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Editors

SusannaMelkas
HannaJokinen
TimoErkinjuntti
SariAtula

Vascular Cognitive Impairment and Dementia

Essentials

  • Vascular cognitive impairment (VCI) can involve symptoms restricted to one or more areas of information processing or, on the other hand, progressive states with extensive symptoms leading to severe memory disorder (old term: vascular dementia).
  • Patients with Alzheimer's disease (AD) and clinically significant cerebrovascular disease (AD + CVD) also belong to the VCI group.
  • The main subtypes of VCI include small vessel disease, large vessel disease, and conditions due to an infarct in an area that is critical for information processing.

Epidemiology and risk factors

  • Symptoms involving memory, perception, executive functions and information processing are common after strokes due to cerebral infarction or haemorrhage. Among 55- to 85-year-old stroke patients, for example, impairment of some area of information processing was found in 83% of all patients and 71% of those who regained functional independence.
  • Common sequelae of stroke include impairment of memory, perception and executive functions.
  • After stroke, more extensive impairment of information processing, dementia, occurs in 25% of patients.
  • Silent brain infarcts, i.e. ones without clinical symptoms, and white matter changes, are associated with an increased risk of a memory disorder.
  • In 15-20% of cases, progressive memory disorder is caused by a CVD, and in about 70% of these by small vessel disease.
    • In Finland, there are about 250 000 patients with small vessel disease and functional impairment.
  • The classic risk factors (hypertension, hypercholesterolaemia, diabetes, obesity, sedentary life style, smoking) of cardiovascular disease and CVD in middle-age are associated with an increased risk of memory disorder in more advanced age. Low educational level has also been found to increase the risk of memory disorders.
  • Extensive lesions caused by small vessel disease involve an increased risk of impaired information processing, dementia, depression, walking difficulty, falls, urinary tract symptoms, strokes, institutionalization, and death.

Symptoms and findings

Small vessel disease

  • A typical early symptom is an executive function deficit associated with slowing down of information processing.
  • Memory impairment is often less pronounced than in AD.
  • Behavioural symptoms include depression, personality changes and slower psychomotor speed.
  • Early clinical findings are:
    • minor signs of an upper motor neurone lesion (pronator drift, unilateral hyperreflexia, coordination problems)
    • gait disturbances (apractic-ataxic, small-stepped, festinating gait)
    • balance disturbances and falls
    • micturition disturbances (urinary frequency and incontinence)
    • pseudobulbar symptoms, such as minor problems with articulation (dysarthria) and swallowing (dysphagia)
    • extrapyramidal symptoms (hypokinesia, rigidity).
  • Focal neurological deficits are very frequently subtle and limited to, for example, mild disturbances of balance and gait.
  • Symptom onset shows variation. The patient's past history often only reveals a transient ischaemic attack (TIA), momentary gait disturbances or confusion without clear focal neurological signs or symptoms suggestive of stroke.
  • Insidious disease onset is more common than sudden onset, and in the majority of patients the symptoms progress steadily without obvious stages of decline. However, symptoms may fluctuate showing day-to-day variation, and sometimes there are phases when no apparent change is noted in the condition even for several months.
  • An MRI scan of the brain will show widespread white matter hyperintensities and/or several lacunar infarcts in the deep grey and white matter. In addition, microhaemorrhages, expansion of perivascular spaces and cerebral atrophy may be found.

Large vessel disease

  • Symptoms related to information processing vary from case to case; symptoms related to executive function and memory, and linguistic and visual symptoms, for example, can often be seen, as well as unilateral neglect.
  • Depending on the location of the infarcts, clinical findings may include hemiplegia and/or gait disturbances (hemiplegic and/or apractic-ataxic gait), visual field defects and/or drooping of the corner of the mouth.
  • Symptom onset is generally acute (hours, days), and the symptoms show stepwise progression (recovery after exacerbation) and fluctuation. If risk factors are well managed, patients can experience phases with no apparent deterioration in their condition often lasting up to a year.
  • Imaging studies typically show several cortical and cortico-subcortical infarcts characteristic of large vessel disease or cardiac emboli. Haemorrhages are also possible.

Other findings

  • No typical findings can be obtained by currently available laboratory tests.
  • No markers specific for VCI alone can be detected in CSF.
  • Functional imaging studies (SPECT, PET) of the brain often show patchy changes.
  • In case of AD + CVD, decreased beta-amyloid 42 in CSF can be seen, which is a biological marker of AD.

Treatment

  • The management of a memory disorder related to CVD concentrates on the causes and risk factors of CVD and on the treatment of other coexisting diseases, such as hypertension, hypercholesterolaemia and diabetes.
  • Preventive measures are very important, and patients should be encouraged to change their lifestyle early enough: no smoking, weight management and sufficient exercise.
  • The benefit from physical exercise is based on its favourable effect on the management of CVD risk factors, and exercise also has a favourable effect on the brain-derived nerve growth factor.
  • Before old age, the risk of memory disorders can be reduced by treating hypertension. Too low blood pressure should be avoided in elderly people and those with extensive white matter changes.
  • Medication to prevent new circulatory disturbances should be prescribed according to stroke treatment guidelines. Clinical studies have not shown any differences in the effects of specific drugs (acetylsalicylic acid, dipyridamole, clopidogrel or anticoagulant therapy) in the symptomatic treatment of VCI.
  • In VCI, medication indicated for memory disorders (galantamine Galantamine for Vascular Cognitive Impairment, donepezil Donepezil for Vascular Cognitive Impairment, memantine Memantine for Dementia, rivastigmine Rivastigmine for Vascular Cognitive Impairment) may be of benefit as far as cognition is concerned but not to improve functional independence.
  • VCI or vascular dementia is not an official indication for any pharmaceutical ingredient that has been studied in Europe (EMA) or in the United States (FDA).

Alzheimer's disease and CVD

  • AD and CVD share many risk factors: hypertension, hypercholesterolaemia, diabetes and arterial diseases.
  • AD + CVD is a significant subtype of progressive memory disease particularly in older age groups; at least half of patients over 80 with memory disorder have this subtype. In the future, this may be the most common single type of memory disorder.
  • Clinical diagnosis is difficult as the patients will have focal neurological symptoms and findings suggestive of CVD and simultaneously changes on cerebral imaging due to both CVD and AD.
  • Factors supporting the diagnosis of concurrent AD include a syndrome with predominantly early impairment of episodic memory, atrophy of the medial temporal lobe on MRI, as well as a decreased concentration of beta-amyloid 42 (Ab42) in CSF.
  • Patients with AD and coexisting CVD may benefit from AD memory medication.
  • Galanthamine is at least as effective here as in the treatment of AD alone. For donepezil, rivastigmine and memantine, there is no equivalent research evidence available.

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