = 2.03, CI = 1.01 to 4.10), were significant independent predictors of recurrence, while education (RR = 1.90, CI = 0.77 to 4.68), admission systolic blood pressure >160 mm Hg (RR = 1.80, CI = 0.94 to 3.44) and alcohol intake exceeding 160 grams per week (RR = 1.86, CI = 0.79 to 4.38) were weakly related. CONCLUSIONS: Our results suggest that dementia significantly increases the risk of long-term stroke recurrence, with additional independent contributions by cardiac disease and sex. Cognitive impairment may be a surrogate marker for multiple vascular risk factors and larger infarct volume that may serve to increase the risk of recurrence. Alternatively, less aggressive medical management of stroke patients with cognitive impairment or noncompliance of such patients with medical therapy may be bases for an increased rate of stroke recurrence.

Aged↗
PubMed1997

Meta-analysis of the Hachinski Ischemic Score in pathologically verified dementias.

Our objectives were to investigate the utility of the Hachinski Ischemic Score (HIS) in differentiating patients with pathologically verified Alzheimer's disease (AD), multi-infarct dementia (MID), and "mixed" (AD plus cerebrovascular disease) dementia, and to identify the specific items of the HIS that best discriminate those dementia subtypes. Investigators from six sites participated in a meta-analysis by contributing original clinical data, HIS, and pathologic diagnoses on 312 patients with dementia (AD, 191; MID, 80; and mixed, 41). Sensitivity and specificity of the HIS were calculated based on varied cutoffs using receiver-operator characteristic curves. Logistic regression analyses were performed to compare each pair of diagnostic groups to obtain the odds ratio (OR) for each HIS item. The mean HIS (+/- SD) was 5.4 +/- 4.5 and differed significantly among the groups (AD, 3.1 +/- 2.5; MID, 10.5 +/- 4.1; mixed, 7.7 +/- 4.3). Receiver-operator characteristic curves showed that the best cutoff was < or = 4 for AD and > or = 7 for MID, as originally proposed, with a sensitivity of 89.0% and a specificity of 89.3%. For the comparison of MID versus mixed the sensitivity was 93.1% and the specificity was 17.2%, whereas for AD versus mixed the sensitivity was 83.8% and the specificity was 29.4%. HIS items distinguishing MID from AD were stepwise deterioration (OR, 6.06), fluctuating course (OR, 7.60), hypertension (OR, 4.30), history of stroke (OR, 4.30), and focal neurologic symptoms (OR, 4.40). Only stepwise deterioration (OR, 3.97) and emotional incontinence (OR, 3.39) distinguished MID from mixed, and only fluctuating course (OR, 0.20) and history of stroke (OR, 0.08) distinguished AD from mixed. Our findings suggest that the HIS performed well in the differentiation between AD and MID, the purpose for which it was originally designed, but that the clinical diagnosis of mixed dementia remains difficult. Further prospective studies of the HIS should include additional clinical and neuroimaging variables to permit objective refinement of the scale and improve its ability to identify patients with mixed dementia.

Brain Ischemia↗
PubMed1996

Recovery of cognitive function after stroke.

BACKGROUND AND PURPOSE: Previous studies have suggested that recovery of cognitive function after stroke is maximal within the first 3 months after onset. We performed the present study to investigate the long-term course and clinical correlates of improvement in generalized cognitive function after ischemic stroke. METHODS: We administered a battery of neuropsychological tests to 151 patients (age, 70.4 +/- 7.7 years; education, 10.4 +/- 4.6 years) at 3 months and then annually after stroke. We transformed their test results into z scores based on the performance of a stroke-free normative group, averaged those scores to create a summary score, and defined improvement in annual examinations as an increase in that summary score greater than two standard deviations above the mean first annual change of the normative group. We then used logistic regression to determine whether stroke location, syndrome, or recurrence; vascular risk factors; dementia status; depression; or demographic variables were associated with improvement. RESULTS: We found that 19 of the 151 patients exhibited improvement, which was evident only at the first annual examination in most cases. Logistic regression determined that improvement was significantly related to left hemisphere infarction relative to brain stem/cerebellar infarction (odds ratio [OR], 5.57), while the presence of a major hemispheral stroke syndrome showed a trend toward significance (OR, 3.32). Diabetes mellitus was significantly associated with a failure to exhibit improvement (OR, 0.12). Based on the logistic model, the probability of long-term improvement would be 54.0% for a patient with a left hemisphere infarct and a major hemispheral syndrome but only 11.9% if diabetes was also present. CONCLUSIONS: Long-term improvement in generalized cognitive function may be evident after stroke in association with left hemisphere infarction and severe hemispheral syndromes, while it may be compromised by diabetes, possibly because of an increased burden of cerebrovascular disease.

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PubMed1996

Risk factors for incident dementia after stroke. Role of hypoxic and ischemic disorders.

BACKGROUND AND PURPOSE: Stroke significantly increases the risk of dementia in the elderly, yet the risk factors for incident dementia after ischemic stroke are not well understood. We attempted to determine whether hypoxic-ischemic (HI) disorders, which may result from comorbid medical conditions (eg. seizures, cardiac arrhythmias, pneumonia), would be an independent risk factor for the development of new dementia after stroke. METHODS: We prospectively followed 185 initially nondemented patients with ischemic stroke (age, 70.3 +/- 7.7 years) for a maximum of 52.8 months. We diagnosed the presence of dementia at annual examinations based on neuropsychological testing and modified DSM-III-R criteria. HI disorders were identified by record review or examination during hospitalization. We used Kaplan-Meier analysis to determine the cumulative proportion of patients with and without HI disorders who survived free of dementia and used Cox models to estimate the relative risk of dementia associated with HI disorders. RESULTS: The cumulative proportion (+/- SE) surviving without dementia was 51.7 +/- 10.9% in the HI group versus 78.2 +/- 4.3% in the non-HI group after 52.8 months of observation. The relative risk of incident dementia associated with HI events was 4.3 (95% confidence interval = 1.9 to 9.6) after we adjusted for demographic factors, recurrent stroke, and baseline cognitive function. CONCLUSIONS: We conclude that HI disorders may be a significant independent risk factor for incident dementia after stroke, even after adjustment for other recognized predictors of cognitive decline. Recognition of HI cerebral damage as a possible pathogenic mechanism for dementia after stroke may allow targeted therapeutic interventions to prevent subsequent cognitive deterioration.

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PubMed1996

Vascular dementia: a construct in evolution.

Since the late 1800s, when Alzheimer and Binswanger proposed the concept of "arteriosclerotic brain degeneration," there has been an evolution in thinking regarding cerebrovascular disease (CVD) as a basis for dementia. While later work recognized the importance of specific infarct characteristics including volume, multiplicity, and location, recent studies have found that many factors may work in combination with those characteristics to produce dementia, including white matter disease; vascular risk factors such as diabetes; comorbid illnesses, particularly those that might produce cerebral ischemia or hypoxia; genetic factors; and host characteristics such as older age and fewer years of education. Studies of the prevalence of vascular dementia (VaD) have suggested that CVD is second only to Alzheimer's disease as a basis for dementia in Western countries and the most common basis in certain Asian countries, but those studies may have underestimated the frequency of dementia associated with CVD due to a failure to perform brain imaging and decreased survival among patients with CVD. Few studies of the incidence of VaD have been performed, but they have also consistently demonstrated an elevated risk associated with CVD. While certain methodologic issues have contributed to the debate regarding the importance of CVD as a basis for dementia, including variability in the techniques that have been used to characterize brain lesions, assess cognitive function, and diagnose dementia; difficulties inherent in the determination of a causal role for CVD in dementia; and the potential confounding effects of aphasia and depression in patients with stroke, it is clear that VaD remains an important public health problem.

Biological Evolution↗
PubMed1995

Dementia associated with bilateral carotid occlusions: neuropsychological and haemodynamic course after extracranial to intracranial bypass surgery.

A 55 year old man with bilateral internal carotid and unilateral vertebral artery occlusions presented subacutely with profound behavioural and cognitive changes featuring frontal lobe deficits. Neuropsychological testing showed severe cognitive impairment compatible with dementia. Anatomical imaging showed only a small right superior frontal infarction. Cerebral blood flow was severely reduced, with profound hypofrontality and limited hypercapnic reactivity, and cerebral metabolism was reduced primarily in the medial frontal lobes. After right sided extracranial to intracranial cerebral bypass surgery, both flow and metabolism improved, as did behavioural and neuropsychological deficits. Perfusion insufficiency from bilateral carotid occlusions, with secondarily reduced metabolism in the frontal zones bilaterally, may be an unusual cause of a reversible frontal dementia syndrome.

Arterial Occlusive Diseases↗
PubMed1995

Strategic infarcts in vascular dementia. A clinical and brain imaging experience.

The mechanisms of dementia resulting from small deep infarctions are incompletely understood. The thesis underlying the concept of "multi-infarct dementia" is that multiple lesions have a synergistic effect on mental functions, resulting in dementia irrespective of specific location or volume. In this report, we summarize our experience with six patients reported previously along with additional patients examined subsequently, whose clinical features and brain imaging findings allow an alternative formulation for dementia resulting from lacunar stroke. The six initial patients presented with an abrupt change in behavior after acute infarction involving the inferior genu of the internal capsule documented by computed tomography (CT) and magnetic resonance imaging (MRI). The acute syndrome featured fluctuating alertness, inattention, memory loss, apathy, abulia, and psychomotor retardation suggesting frontal lobe dysfunction. Contralateral hemiparesis and dysarthria were generally mild, except when the infarct extended into the posterior limb. Neuropsychological testing in five patients with left-sided infarcts revealed severe verbal memory loss. Additional cognitive deficits consistent with dementia were evident in four patients. A right-sided infarct caused transient impairment in visuospatial memory. Functional brain imaging in three patients using 133xenon regional cerebral blood flow (rCBF) and single photon emission computed tomography (SPECT) showed focal reduction in hemispheric perfusion most prominent in the ipsilateral inferior and medial frontal cortex. Perfusion was also defective in the medial and laterial temporal cortex. Important pathways of the limbic system traverse the inferior capsule in the region of the genu. Corticothalamic and thalamocortical fibers form the thalamic peduncles which detach from the internal capsule and enter the thalamus at its rostral and caudal poles and along its dorsal surface. The anterior thalamic peduncle, conveys reciprocal connections between the dorsomedial nucleus and the cingulate gyrus, as well as the prefrontal and orbitofrontal cortex. The inferior thalamic peduncle carries fibers which connect the thalamus with orbitofrontal, insular, and temporal cortex, as well as the amygdala via the ansa peduncularis to the ventral amygdalofugal pathway. Thus, damage to one or both white-matter tracts may occur with infarctions in the region of the inferior genu, causing striking frontal behavioral effects and memory loss in our patients associated with functional deactivation of the ipsilateral frontal and temporal cortex.(ABSTRACT TRUNCATED AT 400 WORDS)

Cerebral Infarction↗
PubMed1994

Disorientation following stroke: frequency, course, and clinical correlates.

To investigate the frequency, course, and clinical correlates of disorientation following stroke, we administered the Mini-Mental State Examination orientation subtest to 177 alert patients 7-10 days and 3 months after stroke and 240 stroke-free nondemented subjects. Disorientation was defined as a score < or = 8/10. Seventy-two (40.7%) of the patients were disoriented 7-10 days after stroke and 39 patients (22.0% of the sample) remained disoriented 3 months later. A logistic regression analysis determined that persistent disorientation was significantly related to stroke status [odds ratio (OR) = 5.8], after adjusting for memory and attentional deficits and demographic variables. Among stroke patients, disorientation was associated with severe hemispheral stroke syndromes (OR = 7.7), but not infarct location or vascular risk factor history, after adjusting for memory and attentional deficits and demographic variables. Sensitivity and specificity analyses determined that disorientation was an inaccurate marker for dementia or deficits in memory or attention, while intact orientation was associated with a low probability of dementia or memory dysfunction in most patients but not preserved attention. We conclude that disorientation is common and persistent following stroke and associated with severe hemispheral stroke syndromes but not infarct location. While disorientation is a poor marker for dementia or deficits in memory or attention, intact orientation should suggest that cognitive functions are likely to be preserved.

Aged↗
PubMed1994

Intrahemispheric localization of drawing dysfunction.

We evaluated drawing disability in 37 patients with right hemispheric stroke and in eight controls with no brain disease. Blinded evaluations included measures of overall recognizability and hemineglect. By mapping the CT lesions of patients, we found that damage to parieto-occipital cortex in poor drawers correlated with poor performance on a line bisection task whereas frontal, subcortical damage in poor drawers did not. We propose that drawing disability may be produced by visual-spatial dysfunction in patients with posterior lesions and by a disturbance of integrated motor function in those with frontal, subcortical damage.

Adult↗
PubMed1994

Cognitive impairment after stroke: frequency, patterns, and relationship to functional abilities.

Cognitive function was examined in 227 patients three months after admission to hospital for ischaemic stroke, and in 240 stroke-free controls, using 17 scored items that assessed memory, orientation, verbal skills, visuospatial ability, abstract reasoning, and attentional skills. After adjusting for demographic factors with standardised residual scores in all subjects, the fifth percentile was used for controls as the criterion for failure on each item. The mean (SD) number of failed items was 3.4 (3.6) for patients with stroke and 0.8 (1.3) for controls (p < 0.001). Cognitive impairment, defined as failure on any four or more items, occurred in 35.2% of patients with stroke and 3.8% of controls (p < 0.001). Cognitive domains most likely to be defective in stroke compared with control subjects were memory, orientation, language, and attention. Among patients with stroke, cognitive impairment was most frequently associated with major cortical syndromes and with infarctions in the left anterior and posterior cerebral artery territories. Functional impairment was greater with cognitive impairment, and dependent living after discharge either at home or nursing home was more likely (55.0% with, v 32.7% without cognitive impairment, p = 0.001). In a logistic model examining the risks related to dependent living after stroke, cognitive impairment was a significant independent correlate (odds ratio, OR = 2.4), after adjusting for age (OR = 5.2, 80 + v 60-70 years) and physical impairment (OR = 3.7, Barthel index < or = 40 v > 40). It is concluded that cognitive impairment occurs frequently after stroke, commonly involving memory, orientation, language, and attention. The presence of cognitive impairment in patients with strike has important functional consequences, independent of the effects of physical impairment. Studies of stroke outcome and intervention should take into account both cognitive and physical impairments.

Cerebrovascular Disorders↗
PubMed1994

Dementia after stroke is a predictor of long-term survival.

BACKGROUND AND PURPOSE: The aim of this study was to determine whether dementia after stroke adversely influences long-term survival. METHODS: Subjects were 251 patients > or = 60 years of age with ischemic stroke who were given neurological, neuropsychological, and functional examinations 3 months after hospitalization and were followed up prospectively. Using criteria modified from the Diagnostic and Statistical Manual of Mental Disorders-III-R, dementia was found in 66 (26.3%) patients at the 3-month baseline examination. Life-table methods were used to estimate mortality rates in the groups with and without dementia after 1 to 5 years of follow-up, Kaplan-Meier curves to estimate the cumulative proportion surviving with and without dementia, and Cox proportional-hazards analysis to compute the relative risk of mortality associated with dementia at baseline, after adjusting for other potential predictors of stroke mortality. RESULTS: The mortality rate was 19.8 deaths per 100 person-years with dementia compared with 6.9 deaths per 100 person-years without dementia. The cumulative proportion surviving after a median follow-up of 58.6 months was 38.9 +/- 0.08% for those with dementia and 74.5 +/- 0.04% for those without dementia. The relative risk associated with dementia was 3.11 (95% confidence interval, 1.79 to 5.41) after adjusting for the effects of demographic factors, cardiac disease, severity of stroke (Barthel Index), stroke type (lacunar versus nonlacunar), and recurrent stroke (examined as a time-dependent variable). When the Mini-Mental State Examination score at baseline was examined instead of the diagnosis of dementia, the results of the model were similar. CONCLUSION: Our study is the first to demonstrate that dementia or cognitive impairment adversely influences long-term survival after stroke, even after adjusting for other commonly accepted predictors of stroke mortality. Impairment in intellectual function after stroke, independent of physical disability, has a significant impact on prognosis. Both cognitive and physical functions should be assessed in clinical studies of stroke outcome.

Aged↗