| Vascular dementia | |
|---|---|
| Other names | Dementia due to cerebrovascular disease;[1] Vascular cognitive impairment[2] |
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| Brain atrophy from vascular dementia | |
| Specialty | Psychiatry,neurology  |
| Symptoms | Cognitive impairment, short-termmemory loss[3] |
| Complications | Heart disease, loss of ability to care for self andinteract,pneumonia[4] |
| Causes | Conditions that impair blood vessels in the brain and therefore interfere with oxygen delivery to the brain[3] |
| Risk factors | High blood pressure,high cholesterol,atrial fibrillation,diabetes[3] |
| Diagnostic method | Lab test, neuroimaging test, neuropsychological testing[5] |
| Differential diagnosis | Alzheimer's disease[5] |
| Treatment | Symptomatic[3][4] |
| Frequency | 15-30% of dementia cases in the United States, Europe, and Asia[5][6] |
Vascular dementia isdementia caused by a series ofstrokes.[2][4] Restricted blood flow due to strokes reducesoxygen andglucose delivery to the brain, causing cell injury and neurological deficits in the affected region.[6] Subtypes of vascular dementia include subcortical vascular dementia, multi-infarct dementia, stroke-related dementia, and mixed dementia.[2][5]
Subcortical vascular dementia occurs fromdamage to small blood vessels in the brain. Multi-infarct dementia results from a series of small strokes affecting several brain regions. Stroke-related dementia involving successive small strokes causes a more gradual decline incognition.[4] Dementia may occur when neurodegenerative and cerebrovascular pathologies are mixed, as in susceptible elderly people (75 years and older).[2][5] Cognitive decline can be traced back to occurrence of successive strokes.[4]
ICD-11 lists vascular dementia asdementia due to cerebrovascular disease.[1]DSM-5 lists vascular dementia as eithermajor or mild vascular neurocognitive disorder.[7]
People with vascular dementia present with progressivecognitive impairment, acutely or sub-acutely as inmild cognitive impairment, frequently step-wise, after multiple strokes.[5]
The disease is described as both amental andbehavioral disorder within theICD-11.[8] Signs and symptoms are cognitive, motor, behavioral, and for a significant proportion of people, alsoaffective. These changes typically occur over a period of 5–10 years. Signs are typically the same as in other dementias, but mainly include cognitive decline and memory impairment of sufficient severity as to interfere with activities of daily living, sometimes with the presence of focal neurological signs, and evidence of features consistent with cerebrovascular disease on brain imaging (CT or MRI).[4][5]
The neurological signs localizing to certain areas of the brain that can be observed arehemiparesis,bradykinesia,hyperreflexia, extensorplantar reflexes,ataxia,pseudobulbar palsy, as well asgait problems andswallowing difficulties. People have patchy deficits on cognitive testing. They tend to have betterfree recall and fewerrecall intrusions when compared with people havingAlzheimer's disease.[9] In the more severely affected people, or those affected by infarcts inWernicke's orBroca's areas, specific problems with speaking calleddysarthria andaphasias may be present.[2][5]
Insmall vessel disease, the frontal lobes are often affected. Consequently, people with vascular dementia tend to perform worse than their Alzheimer's disease counterparts infrontal lobe tasks, such as verbal fluency, and may present with frontal lobe problems:apathy,abulia (lack of will or initiative), problems with attention, orientation, and urinary incontinence. They tend to exhibit moreperseverative behavior. People with vascular dementia may also present with general slowing of processing ability, difficultyshifting sets, and impairment in abstract thinking. Apathy early in the disease is more suggestive of vascular dementia.[2][5]
Rare genetic disorders that cause vascular lesions in the brain exhibit other clinical presentations. As a rule, they tend to occur earlier in life and have a more aggressive course. In addition, infectious disorders, such assyphilis, can cause arterial damage, strokes, and bacterial inflammation of the brain.[10]
Vascular dementia can be caused by ischemic or hemorrhagicinfarcts affecting multiple brain areas, including theanterior cerebral artery territory, theparietal lobes, or thecingulate gyrus.[5] On rare occasions, infarcts in thehippocampus orthalamus are the cause of dementia.[12] A history of stroke increases the risk of developing dementia by around 70%, and recent stroke increases the risk by around 120%.[13] Brain vascular lesions can also be the result of diffusecerebrovascular disease, such assmall vessel disease.[5]
Risk factors for vascular dementia include increasing age,hypertension, smoking,hypercholesterolemia,diabetes mellitus,cardiovascular disease, andcerebrovascular disease.[2][5] Other risk factors include lifestyle, geographic origin, andAPOE-ε4genotype.[2][5]
Vascular dementia can sometimes be triggered bycerebral amyloid angiopathy, which involves accumulation ofamyloid beta plaques in the walls of the cerebral arteries, leading to breakdown and rupture of the vessels.[2][5] Since amyloid plaques are a characteristic feature ofAlzheimer's disease, vascular dementia may occur as a consequence.[2][6]
Several specific diagnostic criteria can be used to diagnose vascular dementia, including theDiagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria, theInternational Classification of Diseases, Tenth Edition (ICD-10) criteria, theNational Institute of Neurological Disorders and Stroke criteria, Association Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS-AIREN) criteria, the Alzheimer's Disease Diagnostic and Treatment Center criteria, and the Hachinski Ischemic Score (afterVladimir Hachinski).[2][6][14]
The recommended investigations for cognitive impairment include: blood tests (for anemia, vitamin deficiency, thyrotoxicosis, infection, among others), chest X-ray,ECG, and neuroimaging, preferably a scan with a functional or metabolic sensitivity beyond a simple CT or MRI.[2][4] When available as a diagnostic tool,single photon emission computed tomography (SPECT) andpositron emission tomography (PET) neuroimaging may be used to confirm a diagnosis of multi-infarct dementia in conjunction with evaluations involvingmental status examination.[2][4][6]
In a person already having dementia, SPECT appears to be superior in differentiating multi-infarct dementia from Alzheimer's disease, compared to the usual mental testing andmedical history analysis.[15][additional citation(s) needed]
The screening blood tests typically includefull blood count,liver function tests,thyroid function tests, lipid profile,erythrocyte sedimentation rate,C reactive protein,syphilis serology, calcium serum level, fasting glucose,urea,electrolytes,vitamin B-12, andfolate.[4][6]
Differentiating dementia syndromes can be challenging, due to the frequently overlapping clinical features and related underlying pathology.Mixed dementia, involving two types of dementia, can occur. In particular,Alzheimer's disease often co-occurs with vascular dementia.[2][5]
Mixed dementia is diagnosed when people have evidence ofAlzheimer's disease and cerebrovascular disease, either clinically or based on neuro-imaging evidence of ischemic lesions.[16]
Gross examination of the brain may reveal noticeable lesions and damage to blood vessels.[2][6] Accumulation of various substances such as lipid deposits and clotted blood appear on microscopic views. Thewhite matter is substantially affected, with noticeable atrophy (tissue loss), in addition to calcification of the arteries.[2][6][17] Microinfarcts may also be present in the gray matter (cerebral cortex), sometimes in large numbers.[2]
Althoughatheroma of the major cerebral arteries is typical in vascular dementia, smaller vessels and arterioles are mainly affected.[2][6]
Early detection and accurate diagnosis are important, as vascular dementia is at least partially preventable.Ischemic changes in the brain are irreversible, but the person with vascular dementia can demonstrate periods of stability or even mild improvement.[18] Since stroke is an essential part of vascular dementia,[13] the goal is to prevent new strokes. This is attempted through reduction of stroke risk factors, such ashigh blood pressure,high blood lipid levels,atrial fibrillation, ordiabetes mellitus.[2][5]
Medications for high blood pressure are used to prevent pre-stroke dementia.[19] These medications includeangiotensin converting enzyme inhibitors,diuretics,calcium channel blockers, sympathetic nerve inhibitors,angiotensin II receptor antagonists oradrenergic antagonists.[medical citation needed]
A 2023 review found that therapy withstatin drugs was ineffective in treating or preventing stroke or dementia in people without a history of cerebrovascular disease.[20]
As of 2025, there are no medications used specifically for prevention or treatment of vascular dementia.[4][3] However, medicines and other therapies can be used to slow progression of the disease.[21]
Many studies have been conducted to determine the average survival of people with dementia. The studies were frequently small and limited, which caused contradictory results in the connection between mortality and the type of dementia and the person's gender. One 2015 study found that the one-year mortality was three to four times higher in people after their first referral to a day clinic for dementia, when compared to the general population.[22] If the person was hospitalized for dementia, the mortality was even higher than in people hospitalized forcardiovascular disease.[22] Vascular dementia was found to have either comparable or worse survival rates when compared to Alzheimer's disease;[23] another 2014 study found that the prognosis for people with vascular dementia was worse for male and older people.[24]
Vascular dementia may be a direct cause of death due to the possibility of a fatal interruption in the brain's blood supply.[25]
Vascular dementia is the second-most-common form of dementia afterAlzheimer's disease in older adults.[4] Theprevalence of the illness is 1.5% in Western countries and approximately 2.2% in Japan. It accounts for 50% of all dementias in Japan, 20% to 40% in Europe, and 15% in Latin America. 25% of people with stroke develop new-onset dementia within one year of their stroke. One study found that in the United States, the prevalence of vascular dementia in all people over the age of 71 is 2.43%, and another found that the prevalence of the dementias doubles with every 5.1 years of age.[citation needed]
The incidence peaks between the fourth and the seventh decades of life and 80% of people have a history ofhypertension.[26][additional citation(s) needed]
A 2018meta-analysis identified 36 studies of prevalent stroke (1.9 million participants) and 12 studies of incident stroke (1.3 million participants).[13] For prevalent stroke, the pooled hazard ratio for all-cause dementia was 1.69; for incident stroke, the pooled risk ratio was 2.18.[13] Study characteristics did not modify these associations, with the exception of sex, which explained 50.2% of between-study heterogeneity for prevalent stroke. These results confirm that stroke is a strong, independent, and potentially modifiable risk factor for all-cause dementia.[13]
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