CLINICAL SYNTHESISFull Access
Quick Reference for Geriatric Psychiatry
Published Online:1 Apr 2004https://doi.org/10.1176/foc.2.2.206
The tables in this section are drawn with permission from Spar JE, La Rue A: Concise Guide to Geriatric Psychiatry, 3rd ed. Washington, DC, American Psychiatric Publishing, 2003.
| Nature of the complaint: what the problem is and when it occurs (e.g., sleep onset, sleep maintenance, early-morning wake up, daytime fatigue, nightmares) |
| Current sleep-wake schedule |
| History of sleep complaint (transient disturbance vs. long-standing complaint) |
| Symptoms of sleep disorders that may not be initially volunteered (e.g., restless legs, periodic limb movements, narcolepsy, gastroesophageal reflux, parasomnias, disruption of sleep-wake schedule) |
| Symptoms of sleep-disordered breathing (disturbed breathing at night, complaints of snoring, headache on waking, partner sleeps in another room) |
| Daytime states, routines, activities (sleepiness, fatigue, functioning, mood, activities, satisfaction with daily routines) |
| Naps, frequency, time of day, length |
| Sleep hygiene (daytime activity, exercise, sleep environment, activity in bed, diet, use of stimulants/depressants) |
| History of professional treatment of the sleep complaint and a review of what the client has tried to remedy the sleep problem |
| Medical/physical problems |
| Use of prescription and nonprescription drugs |
| Psychiatric history and mental status review (symptoms of depression, anxiety, thought disorder, other psychological maladjustment) |
| Stressful circumstances (currently and when sleep problems began) |
| Information regarding antecedents, consequences, secondary gains, precipitating factors, perpetuating factors |
| System | Anatomical Changes With Age | Functional Changes With Age |
|---|---|---|
| Cardiovascular | ||
| Heart | Decreased size, flexibility of collagen matrix; lipofuscin and fat deposition in myocardium; fatty infiltration and calcification of aortic and mitral valves | Impaired left ventricular diastolic filling, reduced β-adrenergic (i.e., chronotropic and inotropic) response to catecholamines, leading to decreased peak exercise cardiac index and ejection fraction |
| Arteries | Redistribution and molecular rearrangement (cross-linking) of elastin and collagen in arterial walls; calcification | Increased systolic blood pressure |
| Respiratory | ||
| Lungs | Enlarged alveolar ducts and alveoli; loss of elasticity | Reduced ventilatory capacity, especially during exercise |
| Musculoskeletal | Increased chest wall and joint rigidity; increased kyphosis; degeneration and calcification of cartilage | Same as above |
| Gastrointestinal | Some loss of smooth muscle cells of intestine; atrophy of gastric mucosa; increase in gastric pH; some loss of hepatocytes; reduction in hepatic blood flow | Reduced eliminatory efficiency: constipation; reduced metabolism of drugs |
| Genitourinary | Loss of renal mass, loss of glomeruli, thickening of basement membrane of glomeruli and tubules, development of tubular diverticula, intimal thickening of arteries, development of afferent-efferent shunts in juxtamedullary glomeruli and obliteration of arterioles in cortical glomeruli; reduced bladder elasticity, especially in women; prostate enlargement in men | Reduced glomerular filtration rate and renal plasma flow; loss of bladder emptying capacity |
| Endocrinologic | Atrophy and fibrosis; loss of vascularity; changes may be very minimal | General decline in secretory rate, but resting hormone blood levels may remain constant as clearance also declines |
| Nervous | Loss of brain weight and volume in most studies; loss of neurons, depending on brain area studied; loss of dendritic arbor with reduced interneuronal connectivity; interneuronal accumulation of lipofuscin and loss of organelles; neurofibrillary degeneration of neurons; accumulation of senile plaques, especially in hippocampus, amygdala, and frontal cortex | Inconsistent evidence of reduced blood flow; reduced metabolism of glucose and oxygen; intellectual changes |
| Musculoskeletal | Reduced muscle and bone mass; demineralization of bone; increased fat in muscles and calcium in cartilage; degeneration of cartilage; loss of elasticity in joints | Loss of muscular strength and stamina |
| Immunologic | Involution of thymus, reduction of the proportion of naïve T cells, increased proportion of activated/memory T cells, decreased expression of IL-2 receptors, decreased cellular proliferative response to T-cell receptor stimulation | Increased susceptibility to cancer |
| Special senses | Yellowing of lens in eye | Loss of auditory and visual acuity, especially night vision |
| Type | History | Physical Findings | Cognitive and Behavioral Function | Imaging/Laboratory Findings |
|---|---|---|---|---|
| Alzheimer’s disease | Gradual onset and progression; ± family history | Typically none until mid/late stages | Language deficits early (word finding, anomia, fluent aphasia); clues not helpful with retrieval; visuospatial deficits early | Cortical atrophy, ventricular enlargement on CT, MRI; temporal/parietal hypometabolism on PET; hypoperfusion on SPECT |
| Vascular dementia | Abrupt onset, stepwise decline; history of hypertension, atherosclerosis | Neurologic signs and symptoms (e.g., gait abnormalities, falls, incontinence) | Patchy impairment; depression, relative preservation of personality common | Stroke; lacunae in basal ganglia, white matter; periventricular lesions very common, required for diagnosis if focal neurologic signs absent |
| HIV dementia | HIV-positive blood test; gradual onset of cognitive changes | Neurologic signs and symptoms may be present (e.g., ataxia, tremor, frontal release signs) | Forgetfulness, apathy, slowness, poor concentration common | Elevated CSF protein; mild lymphocytosis may be present; neuroimaging nonspecific; HIV usually present in CSF |
| Head trauma | Head injury | Depends on location of injury; dysarthria, hemiparesis common | Memory impairment usually present; impulse dyscontrol, irritability, personality change may be seen; nonprogressive unless head trauma repeated (e.g., in dementia pugilistica) | Depends on location, extent of injury |
| Parkinson’s disease | Dementia in later stages of neurologic syndrome | Extrapyramidal signs (e.g., tremor, gait disturbance, rigidity, bradykinesia) | Cognitive slowing, poor recall, frontal signs (e.g., perseveration, decreased word list generation, impaired behavioral sequencing); clues helpful with memory retrieval | Subcortical atrophy on CT (e.g., increased intercaudate distance, ventricular enlargement) common; global cerebral metabolism also may be diminished on PET |
| Huntington’s disease | Autosomal dominant pattern of inheritance; onset generally in 30s–40s; offspring of affected parent 50% likely to be affected | “Fidgeting” progres-sing to choreoathetosis | Personality change, loss of judgment, irritability early, memory impairment later; psychosis common | CT or MRI may show striatal atrophy; PET may show striatal hypometabolism |
| Pick’s disease | Onset in 50s–60s | Frontal release signs (e.g., snout, grasp reflex) common | Personality change, emotional blunting, deterioration of social skills, language deficits early; memory impairment, dyspraxia later | CT or MRI may show frontal and temporal atrophy; PET may show frontal hypometabolism |
| Creutzfeldt-Jakob disease | Onset in 40s–60s; 5%–15% have family history; rapid progression (i.e., 1-year course) typical; can be transmitted by corneal transplant or contact with infected brain tissue or CSF | Myoclonus early, seizures later; ataxia, visual symptoms, gait disturbance variably present | Nonspecific symptoms (e.g., fatigue, diminished sleep and appetite early; global cognitive deficits late) | CT and MRI may be normal; EEG may show sharp, triphasic synchronous discharges at 0.5–2 Hz |
| Test | Potential Diagnosis |
|---|---|
| Complete blood count with differential white cell count | Folate deficiency anemia, viral infection |
| Serum thyroid-stimulating hormone, thyroxine, serum cortisol (a.m. and p.m.) | Hypothyroidism and hyperthyroidism; hypoadrenocorticalism and hyperadrenocorticalism |
| Sequential multiple analysis of 18 chemical constituents of blood (SMA-18) | Hypercalcemia, hypokalemia, hyperglycemia |
| Urinalysis, blood urea nitrogen | Uremia |
| Computed tomography or magnetic resonance imaging of head (as indicated by results of above tests, physical examination) | Brain tumor, stroke |
