Vascular dementia is dementia caused by a series of strokes. Restricted blood flow due to strokes reduces oxygen and glucose delivery to the brain, causing cell injury and neurological deficits in the affected region. Subtypes of vascular dementia include subcortical vascular dementia, multi-infarct dementia, stroke-related dementia, and mixed dementia. Subcortical vascular dementia occurs from damage 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 in cognition. Dementia may occur when neurodegenerative and cerebrovascular pathologies are mixed, as in susceptible elderly people (75 years and older). Cognitive decline can be traced back to occurrence of successive strokes. ICD-11 lists vascular dementia as dementia due to cerebrovascular disease. DSM-5 lists vascular dementia as either major or mild vascular neurocognitive disorder.
Signs and symptoms People with vascular dementia experience progressive cognitive impairment, either acutely or sub-acutely, as seen in mild cognitive impairment, but often in step-wise declines following multiple strokes. The disease is described as both a mental and behavioral disorder within the ICD-11. Signs and symptoms are cognitive, motor, behavioral, and for a significant proportion of people, also affective. These changes typically occur over a period of 5–10 years. Signs are typically similar to those in other dementias but mainly include cognitive decline and memory impairment of sufficient severity to interfere with activities of daily living, sometimes accompanied by focal neurological signs and evidence of cerebrovascular disease features seen on brain imaging (e.g., CT scans or magnetic resonance imaging). The localizing neurological signs observed in areas of the brain include hemiparesis, bradykinesia, hyperreflexia, extensor plantar reflexes, ataxia, pseudobulbar palsy, as well as gait and swallowing difficulties. People have patchy deficits on cognitive testing. They tend to have better free recall and fewer memory errors (a.k.a. recall intrusions) than those with Alzheimer's disease. In more severely affected people, or those with infarcts in Wernicke's or Broca's areas, specific speech problems called dysarthria and aphasia may occur. In small vessel disease, the frontal lobes are often affected. Consequently, people with vascular dementia tend to perform worse than those with Alzheimer's disease on frontal lobe-heavy tasks, such as those involving verbal fluency. They may present with frontal lobe problems, such as apathy, abulia (i.e., lack of will or initiative), difficulties with attention and orientation, and urinary incontinence. They tend to exhibit more perseverative behavior. People with vascular dementia may also present with general slowing of processing ability, difficulty shifting sets, and impairment in abstract thinking. Apathy early in the disease is more suggestive of vascular dementia. 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, some infectious diseases, such as neurosyphilis, can cause arterial damage, strokes, and bacterial inflammation of the brain.
Causes
Vascular dementia can be caused by ischemic or hemorrhagic infarcts affecting multiple brain areas, including the anterior cerebral artery territory, the parietal lobes, or the cingulate gyrus. On rare occasions, infarcts in the hippocampus or thalamus are the cause of dementia. A history of stroke increases the risk of developing dementia by around 70%, and recent stroke increases the risk by around 120%. Brain vascular lesions can also be the result of diffuse cerebrovascular disease, such as small vessel disease.
Risk factors
Risk factors for vascular dementia include increasing age, hypertension, smoking, hypercholesterolemia, diabetes mellitus, cardiovascular disease, and cerebrovascular disease. Other risk factors include lifestyle, geographic origin, and APOE-ε4 genotype. Vascular dementia can sometimes be triggered by cerebral amyloid angiopathy, which involves the accumulation of amyloid beta plaques in the walls of the cerebral arteries, leading to breakdown and rupture of the vessels. Since amyloid plaques are a characteristic feature of Alzheimer's disease, vascular dementia may occur as a consequence.
Diagnosis Several specific diagnostic criteria can be used to diagnose vascular dementia, including the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria, the International Classification of Diseases, Tenth Edition (ICD-10) criteria, the National 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 (after Vladimir Hachinski). 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. When available as a diagnostic tool, single photon emission computed tomography (SPECT) and positron emission tomography (PET) neuroimaging may be used to confirm a diagnosis of multi-infarct dementia in conjunction with evaluations involving mental status examination. 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 and medical history analysis. The screening blood tests typically include full 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, and folate.
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