Treating Vascular Dementia: More of the Same?

David B. Reuben, MD

Disclosures

November 18, 2015

Editorial Collaboration

Medscape &

Question:

How does the treatment for vascular dementia differ from that of other dementias?

Response from David B. Reuben, MD
Professor and Archstone Foundation Endowed Chair, Department of Medicine, University of California, Los Angeles; Chief, Division of Geriatrics, UCLA Medical Center, Santa Monica, California

Although there are considerable similarities between vascular dementia and Alzheimer disease and signs and symptoms commonly overlap, the approach to these different causes of dementia varies. For vascular dementia, there has been an emphasis on the reduction of vascular risk factors to prevent secondary progression of cognitive decline due to subsequent strokes. Hence, standard lifestyle interventions (ie, exercise, smoking cessation, weight loss if obese) are recommended as well as aspirin, antihypertensive therapy, and statins. These treatments have a strong evidence base in prevention of cardiovascular events, including stroke, but the evidence that they specifically reduce the risk for vascular dementia or progression of dementia in those with the disease is less clear.

The benefit of lowering blood pressure and the blood pressure target are controversial. Although lowing blood pressure may prevent further strokes, those who have existing cerebrovascular disease may need higher blood pressure to maintain adequate cerebral perfusion. Recently, the large Systolic Blood Pressure Intervention Trial (SPRINT),[1] which aimed at a target systolic blood pressure <120 mm Hg, was terminated early because of a reduction in overall cardiovascular events. But the effect on incident dementia has not yet been determined. Moreover, the benefit (and potential risk) of aggressive blood pressure management may vary by age and comorbidity. For example, among patients with diabetes, intensive lowering of systolic blood pressure (target <120 mm Hg) was associated with a greater decline in total brain volume (a precursor to cognitive decline) compared with those having a less aggressive target.[2]

Similarly, the benefit of diabetes control is uncertain, with some studies demonstrating worse cognitive function associated with poorer blood sugar control and some showing worse cognition with tighter control. With respect to statins, a recent meta-analysis found inconsistent evidence for an effect of statins on cognition among persons who were cognitively intact.[3] A 2009 Cochrane review identified two large randomized clinical trials that indicated no benefit of statins on cognitive measures despite reductions in serum cholesterol.[4] Nor was low-dose aspirin found to preserve cognition in middle aged or elderly patients at increased cardiovascular risk.[5]

Medications used to treat Alzheimer disease (acetylcholinesterase inhibitors and memantine) are frequently used in the treatment of vascular dementia. Cholinesterase inhibitors may have an effect on cognition in vascular dementia.[6] They may also be beneficial because Alzheimer disease often coexists with vascular dementia. Overall, the effect of these drugs is small, of uncertain clinical significance, and often without effects on functional status.[7] Data on memantine are similar.

In summary, the current approach to treating vascular dementia differs from that of treating Alzheimer disease in that it additionally focuses on treating risk factors for vascular disease. The strength of evidence for effectiveness of risk factor reduction is still not robust, although it may be more convincing for primary prevention of strokes and vascular dementia than for prevention of progression of existing vascular dementia. Medications to treat Alzheimer disease are also used both because of possible effectiveness in treating vascular dementia and for treatment of possible coexisting Alzheimer disease.

Developed in association with the UCLA Alzheimer's and Dementia Care Program

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