Diagnosis, risk factors, and treatment of vascular dementia

Abstract

Although the introduction of modern neuroimaging techniques and standardized clinical evaluations has improved the identification of cerebrovascular disease, the clinical diagnosis of vascular dementia (VaD) is still problematic. Neuropathologic studies have found the current clinical criteria for VaD had low sensitivity with high specificity, suggesting that cerebrovascular disease of sufficient severity to cause cognitive deficits is frequently associated with other disease processes (eg, Alzheimer's disease). The critical factors about the diagnosis of VaD are centered on two issues: definition of dementia and determination of vascular disease. The current clinical criteria for VaD have different definitions of dementia, which are mainly based on an Alzheimer's disease-like presentation, and severe vascular disease can present with or without history of clinical strokes. Therefore, there is a need for a better definition of VaD. This is extremely important to better understand its risk factors, as well as to create homogenous cohorts suitable for drug trials.

Neuroprotection in Vascular Dementia

“…In the current situation, any type of dementia syndrome caused by vascular disease, whether ischemic or hemorrhagic, single or multiple, cortical or subcortical, should be classified under the term VaD [10, 28, 29]. VaD syndrome has been classified in different clinicopathological subtypes (large-vessel VaD, multi-infarct dementia and strategic infarct dementia; small-vessel VaD, subcortical and cortico-subcortical; ischemic-hypoperfusive VaD, and hemorrhagic VaD), and may present clinically in many different forms [29, 30].…”

“…However, the clinical diagnosis of VaD is still a very complex procedure because of the heterogeneous nature of the condition in physiopathological terms and the diversity of individual cases [10, 11]. The clinical data collated thus far has not yielded a clear diagnostic procedure for VaD; the presence of cerebrovascular lesions must also be determined.…”

“…However, the current, limited understanding of the physiopathological mechanisms that produce cognitive deterioration in VaD means that a more specific therapeutic approach cannot yet be established. Several drugs have been used in the treatment of patients diagnosed with VaD, but the results from clinical trials thus far have been largely negative or have shown only very limited efficacy [10]. Unsatisfactory VaD trial results may be attributed in part to the diversity of patients included and to methodological limitations in the trials themselves [10, 17, 18].…”

“…Several drugs have been used in the treatment of patients diagnosed with VaD, but the results from clinical trials thus far have been largely negative or have shown only very limited efficacy [10]. Unsatisfactory VaD trial results may be attributed in part to the diversity of patients included and to methodological limitations in the trials themselves [10, 17, 18]. Preliminary results from recent trials, testing some acetylcholinesterase inhibitors and the NMDA-antagonist memantine, offer some new grounds for hope in the treatment of VaD [17, 18].…”

“…Nevertheless, new clinical trials, designed specifically to evaluate the cases of patients suffering from cognitive impairment of vascular origin, are needed [18, 19]. At the same time, it is possible that vascular cognitive impairment can to some extent be improved, and VaD prevented, if vascular risk factors are brought under control and strokes do not recur [10, 18, 20]. …”