INTRODUCTION — Mild cognitive impairment (MCI) is an intermediate clinical state between normal cognition and dementia. While specific subtle changes in cognition are frequently observed in normal aging, there is increasing evidence that some forms of cognitive impairment are recognizable as an early manifestation of a neurodegenerative condition that will ultimately lead to dementia [1]. MCI is a heterogeneous state, and there remains controversy over aspects of the construct. However, the utility of this paradigm centers around the recognition that dementia is not a dichotomous state; thus, refining our understanding of the layers of transition will improve the understanding of cognitive decline and ultimately benefit patients.
This topic will review the definition of MCI and related terms, as well as the epidemiology, pathology, and clinical assessment of MCI. The prognosis and treatment of MCI and topics related to dementia, including diagnosis, treatment, risk factors, and prevention of dementia, are discussed separately:
●(See "Mild cognitive impairment: Prognosis and treatment".)
●(See "Clinical features and diagnosis of Alzheimer disease".)
●(See "Treatment of Alzheimer disease".)
●(See "Risk factors for cognitive decline and dementia".)
●(See "Prevention of dementia".)
DEFINITIONS — MCI as a syndrome refers to cognitive impairment that does not meet the criteria for dementia but is more than normal aging. Several criteria for, and subtypes of, MCI have been proposed [1-3]. These criteria and subtypes differ somewhat, although there is considerable overlap. In general, these criteria include a measurable deficit in cognition in at least one domain, in the absence of dementia or impairment in everyday functioning.
As originally constructed, the concept of MCI emphasized memory impairment and its status as a precursor state for Alzheimer disease (AD). Subsequently, it was recognized that MCI can be heterogeneous in terms of clinical presentation, etiology, prognosis, and prevalence [3-5], and the construct was expanded to broaden the scope of MCI to other cognitive domains, thereby extending the syndromic early detection of other dementias in their prodromal stages [6-8]. These criteria were developed as a concept relating early changes in specific cognitive domains to those areas most commonly affected in the disorders (eg, memory problems and AD) [8,9].
Considerable judgment is required in making the distinction between impairments that are normal for the older adult population and, on the other extreme, that do not represent dementia. What constitutes impairment in functional status is different for each individual. Such distinctions draw upon clinical expertise and do not rely on psychometric testing alone. These appraisals can differ between assessors and this may account for some of the conflicting results in studies of this disorder, and while the diagnosis of dementia is similarly based on clinical judgment, most clinicians are more comfortable with making determinations of that severity. Some clinicians and investigators have challenged specific aspects of the criteria including the requirements for subjective cognitive complaints and intact daily function [10-12].
Amnestic MCI — Amnestic MCI (aMCI) is often thought of as a precursor to AD [13]. Across all MCI, aMCI is the most common subtype, with a ratio of 2:1 compared with nonamnestic MCI (naMCI), although relative prevalence of MCI subtypes has varied among studies [14,15].
Initially, MCI was used to refer to the amnestic subtype, but other subtypes have since been recognized. (See 'Nonamnestic MCI' below.)
●Single domain – aMCI refers to those individuals with significantly impaired memory who do not meet criteria for dementia. The criteria originally outlined for MCI are understood to identify specifically this type [1,6]:
•Memory complaint, preferably corroborated by an informant
•Objective memory impairment (for age and education)
•Preserved general cognitive function
•Intact general functioning
•Not meeting criteria for dementia
Memory impairments that qualify for MCI are generally represented by defects that are 1.5 standard deviations (SD) or more below age- and education-corrected norms. This is not an absolute threshold, however, since individuals can experience a significant loss of memory without satisfying that criterion. Different tests of memory likely have different sensitivity and specificity, and norms are not available for all populations; this further justifies the necessity for clinical judgment [4].
●Multiple domains – Many individuals with aMCI complain only of memory loss; however, they may have additional impairments in other cognitive domains that are revealed with careful neuropsychological testing [7,16-18]. Such persons may also manifest subtle problems with functioning, but do not meet criteria for a formal diagnosis of dementia [5]. The multiple domains are, by definition, only slightly impaired (ie, less than 1 SD below age- and education-matched normal subjects).
These individuals often progress over several years to meet criteria for AD dementia. The prognostic utility of the multiple-domain form of aMCI remains unclear, as some studies have identified this as the highest risk category for conversion to dementia, while others have exposed instability, with some individuals returning to baseline level of function over time [7,19,20]. Much of this variability derives from different sources of subjects (eg, specialty clinics versus population cohorts).
Nonamnestic MCI
●Single domain – The concept of single-domain naMCI is similar to aMCI, except that this form of MCI is characterized by a relatively isolated impairment in a single nonmemory domain, such as executive functioning, language, or visual spatial skills [5]. Depending upon the domain, individuals with this subtype of MCI may progress to other syndromes, such as vascular cognitive impairment, frontotemporal dementia (FTD), primary progressive aphasia, dementia with Lewy bodies (DLB), progressive supranuclear palsy, or corticobasal degeneration. Individuals within this group appear to be at less of a risk of conversion to dementia, although supporting evidence is limited [9,21-23].
In certain disorders such as behavioral variant FTD, cognitive complaints are often preceded by significant alterations in behavior and comportment. Thus, some have proposed the concept of mild behavioral impairment as a similar paradigm to recognize an additional group with increased risk of dementia [24].
●Multiple domains – Patients who meet these criteria are affected in multiple domains, with a relative sparing of memory problems. The substrate of multidomain naMCI is felt to be that of degenerative disorders associated with tau, TAR DNA binding protein (TDP-43), and alpha-synuclein such as FTD and DLB [25,26].
Other studies have linked MCI in multiple domains to other types of dementia [27]. (See "Etiology, clinical manifestations, and diagnosis of vascular dementia", section on 'Vascular cognitive impairment'.)
Related terminology — There are many loosely related terms that have been used to describe constructs that are similar to or perhaps even the same as MCI (eg, incipient dementia, isolated memory impairment, dementia prodrome, minimal AD, predementia AD, prodromal AD, and early AD) [1,2,5,6,28,29]. Most of these definitions do not overlap fully with the definition of MCI [30].
●The concept of MCI perhaps reflects most closely the idea of "cognitive impairment, no dementia" (CIND) [31]. However, in contrast to the definition for the amnestic form of MCI, CIND does not require the presence of prominent memory deficits and includes in its definition the presence of a functional disability. In addition, CIND does not necessarily require a change in cognition, such that individuals with longstanding low levels of cognition could qualify. It is a more inclusive definition than MCI, as is reflected by its higher prevalence. (See 'Epidemiology' below.)
●The construct of "mild neurocognitive disorder" was introduced in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) [32]. Mild neurocognitive disorder is similar to MCI as defined here, and for the clinician, the two entities are equivalent. Mild neurocognitive disorder refers to a condition involving cognitive impairment in one or more domains, often memory, with relative preservation of functioning and the absence of dementia.
●"Age-associated memory impairment" and "age-associated cognitive decline" (AACD) are also widely used and fairly well-known terms. However, these terms differ from MCI in that they were originally devised to define normal age-associated memory and cognitive changes in older adults as referenced to young normal adult individuals [1,33,34]. AACD was developed as a way of better defining the cognitive changes in older adult patients compared with age-adjusted norms. AACD has more recently been recognized as identifying a state of impairment similar to MCI [35]. By contrast, MCI refers to an abnormal change in cognitive function.
●Studies of "preclinical AD" should be distinguished from studies of MCI [36]. In MCI studies, patients meet cognitive criteria for diagnosis, and are then followed prospectively to assess for conversion to dementia. By contrast, preclinical AD refers to individuals with normal cognition who possess positive biomarkers for AD, such as a positive amyloid positron emission tomography (PET) scan or evidence of AD biomarkers in the cerebrospinal fluid (CSF) [37]. (See "Clinical features and diagnosis of Alzheimer disease", section on 'Preclinical Alzheimer disease'.)
●"Suspected non-AD pathology (SNAP) MCI" is a term that is increasingly used in research studies to denote individuals who meet clinical criteria for MCI, show no evidence of amyloid pathology based on CSF biomarker and/or amyloid PET imaging, but have evidence of neuronal injury as measured by either medial temporal lobe atrophy or hypometabolism on 18-F fluorodeoxyglucose PET (FDG-PET) [38,39]. The SNAP designation may be relevant prognostically as well [38]. (See "Mild cognitive impairment: Prognosis and treatment", section on 'MRI'.)
EPIDEMIOLOGY — MCI is common in older adult populations, although individual study estimates vary significantly due to differing diagnostic criteria, measuring instruments, and sample populations studied. Based on a meta-analysis of 34 studies conducted by the American Academy of Neurology, the estimated prevalences by age are [40]:
●Age 60 to 64 years: 6.7 percent
●Age 65 to 69 years: 8.4 percent
●Age 70 to 74 years: 10.1 percent
●Age 75 to 79 years: 14.8 percent
●Age 80 to 84 years: 25.2 percent
Estimates of incidence rates for MCI vary as well; a variety of population-based cohort studies have reported incidence rates in their older adult populations (>65 to 75 years) of between 14 and 111 per 1000 patient-years [41-48]. Amnestic MCI (aMCI) appears to occur more commonly than other subtypes [46]. In the Mayo Clinic Study of Aging, the population-based incidence of MCI in individuals over age 70 years was estimated at 5 to 6 percent per year [46].
Aside from advancing age, factors most consistently associated with an increased prevalence of MCI include [4,10,40,46,48-62]:
●Lower educational level
●Vascular risk factors, including hypertension, midlife diabetes, obesity
●History of stroke or heart disease
●Apolipoprotein E (APOE) epsilon 4 genotype
●Neuropsychiatric symptoms (agitation, apathy, depression, anxiety)
PATHOLOGY — Neuropathologic studies suggest that MCI represents an early clinical expression of neurodegenerative disease. Several autopsy studies have found that individuals with MCI (particularly amnestic MCI [aMCI]), as a group, have Alzheimer disease (AD) pathology that is intermediate in severity between normal controls and persons with more advanced AD [14,63-69]. A predominant feature of these studies is the presence of tau deposition in the medial temporal lobes [64].
Some, but not all, studies find that pathologies consistent with other dementing processes (eg, Lewy body disease and cerebrovascular disease) are also over-represented in the MCI population compared with normal controls, although AD pathology usually predominates [13,63,70-72]. Cerebrovascular and mixed pathologies are especially common among individuals who carry a diagnosis of MCI for a longer interval or die without having progressed to dementia [73].
Studies of cholinergic markers in patients with MCI and early to late stages of AD are helping to elucidate the pathogenesis of AD and have challenged the hypothesis that cholinergic dysfunction is responsible for early cognitive dysfunction in this disorder [66,67].
SYMPTOMS
Cognitive complaints — Patients with MCI, particularly the amnestic subtype, complain primarily of impaired memory. It is important to ascertain that this represents a change from baseline. Subjective memory complaints have been demonstrated to predict cognitive decline, even when patients appear unimpaired on objective testing [74-78]. It is important to note, however, that difficulties with certain aspects of memory, such as recalling names, are frequently reported by normal older adult patients. Subjective reports of memory complaints can often reflect mood or affective state, as well as poor sleep and pain [74,79]. Subjective cognitive complaints may be an insensitive clinical criterion as well as a nonspecific one; some individuals who meet neuropsychological test criteria for MCI deny having significant memory problems [12].
In contrast to the impaired awareness of deficits commonly present in patients with Alzheimer disease (AD), patients with MCI may be particularly troubled by their symptoms [76,80,81]. However, over time, patients with MCI who convert to AD shift to a relatively greater preponderance of informant-reported symptoms over self-reported symptoms [82]. This phenomenon may be helpful in following an individual patient's progression to dementia.
Neuropsychiatric symptoms — As with dementia, mood and behavioral symptoms are more common in patients with MCI than in cognitively unimpaired, age-matched controls [83-88]. The prevalence of depression ranges from 25 to 40 percent [89]; other common symptoms include irritability, anxiety, aggression, and apathy [85]. Patients with behavioral symptoms may be more impaired on cognitive measures than those without behavioral symptoms [85]. Population-based studies comparing MCI and AD patients find a similar range of neuropsychiatric symptoms, with AD patients having them in somewhat higher frequency and severity [86,90,91]. (See "Management of neuropsychiatric symptoms of dementia".)
The relationship between depression and cognitive impairment is complicated. Cognitive impairment may be a presenting symptom of depression, so-called pseudodementia or dementia syndrome of depression. Depression may also be an early manifestation of cognitive impairment. (See "Diagnosis and management of late-life unipolar depression".)
A number of population-based studies have found an association between various measures of depression and either the presence or incidence of MCI [83,92-98]. However, follow-up data have yielded somewhat mixed results. In the aggregate, these results appear to suggest that depression may be an early manifestation of cognitive decline and possibly an independent risk factor for MCI or progression to dementia. At the least, these studies highlight the importance of recognizing the symptoms of mood and behavioral changes in patients reporting memory problems, as they may represent a group at increased risk of developing dementia, and warrant closer follow-up.
EVALUATION
Goals of the evaluation — The evaluation of patients who present with cognitive complaints is focused on establishing the severity of the impairments and providing a baseline for follow-up. Individuals with MCI are at increased risk of progressing to dementia, and clinicians should not assume that concerns about impaired cognition are related to normal aging without proper evaluation. Accurate diagnosis of MCI is important in order to [40]:
●Assess for reversible causes of cognitive impairment
●Help patients and families understand the cause of their cognitive concerns
●Discuss prognostic significance of a diagnosis of MCI and help patients and families plan for the future
Office evaluation — The cornerstone of any evaluation of someone with memory loss is the clinical interview. Ideally, an informant will be available, and if not, attempts should be made to contact one. The goals are to assess the severity of memory loss and the degree, if any, of functional impairment that limits independence in daily activities [40]. Although the boundary is not always clear, functional impairment is a key indicator that distinguishes dementia from MCI.
By discussing current events involving a variety of topics, it is often possible to develop a sense of the degree of amnestic problems. Discussing premorbid and current financial competence with patients and family members can be another useful measure of cognitive status that may be particularly sensitive to early decline [99]. Clear functional decline such as difficulties with activities of daily living may be a later, but more specific, finding for early dementia [100].
A brief, comprehensive evaluation of the patient's cognitive profile should also be performed. Clinicians should not rely on historical report of subjective memory concerns alone. Examples of brief, validated cognitive assessments include the Folstein Mini-Mental State Examination (MMSE) and the Montreal Cognitive Assessment (MoCA) [101-104]. (See "Evaluation of cognitive impairment and dementia", section on 'Cognitive testing'.)
Other essential aspects of the office evaluation include:
●A comprehensive medical and neurologic examination must be performed to identify sources of nondegenerative causes of cognitive change.
●A medication list should be reviewed to identify those medications associated with adverse cognitive effects.
●A sleep history should be obtained to identify potential dementia-related sleep disturbances as well as sleep disorders that might be contributing to cognitive impairment. (See "Risk factors for cognitive decline and dementia", section on 'Sleep disturbances' and "Risk factors for cognitive decline and dementia", section on 'Obstructive sleep apnea'.)
●Underlying psychiatric conditions should also be probed. (See "Screening for depression in adults", section on 'Screening instruments'.)
Neuropsychological testing — Patients who screen positive for MCI by history and brief cognitive assessment should have more in-depth cognitive testing, such as neuropsychological testing with interpretation based on appropriate normative data [40].
Neuropsychological testing includes an objective measure of memory impairment [5]. It may also have additional value in the detection of contributing or causative depression.
Neuropsychological testing should not be used in isolation; clinical judgment is critical to diagnosing both dementia and MCI [10,80]. There are no uniformly accepted criteria for the diagnosis of MCI using neuropsychological testing. Some suggest a 1.5 standard deviation (SD) threshold value for tests of memory impairment; others have used 1 SD [1,4,33,105]. These appear to be the appropriate ranges for most individuals diagnosed with MCI, but these data must be used in the context of the history of the individual. In amnestic MCI (aMCI), other cognitive domains may be impaired, but test abnormalities are generally milder and are usually within 0.5 SD of appropriate comparison groups. In multiple-domain MCI, several cognitive domains may be impaired in the 0.5 to 1.0 SD range. These ranges are not used as cutoff scores, but they provide a sense of the impairments seen in MCI.
Some rating scales are useful for characterizing the stage of impairment but are not substitutes for the clinical diagnosis of MCI. The Clinical Dementia Rating (CDR) scale and the Global Deterioration Scale (GDS) are useful adjuncts for the clinician in characterizing the degree of impairment. For example, a CDR of 0.5 commonly refers to the degree of impairment between normal aging and mild dementia. However, patients with MCI can have a CDR rating of 0 or 0.5 due to the subtle degrees of impairment without a functional decline. Since the CDR largely involves the subjective perceptions of the patient and an informant, judgments may vary from the clinician's impression of the degree of impairment. Similarly, with the GDS, Stages 2 and 3 can be conflated due to the patient's and informant's perception. Thus, while the scales are useful for estimating impairment, they are not adequate for the diagnosis of MCI [106].
For patients who meet criteria for MCI or have persistent cognitive complaints, neuropsychological reassessment in approximately one year is recommended to monitor cognitive and functional decline [6]. Improved performance on the examination argues against neurodegenerative disease, while declining performance supports that diagnosis, even before a threshold level for dementia has been reached [99]. (See "Mild cognitive impairment: Prognosis and treatment", section on 'Progression to dementia' and "Mild cognitive impairment: Prognosis and treatment", section on 'Neuropsychological testing'.)
Neuroimaging — The role of neuroimaging, brain computed tomography (CT) or magnetic resonance imaging (MRI), in the evaluation of MCI is evolving.
We order noncontrast brain MRI with coronal slices to image the hippocampus in patients with MCI. Others may take the view that CT scan can adequately evaluate for cerebrovascular disease, subdural hematoma, normal pressure hydrocephalus, or mass lesion that might cause clinically significant cognitive deficits. However, MRI is more sensitive than CT in assessing focal patterns of atrophy, such as temporal lobe volume loss; this last finding may indicate an individual at particularly high risk of converting from MCI to dementia. (See "Mild cognitive impairment: Prognosis and treatment", section on 'MRI'.)
In addition, MRI may be more sensitive than CT in identifying cerebrovascular disease, another finding that may identify patients at higher risk of progressing to dementia and who might additionally benefit from more aggressive treatment of vascular comorbidities. (See "Treatment of vascular cognitive impairment and dementia", section on 'Vascular risk modification' and "Mild cognitive impairment: Prognosis and treatment", section on 'Cerebrovascular risk factors'.)
The role of other neuroimaging tests, including positron emission tomography (PET), functional MRI, PET amyloid imaging, and single-photon emission CT (SPECT), in assessing the risk for and type of neurodegenerative dementia is evolving. (See "Clinical features and diagnosis of Alzheimer disease", section on 'Neuroimaging'.)
Data from the Alzheimer Disease Neuroimaging Initiative document the utility of imaging biomarkers such as amyloid PET in predicting progression [107]. (See "Mild cognitive impairment: Prognosis and treatment", section on 'Amyloid PET'.)
Other testing — Treatable conditions should also be ruled out. In general, the evaluation of patients with MCI should be similar to that performed in patients presenting with dementia and include a neuroimaging study (brain CT or MRI) and screening for B12 deficiency, hypothyroidism, and evaluation for depression. (See "Evaluation of cognitive impairment and dementia".)
Ongoing investigations are examining the relationship between apolipoprotein E (APOE) genotype and/or the levels of certain biomarkers within the cerebrospinal fluid (CSF) and the risk of converting from MCI to dementia. At the present time, there is no clinical imperative for these tests. (See "Mild cognitive impairment: Prognosis and treatment", section on 'Predictors'.)
DIAGNOSIS — Clinical judgment is critical to diagnosing MCI [10,80]. There are no uniformly accepted criteria for the diagnosis of MCI using neuropsychological testing or other cognitive assessments. MCI is ultimately a clinical diagnosis that considers the individual's expected level of cognitive function. In the absence of clear evidence that an individual's performance on cognitive testing represents a clear decline, a diagnosis of MCI should be withheld, even if scores meet criteria for MCI.
A workgroup on diagnostic guidelines from the National Institute on Aging and the Alzheimer's Association identified the following core clinical features that indicate MCI due to Alzheimer disease (AD) [108]:
●Cognitive concern reflecting a change in cognition reported by patient or informant or observed by clinician
●Objective evidence of impairment in one or more cognitive domains, typically including memory
●Preservation of independence in functional abilities
●Not demented
These criteria only refer to the subset of all MCI that is thought be due to AD, and not to MCI due to other etiologies, eg, vascular disease, other neurodegenerative conditions, or psychiatric conditions [8].
In addition, the etiology of MCI should be evaluated to identify a cause other than AD (see 'Evaluation' above):
●Identify or rule out vascular, traumatic, medical causes of cognitive decline, where possible
●Provide evidence of longitudinal decline in cognition, when feasible
●Identify other clinical features that may suggest a specific neurodegenerative syndrome (eg, parkinsonism)
●Report history consistent with AD genetic factors, where relevant
DIFFERENTIAL DIAGNOSIS — While MCI is associated with the risk of Alzheimer disease (AD), other neurodegenerative dementias, and vascular dementia, other conditions can also present with MCI.
●Psychiatric disease, particularly depression, may present with cognitive rather than mood complaints.
●Adverse effects of medications (eg, anticholinergic, antihistamine use) and sleep disturbances are also common causes of cognitive complaints, particularly in older adult populations [109,110].
●Metabolic disturbances, particularly vitamin B12 deficiency and hypothyroidism, should be considered in the differential diagnosis of MCI.
●Normal aging can be associated with both subjective and objective cognitive changes. In general, these are not sufficiently severe to be of concern and are not accompanied by loss of functional abilities in daily life.
●Structural brain disease is an uncommon cause of MCI in the absence of focal neurologic findings.
In one community sample, patients with "cognitive impairment, no dementia" (CIND) were diagnosed with depression and other psychiatric disease (10.2 percent), alcohol- and drug-related causes (6.9 percent), and delirium (1 percent) [31]. Approximately one-quarter of cases had neurologic disease (brain tumor, Parkinson disease, multiple sclerosis, cerebrovascular disease, and epilepsy). Among the remaining 57.5 percent, most (31.7 percent) had circumscribed memory impairment.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cognitive impairment and dementia".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Evaluating memory and thinking problems (The Basics)" and "Patient education: Mild cognitive impairment (The Basics)")
●Beyond the Basics topic (see "Patient education: Dementia (including Alzheimer disease) (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS — Mild cognitive impairment (MCI) represents a state between normal aging and dementia.
●MCI includes patients with cognitive deficits that are insufficiently severe to meet criteria for dementia but are more severe than those associated with normal aging. (See 'Definitions' above.)
●Types of MCI based on the affected cognitive domains (amnestic MCI [aMCI], nonamnestic MCI [naMCI]) are individually recognized with subtypes of single- and multiple-domain classifications. These clinical subtypes are believed to have value in predicting conversion to a specific type of dementia. (See 'Definitions' above.)
●Pathologic studies of individuals with MCI generally reveal pathology of neurodegenerative or cerebrovascular disease that is intermediate between cognitively normal and demented adults. Alzheimer-type pathology typically predominates, particularly among those with aMCI. (See 'Pathology' above.)
●Clinicians should consider potentially treatable causes of cognitive impairment, such as psychiatric disease, the effects of medications, and underlying medical conditions. (See 'Differential diagnosis' above and 'Office evaluation' above and 'Other testing' above.)
●We recommend neuropsychological testing in individuals suspected of having MCI. Those meeting criteria for MCI and those with prominent subjective complaints should have follow-up testing to evaluate for progression between one and two years after the initial assessment. (See 'Neuropsychological testing' above.)
●In addition, a number of screening mental status scales can be performed during office examinations for evidence of cognitive decline. (See 'Office evaluation' above.)
●We recommend a brain magnetic resonance imaging (MRI) study be performed in individuals with MCI to exclude structural disease and assess the extent of cerebrovascular disease and regional atrophy. (See 'Neuroimaging' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Eric M McDade, DO, who contributed to an earlier version of this topic review.
