Changes in the Elderly

Normal Changes in the Elderly

Normal changes in the elderly should not impair daily functioning, such as self-care, everyday activities, managing finances, and medication management.

Neurocognitive changes

Anatomic and physiologic changes:

• ↓ Brain volume:
  • Greatest in the frontal and temporal lobes
  • White matter affected more than gray matter
• ↓ Cerebral blood flow
• ↓ Levels of neurotransmitters

Effects:

• Intelligence: 
  • Decline in reaction time and psychomotor skills
  • Decline in ability to process new information quickly (fluid intelligence)
• Memory:
  • Decline in declarative memory, which includes:
    • Semantic memory (language, meaning of words)
    • Episodic memory (memory of past events)
  • Nondeclarative memory (learned skills) does not decline with aging.
  • Decline in recall ability
• Attention and concentration: 
  • Decline in multitasking abilities
  • ↓ Concentration
• Language: decline in verbal fluency and naming objects (expressive aphasia)
• Decline in visuospatial abilities
• Decline in executive functioning (ability to plan, solve problems)

Sensory function

Anatomic and physiologic changes:

• Eyes:
  • Periorbital tissue atrophy
  • ↑ Flaccidity of the eyelids
  • ↓ Lacrimal gland function
  • Conjunctival atrophy
  • Corneal deposits
  • ↓ Lens elasticity
  • ↓ Ciliary muscle strength
• Ears:
  • Thinning of the external auditory canal walls
  • Cerumen is drier.
  • Loss of hair cells in the organ of Corti

Effects:

• Visual acuity
• Presbyopia (↓ ability to focus on nearby objects)
• Presbycusis (↓ in high-frequency hearing acuity)
• Trouble with speech discrimination and sound localization
• ↓ Olfaction → loss of taste (cause is not entirely clear)

Sleep patterns

• ↓ REM and slow-wave sleep
• ↑ Sleep onset latency
• ↑ Early awakenings
• ↑ Frequency of nighttime awakenings

Organ system changes

• Cardiovascular function:
  • Mild ↓ in heart rate and ↓ response to exertion/stressors
  • ↑ Stiffness of vessels → ↑ BP
  • Thickening and calcification of heart valves
  • Impaired diastolic function
• Pulmonary function:
  • ↓ Elastic tissue → ↓ elastic recoil → enlarged alveolar ducts → loss of ⅓ of surface area per volume of lung tissue → ↑ anatomic dead space
  • ↑ Chest wall stiffness
  • ↓ Functional reserves
    • ↑ Residual volume and FRC
    • ↓ Forced vital capacity
  • ↑ Alveolar-arterial (A-a) oxygen gradient and V/Q mismatch
• GI function:
  • ↓ Esophageal muscle strength and coordination → dysphagia
  • ↑ In reflux esophagitis, due to altered contractions and sphincter tone
  • ↓ Transit time → ↑ in constipation
• Renal function:
  • ↓ Renal mass and ↑ fibrosis
  • ↓ Renal blood flow
  • ↓ Renal function
  • ↓ Creatinine clearance
• Immune function: 
  • ↓ Immune response
  • ↑ Susceptibility to infection and malignancy
• Skin:
  • Epidermal thinning
  • ↓ Elasticity
  • ↑ Fragility

Body mass and metabolism

• ↓ Lean muscle mass 
• ↑ Body fat
• ↓ Bone density 
• ↓ Basal metabolic rate
• ↓ Caloric consumption needs

Sexual changes

• Men:
  • Slower erection and ejaculation
  • Longer refractory period
• Women: vaginal atrophy, thinning, and dryness (due to ↓ in estrogen)

Pathologic Cognitive Decline

While some changes in cognition are observed in normal aging, some patients may experience more cognitive impairment than expected, which affects intellectual performance or daily functioning. This unexpected impairment should prompt an evaluation.

Clinical presentation

• Memory lapses and forgetfulness
• Inability to focus
• Difficulty finding words
• Inability to complete tasks independently
• Decline in reasoning and judgment
• Personality changes
• Mood changes

Screening for cognitive decline

• Recommended only if clinical suspicion is present
• Mini–Mental State Examination (MMSE): 
  • 30-point questionnaire 
  • Used extensively in clinical settings to measure cognitive impairment
  • Includes the following:
    • Orientation to time  
    • Orientation to place 
    • Registration 
    • Attention and calculation 
    • Recall 
    • Language 
    • Repetition
    • Complex commands
  • Interpretation:
    • ≥ 24 points is considered normal.
    • 19–23 points indicates mild dementia.
    • 10–18 points indicates moderate dementia.
    • ≤ 9 points indicates severe dementia. 
• Mini–cognitive test has 89% specificity for dementia, involving the following: 
  • 3-item recall
  • Clock draw test

Evaluation

• Review medications.
• Screen for depression.
• Laboratory evaluation:
  • TSH → hypothyroidism
  • Vitamin B₁₂ and CBC → vitamin B₁₂ deficiency
  • Rapid plasma reagin → tertiary syphilis
• Neuroimaging (CT or MRI) to evaluate for:
  • Cerebrovascular disease
  • Normal-pressure hydrocephalus
  • Subdural hematoma
  • Mass lesion
• Neuropsychological testing (in-depth cognitive testing)

Differentiating mild versus more severe neurocognitive changes

• Mild neurocognitive decline:
  • Mild decline in ≥ 1 cognitive domain
  • Normal functioning in all daily activities 
• Major neurocognitive decline (dementia):
  • Severe decline in ≥ 1 cognitive domain
  • Significant irreversible decline in all daily activities 
  • Marked functional impairment

Differential Diagnosis

• Major depressive disorder: mood disorder marked by depressed mood, sleep disturbances, anhedonia, feelings of guilt or worthlessness, loss of energy, low concentration, weight or appetite changes, psychomotor retardation or agitation, and suicidal ideation. In elderly patients, pseudodementia may also be present. Diagnosis is clinical but requires ruling out other potential diagnoses. Treatment options include pharmacotherapy, psychotherapy, and electroconvulsive therapy.
• Alzheimer disease: chronic neurodegenerative disease. Alzheimer disease is the most common cause of dementia. The etiology of this disease is unclear but is thought to be multifactorial. Alzheimer disease causes a decline in memory, thought processes, behavior, and functional abilities. Diagnostic considerations involve history, exam, imaging, lab test, and neuropsychological testing; however, definitive diagnosis is made only postmortem with evidence of amyloid plaques and neurofibrillary tangles at autopsy. There is no cure.
• Vascular dementia: declines in mental function caused by brain damage after insufficient or impaired blood supply to the brain. This type of dementia characteristically causes stepwise progression of decline in thought processes, executive functioning, and daily functional abilities. Exact symptoms vary by area of the brain impacted by impaired blood flow. Diagnosis is aided by imaging studies. Management is focused on control of risk factors and conditions such as hypertension, dyslipidemia, and diabetes.
• Frontotemporal dementia: group of rare brain disorders, including Pick disease, associated with atrophy in the frontal and temporal lobes of the brain. This atrophy leads to personality and behavioral changes, as well as diminished thought processes and language abilities. Diagnosis is made clinically in combination with imaging, neuropsychological tests, and other tests to rule out other conditions. Management involves antipsychotics and antidepressants, as well as speech therapy.
• Lewy body dementia: 2nd most common progressive dementia. Lewy body dementia develops because of abnormal deposition of Lewy bodies in the nerve cells of the brain, leading to impaired mental functions related to thinking, movement, behavior, and mood. Patients will also have visual hallucinations, Parkinson’s disease–like movement abnormalities, and fluctuating cognition. The diagnosis is made clinically and through imaging and testing to rule out other conditions. There is no cure, but medications may help manage symptoms. 
• Normal-pressure hydrocephalus: abnormal accumulation of CSF inside the ventricles of the brain, typically due to a blockage in the drainage pathway. This accumulation causes pressure and stretching of the periventricular white matter, Normal-pressure hydrocephalus is marked by gait abnormalities, incontinence, and dementia. Imaging of the brain, lumbar puncture, and intracranial pressure monitoring help make the diagnosis. Management involves placing a shunt in the brain to drain the CSF. 
• Prion diseases: also known as transmissible spongiform encephalopathies. Prion diseases are a large group of rare, progressive neurodegenerative diseases that can affect both humans and animals. Symptoms include behavioral changes, ataxia, myoclonus, and seizures. Unfortunately, these diseases are associated with long incubation periods (≥ 20 years), and once symptoms occur, progression to death is rapid. Diagnosis is often made on postmortem brain biopsy. 
• Vitamin B₁₂ deficiency: potential cause of reversible cognitive decline. Low levels of vitamin B₁₂ can be due to a decline in absorption with increasing age, poor diet, alcoholism, and pernicious anemia. Clinical manifestations include fatigue, psychotic symptoms, and decline in concentration, visual-spatial tasks, and executive functioning. Diagnosis is made via vitamin B₁₂ blood testing and neuropsychological evaluation. Management involves vitamin B₁₂ replacement.