ACCT-AD Instruction Manual

The Assessment of Cognitive Complaints Toolkit for Alzheimer's Disease (ACCT-AD) Instruction Manual provides guidance on diagnosing cognitive impairment and introduces the toolkit’s design and approach.

Approach to Assessment

For both detection and full cognitive assessment, the toolkit relies primarily on the clinical history and assumes the availability of a knowledgeable informant (for example, a spouse, family member, or friend) who can provide collateral information.

Information from both the patient and the informant is essential for accurate diagnosis. Currently, no objective test can capture all of the information needed to determine the cause of cognitive impairment, and patient self-report may be unreliable when cognitive symptoms are present.

Use of the toolkit may lead to the following conclusions (see the workflow diagram below and the Outcome Scenarios and Decision Tree in the Reference and Interpretation Manual for additional details):

  • The reported concerns are consistent with normal aging and do not require further assessment.
  • The concerns exceed what would be expected for age and warrant further evaluation.

When symptoms exceed expectations for age, the toolkit helps determine severity:

  • Mild cognitive impairment (MCI): Cognitive changes that do not affect, or minimally affect, daily functioning.
  • Dementia: Cognitive changes that interfere with daily functioning.

We strongly recommend reviewing the section on distinguishing mild cognitive impairment from dementia.

Regardless of severity, findings are organized into three categories:

  1. Findings consistent with Alzheimer's disease (AD).
  2. Findings that suggest another neurodegenerative disorder and warrant specialist referral.
  3. Findings that suggest an alternative neurological or non-neurological cause that should be addressed before determining whether a neurodegenerative condition is present. Examples include symptoms with sudden onset (e.g., stroke), sleep apnea, or significant mood symptoms.
ACCT-AD Assessment Workflow

The foundation of this toolkit is the clinical history, which provides most of the information needed to establish a diagnosis. The toolkit includes suggested wording for open-ended questions in the Patient Assessment Forms section. These questions reflect the approach used by the experts who developed the toolkit.

The toolkit also provides optional prompts to use when patients or informants need clarification or provide responses that are unclear or not relevant. These prompts are not necessary when a clear and relevant answer has already been provided.

To support interpretation of cognitive and behavioral concerns, the Reference and Interpretation Manual includes common responses to each question and color-coded guidance for interpretation.

Potential outcomes are categorized as follows:

  • Green: Consistent with normal aging
  • Yellow: Consistent with Alzheimer's disease
  • Red: Not consistent with normal aging or Alzheimer's disease; may indicate another cause of dementia
  • Orange: Indeterminate or potentially due to a non-neurological cause

The same color-coding system is used throughout the assessment, including the neurological examination, cognitive testing, laboratory studies, and imaging. Clinicians who are new to the toolkit may find themselves consulting the Reference and Interpretation Manual frequently. As familiarity with the assessment process increases, consultation should become less necessary.

For example, in the language symptoms interpretation table, the questions and prompts are highlighted in gray, and potential responses are color-coded by clinical significance.

ACCT-AD Language and Color Coding Sample

To establish a diagnosis, clinicians should obtain answers to all history questions included in the assessment. If a diagnosis of normal aging, mild cognitive impairment, or Alzheimer's disease dementia is made, no findings should be coded red. Red findings are not typical of normal aging or Alzheimer's disease and should prompt consideration of referral to a specialist.

If red findings are identified, clinicians may choose to stop the diagnostic process and inform the patient that a specialist referral is recommended. However, it may still be useful to complete additional portions of the assessment, including the neurological examination, to better characterize findings for the consulting provider. Laboratory studies and imaging may be deferred to the specialist. See the referral section for additional guidance.

The toolkit also provides guidance on cognitive testing. It is important to use tests appropriate to the patient's educational background. Inappropriate testing may yield results inconsistent with the clinical picture and may not accurately reflect cognitive status.

If an appropriate cognitive test is unavailable, it is generally preferable to rely on the clinical history rather than attempt to interpret an unsuitable test. In these situations, referral for expert evaluation, such as neuropsychological testing, may be warranted. The toolkit also includes recommendations for cognitive testing in individuals with limited formal education and for select language groups.

The full evaluation assumes familiarity with the patient's medical, family, and social histories, as well as the patient's medication list. Additional time may be needed to gather this information for new patients. The assessment may be completed over multiple visits to accommodate patient and provider schedules.

Not all questions must be asked by the primary clinician. Information may be collected by other members of the care team. However, the clinician interpreting the responses should have sufficient training to determine whether the patient understood the question and provided a meaningful response.

 

Definition of key terms
  • Cognitive and behavioral concerns: your judgment that there is a possible cognitive decline based on patient or informant- expressed concern or your own observation of a change in cognition or behavior.
  • Cognitive Impairment: Cognitive impairment is when a person has trouble remembering, learning new things, concentrating, or making decisions that affect their everyday life. Cognitive impairment ranges from mild to severe. It can be documented using standardized cognitive tests, but such tests are only reliable if they have been validated for the patient’s level of education, language, and cultural background.
  • Neurocognitive disorder/syndrome/disease: a disorder of cognition or behavior that results from neurologic dysfunction due to injury or disease.
  • Neurodegenerative disorder: a progressive disorder of the nervous system characterized clinically by insidious onset, gradual progression, and eventual functional impairment in most cases, and pathologically by neuronal morphological changes and neuronal loss, and usually by accumulation of microscopic collections of proteins within and/or outside of neurons.
  • Dementia, also called Major Neurocognitive Disorder in DSM-5: a neurocognitive disorder that is severe enough to interfere with the ability to function at work and or other daily activities. A deterioration of intellectual faculties, such as memory, concentration, and judgment, or socioemotional behavior resulting from an organic disease or disorder of the brain.
  • Alzheimer’s disease: Alzheimer’s disease (AD) is usually considered the most common cause of dementia. The most common symptoms in AD are forgetting recent events and conversations. A dementia where the earliest and most prominent symptoms are this type of forgetfulness is often called a “typical” dementia syndrome.
  • Atypical dementia: Dementia where symptoms other than memory are the earliest and most important symptoms. Atypical dementias can begin with declines in language, visuospatial, or socioemotional function. Any dementia where motor symptoms are early or very prominent would also be considered atypical. In addition, any dementia where the symptoms begin before the age of 65 would be considered early age of onset, and therefore atypical. When a dementia syndrome is atypical, it suggests that the cause may not be Alzheimer’s (see table below), although Alzheimer’s can also present with atypical symptoms.
  • Mild Cognitive Impairment (MCI), also called Minor Neurocognitive Disorder in DSM-5: Deficits in memory or other cognitive functions that do not significantly impact daily functioning.
  • Cognitive testing: assesses cognitive function. Cognition is a combination of processes that involve storing, utilizing, and manipulating information. Tests of cognitive function typically assess domains such as memory, language, executive function, and visuospatial function. A problem with cognition is called cognitive impairment, which can range from mild to severe. Cognitive tests are only reliable if they have been validated for the patient’s level of education, language, and cultural background.
  • Functional Impairment: Functional impairment refers to the loss of ability to independently conduct activities of daily living (ADLs). Such activities are usually divided into instrumental ADLs (IADLs), such as working, bill paying, and other financial activities; cooking, shopping, and other home activities; and basic ADLs, such as dressing and hygiene. Functional impairment is a required criterion for the diagnosis of major neuropsychiatric disorders/dementias.
  • Biomarkers: Biologically based measures that capture some element of the biology of disease. These typically include brain imaging, measurements of proteins or other molecules in cerebrospinal fluid (CSF) or blood. Biomarkers can be used to detect the presence of a disease, track its progression, or both. Some biomarkers provide information about a certain aspect of a disease (such as the severity of neurodegeneration) but are not very specific, whereas others target specific biological mechanisms to help identify the cause of symptoms.
Causes of dementia and principles of diagnosis

This toolkit is designed primarily as a practical resource for evaluating cognitive complaints in clinical practice. It may also serve as a training tool for clinicians with less experience in cognitive assessment. It is not intended to be a comprehensive review of dementia etiologies. For additional background, readers may consult resources such as the Gerontological Society of America’s KAER Toolkit and the Health Resources and Services Administration’s Training Curriculum: Alzheimer’s Disease and Related Dementias.

Defining dementia

Dementia is a clinical syndrome characterized by progressive decline in cognitive and/or behavioral function over time, typically for at least 6 months, resulting in loss of independence in activities the individual previously performed independently. Determining when this threshold has been reached can be challenging and may vary according to an individual’s occupational demands, educational background, and baseline level of functioning. Despite this variability, impairment in daily functioning remains the defining criterion for a diagnosis of dementia.

In the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), the term major neurocognitive disorder replaced dementia. However, the term dementia remains widely used in neurology, geriatrics, and psychiatry. When cognitive and behavioral symptoms have progressed to the point of dementia, a neurological disease is often the underlying cause.

Dementia is a syndrome, not a specific diagnosis

Dementia describes the severity and functional consequences of cognitive decline but does not identify the underlying cause. Establishing the etiology is therefore a critical component of the diagnostic evaluation.

Neurodegenerative disease is the most common cause of dementia. These disorders are characterized by progressive accumulation of abnormal proteins within the central nervous system, leading to neuronal dysfunction and cell death. Examples include Alzheimer’s disease (AD), Parkinson’s disease, dementia with Lewy bodies, frontotemporal dementia, and other neurodegenerative syndromes.

Although AD is the most common cause of dementia overall, non-AD neurodegenerative disorders account for a substantial proportion of cases, particularly among individuals with symptom onset before age 65. In this population, at least half of the patients may have a non-AD dementia syndrome (Garre-Olmo et al., 2010).

Principles of neurodegenerative disease diagnosis

In many neurodegenerative diseases, the underlying pathological proteins cannot be definitively identified in living individuals. As a result, diagnosis relies largely on recognition of characteristic clinical syndromes.

Different neurodegenerative diseases tend to affect specific neural systems early in their course and then spread to additional regions over time. A careful clinical history is therefore essential. Particular attention should be paid to the earliest symptoms, their progression, and the sequence in which cognitive, behavioral, language, motor, and other neurological features emerged. This pattern often provides the strongest clues to the underlying diagnosis.

Importance of clinical history and neurological examination

Many clinically important manifestations of neurodegenerative disease—including hallucinations, personality changes, loss of empathy, and other socioemotional symptoms—may not be adequately captured by standardized cognitive tests. Conversely, similar patterns of impairment on neuropsychological testing may occur across multiple dementia syndromes.

Although cognitive testing is an important component of the evaluation, it should not be used as a substitute for a thorough clinical history. A neurological examination is equally important because certain neurodegenerative disorders involve characteristic motor findings, whereas others do not.

The Dementia Causes Table below summarizes the major neurodegenerative syndromes encountered in clinical practice and highlights key clinical features that may help differentiate them.

Dementia Causes Table. Brief summary of the major neurodegenerative syndromes that are commonly seen in clinical practice and the main clinical features that distinguish them.
 Alzheimer's Disease (AD)Vascular Dementia (VaD)Lewy Body Dementia (LBD)Behavioral Variant Frontotemporal Dementia (bvFTD)Corticobasal Degeneration (CBD)Progressive Supranuclear Palsy (PSP)FTD Language Variants
OnsetGradual, usually after age 65Maybe sudden or stepwiseGradualGradual, usually before age 65Gradual, between 60–80 (mean 64)Gradual, between 50–80 (mean 63)Gradual
Causative ProteinBeta amyloid and tauN/AAlpha-synucleinTau, TDP-43, FUSTauTauTDP-43, tau
Typical First SymptomMemory difficultiesDepends on ischemiaVaries, hallucinations, or visuospatialBehavior or personality changesUnilateral motor changesFallsLanguage
Cognitive Domain, SymptomsMemory, language, and visuospatialDepends on the anatomy of ischemiaMemory, visuospatial, fluctuating symptomsExecutive: ± memoryExecutive: ± memorySpared memory, frontal subcortical deficitsLanguage, loss of knowledge of word meaning
Psychiatric/ BehavioralDelusions are commonDepression, irritabilityHallucinations, usually visualDisinhibition, apathyDisinhibition, apathyDepression, impulsivityComplusions
Motor Symptoms

Rare early, apraxia later

 

Correlated with the location of ischemiaParkinsonismSome rare cases with motor neuron diseaseAlien limb, unilateral dystoniaFalls, supranuclear gaze palsy, axial rigidity, dysarthria, dysphagiaEffortful speech
ProgressionGradual, over 8 to 10 yearsStepwise with further ischemiaGradual, but faster than ADGradual, but faster than ADGradual, motor symptomsGradual, mean survival 6–9 yearsGradual
Laboratory TestsNormalNormalNormalNormalNormalNormalNormal
ImagingPossible global atrophy, small hippocampusCortical or subcortical white matter lesions on MRIPossible global atrophyAtrophy in the frontal and temporal lobesAsymmetrical parietal and frontal atrophyMidbrain atrophyLeft frontoinsular or anterior temporal atrophy

Role of other medical conditions

Many non-neurodegenerative conditions can contribute to cognitive impairment. Common examples include medication effects, obstructive sleep apnea, psychiatric disorders, substance use, and chronic medical illnesses. These conditions may be identified through the medical history, social history, medication review, or history of present illness.

When such conditions are present, the temporal relationship between their onset and the emergence of cognitive symptoms is particularly important. However, clinicians should recognize that these factors may coexist with, rather than fully explain, an underlying neurodegenerative disease.

For example, a patient whose history is highly consistent with Alzheimer’s disease may also have depression or sleep apnea. Treatment of these comorbid conditions is appropriate, but lack of improvement—or continued decline despite treatment—should prompt reconsideration of a neurodegenerative etiology.

In patients with milder cognitive symptoms, including those meeting criteria for mild cognitive impairment (MCI), non-neurological medical conditions are more likely to contribute substantially to the clinical presentation. Nevertheless, longitudinal follow-up remains important to determine whether symptoms improve, remain stable, or progress.

Dementia versus mild cognitive changes

Key Points

  • Mild cognitive impairment (MCI) involves measurable cognitive decline with little or no impairment in daily functioning.
  • MCI is often caused by a neurodegenerative disease, but it can also result from other medical, psychiatric, or age-related conditions.
  • Identifying MCI is important because it allows clinicians to monitor patients more closely and helps patients and families plan for the future.
  • MCI can be evaluated using the same assessment tools used to evaluate dementia.

Dementia and functional impairment

In this toolkit, the term dementia refers to cognitive and behavioral changes that are severe enough to interfere with independent daily functioning. For example, a person who was previously able to manage finances, prepare meals, shop independently, or perform work responsibilities may require assistance because cognitive errors are affecting these activities. In DSM-5 terminology, this condition is classified as Major Neurocognitive Disorder.

Recognizing dementia is important because normal aging does not cause cognitive changes severe enough to impair independent function. When dementia is present, an underlying disease process is assumed, even if the specific cause cannot yet be confirmed through diagnostic testing.

Because functional decline is central to the diagnosis of dementia, this ACCT-AD toolkit includes questions designed to identify changes in daily activities. Functional impairment should be considered evidence of dementia only when the patient continues attempting these activities but can no longer perform them successfully, leading others to take over. For example, voluntarily stopping work because of concern about memory would not, by itself, constitute evidence of dementia.

Understanding mild cognitive impairment

Many individuals experience memory or other cognitive changes that are noticeable to themselves, family members, or friends. Long-term follow-up studies show that some of these individuals eventually develop dementia. The term mild cognitive impairment (MCI) is commonly used to describe this stage of cognitive decline, when daily functioning remains largely intact.

Symptoms of MCI may resemble those seen in Alzheimer’s disease, particularly difficulties with recent memories, conversations, or events. Others may present with symptoms more suggestive of different neurodegenerative disorders. Many individuals with MCI maintain independence through compensatory strategies such as calendars, reminders, note-taking, and strong organizational habits.

Research using imaging and biological markers has shown that many people with MCI already have evidence of Alzheimer’s disease or another neurodegenerative condition. Current models suggest that these diseases often begin years before symptoms appear, progress through a stage of MCI, and eventually lead to dementia.

However, not all MCI is caused by neurodegenerative disease. Some individuals remain stable for years, never progress, or even improve. In these cases, symptoms may be related to normal aging, cerebrovascular disease, mood disorders, medications, sleep disorders, or other medical conditions. Although these causes are often apparent from the clinical history, they are not always easily identified. Therefore, MCI should not automatically be considered an early stage of neurodegenerative disease.

As biomarkers continue to improve, clinicians will increasingly be able to determine whether MCI is related to Alzheimer’s disease or another neurodegenerative process.

Why diagnosing MCI matters

Patients with MCI are at increased risk of developing dementia and should be monitored over time. Early identification also provides an opportunity to address modifiable risk factors, evaluate potential underlying causes, and plan for the future.

The evaluation of MCI should include the same core assessment used for dementia, including:

  • Clinical history
  • Physical and neurologic examination
  • Laboratory testing
  • Brain imaging when appropriate
  • Biomarker testing when clinically indicated

Because some cases of MCI may progress, clinicians should encourage patients to consider advance care planning and ensure that trusted family members or caregivers remain aware of changes in daily functioning, particularly in financial management.

Diagnosing MCI also helps provide patients and families with the most accurate assessment of their concerns. Labeling a person as having dementia when the evidence does not support that diagnosis can cause unnecessary distress. Conversely, describing significant cognitive decline as normal aging may fail to address legitimate concerns. An MCI diagnosis acknowledges that meaningful cognitive change is present while recognizing uncertainty regarding future progression.

Terminology and diagnostic considerations

MCI has been described using several related terms, including Cognitive Impairment No Dementia (CIND) and Minor Neurocognitive Disorder, the DSM-5 term.

Some clinicians further classify MCI based on the primary cognitive domain affected. For example:

  • Amnestic MCI: primarily memory impairment
  • Non-amnestic MCI: impairment in other domains, such as executive function, language, or visuospatial abilities

Experts differ on how MCI should be defined. Some reserve the diagnosis for patients with objective evidence of impairment on cognitive testing. The assessments included in this toolkit can provide such evidence. However, some patients with clinically significant cognitive decline may perform normally on brief screening tests and require more detailed neuropsychological testing to demonstrate impairment.

For the purposes of this toolkit, MCI may be diagnosed when clinical judgment supports the presence of meaningful cognitive decline that does not yet impair independent functioning, even if basic cognitive screening results are normal. Referral for formal neuropsychological evaluation may be helpful when diagnostic uncertainty remains.

A graph illustrating cognitive decline over time as disease-causing proteins accumulate.
Cerebrovascular disease and cognitive impairment

Key Points

  • Stroke-related cognitive impairment typically has a sudden onset and may lead to partial recovery or stabilization over time.
  • Small-vessel cerebrovascular disease can cause brain injury that appears as white-matter hyperintensities on T2-weighted MRI, including FLAIR sequences.
  • Small vessel disease can contribute to cognitive impairment, but it is unlikely to be the sole cause when cognitive changes are severe enough to meet criteria for dementia.
  • Some patients with mild cognitive impairment may have cognitive symptoms primarily related to vascular disease, but many also have underlying neurodegenerative pathology.
  • Mild white matter changes reported on MRI are unlikely to be a major cause of cognitive symptoms.
  • Patients with insidiously progressive cognitive or behavioral decline should be evaluated for possible neurodegenerative disease, even when significant vascular disease is present on imaging.

Cerebrovascular disease warrants special consideration in the evaluation of cognitive impairment.

Patients with sudden onset of cognitive symptoms or other focal neurological deficits may have experienced a stroke or another acute neurological event. These patients require urgent neurological evaluation.

In contrast, chronic small-vessel cerebrovascular disease may contribute to cognitive decline through cumulative brain injury and is an established cause of vascular cognitive impairment and dementia. The role of vascular disease in cognitive decline is discussed in more detail in a dedicated section below.

Stroke and cognitive impairment

Cerebrovascular disease associated with aging and vascular risk factors, such as hypertension and diabetes, can affect cognition in several ways. The clearest relationship occurs when cognitive symptoms develop after an ischemic or hemorrhagic stroke.

Depending on the location of the lesion, stroke can cause aphasia, memory impairment, visuospatial dysfunction, or other cognitive deficits. Stroke-related cognitive impairment is usually identifiable from the clinical history. Symptoms typically begin suddenly, are most severe at onset, improve to some degree over weeks to months, and then remain relatively stable.

Progressive cognitive decline is not characteristic of stroke-related cognitive impairment and should prompt consideration of an alternative or additional diagnosis, particularly a neurodegenerative disease. Neuroimaging should demonstrate a lesion capable of explaining the patient's symptoms, such as a cortical infarct or a strategically located lacunar infarct. While an MRI obtained shortly after a stroke may identify features of a recent event, accurately determining the age of an infarct becomes increasingly difficult after the acute period.

Small vessel disease and cognitive impairment

Chronic ischemic injury affecting small cerebral vessels is another common contributor to cognitive impairment. On MRI, these changes appear as white matter hyperintensities on T2-weighted and FLAIR sequences. On CT, they may appear as areas of low attenuation within the white matter.

These abnormalities commonly occur around the lateral ventricles and within the deep white matter. Lacunar infarcts, often involving the basal ganglia, may also be present even in patients without a history of recognized stroke.

Research demonstrates that larger volumes of white matter hyperintensities and the presence of lacunes are associated with an increased risk of cognitive impairment. However, these imaging findings correlate only modestly with symptoms. Many older adults have substantial white matter disease on MRI without clinically significant cognitive or behavioral changes.

Vascular dementia and mixed pathology

The term vascular dementia is often applied when a patient with dementia also has evidence of cerebrovascular disease on imaging. However, this term can imply that vascular injury is the sole cause of dementia, which is frequently not the case.

Neuropathologic studies have shown that most patients diagnosed with dementia during life have underlying neurodegenerative disease, most commonly Alzheimer's disease, often in combination with vascular pathology. As a result, many patients with dementia and significant cerebrovascular disease have mixed pathology.

Among patients with mild cognitive impairment, vascular disease may be the primary cause of symptoms in some cases, although mixed vascular and neurodegenerative disease remains common. Estimates vary across studies, and available data may not fully reflect the diversity of populations.

For this reason, the term vascular cognitive impairment is often preferred because it recognizes that vascular injury may contribute to cognitive decline without necessarily being the sole cause.

Clinically, cognitive impairment related to small vessel disease often produces greater executive dysfunction than typical Alzheimer's disease. However, memory complaints can be similar, and clinical features alone are often insufficient to distinguish vascular from neurodegenerative causes.

Clinical interpretation of imaging findings

White matter hyperintensities on MRI

Determining whether vascular disease is responsible for a patient's cognitive symptoms depends on the clinical context.

A vascular etiology is most convincing when all of the following are present:

  • A clear temporal relationship between a stroke and symptom onset.
  • Cognitive deficits that remain stable or improve over time.
  • Imaging findings that plausibly explain the observed deficits.

Outside this scenario, attributing cognitive symptoms to small-vessel disease is more challenging.

Although formal rating scales for white matter hyperintensities exist, they are rarely used in routine clinical practice. Radiology reports typically describe these findings as mild, moderate, or severe.

In general, mild white matter changes are unlikely to make a substantial contribution to cognitive symptoms, except possibly in patients with very mild cognitive complaints. This interpretation applies regardless of the presence of vascular risk factors.

Conversely, even moderate or severe small vessel disease is unlikely to be the sole explanation for established dementia. Because neurodegenerative diseases cannot be excluded on the basis of vascular imaging findings alone, clinicians should maintain a high index of suspicion for concurrent neurodegenerative pathology.

Diagnostic approach

Patients with insidiously progressive cognitive or behavioral decline should be considered to have possible neurodegenerative disease, even when significant cerebrovascular disease is present on imaging.

Diagnostic evaluation should proceed as it would in the absence of vascular disease. If the clinical presentation is consistent with Alzheimer's disease, it is reasonable to diagnose an Alzheimer's-type clinical syndrome while recognizing cerebrovascular disease as a potential contributor. In people with mild cognitive impairment, vascular disease may represent either a contributing factor or the primary cause.

Similarly, features suggestive of atypical neurodegenerative syndromes or other neurologic conditions should be evaluated according to standard diagnostic approaches, regardless of the presence of vascular imaging abnormalities.

Assessment recommendations and guidelines

Detection of symptoms

When does a provider know that a patient needs an assessment of cognitive symptoms? Current expert guidelines do not recommend routine formal cognitive testing of patients based on arbitrary cutoffs such as age (US Preventive Services Task Force – Screening for cognitive impairment). Rather, the clinician should be alert to signs of cognitive changes. These can include: 

  • The patient brings up cognitive concerns during a visit.
  • The patient’s informant (caregiver, family member, or friend) raises cognitive concerns with the provider or medical staff.
  • The medical staff and/or provider notice potential cognitive concerns (e.g., missed appointments, medication errors).

In addition, current guidelines suggest that a few brief, routine questions can be used to identify patients with cognitive concerns. One example of when these might be used is in a health risk assessment (HRA) conducted during the Medicare Annual Wellness Visit. The CDC provides additional direction on the potential contents and approaches for performing an HRA.

The CDC guidelines anticipate that the HRA questions can be obtained in many ways, including paper or online questionnaires, in person, and other options.

There are no requirements for using specific questions, and different sources recommend different versions (e.g., the Alzheimer's Association Cognitive Screen Toolkit).

The ACCT-AD toolkit provides questions and procedures for detecting significant cognitive complaints. 

While ACCT-AD Detection Questions may be suitable for detecting concerns using pre-visit questionnaires and similar approaches, the ACCT-AD toolkit recommends that a trained medical staff member ask these questions in person, as there is currently insufficient data to indicate that they are adequately sensitive when self-administered. These questions should be asked of a patient and informant, and if no informant is available, they should be supplemented with a brief cognitive test.

Diagnosis of cause: Full evaluation

Expert guidelines recommend that, if detection procedures or similar tools indicate significant cognitive and/or behavioral changes, a full assessment be conducted. The full assessment provides the opportunity to quantify the severity of the problem and its impact on daily function, to obtain a detailed inventory of all of the problems beyond the primary complaint, to identify medical issues that may be contributing or causing the cognitive and behavioral changes, and, if the conclusion is that the patient may be suffering from mild cognitive changes or dementia due to a neurodegenerative disease, to specify the potential cause of the symptoms.

Referral

Once a probable etiology for the symptoms has been established, the clinician should decide whether a referral is needed, who should be consulted, and the goals of the referral.

Cognitive testing information

The following PowerPoint tutorials are available upon request. We have provided PDF versions of these PowerPoints in Section 3: Patient Assessment Forms.

  • Best practices for cognitive testing
  • Mini-Cog
  • Mini-Mental State Examination (MMSE)
  • Montreal Cognitive Assessment (MoCA)
  • Saint Louis University Mental Status (SLUMS) Examination
  • Modified Mini-Mental State (3MS)

Cognitive testing with low literacy and language constraints

The recommendations in this toolkit are based on available research and the clinical experience of the toolkit developers. However, most studies of cognitive screening tools have been conducted in highly educated populations living in high-income countries. Educational background, language, culture, and literacy can significantly influence performance on cognitive tests.

As a result, clinicians should adapt the toolkit’s recommendations when evaluating patients with limited formal education, low literacy, or limited English proficiency. Patients in California and across the United States represent a wide range of cultural and linguistic backgrounds, and the evidence supporting cognitive screening tools varies considerably across languages and populations.

For many cultural and language groups, there is insufficient evidence to recommend a specific cognitive assessment approach. As noted in the toolkit limitations section, concerns about cognitive or behavioral decline in a patient with limited education and/or limited English proficiency are an appropriate reason for referral to a specialist with expertise in cognitive evaluation.

Where evidence is available, the toolkit identifies appropriate cognitive screening instruments for commonly encountered clinical situations. In addition to selecting the appropriate test, clinicians should use education-adjusted interpretation guidelines. Alternative cutoff scores for individuals with lower levels of education are provided in the Reference and Interpretation Manual.

ContextBrief Cognitive Test for DetectionCognitive Testing for Full Assessment
Spanish >6 yrs. of educationMini-CogMontreal Cognitive Assessment (MoCA)
Spanish ≤6 yrs. of educationModified version of the Mini-Mental State Exam (MMSE)Modified version of the Mini-Mental State Exam (MMSE)
Chinese >6 yrs. of educationBrain Health Test (BHT)Montreal Cognitive Assessment (MoCA)
Chinese ≤6 yrs. of educationBrain Health Test (BHT)Montreal Cognitive Assessment – basic (MoCA basic)

Using interpreters during cognitive testing

Formal cognitive testing is only one component of a comprehensive evaluation of cognitive concerns. The accuracy and validity of cognitive test results can be influenced by many factors, including differences between the clinician and patient in language, culture, country of origin, education, health literacy, and attitudes toward testing.

Whenever possible, patients should be assessed in their preferred language by a clinician or examiner who is trained in cognitive assessment and understands how cultural, educational, linguistic, and dialect differences may affect test performance and interpretation.

Unless the clinician is fully bilingual and trained to conduct cognitive testing in the patient’s language, a multidisciplinary approach is often necessary. When language, cultural, or educational factors are likely to substantially affect test validity, clinicians may obtain more useful information from a careful history than from formal cognitive testing. If cognitive testing is necessary despite these barriers, referral to a neuropsychologist or other qualified specialist should be considered.

Clinicians often use interpreters to bridge language differences. This approach may be appropriate in some circumstances, but only when specific conditions are met. Practices that work regularly with trained medical interpreters may be better positioned to conduct interpreter-assisted cognitive testing.

Before administering cognitive testing through an interpreter, consider the following:

  1. Interpreter familiarity with cognitive testing

    The individual assisting with testing should have training or experience with the planned cognitive assessment and should be familiar with the testing materials and administration procedures. Clinicians should confirm that the interpreter understands the importance of standardized administration and, whenever possible, has reviewed relevant training materials.

  2. Maintaining standardized test administration

    The use of an interpreter introduces additional challenges to test administration. Cognitive test scores are only valid when instructions, prompts, and test materials are delivered according to standardized procedures.

  3. Interpreters should translate the clinician’s instructions as accurately and directly as possible without adding explanations, coaching, prompts, or other interactions.

    Because maintaining standardization can be difficult, family members should rarely be used as interpreters during cognitive testing.

  4. Use of validated assessment tools

    Whenever possible, clinicians should use cognitive measures that have been validated for the patient’s language, cultural background, education level, and country of origin. Appropriate interpretation guidelines and validated cutoff scores should also be available. Dialect differences may further affect the suitability of a particular measure.

  5. Assessing barriers to engagement and understanding

    After testing, clinicians should discuss the process with the interpreter to identify any factors that may have affected the patient’s performance, including language comprehension difficulties, cultural differences, educational background, or engagement with the testing process.

Interpreting results obtained through an interpreter

If cognitive testing is conducted through an interpreter, clinicians should interpret the results cautiously and within the broader clinical context.

Compare test results with the overall clinical picture

Clinicians should consider whether cognitive test results are consistent with the patient’s history, functional abilities, informant reports, and other clinical findings. If test results conflict with other aspects of the evaluation—particularly when the discrepancy could affect diagnosis or management—greater weight should be placed on the clinical history, and referral to a specialist should be considered.

Refer when results are borderline or uncertain

Referral is appropriate when test scores fall near diagnostic cutoff points or when uncertainty remains regarding the validity or interpretation of the results. Specialist evaluation may help clarify the diagnosis and guide management.

Guidance on the neurological exam

The assessment of any patient with cognitive complaints must include a neurological examination. For those who need a review of how to conduct and interpret a neurological examination, there are many resources available. Some good ones include:

  1. The book titled Clinical Neuroanatomy Made Ridiculously Simple by Stephen Goldberg. This book presents clinical neuroanatomy with mnemonics, humor, and case presentations. It includes a tutorial on localizing neurologic injuries and an interactive quiz on classic neurologic cases. Windows/Macintosh CD and book.
  2. The website at neuroexam.com. This website is an interactive online guide to the main components of the neurologic examination with video demonstrations. It is based on the book Neuroanatomy through Clinical Cases by Hal Blumenfeld, MD, PhD, Yale University School of Medicine.
Reference and interpretation pages

This section provides reference materials that primary care physicians can consult before, during, or after an assessment to support interpretation of collected data and clinical decision-making.

For guidance on interpreting responses that arise during the detection process, visit the Brief Assessment Responses section. Direct links to relevant interpretation guidance are also available within the Brief Assessment, following each question.

Family and caregiver resources for care

Dementia caregiving

Finding local resources

Information about long term care

Finding legal help

Home safety

Self-Care resources

Activities

Caregiving videos

Off