Vascular Dementia
Original Editor - Lucinda hampton
Top Contributors - Lucinda hampton, Angeliki Chorti, Kim Jackson and Ewa Jaraczewska
Introduction
Vascular dementia (VaD) ranks as the second most common dementia after Alzheimer's, caused primarily by brain hypoperfusion and hypoxia from vascular pathologies. [1] Unlike Alzheimer's, VaD incidence is declining due to improved cardiovascular risk management.
Clinical Challenge: VaD symptoms significantly overlap with Alzheimer's disease, making diagnosis difficult. Currently, no FDA-approved treatments exist specifically for VaD - management focuses on symptom control rather than disease modification.[2]
Watch this 3 minute informative video.
Epidemiology
Incidence is hard to discover but some support that it may be strongly matched with age, occurring in 1% of patients greater than 55 years and in greater than 4% of patients over 71 years; [4] others argue that this is no longer the case due to individuals being less susceptible to the negative consequences of vascular disorders and differences in follow-up time between individuals with and without a vascular disorder. [5] To add to this uncertainty Alzheimer disease often co-occurs with vascular dementia. Also, accelerated vascular changes occur in some people due to specific underlying disease not shown on vascular dementia studies.[6] Risk factors for the development of vascular dementia include hyperlipidemia, hypertension, diabetes mellitus, and tobacco use.[7]
Pathophysiology
Vascular dementia is an integral part of Alzheimer's and other geriatric neurodegenerative conditions associated with dementia. All form of vascular dementia have a similar pathogenic origin, resulting from hypoperfusion, oxidative stress and inflammation, which contribute to hemispheric white matter alterations. Demyelination and axonal loss also play a part in the wide ranging functional brain changes that underly cognitive impairment and the associated atrophy of the cerebral hemispheres.[8]
Diagnostic Criteria
An international panel of experts has recently updated the diagnostic criteria for vascular cognitive impairment and dementia to reflect recent advances in neuroimaging and biomarker research. [9] This is the first update of the International Society for Vascular Cognitive and Behavioral Disorders (VasCog) standards in more than a decade (2014), with the World Stroke Organisation (WSO) endorsing the criteria, hence named VasCog-2-WSO. [9] According to the VasCog-2-WSO criteria, mild cognitive impairment (MCI) refers to an acquired cognitive decline in at least 1 cognitive domain that does not affect independence, whereas VaD is defined as substantial cognitive decline in at least 1 cognitive domain that affects independence. [9] Agreed cognitive domains were attention and processing speed, executive function, learning and memory, language, perceptual-motor function, and social cognition. [9]The vascular etiology of cognitive impairment / dementia was substantiated by cognitive deficits related with 1 or more clinical strokes, in which the onset of cognitive decline is sudden and continues to be observed more than 3 months after stroke, or when there is no stroke history, with subcortical ischemic pathology, which typically affects attention and processing speed or executive functioning. [9]
Classification
According to the VasCog-2-WSO, there are 3 subtypes of VaD: hemorrhagic, ischemic, and mixed. Patients with preclinical or at risk for VaD should demonstrate significant neuroimaging evidence of cerebrovascular disease but without mild cognitive impairment or dementia criteria met.[9]
Management
Dementias have no single treatments, with the focus being on treating individual risk factors (e.g. hypertension, smoking, hypercoagulation, atherosclerosis).[6]
Alongside drug interventions, non-pharmacological interventions are used to treat the symptoms of dementia.
- Non-pharmacological Management e.g. Cognitive stimulation therapy; reminiscence therapy for mild to moderate dementia; cognitive rehabilitation or occupational therapy (working on functional goals of the individual and/or their carers).
- Diet: A healthy diet may decrease VaD risk, but evidence is limited. [10]
- Lifestyle Modifications: Regular exercise and an active lifestyle; stimulating, personalised daily activities.
Prevention
In the absence of successful therapies, promoting and maintaining vascular health is critical to prevent both the vascular and neurodegenerative components of the VaD. Vascular health is addressed by treating the risk factors e.g. diabetes, hypertension, smoking, and hyperlipidemia. Many studies indicate that using antihypertensive medications reduces the risk of VaD. [7] Furthermore, the early identification of associated vascular cognitive impairment that is usually present before VaD, may contribute to the prevention or decrease in progress of VaD by allowing early intervention. [11]
Physiotherapy Management
Prevention is key: Since VaD stems from vascular pathologies, physiotherapists may play a crucial role in:
- Managing modifiable cardiovascular risk factors through exercise prescription
- Implementing lifestyle modifications that directly impact vascular health
- Addressing comorbid conditions that contribute to vascular compromise
Treatment focus: With limited pharmaceutical options, non-pharmacological interventions become essential. Physiotherapy interventions targeting cardiovascular fitness, mobility maintenance, and fall prevention take on heightened importance in VaD management.
The declining incidence of VaD demonstrates that vascular risk factor modification works - positioning physiotherapists as key players in both prevention and management strategies. VaD is cognitive impairment caused by damaged or blocked blood vessels in the brain. The symptoms of vascular dementia can vary from person to person, depending on what part of the brain is damaged and other health factors. [2]
Case Studies
Physiopedia's Case Study on Subcortical Vascular Dementia
Vascular Dementia Case Study and Radiological Findings by Radiopedia
Case report on a family's experience of managing Vascular Dementia at home
References
- ↑ Morgan AE, Mc Auley MT. Vascular dementia: From pathobiology to emerging perspectives. Ageing Res Rev. 2024 Apr;96:102278.
- ↑ 2.0 2.1 Ng S, Hornblass A, Habibi P, Ikramuddin S, Chen J, Feng W, Cai D. Updates on vascular dementia. Stroke and Vascular Neurology. 2025 Feb 24; 0.
- ↑ Dementia Australia. What is Vascular Dementia?. Available from: https://www.youtube.com/watch?v=hcgT9KaPtAY [accessed 10/12/2025]
- ↑ van Straaten EC, Scheltens P, Knol DL, van Buchem MA, van Dijk EJ, Hofman PA, Karas G, Kjartansson O, de Leeuw FE, Prins ND, Schmidt R, Visser MC, Weinstein HC, Barkhof F. Operational definitions for the NINDS-AIREN criteria for vascular dementia: an interobserver study. Stroke. 2003 Aug;34(8):1907-12.
- ↑ Legdeur N, van der Lee SJ, de Wilde M, van der Lei J, Muller M, Maier AB, Visser PJ. The association of vascular disorders with incident dementia in different age groups. Alzheimers Res Ther. 2019 May 17;11(1):47.
- ↑ 6.0 6.1 Radiopedia Vascular dementia Available from:https://radiopaedia.org/articles/vascular-dementia [accessed 12/10/2025]
- ↑ 7.0 7.1 Sanders AE, Schoo C, Kalish VB. Vascular Dementia. [Updated 2023 Oct 22]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-.
- ↑ Iadecola C. The pathobiology of vascular dementia. Neuron. 2013 Nov 20;80(4):844-66.
- ↑ 9.0 9.1 9.2 9.3 9.4 9.5 VasCog-2-WSO Criteria Consortium; Sachdev PS, Bentvelzen AC, Kochan NA, Jiang J, Hosoki S, et al. Revised Diagnostic Criteria for Vascular Cognitive Impairment and Dementia-The VasCog-2-WSO Criteria. JAMA Neurol. 2025 Sep 16:e253242.
- ↑ Griffiths A, Matu J, Tang EYH, Gregory S, Anderson E, Fairley A, Townsend R, Stevenson E, Stephan BCM, Siervo M, Shannon OM. Foods, dietary patterns, and risk of vascular dementia: a systematic review. Nutr Metab (Lond). 2024 Dec 18;21(1):105.
- ↑ Bir SC, Khan MW, Javalkar V, Toledo EG, Kelley RE. Emerging Concepts in Vascular Dementia: A Review. J Stroke Cerebrovasc Dis. 2021 Aug;30(8):105864.