Vascular dementia is the second most common cause of dementia, although it is neglected by some authors. Inadequate circulation, silent brain infarcts, and symptomatic strokes all increase dementia. High blood pressure increases the risk of both dementia and stroke.
Many of my articles on vascular dementia are groups under causes of dementia. No specific treatment has been proposed except to control blood pressure. Some of the treatments which help Alzheimer's seem to help vascular dementia although many studies to not differentiate. Extensive animal research suggests that melatonin may help prevent vascular dementia.
Lack of Nighttime BP Drop Linked to Cognitive Impairment: Twenty-four-hour blood pressure (BP) readings have been found to correlate with hypertensive target organ damage. Lacunar infarcts (LI) and white matter lesions (WML) represent manifestations of cerebral hypertensive target organ damage. In a study of 200 patients with first-time symptomatic LI, 50% had no drop in nighttime BP (nondippers), 27.5% an increase in nighttime BP (reverse dippers) and 22.5% the normal drop in nighttime BP (dippers). Forty-one patients had cognitive impairment (CI). Males (OR 3.35), advanced periventricular hyperdensities (PVH) (OR 14.42) and absence of a dipping status (nondipper: OR 12.62; reverse dipper: OR 11.95) were independently associated with CI. High nighttime systolic BP (OR 3.93), high daytime (OR 2.06) and nighttime diastolic BP (OR 2.48) and absence of a dipping status (nondipper: OR 2.7; reverse dipper: OR 3.78) were significantly associated with PVH. The Relationship between 24-Hour Blood Pressure Readings, Subcortical Ischemic Lesions and Vascular Dementia. Yamamoto Y, Akiguchi I, et al. Kyoto, Japan. Cerebrovasc Dis. 2005 Mar 17;19(5):302-308. Ed: Non-dipping could be related to a lack of melatonin.
Vascular Stroke Dementia Show Deterioration 3 Years Before Stroke: Population-based samples of 15 incident VaD cases, 43 incident AD cases, and 149 normal controls were compared on tests of episodic and short-term memory, verbal fluency, and visuospatial skill. Both dementia groups showed preclinical impairment relative controls on tasks assessing episodic memory 3 years before diagnosis, and there were no differences between these groups on any cognitive measure. The existence of a preclinical phase in the present VaD cases suggests that circulatory disturbance may affect cognitive performance before the occurrence of stroke that leads to clinical VaD. These results extend previous findings of similar patterns of cognitive deficits in the early clinical phases of AD and VaD to the preclinical phases of these diseases. Similar patterns of cognitive deficits in the preclinical phases of vascular dementia and Alzheimer's disease. Laukka EJ, Jones S, et al. Karolinska Institutet, Stockholm, Sweden. J Int Neuropsychol Soc. 2004 May;10(3):382-91
Less Educated, Older, Heavy Drinking, Atrial Fibrillation, Left Carotid Area are Dementia Risk Factors After Stroke:
Metalloproteinase Marker MMP-9 Distinguishes Vascular Dementia: Cerebrovascular disease increases expression of brain matrix metalloproteinases (MMPs) and tissue inhibitors to metalloproteinases (TIMPs). Fifteen patients with dementia caused by multiple infarcts and progressive dementia caused by disease of the small cerebral blood vessels were compared to 30 patients with AD. Gelatinase B (MMP-9) levels were significantly elevated in the CSF of VaD patients compared either to those with AD (P<0.0001) or to controls. MMP-2, TIMP-1, and TIMP-2 were similar in patient groups and controls. CSF MMP-9 increases in other neurological conditions and is not specific for VaD. Still, it could provide an additional biological marker for the separation of patients with VaD and AD. Measurement of gelatinase B (MMP-9) in the cerebrospinal fluid of patients with vascular dementia and Alzheimer disease. Adair JC, Charlie J, et al. University of New Mexico. Stroke. 2004 Jun;35(6):e159-62
Brain Infarcts and Alzheimer's Pathology Affect Dementia Independently: 153 deceased Catholic clergy who participated in the Religious Orders Study had had annual cognitive testing. At autopsy, neuritic and diffuse plaques and neurofibrillary tangles were counted and combined into a standardized summary measure of AD pathology. Number, volume, side, and distribution of old macroscopic infarctions were recorded. There was no relationship between AD pathology and infarctions (r = 0.04, p = 0.56). Each unit of AD pathology increased the odds of dementia by 4.40-fold, and this was essentially unchanged after accounting for infarctions. The presence of one or more infarctions independently increased the odds of dementia by 2.80-fold. There was no interaction between AD pathology and infarctions to further increase the likelihood of dementia (p = 0.39). The number, size, and distribution of infarctions added to the odds of dementia but also did not show an interaction with AD pathology. Similar results were found in analyses with global cognitive function and five different cognitive systems. Cerebral infarctions and the likelihood of dementia from Alzheimer disease pathology. Schneider JA, Wilson RS, et al. Rush Alzheimer's Disease Center. Neurology. 2004 Apr 13;62(7):1148-55
Reducing BP After Stroke No Impact On Silent Brain Infarct or Atrophy: In a DB PC study of 667 patients, the angiotensin-converting enzyme (ACE) inhibitor perindopril (4 mg daily), with or without the diuretic indapamide (2 mg daily) over 3.9 years reduced the blood pressure (systolic/diastolic) by 5.2/2.6 mmHg but had no effect on recurrent symptomatic stroke or new SBI. The baseline diastolic blood pressure was significantly associated with the risk of new SBI (p = 0.004). Effects of perindopril-based blood pressure lowering and of patient characteristics on the progression of silent brain infarct: the Perindopril Protection against Recurrent Stroke Study (PROGRESS) CT Substudy in Japan. Hasegawa Y, Yamaguchi T, et al; PROGRESS CT Substudy Investigators. Japan. Hypertens Res. 2004 Mar;27(3):147-56
Nimodipine Calcium Channel Blocker Might Have Helped Some: In a much smaller 1-year DB PC study of 230 patients with subcortical VaD, those on nimodipine 90 mg/d did no better on the Sandoz Clinical Assessment Geriatric scale 5-point variation, the primary outcome measure. They did show less frequent deterioration (3 or more point-drop versus baseline) on a Mini-Mental State Examination (28.1% versus 50.5%; P<0.01) and Global Deterioration Scale (P<0.05). Dropouts and adverse events were all significantly more common among placebo than nimodipine patients, particularly cardiovascular (30 versus 13; RR, 2.26) and cerebrovascular events (28 versus 10; RR, 2.48), and behavioral disturbances requiring intervention (22 versus 5; RR, 3.88). Efficacy and safety of nimodipine in subcortical vascular dementia: a randomized placebo-controlled trial. Pantoni L, del Ser T, et al. University of Florence, Italy. Stroke. 2005 Mar;36(3):619-24.
Thomas E. Radecki, M.D., J.D.