2024 Volume 10 Pages 3-4
Ischemic changes in vascular dementia (VaD) are often associated with other dementias, such as Alzheimer's disease, and have been shown to accelerate the disease process. It is therefore important to control risk factors for cerebrovascular disease in all dementias. This review outlines the vascular lesions underlying VaD and describes practical treatments based on this condition.
Vascular dementia (VaD) is caused by cerebrovascular disease and is the second most common neurocognitive disorders after Alzheimer’s disease. Most VaDs are classified into three types: small vessel disease with dementia, multiple infarct dementia, and strategic single infarct dementia. Other dementias include hypoperfusion vascular dementia, cerebral hemorrhagic vascular dementia, and hereditary vascular dementia. Hereditary vascular dementia is known to include subcortical infarcts and leukoencephalopathy (CADASIL), cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL), hereditary cerebral amyloid angiopathy, mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), Fabry disease, and retinal vasculopathy with cerebral leukoencephalopathy (RVCL), etc. It has been discussed that it is important to control the risk factors of lifestyle-related diseases such as hypertension for many vascular dementias, except for hereditary vascular dementia, and that it may lead to the prevention of the onset of the disease1–3).
Small vessel disease with dementia accounts for about 50% of VaD. This type of dementia is classified into subcortical vascular dementias caused by hypertensive cerebral small vessel disease and cerebral amyloid angiopathy. Among subcortical vascular dementias, those mainly caused by lacunar infarction are called multiple lacunar infarct dementia, while those mainly caused by white matter lesions are called Binswanger’s disease. The main clinical symptoms of small vessel disease with dementia are frontal lobe dysfunction, i.e., psychiatric symptoms such as apathy, decreased spontaneity, irritability, and depression. In addition, gait disorders called vascular parkinsonism, forced crying and laughing, pseudobulbar palsy, and dysuria are common in this type of dementia. Morphological imaging studies such as MRI and CT are required for diagnosis. It is necessary to verify whether the cerebrovascular lesions indicated by these studies is temporally related to dementia and whether the imaging findings and symptoms match. Cognitive decline within 3 months after a stroke should be checked. If dementia is present before the onset of stroke, latent Alzheimer’s disease is considered. Cerebral blood flow single photon emission computed tomography (SPECT) is also useful for diagnosis. MRI fluid attenuated inversion recovery (FLAIR) images are beneficial for evaluating white matter lesions, especially in the frontal lobe. Early emphasis on the temporal pole is suspicious of CADASIL or CARASIL and requires a detailed medical history. CADASIL is characterized by midlife migraine and recurrent stroke, and CARASIL is characterized by juvenile low back pain and baldness.
Lacunar infarction is 3–15 mm round in FLAIR, with high margin brightness, and is frequently observed in the basal ganglia, thalamus, white matter, and pons. The enlargement of the perivascular space is usually less than or equal to 2 mm and there is no increase in marginal brightness. Attention should be paid to cerebral hemorrhage because the findings change depending on the onset and the time of imaging. In CT, the acute phase is a high density area, and in the chronic phase, the hematoma is absorbed and the slit-like low density area is formed. MRI is particularly useful in the chronic phase, where hemosiderin is low in T2-weighted imaging, and the most common sites are putamen, thalamus, cerebellum, and brainstem. MRI T2* and susceptibility-weighted imaging (SWI) are valuable for confirming microbleeds. There are three types of microbleeds: those that occur mainly in the basal ganglia and thalamus, those that occur frequently in the cortical regions where cerebral amyloid angiopathy is suspected, and those that are a mixture of both.
Multiple infarction dementia accounts for about 30% of VaD. This type of VaD presents with a variety of symptoms that depend on the region of cerebral blood vessels. The main clinical symptoms are motor paralysis, aphasia, apraxia, agnosia, Gerstmann syndrome, dyslexia, and memory impairment.
Strategic single infarct dementia is characterized be memory impairment, apathy, decreased motivation and spontaneity, delirium, dementia, etc. These symptoms appear rapidly and tend to get better with the passage of time. The responsible foci of strategic single infarct dementia are divided into cortical and subcortical lesions. Cortical lesions include the hippocampus, angular gyrus, posterior cerebral artery region, and middle cerebral artery region. Subcortical lesions include the thalamus and the basal forebrain. In addition, the cingulate gyrus, mammillary bodies, caudate nucleus, genu of internal capsule, and posterior corpus callosum are also important lesion sites. Medial thalamic lesions are well known to cause acute somnolence, impaired memory, decreased consciousness and motivation, Horner’s syndrome, and vertical eye movement disorders. Hippocampal lesions cause impaired memory dysfunction, hemianopsia, agitation and confusion in the acute phase. Angular gyrus syndrome is an important symptom of this type of VaD2).
Treatment of VaD is essential to control risk factors such as hypertension, diabetes, dyslipidemia, atrial fibrillation, smoking, obesity, and excessive drinking. For hypertension, it is necessary to pay attention to home blood pressure and diurnal fluctuations, and keep in mind that excessive lowering of blood pressure is not only a risk of falls in the elderly, but also there is no evidence for suppression of VaD. Consideration should also be given to medication adherence, polypharmacy, chronic kidney disease (CKD), etc. After verifying the evaluation of microbleeds with imaging studies, antithrombotic therapy will be considered3).
As treatment for atherothrombotic cerebral infarction and lacunar infarction, use aspirin, clopidogrel, or cilostazol as an antithrombotic drug, and avoid dual combination therapy (DAPT). For treatment for cardiogenic cerebral embolism, use dose adjustment of warfarin with PT-INR 2.0–3.0 (INR 1.6–2.6 for the elderly over 70 years old), and for non-valvular atrial fibrillation, edoxaban (60 mg) once a day (30 mg for underweight and renal impairment). When complication of Alzheimer’s disease is suspected, galantamine hydrobromide in early to middle phase and Memantine hydrochloride in middle to late phase of the disease should be considered as appropriate. At the time of behavioral and psychological symptoms of dementia (BPSD) merger, amantadine for apathy, quetiapine for irritability and agitation if it is confirmed that there is no diabetes mellitus. In patients with diabetes mellitus, risperidone should be considered.
It is broadly classified into inhibition of the progression of cerebrovascular disease, prevention of recurrence, and symptomatic treatment. Cerebrovascular accident is largely related to lifestyle-related diseases, and it is important to control hypertension, dyslipidemia, and diabetes. Cilostazol and clopidogrel should be considered for small vessel lesions confirmed by MRI, etc., and cholinesterase inhibitors and n-methyl-d-asparatate (NMDA) receptor antagonist should be considered for cognitive impairment. Selective serotonin reuptake inhibitors (SSRIs) and serotonin and norepinephrine reuptake inhibitors (SNRIs) are used for depression, and atypical antipsychotics are used for anxiety and irritability. Amantadine is considered for decreased spontaneity and apathy, and levodopa is considered for parkinsonism. Cerebral amyloid angiopathy is broadly classified into type 1 cerebral amyloid angiopathy, in which capillaries are also damaged, and type 2 cerebral amyloid angiopathy, in which lesions are localized to small arteries. Hypoperfusion vascular dementia is caused by cerebral circulatory failure and hypoxia. Cerebral hemorrhagic vascular dementia is caused by cerebral hemorrhage and subarachnoid hemorrhage. Hereditary vascular dementia includes CADASIL, CARASIL, hereditary cerebral amyloid angiopathy, MELAS, Fabry disease, and RVCL. Although they are relatively rare, they should not be overlooked. If there is inconsistency between the symptoms and imaging findings of VaD, Parkinson’s signs, or significant ventricular enlargement, consultation with a specialist is advisable. Most VaD cases are not urgent, but caution should be exercised when accompanied by acute disease. Explain to patients that hypertension is the biggest risk factor for VaD, and that hypertension treatment is important for inhibiting the progression of VaD3). In addition to medication adherence and BPSD management, it is also necessary to consider the risk of aspiration associated with pseudobulbar palsy.
The author has no conflict of interest.
