Dementia is a syndrome of chronic progressive cognitive decline resulting in functional impairment . In the Diagnostic Manual of Mental Disorders, Fifth Edition (DSM-V), cognitive decline is quantified as deficits in one or more domains (e.g., memory, executive function, visuospatial, language, attention). Second only to Alzheimer disease (AD), vascular dementia (VD) is one of the most common causes of dementia affecting the elderly (aged greater than 65 years), with a variable presentation and unpredictable disease progression   . The diagnosis of VD is obtained by a thorough history and physical examination, including a measure of cognitive performance . VD is diagnostically challenging and not precise given the many causes of dementia, including the potential for a mixed dementia syndrome .
VD is distinguished from other forms of dementia in that it results from brain ischemia, although the temporal relationship to the ischemic event may be subtle or go unnoticed. There are various subtypes and multiple terms to describe the vascular pathology and affected brain tissue, such as multi-infarct dementia, small vessel disease or Binswanger disease, strategic infarct dementia, hypoperfusion dementia, hemorrhagic dementia, hereditary vascular dementia, and AD with cardiovascular disease  .
Approximately 15% to 17% of all dementia syndromes are vascular in etiology  . The incidence of VD increases with age, with the risk doubling approximately every five years. Risk factors for the development of VD include hyperlipidemia, hypertension, diabetes mellitus, and tobacco use  .
VD occurs as a result of cerebral tissue ischemia causing gliosis and demyelination. Ischemia may occur as a result of atherosclerosis, thrombosis, or vasculopathy   . There are several subtypes of VD, including the following:
A thorough history should be obtained from the patient, focusing on cognitive and functional deficits, onset, and progression of symptoms. Interviewing family members and caregivers is important as patients with cognitive decline rarely have insight into their cognitive and functional limitations. Caregivers may report an abrupt or stepwise onset of cognitive decline, or the appearance of symptoms may be subtle without connection to an ischemic event. The functional assessment should evaluate for impairments in instrumental activities of daily living (IADLs), such as cooking, driving, and financial and medication management, and basic activities of daily living (ADLs), such as dressing, bathing, and toileting. Additionally, patient past medical history, current medications, and surgical history should be obtained. Regarding physical examination, one should assess patients for focal neurologic deficits .
If there is a suspicion for VD, then patients should undergo cognitive testing. There are a variety of cognitive performance tests available which enable the practitioner to assess for cognitive domain deficits. Rule-out secondary etiologies of cognitive decline, to include depression, thyroid disorder, medications (e.g., benzodiazepines or anticholinergics), alcohol abuse, or infectious causes (e.g., neurosyphilis or human immunodeficiency virus-associated dementia). Recommended laboratory studies include complete blood count, complete metabolic panel, thyroid-stimulating hormone level, rapid plasma regain (RPR), and vitamin B12. For depression assessment, practitioners can utilize the Geriatric Depression Scale (validated in mild dementia) or PHQ-9. If warranted, practitioners should obtain imaging studies. For example, if the patient demonstrates focal neurologic deficits, then MRI without contrast would be the preferred imaging modality .
Today vascular dementia also is diagnosed using the DSM 5 criteria, the International Classification of Diseases, Tenth Edition criteria, the Alzheimer's Disease Diagnostic and Treatment criteria, the National Institute of Neurological Disorders and Stroke-Association Internationale pour la Recherche at L'Enseignement en Neurosciences (NINDS-AIREN) criteria, and the Hachinski ischemic score.
There are no present curative treatments for VD. Treatment of VD includes two approaches: (1) management of progression and behaviors, and (2) prevention by modifying risk factors. Cholinesterase inhibitors have been shown to slow the progression of cognitive decline . The side effect profile is significant, to include gastrointestinal distress, symptomatic bradycardia, and agitation. Memantine, an NMDA antagonist, is FDA approved for moderate to severe dementia and has been shown to improve patient functional levels and lessen care dependency . Whether to offer these medications takes a careful conversation with patients and caregivers, weighing the benefits and side effects individualized to their health condition and goals of care.
Medication management includes the elimination of medications which are unnecessary or have the potential to exacerbate symptoms (e.g., anticholinergics). Identification and optimization of comorbidities, such as hypertension, diabetes mellitus, and hyperlipidemia, will assist in lowering patient vascular risk factors but have not demonstrated an impact on cognitive function. Additionally, providers should encourage smoking cessation in tobacco users, advise a decrease in alcohol use, and assess for other potential geriatric syndromes such as falls, depression, and urinary incontinence.
VD is preventable by modifying the risk factors like diabetes, hypertension, smoking, and hyperlipidemia. The one very important risk factor that should be modified is hypertension. Countless studies show that use of antihypertensive medications can reduce the risk of vascular dementia. In addition, the patient’s coronary artery disease, atrial fibrillation, and ischemic heart disease have to be appropriately managed.
In patients who show early impairment in cognition or have MRI or CT evidence of stroke or carotid artery disease, data show that secondary prevention with the use of stroke preventive treatments like carotid endarterectomy, antiplatelet agents, warfarin or physical exercise can slow down the progression of the disease.
Overall, patients with VD have a shortened life expectancy. Those who have already had a cerebrovascular accident have the highest mortality, with a 5-year survival of only 39%. Patients with VD also have coexisting atherosclerotic disease, and death from cardiovascular causes is common.
Besides death, other complications of VD include the following:
Diagnosis of VD allows physicians to provide patients and caregivers with valuable counseling regarding secondary prevention, safety, advance care planning, and caregiver burden. Secondary prevention discussions may focus on healthy diet, exercise, cognitive stimulation, and socialization. As healthcare providers, our goal is to ensure safety while optimizing independence.
There are no present curative treatments for VD. Treatment of VD includes two approaches: (1) management of progression and behaviors, and (2) prevention by modifying risk factors. Cholinesterase inhibitors have been shown to slow the progression of cognitive decline . The side effect profile is significant, to include gastrointestinal distress, symptomatic bradycardia, and agitation. Memantine, an NMDA antagonist, is FDA approved for moderate to severe dementia and has been shown to improve patient functional levels and lessen care dependency . Whether to offer these medications takes a careful conversation with patients and caregivers, weighing the benefits and side effects individualized to their health condition and goal.
Issues of driving, medication management, financial management, and cooking are just some issues that should be evaluated. Advanced-care planning should explore the patient’s values as they relate to interventions, quality of life, and longevity. Lastly, provide caregivers with support and education, which may consist of support groups or respite care for the management of caregiver burden.
|||The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease., McKhann GM,Knopman DS,Chertkow H,Hyman BT,Jack CR Jr,Kawas CH,Klunk WE,Koroshetz WJ,Manly JJ,Mayeux R,Mohs RC,Morris JC,Rossor MN,Scheltens P,Carrillo MC,Thies B,Weintraub S,Phelps CH,, Alzheimer's & dementia : the journal of the Alzheimer's Association, 2011 May [PubMed PMID: 21514250]|
|||Epidemiology and risk factors of dementia., van der Flier WM,Scheltens P,, Journal of neurology, neurosurgery, and psychiatry, 2005 Dec [PubMed PMID: 16291918]|
|||Vascular dementia: prevention and treatment., McVeigh C,Passmore P,, Clinical interventions in aging, 2006 [PubMed PMID: 18046875]|
|||Vascular dementia., O'Brien JT,Thomas A,, Lancet (London, England), 2015 Oct 24 [PubMed PMID: 26595643]|
|||Evaluation of suspected dementia., Simmons BB,Hartmann B,Dejoseph D,, American family physician, 2011 Oct 15 [PubMed PMID: 22010769]|
|||Vascular dementia., Strub RL,, The Ochsner journal, 2003 Winter [PubMed PMID: 22470255]|
|||Moulin S,Cordonnier C, Role of Cerebral Microbleeds for Intracerebral Haemorrhage and Dementia. Current neurology and neuroscience reports. 2019 Jun 19; [PubMed PMID: 31218453]|
|||Assal F, History of Dementia. Frontiers of neurology and neuroscience. 2019; [PubMed PMID: 31220848]|
|||Jiménez-Pavón D,Carbonell-Baeza A,Lavie CJ, Promoting the Assessment of Physical Activity and Cardiorespiratory Fitness in Assessing the Role of Vascular Risk on Cognitive Decline in Older Adults. Frontiers in physiology. 2019; [PubMed PMID: 31214046]|
|||Eggink E,Moll van Charante EP,van Gool WA,Richard E, A Population Perspective on Prevention of Dementia. Journal of clinical medicine. 2019 Jun 12; [PubMed PMID: 31212802]|
|||Gómez-Gómez ME,Zapico SC, Frailty, Cognitive Decline, Neurodegenerative Diseases and Nutrition Interventions. International journal of molecular sciences. 2019 Jun 11; [PubMed PMID: 31212645]|