Vascular dementia is a condition arising secondarily to cerebrovascular disease. It is characterized by executive dysfunction and difficulty in performing activities of daily living. It must be differentiated from other causes of dementia, primarily Alzheimer's disease.
Vascular dementia (VaD) is the second most common cause of dementia and its prevalence increases after the sixth decade of life [1] [2]. It is defined as a condition characterized by features of stroke or subclinical vascular brain injury which involves malfunction of at least two cognitive domains leading to a decrease in the ability to perform activities of daily living [3]. The cognitive features of VaD depend on the anatomical location of the vascular injury and this has led to the classification of VaD into different subtypes: small, large, or mixed vessel disease [4] [5]. Patients with small vessel disease present with a higher incidence of executive dysfunction whereas dysfunctional language and visuospatial perception are noticed more often in patients with large vessel VaD [6]. Clinical presentation of VaD in cortical injury includes speech abnormalities and neglect while a subcortical injury is associated with cognitive, emotional and behavioral difficulties, psychomotor retardation, pseudobulbar palsy, and gait dysfunction [1] [3]. Other features of VaD are restlessness, agitation, aggressive behavior, hallucinations, delusions, paranoia, circadian mood disturbances (sundowning), disorientation, and depression. As the brain injury is variable in VaD, memory disturbances may also be variable or may be completely absent [1]. The intellectual decline in VaD is classically described as "step-wise" (multi-infarct dementia) but can be continuous (lacunar infarcts) too.
Clinical presentation of VaD may resemble that of Alzheimer's disease (AD) although the following features help to differentiate between the two conditions:
A physician should suspect VaD in a patient with cognitive dysfunction which follows a neurologic episode/deficit. The workup should commence with a detailed history eliciting onset and progression of cognitive and neuropsychiatric symptoms as well as a history of atherosclerotic conditions like angina pectoris. A detailed neurological and psychiatric assessment is essential. The Mini-Mental Status Exam (MMSE) is likely to reveal patchy cognitive deficits in VaD compared to global deficits in AD [7]. Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5) criteria provide the guidelines to help in the diagnosis of VaD [8].
Laboratory tests are performed to exclude other etiologies of dementia. They include a complete blood count (CBC), erythrocyte sedimentation rate (ESR), blood glucose levels, thyroid, liver, and kidney function tests, vitamin B12 levels, and Venereal Disease Research Laboratory (VDRL) test for syphilis. In addition, other tests like human immunodeficiency virus (HIV) testing, and tests to rule out autoimmune diseases should be ordered.
Neuroimaging with computed tomography (CT) and magnetic resonance imaging (MRI) help to confirm the diagnosis with MRI being considered the gold standard. A vascular cause of dementia mainly can be excluded if CT and MRI do not demonstrate any cerebrovascular pathology. MRI findings in VaD include multiple white matter infarcts or lesions in the periventricular white matter, lacunar infarcts, and atrophy of the hippocampal or entorhinal cortical areas. Positron emission tomography (PET) helps in the identification of VaD and differentiates it from AD [9]. Cerebral angiography is only indicated prior to carotid endarterectomy and is likely to show beading of the cortical blood vessels. Other tests which may be performed include an electrocardiogram, echocardiography, Holter monitoring, and carotid Doppler studies.