Encyclopedia of Gerontology and Population Aging

Living Edition
| Editors: Danan Gu, Matthew E. Dupre

Vascular Dementia

  • Margaret E. WigginsEmail author
  • Catherine Price
Living reference work entry
DOI: https://doi.org/10.1007/978-3-319-69892-2_719-1

Synonym

VaD

Definition

Vascular dementia (VaD) is the second most common form of dementia (See “Dementia”), after Alzheimer’s disease (O’Brien and Thomas 2015). The etiology of VaD is believed to be due to the blood vessels to the brain becoming blocked or narrowed, therefore leading to clinical stroke(s) or insults that in turn impact brain integrity and functioning (See “Vascular Diseases of Aging”). Cognitive changes associated with VaD are variable and highly dependent on the vascular pathology leading to the disease, but deficits in executive function and attention are considered a salient feature of neurocognitive presentation (O’Brien et al. 2003).

Overview

Diagnostic Criteria: In the 1970s, the term multi-infarct dementia (MID) was used to describe patients who developed a dementia syndrome after a single vascular insult or a series of vascular insults/strokes (Hachinski et al. 1974). Now, the term vascular dementia is used regardless of the etiology or pathogenesis of the brain lesion(s) involved (Román et al. 1993). It is generally agreed upon that diagnosis of VaD should consider two factors: (1) the presence of a dementia by neuropsychological findings and (2) a history of stroke(s) or presence of vascular disease confirmed by the use of neuroimaging that can then suggest a possible link between the neurocognitive profile and brain pathology (Gorelick et al. 2011). In 2013, the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) replaced the category “delirium, dementia, amnestic and other geriatric cognitive disorders” with a new term for use in clinical practice, “neurocognitive disorders” (American Psychiatric Association 2013). Major neurocognitive disorder is the DSM-5 term for dementia, with major vascular neurocognitive disorder being the clinical term for VaD (American Psychiatric Association 2013). Additional specifiers can indicate whether it is a “probable” or “possible” etiology and whether or not behavioral disturbances are present (American Psychiatric Association 2013).

Key Research Findings

Etiology and Risk Factors: The etiology of vascular dementia varies greatly in regard to brain pathology and vascular insults though it typically occurs when blood vessels leading to the brain become blocked or narrowed, causing strokes. Multi-infarct dementia is caused by multiple large or small vascular infarcts, with larger overall infarct volume and a higher frequency of small infarcts being associated with greater impairments in cognitive functioning and incidence of dementia (Hachinski et al. 1974; Schneider et al. 2003; Sonnen et al. 2007). Strategic infarct dementia occurs when a single, small infarct in a specific brain region such as the thalamus leads to cognitive deficits (Szirmai et al. 2002). Subcortical ischemic vascular dementia (SIVD) is the result of small vessel disease (Román et al. 2002). Regardless of the specific etiology, all forms of dementia due to vascular diseases are encompassed by the umbrella term of vascular dementia.

Incidence: True incidence rates of VaD are unknown, as there are multiple diagnostic thresholds and criteria available (Román et al. 1993; Hachinski et al. 1974). However, up to 1/3 of stroke survivors over the age of 65 develop vascular dementia after the vascular incident(s) occur (Tatemichi et al. 1990; Pohjasvaara et al. 1997; Pendlebury and Rothwell 2009), suggesting that approximately 125,000 newly diagnosed cases of VaD occur after stroke every year in the United States alone (Román et al. 2002). The incidence rates of VaD rise with age, with the prevalence of vascular dementia doubling approximately every 5.3 years (Jorm et al. 1987), and accounting for approximately 20% of all known cases of dementia (Gorelick et al. 2011). A systematic review and meta-analysis assessing risk factors associated with dementia found that risk factors associated with dementia after stroke include increased age, low educational attainment, pre-existing cognitive decline, premorbid disability, diabetes, and atrial fibrillation and factors related to the stroke itself including lesion hemisphere, severity, number of strokes across time and space, recurrent strokes, incontinence, seizures, hypoxic ischemic episodes, and hypertension (Pendlebury and Rothwell 2009). Similar risk factors have been found for VaD not related to stroke, most commonly increased age and vascular risk factors (Wiesmann et al. 2013).

Neuropsychological Findings: The neuropsychological impact of VaD is variable and depends on the specific neural substrates impacted by the vascular pathology (O’Brien and Thomas 2015). However, due to subcortical vascular pathology frequently causing disruption to frontal striatal circuits including the thalamus, deficits in executive function, attention, speed of processing, and motor performance are common (O’Brien et al. 2003; Stebbins et al. 2008). Memory is thought to be relatively spared in comparison with individuals with dementia of the Alzheimer’s type, though the literature assessing memory deficits in VaD is mixed (Reed et al. 2007; Price et al. 2005). The disease progression of vascular dementia is often “step-wise” in nature. A step-wise disease progression is characterized by periods of stable cognitive functioning, followed by a quick drop in cognitive function following a stroke or vascular event. This cycle continues with periods of stability and drops after each additional vascular insult.

Brain Imaging: Neuroimaging is a critical component in the diagnosis of VaD (See “Neuroimaging”). While computed tomography (CT) scanning is sufficient for determining neuropathology including infarcts and white matter lesions (leukoaraiosis), magnetic resonance imaging (MRI) is the gold standard as it has greater precision for determining the degree, location, and severity of the vascular pathology (O’Brien and Thomas 2015). Several studies have suggested that multiple lacunes, strategic infarcts, or significant white matter lesion burden (>25%) as seen on MRI is consistent with a diagnosis of VaD (Pendlebury and Rothwell 2009; Price et al. 2005).

Treatment: Primary prevention is a key goal in regard to vascular dementia. Given that VaD may result from varying pathologies, strategies for disease prevention will vary on an individual level. However, it is important to recognize and distinguish primary processes such as vascular risk factors from secondary events such as vascular disease leading to a stroke (O’Brien et al. 2003). Therefore, identification and treatment of primary processes are critical for disease prevention. Secondary prevention includes treatment of acute and recurrent stroke. Once a dementia process has evolved, clinical trials have recently demonstrated efficacy for cholinesterase inhibitors such as donepezil in the treatment of VaD. When treated with donepezil, patients with VaD have demonstrated significant improvements in cognitive abilities, global functioning, and independent activities of daily living (IADLs; Román et al. 2005).

Future Directions of Research

There is a recent surge in research assessing and comparing the mechanisms and biomarkers associated with VaD and other dementias such as Alzheimer’s disease dementia, Lewy body dementia, and frontotemporal dementia (Maclin et al. 2019). Additionally, research involving the effects of various drugs for the treatment of VaD are being conducted in mouse models (Zacharek et al. 2019). This literature is then paving the way for clinical trials to assess safety and efficacy of such drugs for the treatment of VaD including acetylcholinesterase inhibitors. Additionally, research examining biomarkers such as genetic predispositions for vascular dementia is still relatively new when compared to literature on other dementias such as the Alzheimer’s type and warrants further investigation.

Summary

Vascular dementia (VaD) is the second most common form of dementia with at least 125,000 new cases diagnosed each year in the United States alone, second only to Alzheimer’s disease. Though the etiology varies on an individual basis, it is most often caused by the blood vessels to the brain becoming blocked or narrowed, leading to stroke(s). Cognitively, individuals with VaD may experience a step-wise decline in cognitive functioning. This cognitive decline most often occurs in the domains of executive function and attention, while memory is relatively spared. Neuroimaging is a critical component in the diagnosis of VaD, with MRI being used to determine the degree, location, and severity of infarcts that may correspond with cognitive performance. While identification and treatment of vascular risk factors are key components in the prevention of VaD, there is an increasing interest in clinical trials assessing various drugs for the treatment of vascular dementia such as acetylcholinesterase inhibitors. Future research will continue to assess biomarkers and mechanisms behind the disease, as well as various forms of treatment.

Cross-References

References

  1. American Psychiatric Association (2013) Diagnostic and statistical manual of mental disorders (DSM-5). Washington, DC: American Psychiatric PubGoogle Scholar
  2. Gorelick PB, Scuteri A, Black SE, DeCarli C, Greenberg SM, Iadecola C et al (2011) Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 42(9):2672–2713CrossRefGoogle Scholar
  3. Hachinski VC, Lassen NA, Marshall J (1974) Multi-infarct dementia: a cause of mental deterioration in the elderly. Lancet 304(7874):207–209CrossRefGoogle Scholar
  4. Jorm AF, Korten AE, Henderson AS (1987) The prevalence of dementia: a quantitative integration of the literature. Acta Psychiatr Scand 76(5):465–479CrossRefGoogle Scholar
  5. Maclin JMA, Wang T, Xiao S (2019) Biomarkers for the diagnosis of Alzheimer’s disease, dementia Lewy body, frontotemporal dementia and vascular dementia. Gen Psych 32(1):e100054CrossRefGoogle Scholar
  6. O’Brien JT, Thomas A (2015) Vascular dementia. Lancet 386(10004):1698–1706CrossRefGoogle Scholar
  7. O’Brien JT, Erkinjuntti T, Reisberg B, Roman G, Sawada T, Pantoni L et al (2003) Vascular cognitive impairment. Lancet Neurol 2(2):89–98CrossRefGoogle Scholar
  8. Pendlebury ST, Rothwell PM (2009) Prevalence, incidence, and factors associated with pre-stroke and post-stroke dementia: a systematic review and meta-analysis. Lancet Neurol 8(11):1006–1018CrossRefGoogle Scholar
  9. Pohjasvaara T, Erkinjuntti T, Vataja R, Kaste M (1997) Dementia three months after stroke: baseline frequency and effect of different definitions of dementia in the Helsinki Stroke Aging Memory Study (SAM) cohort. Stroke 28(4):785–792CrossRefGoogle Scholar
  10. Price CC, Jefferson AL, Merino JG, Heilman KM, Libon DJ (2005) Subcortical vascular dementia: integrating neuropsychological and neuroradiologic data. Neurology 65(3):376–382CrossRefGoogle Scholar
  11. Reed BR, Mungas DM, Kramer JH, Ellis W, Vinters HV, Zarow C et al (2007) Profiles of neuropsychological impairment in autopsy-defined Alzheimer’s disease and cerebrovascular disease. Brain 130(3):731–739CrossRefGoogle Scholar
  12. Román GC, Tatemichi TK, Erkinjuntti T, Cummings JL, Masdeu JC, Garcia JH et al (1993) Vascular dementia: diagnostic criteria for research studies: report of the NINDS-AIREN international workshop. Neurology 43(2):250–250CrossRefGoogle Scholar
  13. Román GC, Erkinjuntti T, Wallin A, Pantoni L, Chui HC (2002) Subcortical ischaemic vascular dementia. Lancet Neurol 1(7):426–436CrossRefGoogle Scholar
  14. Román GC, Wilkinson DG, Doody RS, Black SE, Salloway SP, Schindler RJ (2005) Donepezil in vascular dementia: combined analysis of two large-scale clinical trials. Dement Geriatr Cogn Disord 20(6):338–344CrossRefGoogle Scholar
  15. Schneider JA, Wilson RS, Cochran EJ, Bienias JL, Arnold SE, Evans DA, Bennett DA (2003) Relation of cerebral infarctions to dementia and cognitive function in older persons. Neurology 60(7):1082–1088CrossRefGoogle Scholar
  16. Sonnen JA, Larson EB, Crane PK, Haneuse S, Li G, Schellenberg GD et al (2007) Pathological correlates of dementia in a longitudinal, population-based sample of aging. Ann Neurol 62(4):406–413CrossRefGoogle Scholar
  17. Stebbins GT, Nyenhuis DL, Wang C, Cox JL, Freels S, Bangen K et al (2008) Gray matter atrophy in patients with ischemic stroke with cognitive impairment. Stroke 39(3):785–793CrossRefGoogle Scholar
  18. Szirmai I, Vastagh I, Szombathelyi É, Kamondi A (2002) Strategic infarcts of the thalamus in vascular dementia. J Neurol Sci 203:91–97CrossRefGoogle Scholar
  19. Tatemichi TK, Foulkes MA, Mohr JP, Hewitt JR, Hier DB, Price TR, Wolf PA (1990) Dementia in stroke survivors in the stroke data bank cohort. Prevalence, incidence, risk factors, and computed tomographic findings. Stroke 21(6):858–866CrossRefGoogle Scholar
  20. Wiesmann M, Kiliaan AJ, Claassen JA (2013) Vascular aspects of cognitive impairment and dementia. J Cereb Blood Flow Metab 33(11):1696–1706CrossRefGoogle Scholar
  21. Zacharek A, Venkat P, Chopp M, Landschoot-Ward J, Chen J (2019) Abstract TMP120: sildenafil treatment of vascular dementia in aged rats. Stroke 50(Suppl_1):ATMP120-ATMP120CrossRefGoogle Scholar

Copyright information

© Springer Nature Switzerland AG 2019

Authors and Affiliations

  1. 1.Department of Clinical and Health Psychology, College of Public Health and Health ProfessionsUniversity of FloridaGainesvilleUSA

Section editors and affiliations

  • Adam J. Woods
    • 1
    • 2
  1. 1.Center for Cognitive aging and Memory, Department of Aging and Geriatric ResearchMcNight Brain Institute, University of FloridaGainesvilleUSA
  2. 2.Department of Clinical and Health PsychologyUniversity of FloridaGainesvilleUSA