Vascular Dementia (also know as multi-infarct dementia) is acute or chronic cognitive deterioration due to diffuse or local cerebral infarction that is most often related to cerebrovascular disease.  It is the second most common dementia, and usually begins after the age of 70.  Causative factors include hypertension, diabetes mellitus, hyperlipidemia, and smoking.    

The onset of multi-infarct dementia often goes unnoticed in the early stages, particularly if the strokes are minor. If the strokes are minor, symptoms caused by each stroke may include mild weakness in the limbs, slurred speech, dizziness and a slight impairment to the short-term memory, though these do not last for long.  Small cerebral infracts cause enough neuronal or axonal loss to impair brain function.  It is a disease of the small and medium sized vessels. 

However, the cumulative effects of these strokes will eventually result in noticeable symptoms being displayed. These symptoms include: exaggeration of deep tendon reflexes, extensor plantar response, gait abnormalities, weakness of an extremity, hemiplegias, pseudobulbar palsy with pathologic laughing and crying, and other signs of extrapyrmidal dysfunction.  Cognitive loss may be focal. 

Diagnosis

CT and MRI may show bilateral multiple infracts in the dominant hemisphere and limbic structures, multiple lacunar strokes, or periventicular white matter.  .   

The incidence is 9 times higher in patients who have had a stroke than the control group, with 25% developing new-onset dementia within 1 year of their stroke.  The 5-year survival is 39% compared with 75% for aged match control group.  Vascular dementia is associated with a higher mortality than 'Alzheimer's', presumably because of the excess in cardiovascular risk factors. 

Vascular Dementia:  Distinguishing Characteristics, Treatment, and Prevention

Gustavo C. Roman, MD, U. of Texas

Vascular dementia (VaD) is the second-most-common cause of dementia in the elderly, after Alzheimer's disease (AD). VaD is defined as loss of cognitive function resulting from ischemic, hypoperfusive, or hemorrhagic brain lesions due to cerebrovascular disease or cardiovascular pathology. Diagnosis requires the following criteria: cognitive loss, often predominantly subcortical; vascular brain lesions demonstrated by imaging; a temporal link between stroke and dementia; and exclusion of other causes of dementia. Poststroke VaD may be caused by large-vessel disease with multiple strokes (multiinfarct dementia) or by a single stroke (strategic stroke VaD). A common form is subcortical ischemic VaD caused by small-vessel occlusions with multiple lacunas and by hypoperfusive lesions resulting from stenosis of medullary arterioles, as in Binswanger's disease. Unlike with AD, in VaD, executive dysfunction is commonly seen, but memory impairment is mild or may not even be present. The cholinesterase inhibitors used for AD are also useful in VaD. Prevention strategies should focus on reduction of stroke and cardiovascular disease, with attention to control of risk factors such as hypertension, diabetes mellitus, hypercholesterolemia, and hyperhomocysteinemia

Mixed Dementia

Emerging Concepts and Therapeutic Implications

JAMA. 2004;292:2901-2908.

Context  The prevalence of mixed dementia, defined as the coexistence of Alzheimer disease (AD) and vascular dementia (VaD), is likely to increase as the population ages.

Objectives  To provide an overview of the diagnosis, pathophysiology, and interaction of AD and VaD in mixed dementia, and to provide a systematic literature review of the current evidence for the pharmacologic therapy of mixed dementia.

Data Sources, Study Selection, and Data Extraction  The Cochrane Database of Systematic Reviews was searched using the keyword dementia. MEDLINE was searched for English-language articles published within the last 10 years using the keywords mixed dementia, the combination of keywords Alzheimer disease, cerebrovascular disorders, and drug therapy, and the combination of keywords vascular dementia and drug therapy.

Evidence Synthesis  Dementia is more likely to be present when vascular and AD lesions coexist, a situation that is especially common with increasing age. The measured benefits in clinical trials for the treatment of mixed dementia are best described as statistically significant differences in cognitive test scores and clinician and caregiver impressions of change. In these studies, the control groups’ scores typically decline while the treatment groups improve slightly or decline to a lesser degree over the study period. Nevertheless, even the patients who experience treatment benefits eventually decline. Cholinesterase inhibitor (ChI) therapy for mixed dementia shows modest clinical benefits that are similar to those found for ChI treatment of AD. The N-methyl-D-aspartate (NMDA) antagonist memantine also shows modest clinical benefits for the treatment of moderate to severe AD and mild to moderate VaD, but it has not been studied specifically in mixed dementia. The treatment of cardiovascular risk factors, especially hypertension, may be a more effective way to protect brain function as primary, secondary, and tertiary prevention for mixed dementia.

Conclusions  Currently available medications provide only modest clinical benefits once a patient has developed mixed dementia. Cardiovascular risk factor control, especially for hypertension and hyperlipidemia, as well as other interventions to prevent recurrent stroke, likely represent important strategies for preventing or slowing the progression of mixed dementia. Additional research is needed to define better what individuals and families hope to achieve from dementia treatment and to determine the most appropriate use of medication to achieve these goals.