No abstract available.
Dementia* ; Pathology*

No abstract available.
Dementia* ; Neuropsychiatry* ; Pathology*

No abstract available.
Dementia* ; Neuropsychiatry* ; Pathology*

Background: Dementia is one of the major causes of dependency after stroke. The prevalence of poststroke dementia (PSD)defined as any dementia occurring after stroke is likely to increase in the future.Objectives: This study have two purposes: 1) Clinical study of MCI and dementia after the first stroke of patients with age of 60 years and older; 2) Overview on clinical characteristics of memory disorders. Subjects and method: 30 patients with were diagnosed with the first ischemic stroke in Huu nghi hospital together with the same number in the control group were involved in this study. The subjects in the two groups were all satisfied with included/excluded criteria diagnosis. Clinical diagnosis of new - onset dementia or other mental disorders was determined using neuropsychological tests. Results: Many functions of the brain were impaired including: logical memory, visiospatial skills, executive function were statistically reduced in the research group compared to the control. However, language function was also impacted but not as much as others. The frequency of the poststrocke dementia in this study was 12.3% while the poststrocke mild cognitive impairment rate was 47%. Conclusions: Global cognitive functioning together with memory state was significantly declined in the ischemic stroke compared to the control group.
Stroke/ pathology ; complications ; Dementia/ pathology ; complications

BACKGROUNDS: Behavioral and psychological symptoms as well as cognitive impairement are very disturbing symptoms in dementia. It is important in managing dementia patient to control these behavioral and psychological symptoms. In this study, we examined the effect of risperidone and optimal therapeutic dosage on controlling these behavioral and psychological symptoms of dementia (BPSD). METHODS: 57 patients (male: 19, female: 38) with dementia, aged 65 and older in Buyeo geriatric hospital located in Buyeo-gun, chung-nam, were finally included in this study. risperidone was administrated to these subjects for 10 weeks to control BPSD. Behavioral Pathology in Alzheimer's Disease Rating Scale (BEHAVE-AD) was rated before administration of risperidone and after administration of risperidone for 10 weeks to evaluate the improvement of BPSD. Global Deterioration Scale (GDS) was rated before administration of risperidone. The correlation between baseline GDS score and the change of sum score of BEHAVE-AD was analyzed. RESULT: The mean dose of resperidone at the endpoint was 0.706+/-0.522 mg/d. The significant reduction of the sum score of BEHAVE-AD was observed in subjects after administration of risperidone for 10 weeks. Clinical improvement (> or =50% reduction of sum score of BEHAVE-AD from baseline sum score) was showed in 32 subjects (56.1%) among 57 subjects. Also there was weakly negative correlation between baseline GDS score and the change of sum score of BEHAVE0AD. CONCLUSION: Risperidone was effective in controlling BPSD of dementia patients at 0.706+/-0.522 mg/d.
Alzheimer Disease ; Dementia* ; Female ; Humans ; Pathology ; Risperidone*

Humans ; AIDS Dementia Complex/pathology* ; HIV Infections

The dementia with Lewy bodies which was common next to the Alzheimer's dementia had been oftenly misdiagnozed as vascular dementia. The pathologic diagnosis of dementia with Lewy bodies was increasing with the development of immunocytochemical techniques, and it also drew much interest recently. The clinical criteria included core symptoms such as fluctuation of cognitive function, well-formed visual hallucination and extrapyramidal symptoms. For the pathologic criteria, presence of brainstem or cortical Lewy bodies were essential, besides of other pathology. However, it was difficult to obtain satisfactory consensus between investigators about the clinical and pathologic criteria of the dementia with Lewy bodies. There were several reports which suggested good response to the cholinesterase inhibitors.
Brain Stem ; Cholinesterase Inhibitors ; Consensus ; Dementia* ; Dementia, Vascular ; Diagnosis ; Hallucinations ; Humans ; Lewy Bodies* ; Pathology ; Research Personnel

Dementia ; pathology ; Hallucinations ; pathology ; Humans ; Lewy Body Disease ; pathology ; Nerve Net ; pathology

Vascular dementia (VaD) is a history-laden disease entity that dates back to the 19th century when arteriosclerotic brain atrophy due to hardening of the arteries was perceived as the major cause of senile dementia. Its existence had been overshadowed by the emergence of Alzheimer's disease (AD) in the past century and research on AD dominated the field of dementia. Interest in VaD has been revived in recent years as vascular lesions have been shown to make great contributions to the development of dementia, particularly in the elderly. VaD has now evolved into the concept of vascular cognitive impairment (VCI), which encompasses not only VaD but also AD with cerebrovascular disorder and VCI with no dementia. The concept of VCI is intended to maximize the therapeutic potential in dementia management because the vascular component may be amenable to therapeutic intervention particularly in the early stages of cognitive impairment. Subcortical ischemic vascular dementia (SIVD) is pathologically driven by severe stenosis and the occlusion of small vessels that culminate into white matter ischemia and multiple lacunar infarctions in the subcortical structures. The relatively slow progression of symptoms and clinical manifestations associated with cholinergic deficits often make the differentiation of SIVD from AD difficult. The recent development of in vivo amyloid imaging enabled further pathological breakdown of SIVD into pure SIVD and mixed dementia with subcortical ischemia based on the absence or existence of amyloid pathology in the brain. In this article, the authors reviewed the emerging concepts of VaD/VCI and the clinical manifestations, biomarkers, treatments, and preclinical models of SIVD based on the pathophysiologic mechanisms of the disease.
Aged ; Alzheimer Disease ; Amyloid ; Arteries ; Atrophy ; Biomarkers ; Brain ; Cerebrovascular Disorders ; Constriction, Pathologic ; Dementia ; Dementia, Vascular* ; Humans ; Ischemia ; Pathology ; Stroke, Lacunar

Frontotemporal lobar degeneration (FTLD) is a progressive dementia with prominent neuropsychiatric features, aphasia or both. FTLD predominantly affects the frontal and anterior part of temporal cortex. FTLD is classified into frontotemporal dementia (FTD), progressive nonfluent aphasia (PA), and semantic dementia (SD). FTLD is estimated to account for 20% of cases of degenerative dementia with presenile onset. This disease typically has onset in the mid- or early fifties. FTD is characterized by behavioral change and executive dysfunction, PA features a progressive nonfluent aphasia. SD is characterized by a progressive semantic aphasia and associative agnosia. Structural imaging shows atrophy of the frontal lobe and the anterior portion of the temporal lobe, bilaterally symmetric or asymmetric. Pathologically, FTLD can be classified into tau-positive pathology, tau-negative, ubiquitin positive pathology, dementia lacking distinctive histology. At present, there are no specific pharmacological therapies approved for use in any of the FTLD syndrome.
Agnosia ; Aphasia ; Atrophy ; Dementia ; Frontal Lobe ; Frontotemporal Dementia ; Frontotemporal Lobar Degeneration* ; Pathology ; Primary Progressive Nonfluent Aphasia ; Temporal Lobe ; Ubiquitin