| 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 |
| Note: CSF=cerebrospinal fluid; CT=computed tomography; EEG=electroencephalogram; HIV=human immunodeficiency virus; MRI=magnetic resonance imaging; PET=positron emission tomography; SPECT=single photon emission computed tomography |