How do I evaluate and manage an older adult with memory or cognitive impairment?

Evaluation and Management of Older Adults with Memory or Cognitive Impairment

When to Evaluate

Evaluate all patients who self-report cognitive concerns, have family members reporting concerns, or in whom you suspect cognitive changes based on observed difficulties with appointments, medication adherence, or decision-making. 1 Do not wait for universal screening—the USPSTF concludes evidence is insufficient to recommend routine screening in asymptomatic older adults because no trials demonstrate that screening improves mortality, quality of life, or functional status. 2, 1

However, remain vigilant for early signs including:

• Memory problems or language difficulties 2
• Difficulty managing finances, medications, transportation, or household tasks 3
• Missed appointments or medication non-adherence 1
• Family member concerns (often the first indicator) 4, 5

Initial Cognitive Screening

Use the Mini-Cog as your first-line screening tool—it takes only 2-4 minutes with 76% sensitivity and 89% specificity, combining three-word recall with clock drawing. 1, 5 This is superior to longer instruments for initial assessment.

Alternative brief tools include: 2, 5

• Memory Impairment Screen (MIS)
• AD8 informant questionnaire
• Clock Drawing Test alone

Critical caveat: Screening scores alone are not diagnostic and must be interpreted within comprehensive clinical context including medical history and functional assessment. 1 Education level, language, and cultural factors significantly affect test performance—the MMSE particularly yields false-positives in older adults with lower education and false-negatives in younger, highly educated individuals. 1

Comprehensive History

Obtain detailed information on: 4, 5, 6

Cognitive domains:

• Memory (episodic, working, semantic)
• Language (word-finding, comprehension)
• Attention and concentration
• Visuospatial abilities (getting lost, spatial orientation)
• Executive function (planning, judgment, problem-solving)
• Behavioral changes

Functional impact on instrumental activities of daily living: 3, 5

• Managing finances
• Medication management
• Transportation/driving
• Household management
• Cooking and shopping

Timeline and progression: 4, 6

• Onset (gradual vs. rapid)
• Duration of symptoms
• Rate of decline
• Fluctuations in cognition

Corroboration from family/caregiver is essential—many patients with dementia lack insight into their deficits. 4, 5

Medication Review for Reversible Causes

Immediately review and discontinue medications that impair cognition, as this is often the most reversible cause of memory deficits. 3

High-priority medications to taper or discontinue: 3

• Benzodiazepines (lorazepam, clonazepam, diazepam)—cause sedation, cognitive impairment, falls
• Sedative-hypnotics (zolpidem, zaleplon)—directly impair cognition
• Anticholinergics (diphenhydramine, hydroxyzine, oxybutynin)—cause delirium and memory impairment
• Opioids—contribute to sedation and cognitive dysfunction

Also review antiepileptics for toxic levels and polypharmacy interactions. 2

Physical Examination

Focus on: 4, 5

• Neurologic examination: Focal deficits suggest stroke; parkinsonism suggests Lewy body or Parkinson's dementia
• Cardiovascular examination: Atrial fibrillation, carotid bruits
• Vision and hearing assessment: Sensory deficits mimic or worsen cognitive impairment 2, 5
• Gait and balance: Fall risk assessment
• Nutritional status: Weight loss, signs of malnutrition

Laboratory Evaluation for Reversible Causes

Order comprehensive metabolic screening to identify treatable contributors: 7, 3, 5

Essential tests:

• Complete blood count with differential (anemia, infection) 7
• Comprehensive metabolic panel (electrolytes, renal function, glucose) 7
• Thyroid function tests (TSH, free T4) 7, 3, 5
• Vitamin B12 and folate levels 7, 5
• Fasting glucose and lipid panel (cardiometabolic risk) 7
• Urinalysis with culture (occult infection) 7

Additional tests for diabetic patients: 7, 3

• HbA1c
• Microalbuminuria

Common reversible contributors include hypothyroidism, B12 deficiency, electrolyte abnormalities, hypoglycemia/hyperglycemia, anemia, and undetected infections. 2, 7

Brain Imaging

Obtain non-contrast MRI of the brain (or CT if MRI unavailable/contraindicated) to rule out structural causes: 4, 5

• Stroke/infarcts
• Subdural hematoma
• Brain tumor
• Normal pressure hydrocephalus
• Focal atrophy patterns

Detailed Cognitive Assessment if Initial Screen Abnormal

If the Mini-Cog is abnormal, perform more detailed cognitive testing using: 1, 3, 5

• Montreal Cognitive Assessment (MoCA)—preferred for detailed assessment
• Saint Louis University Mental Status (SLUMS)
• Rowland Universal Dementia Assessment Scale (RUDAS)

Combining cognitive tests with informant reports significantly improves diagnostic accuracy. 1

For patients with intellectual/developmental disabilities, use specialized instruments: 2

• Dementia Scale for Down's Syndrome
• Test for Severe Impairment
• Focus on recognizing change from premorbid baseline

When to Refer to Neurology/Neuropsychology

Refer when: 1, 5, 8

• Early-onset symptoms (before age 60-65)
• Screening abnormalities require clarification of the cognitive-behavioral syndrome
• Patient has subjective concerns but normal screening tests
• Atypical features present (rapid progression, prominent behavioral changes, focal neurologic signs)
• Severe behavioral disturbances
• Diagnosis remains unclear after initial workup

Abbreviated neuropsychological assessment programs can provide expedited diagnosis—30% receive dementia diagnosis, 50% mild cognitive impairment, and one-third receive new psychiatric diagnoses. 8

Differentiate from Depression and Delirium

Depression can cause "pseudodementia" with cognitive symptoms: 2, 3

• Screen with standardized depression tools
• Depression and early dementia frequently co-occur
• Late-life depression has 4% period prevalence when comorbid with anxiety 3

Delirium presents with: 5

• Acute onset (hours to days)
• Fluctuating course
• Inattention as primary feature
• Often reversible with treatment of underlying cause

High-Risk Populations Requiring Proactive Evaluation

Prioritize serial evaluation in: 1, 7

• Advanced age: Prevalence increases from 5% at ages 71-79 to 37% over age 90
• Family history of Alzheimer's disease
• Cardiovascular risk factors: Midlife hypertension, obesity, diabetes
• Race/ethnicity: 21.3% prevalence in Black adults vs. 11.2% in white adults aged 71+; 1.5× higher in Hispanic populations
• Down syndrome and intellectual disabilities: Earlier onset, higher prevalence 2

Initial Management After Diagnosis

Non-pharmacologic interventions (first-line): 4, 5

• Cognitively engaging activities (reading, puzzles)
• Physical exercise (walking, structured programs)
• Socialization (family gatherings, group activities)
• Cognitive stimulation therapy 3
• Caregiver education on communication strategies and structured routines 3

Pharmacologic treatment for Alzheimer's disease: 4

• Mild to moderate dementia: Donepezil (acetylcholinesterase inhibitor) 5-10 mg daily
• Moderate to severe dementia: Memantine 10-20 mg daily (alone or added to donepezil)
• Parkinson's disease dementia: Rivastigmine

Realistic expectations: Available treatments provide only modest benefits—cognitive scores improve by 1-3 points on ADAS-cog (equivalent to delaying natural progression by 2-7 months) with inconsistent effects on daily functioning. 1

Safety and Planning

Address: 1, 8

• Driving safety and decision-making capacity
• Fall prevention strategies 3
• Advance care planning while patient can still participate
• Financial and legal planning (power of attorney, healthcare proxy)
• Caregiver support and respite services

Monitoring

Schedule reassessment every 6-12 months to track: 3

• Cognitive function (repeat screening tools)
• Functional autonomy
• Behavioral symptoms
• Medication side effects
• Caregiver burden

Repeat cognitive screening with any significant decline in clinical status or increased difficulty with self-care. 3