Poststroke dementia

The association between stroke and dementia is frequent. The prevalence of poststroke dementia (PSD) ranges from 6 to 32%, depending on the population studied, the criteria used for the diagnosis of dementia, and the time interval between the stroke and the neuropsychological assessment. The risk of PSD is high immediately after stroke and remains higher than in controls in stroke patients nondemented 3 months after stroke. Not all cases of PSD are vascular in origin, with about one third of demented patients diagnosed as having Alzheimer's disease plus stroke. The pathophysiology of PSD is probably multifactorial, with an influence of vascular lesions, associated Alzheimer's lesions and white matter changes. The risk of dementia is higher in older patients and in patients with preexisting cognitive decline - no dementia, severe stroke, a history of stroke, white matter changes and cerebral atrophy. The influence of stroke location, vascular risk factors and silent infarcts remains to be determined. PSD adversely influences the outcome in stroke patients.     

Poststroke dementia: influence of hippocampal atrophy

BACKGROUND: The prevalence of dementia is increased after stroke. Medial temporal lobe atrophy (MTLA) is associated with Alzheimer disease, and with prestroke dementia in patients who have had a stroke. OBJECTIVE: To determine the influence of MTLA on the long-term risk of dementia after stroke, after excluding the patients who had prestroke dementia. METHODS: The study was conducted in 144 consecutive patients who had a stroke, who were aged 40 years or older (66 women and 78 men; median age, 72 years), and who had an Informant Questionnaire on Cognitive Decline in the Elderly score lower than 104. On admission to the hospital all patients underwent a noncontrast computed tomographic scan including temporal lobe-positioned slices. A cut-off of 11.5 mm was used to differentiate patients with MTLA from those without MTLA. Patients were followed up with clinical and cognitive assessments over a 3-year period. RESULTS: Three years after stroke, 34 patients (23.6%) had developed new-onset dementia. The cumulative proportion of survivors without dementia was 57.6% in patients with MTLA and 80.8% in patients without MTLA (P =.02). The unadjusted relative risk of poststroke dementia associated with MTLA was 2.3 (95% confidence interval, 1.1-4.7). However, using the Cox proportional hazards model, MTLA did not seem to be an independent predictor of poststroke dementia. Independent predictors of poststroke dementia were increasing age, diabetes mellitus, severity of the clinical deficit at admission, and severity of leukoaraiosis on computed tomography. CONCLUSIONS: Patients who had a stroke and MTLA more frequently develop dementia than patients without MTLA, but our study does not suggest that MTLA independently contributes to dementia. A longer follow-up may be necessary to reevaluate the influence of MTLA.     

Poststroke dementia : clinical features and risk factors

BACKGROUND AND PURPOSE: The goal of the present study was to examine a series of putative risk factors of poststroke dementia (PSD), especially those factors usually associated with cerebrovascular disease and degenerative dementia, in a series of 251 consecutive unselected stroke patients. METHODS: A standard protocol was prospectively applied at admission and 3 months after stroke; this protocol included clinical, functional, and cognitive assessments, hemogram and serum biochemistry, ECG and CT exams, apolipoprotein E and angiotensin-converting enzyme genotype, and neuropsychological examination. After a neuropsychological examination and an interview with a relative, the following diagnostic criteria were used: the Diagnostic and Statistical Manual of Mental Disorders (DSM)-IV for dementia after stroke, DSM-III-R for previous dementia and dementia stage, and Association Internationale pour la Recherche et l'Enseignement en Neurologie (NINDS-AIREN) for vascular dementia. RESULTS: Seventy-five cases (30%) demonstrated dementia at 3-month follow up; 25 of them (10%) had demonstrated dementia before the stroke. Dementia was unrelated to type (ischemic/hemorrhagic) or location of stroke, vascular factors (hypertension, diabetes, ischemic heart disease, or hypercholesterolemia), apolipoprotein E or angiotensin-converting enzyme genotype, and serum homocysteine. Age (odds ratio [OR] 1.1, 95% CI 1.03 to 1.2), previous nephropathy (OR 6.1, 95% CI 1.5 to 24.3), atrial fibrillation (OR 4.4, 95% CI 1. 4 to 13.9), low Canadian Neurological Scale score at discharge (OR 0. 5, 95% CI 0.4 to 0.6), and previous mental decline assessed by the shortened Spanish version of the Informant Questionnaire on Cognitive Decline in the Elderly (SS-IQCODE; OR 1.2, 95% CI 1.1 to 1. 4) were the correlates of dementia in logistic regression analyses. The same risks factors were found when cases with previous dementia and with hemorrhagic stroke were excluded. CONCLUSIONS: Dementia is frequent after ischemic or hemorrhagic stroke. Age, nephropathy, atrial fibrillation, previous mental decline, and stroke severity independently contribute to the risk.     

Poststroke dementia: incidence and relationship to prestroke cognitive decline

OBJECTIVE: To evaluate the 3-year incidence of poststroke dementia (PSD) and the influence of prestroke cognitive decline. METHODS: The authors evaluated prestroke cognitive functions in 202 consecutive stroke patients > or =40 years old using the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE), with a cut-off of 104 for the diagnosis of dementia. Six months and then annually after stroke, dementia was reassessed. The diagnosis of dementia was based on the International Classification of Diseases, 10th revision criteria in survivors who underwent a visit with a neurologist, or on the IQCODE score obtained by telephone contact with the family in survivors who did not. Statistics were performed using life-table methods. RESULTS: Thirty-three patients were excluded because of prestroke dementia. In the 169 remaining patients, the cumulative proportion of patients with dementia was 28.5% at the end of the follow-up period, with most of PSD occurring during the first 6 months. Using multivariate analysis, independent predictors of PSD were aging, preexisting cognitive decline, severity of deficit at admission, diabetes mellitus, and silent infarcts. Leukoaraiosis was an independent predictor of PSD when prestroke cognitive decline was not taken into account. The presumed etiology of dementia was vascular dementia (VaD) in two-thirds of patients and AD in one-third. CONCLUSIONS: The risk of PSD is high, and increased in patients with prestroke cognitive decline, with about one-third of patients meeting the criteria for AD and two-thirds meeting the criteria for VaD. These results confirm that, in stroke patients, an underlying degenerative pathology may play a role in the development of PSD.     

Poststroke seizures

Stroke is the most common cause of seizures in the elderly, and seizures are among the most common neurologic sequelae of stroke. About 10% of all stroke patients experience seizures, from stroke onset until several years later. This review discusses current understanding of the epidemiology, pathogenesis, classification, clinical manifestations, diagnostic studies, differential diagnosis, and management issues of seizures associated with various cerebrovascular lesions, with a focus on anticonvulsant use in the elderly.     

Poststroke depression

Neuropsychological symptoms are probably among the most commonly ignored complications in stroke patients. Depression is a common yet often unrecognized neuropsychological consequence of stroke, having biological, psycho-behavioral, and social dimensions. The reported prevalence of depression following a stroke varies from 20% to 50% within the first year, with an apparent peak within the first 6 months of onset event. The disparity of reported prevalence rates significantly depends on study methodology, diagnostic assessment tools, and time elapsed after stroke onset. The etiology of depression after a stroke is complex; it is likely determined by multiple factors, including lesion location, social handicap, and family support. Depression impedes rehabilitation progress following stroke and is associated with impaired functional outcome, cognitive decline, and increased mortality. Similarly, depression has been linked to increased risk of stroke occurrence. Despite high prevalence and serious sequels, poststroke depression (PSD) remains undetected and untreated. Early diagnosis and successful intervention may improve clinical outcome and should be considered a key for better stroke care. In this article, we review the clinical presentation, epidemiology, pathogenesis, and consequences of PSD and summarize current recommendations for therapeutic intervention.     

Dementia Poststroke

Abstract : The frequency of dementia poststroke is high, and stroke considerably increases the risk of dementia. The risk factors for dementia related to stroke are still incompletely understood. In addition to age and low level of education, different combinations of vascular risk factors and stroke features have been associated with poststroke dementia. A single explanation for poststroke dementia is not adequate; rather, multiple factors including stroke features (dysphasia, major dominant stroke syndrome), infarct features (type, side, site, number, and volume), extent and type of white matter lesions (WMLs), degree and site of atrophy, host characteristics (e.g. age, educational level), and risk factors for stroke (e.g. prior cerebrovascular disease, diabetes) each contribute to the risk of dementia poststroke.
Dementia after first ever clinical stroke is also frequent. Cognitive decline is present prior to stroke in up to one-third of patients developing post-stroke dementia. Medial temporal lobe atrophy, a marker of an increased risk of Alzheimer's disease (AD), is more frequent in stroke patients who have preexisting dementia or cognitive decline, as well as poststroke dementia. This may be explained by co-existing AD and cerebrovascular disease (CVD). The magnitude of this mixed dementia (AD with CVD/Vascular Dementia (VaD)) group has been previously underestimated, and it is a diagnostic challenge in the older population.
Dementia due to CVD is a rather advanced stage of is chemic brain changes, and outcome of treatment and prevention may be limited. Accordingly, the focus should be placed on the entire spectrum of cognitive impairment related to CVD, focusing especially the early cognitive changes.     

脑卒中后中枢性疼痛

脑卒中后中枢性疼痛（CPSP）是脑卒中后与病灶有关的、在瘫痪躯体的一部分、持续或间断的及同时伴有感觉异常为主要特点的疼痛。由于临床医生对CPSP重视不足,导致患者长期处于疼痛状态,影响日常生活质量。为更好了解CPSP,本文就其流行病学、病理生理、临床特点及药物治疗做一综述。     

Poststroke depression and psychosis

Stroke is capable of producing a varied spectrum of neurobehavioral syndromes that may come to the attention of the mental health professional evaluating psychiatric symptoms in elderly individuals. The neurobehavioral effects may include affective or psychotic symptoms and may occur immediately after the stroke or months to years later. The presence of underlying (or pre-existing) brain disease may have an adverse effect on the resolution of the neuropsychiatric symptoms. Although there are no treatment response studies in the area of psychosis following stroke, the response of poststroke depression to antidepressants makes attempted pharmacologic treatment of symptoms justified.     

Poststroke depression: psychopharmacological considerations

PSD is a common psychiatric complication of stroke. It is often underrecognized and untreated. Numerous studies show that untreated PSD impedes the rehabilitation and recovery process, jeopardizes quality of life, and increases mortality. Successful management of the PSD requires early recognition and initiation of appropriate treatment to facilitate an optimal level of functioning. As active members of the interdisciplinary treatment team, psychiatric consultative-liaison nurses play a pivotal role in facilitating positive treatment outcomes during both the acute and rehabilitation phases in the management of PSD.     

Poststroke depression: A biopsychosocial approach

Poststroke depression (PSD) is a form of geriatric depression that is associated with various negative outcomes. This article reviews existing research concerning the etiology, treatment, and prevention of PSD with particular emphasis on the development of a biopsychosocial conceptualization of PSD etiology and treatment. Existing intervention trials are reviewed. A behavioral model of PSD treatment is presented based on a biopsychosocial understanding of PSD that highlights the potential utility of the lesion location hypothesis in the early poststroke period and the behavioral and social changes that may be linked to depression in the postacute period after stroke.     

Poststroke depression and lesion location revisited

Seventy patients with one brain infarct on magnetic resonance imaging (MRI) were studied 3 months after ischemic stroke by a standardized protocol to detail side, site, type, and extent of the brain infarct, as well as severity of white matter lesions and brain atrophy. Depression was diagnosed by DSM-III-R and DSM-IV criteria. The brain infarcts that affected structures of the frontal-subcortical circuits, (i.e., the pallidum and caudate, especially on the left side) predisposed stroke patients to depression. The size of the infarcts at these sites in the depressed patients was larger. Using a logistic regression analysis, the authors found that a brain infarct that affected pallidum was a strong independent MRI correlate for poststroke depression (odds ratio = 7.2).