3.10.3 Vascular dementia

The Neuropathology of Vascular Dementia

Vascular dementia is the second most frequent cause of dementia. This prevalent form of dementia called vascular dementia is brought on by inadequate blood supply to the brain. In the UK, it is predicted to have an impact on about 150,000 people per year.

Vascular dementia (VaD) is a type of dementia that results from damage to the brain’s blood vessels, leading to reduced blood flow and oxygen supply to the brain. This results in the death of brain cells, leading to a decline in cognitive function and memory. VaD is a common form of dementia, accounting for around 10-20% of all cases, and is particularly prevalent in older individuals with a history of cardiovascular disease, stroke, or hypertension.

The neuropathology of VaD is characterized by a combination of macroscopic and microscopic changes in the brain. At a macroscopic level, VaD is characterized by the presence of small infarcts, or areas of dead brain tissue, in the white matter and basal ganglia. These infarcts result from reduced blood flow to the brain, which can be caused by a variety of factors, including atherosclerosis, emboli, or lacunar infarcts (Erkinjuntti, 2002).

At a microscopic level, the neuropathology of VaD is characterized by changes in the brain’s microvasculature, including the formation of microinfarcts, and degeneration of the white matter and basal ganglia. In addition, there may be evidence of oxidative stress, neuroinflammation, and glial activation, which can further contribute to the degeneration of brain cells (Chen, 2010).

There are various aetiologies to vascular dementia:

Aetiology:Example:
Neuropathological lesionMulti-infarct dementia, strategic infarct dementia, small vessel disease with dementia (Binswanger’s disease and CADASIL), hypoperfusion dementia and haemorrhagic dementia.
Clinical presentationVarious presentations are determined by a multitude of factors. Consistently all patients will show cognitive impairment.
CauseIschaemic infarction, brain haemorrhage and hypoperfusion brain ischaemia. Each has individual features at the gross anatomical level.

Following ischaemic infarction, brain tissues become necrotic and undergo three stages of healing: acute, subacute and chronic. At different stages, different types of cells predominate depending on the process involved. Similar changes are seen even in a border-zone infarction.

Notable types of vascular dementia:

Binswanger’s disease: also called subcortical vascular dementia, is a type of dementia caused by widespread, microscopic areas of damage to the deep layers of white matter in the brain.

CADASIL: often referred to as hereditary multi-infarct dementia is a cause of vascular dementia. It is an autosomal dominant inheritance disorder.

Symptoms:

The cognitive dysfunction of vascular dementia is distinguished by executive dysfunction rather than abnormalities in memory and language function. Although cognitive decline can occur in stages, it is usually gradual and may include periods of stability or even improvement (Gelder 2012).

Other symptoms include changes to their attitude, demeanour, or behaviour. Plus having trouble planning and understanding plans. Patients often struggle to focus their attention, leaving them feeling disorientated and confused.

Risk factors:

The risk rises with age, with persons over 65 having the highest prevalence of vascular dementia.

However, it is the second most prevalent type of young-onset dementia and can as per the name affect younger people (where symptoms develop before the age of 65).

Men are slightly more likely to get vascular dementia than women are, and persons with South Asian and African-Caribbean ancestry are at higher risk.

Additionally, there may be a modest increase in risk for those with a family history of vascular dementia.

The following are additional risk elements for vascular dementia:

  • Hypertension
  • Defective hearing
  • Smoking
  • Obesity
  • Depression
  • Heavy drinking and social isolation
  • Trauma to the brain

(T O’Brien & Thomas, 2015)

Diagnosis:

Diagnosis of VaD typically involves a comprehensive evaluation, including medical history, physical examination, and imaging studies, such as magnetic resonance imaging (MRI) or computed tomography (CT) scans. While there is no cure for VaD, various treatments and therapies are available to help manage the symptoms of the disease, improve quality of life, and delay progression. These may include anti-hypertensive drugs, anticoagulants, and antiplatelet agents, as well as lifestyle modifications, such as exercise and a healthy diet.

References:

(1) Chen, J., & Wong, T. (2010). Vascular dementia. The Lancet Neurology, 9(9), 817-827.

(2) Gelder, M., Andreasen, N., Lopez-Ibor, J. and Geddes, J. (2012). New Oxford Textbook of Psychiatry. Oxford: Oxford University Press.

(3) Erkinjuntti, T., Roman, G., Gauthier, S., & Bullock, R. (2002). Vascular dementia. The Lancet Neurology, 1(1), 27-36.

(4) T O’Brien, J., & Thomas, A. (2015). Vascular dementia. The Lancet, 386(10004), 1698-1706.