Search

In this review, we report current data on spoken and written language disorders in the most frequent dementia syndromes, namely Alzheimer' disease, vascular cognitive impairment and dementia with Lewy bodies. Language deficits are also the core features of three variants of primary progressive aphasia, namely the nonfluent/agrammatic, semantic and logopenic variants. This review reveals that, like other cognitive functions, language is highly vulnerable to neurodegenerative diseases. For some, language deficits result from impairment in linguistic processes per se, while for others, they are the direct consequence of impairments affecting working memory and executive functions. Language deficits in Alzheimer's disease and in nonfluent/agrammatic and semantic variants of primary progressive aphasia are well documented. By contrast, those about vascular cognitive impairment and dementia with Lewy bodies remain scarce and limited to large cognitive domains. The identification of logopenic variant of primary progressive aphasia is very recent, and more research is needed to complete the clinical description and identification of the functional origin of the disorders. Finally, knowledge on the impairment of written language in neurodegenerative diseases is less well documented than those on spoken language deficits. Other studies are therefore needed to improve the description of linguistic profiles and to provide additional elements to help in the differential diagnosis.

The concept of vascular dementia has evolved over the past century to include multiple underlying pathophysiological mechanisms. Neuroimaging techniques offer new and better ways to identify the presence of cerebrovascular pathology, although they do not improve our ability to link these changes to the onset of clinical cognitive impairment. Clinical criteria for vascular dementia have also evolved but they remain imperfect. Most epidemiological studies define mixed dementia as the coexistence of Alzheimer's disease and vascular dementia. Clinicopathologic correlations show a clear association between the concomitant presence of vascular and Alzheimer lesions and the severity of cognitive impairment in mixed dementia and provide strong support for the validity of the mixed dementia concept. Mixed dementia is a very frequent disease that remains underdiagnosed, especially in the elderly. The diagnosis of vascular and mixed dementia remains a clinical challenge and cannot be improved without further studies of clinicopathological correlations and functional neuroimaging. Preventive therapeutic interventions include control of vascular risk factors and especially treatment of hypertension.

Alzheimer's disease (AD) and vascular dementia (VaD) are the most frequent causes of dementia in the elderly. Although AD can be diagnosed with a very high degree of accuracy, the distinction between pure AD, VaD and mixed dementia (MD), where both pathologies co-exist in the same patient, remains a controversial issue and one of the most difficult diagnostic challenges. MD represents a very frequent pathology, especially in the elderly, as underlined by the neuropathological studies. However, the respective importance of degenerative and vascular lesions, their interaction in the genesis of dementia and the mere existence of mixed dementia are still debated. Accurate diagnosis of MD is of crucial significance for epidemiologic purposes and for preventive and therapeutic strategies. Until recently, pharmacological studies have generally focused on pure diseases, either AD or VaD, and have provided little data on the best therapeutic approach to MD. This review will provide an overview of neuropathological aspects of MD in the elderly, which appears to be one of the most common forms of dementia.

Vascular dementia is the second cause of dementia after Alzheimer's disease. It is a broad term which includes dementia due to: single or multiple infarcts related to large vessel disease, subcortical ischemic pathology linked to small vessel disease, hemorrhages, and hypoperfusion. Furthermore, vascular and Alzheimer lesions often coexist leading to a mixed dementia. The diagnosis should be considered in the presence of dementia, clinical or neuroradiological signs of cerebrovascular disease and a plausible link between the two. Newly identified preventive strategies and encouraging results of recent trials using cholinesterase inhibitors or memantine suggest therapeutic potential.

Aspirin given as a platelet antiaggregant has been shown to be effective for secondary prevention both in cardiology (myocardial infarction, uncontrolled angina pectoris, coronary bypass, etc.) and in neurology (after a cerebral vascular event or an episode of temporary ischaemia). For example, the risk of non-fatal recurrence is reduced by 31% after myocardial infarction and by 22% after cerebral vascular events. In the large scale trials which led to these findings, patients were usually included on the basis of one type of illness, heart disease of neurological disorder. However, these studies have also revealed a cross-over effect. For example a 35% reduction in non-fatal myocardial infarction after secondary preventive treatment for cerebral vascular events and a 42% reduction in cerebral vascular events after secondary preventive treatment for myocardial infarction. Such arguments suggest the importance of evaluating the dual brain/heart and heart/brain impact of secondary prevention. In addition, aspirin has been shown to be effective in certain forms of non-valvular atrial fibrillation and in vascular dementia. Recommended doses vary between 160 and 300 mg/day. Secondary cardiologic prevention with such doses has a favourable effect both on the cardiologic indications after infarction or poorly controlled angina pectoris and has an additional impact on primary prevention of neurological events. The Scientific Committee of the American Heart Association recommends the dose of 160 mg/day after myocardial infarction. For secondary neurological indications, recent studies demonstrate that the dose of 300 mg/day is as effective as higher doses which are less well tolerated and haematologists have underscored that doses below 160 mg/day would not have a sufficient anti-thrombotic effect. The recommended doses for neurological indications would thus be within this range. It is reasonable to expect a dual impact of secondary prevention with doses near 300 mg/day.

In the past decades, the recognition of polymorbidity as an important characteristic of geriatric medicine lead to important improvements in the multidisciplinary approach of the elderly. Coexistence of somatic and psychiatric diseases with various forms of etiopathogenic relations has been described early in this century. Dementia may be caused, aggravated, revealed or randomly accompanied by somatic diseases and inversely. However, very few attempts have been made in order to analyze the significance of these associations. This study is meant to give a better epidemiological knowledge of the relation between cardiovascular diseases and cerebral aging. This could lead to a better diagnostic approach and to a more complete physiopathological conception of dementia. 904 autopsy reports (patients who died between 1972 and 1986 in the Hôpital de Gériatrie of Genova) have been reviewed and classified in three groups according to neuropathological findings: 335 subjects with vascular encephalopathy of various types, 382 patients with degenerative diseases of Alzheimer type and 187 patients with normal brain. The subjects of these three groups had not all been considered demented. For each patient, age, sex, cause of death and 14 cardiovascular items have been appointed. The patients of the Alzheimer group died older and were more often women than those of the two other groups. The subjects of the vascular group died older than those of the normal group and were more often men than those of the two other groups. Stoke was considered to be the cause of death in 3% of the vascular patients whereas, by definition, it was absent from the two other groups.(ABSTRACT TRUNCATED AT 250 WORDS)