Examine for the numerous medical causes of dementia (e.g., endocrine, heart, kidney, lung, liver, infection). Always perform a careful neurologic examination, and identify any focal CNS causes of dementia. Always test for sense of smell (first cranial nerve)—may identify a large unrecognized frontal lobe lesion. Always test hearing. Advanced diffuse disease displays ataxia, facial grimaces, agnosias, apraxias, motor impersistence, and/or perseveration and pathologic reflexes (grasp, snout, suck, glabella tap, tonic foot, etc.). Recognize that all types of physical illnesses occur more frequently in the demented patient (reasons for this are unclear). Survival time is reduced.

Selected tests based on suspected etiology. Consider screening with ESR, CBC, STS, SMA-12, T₃ and T₄, vitamin B₁₂ and folate assays, UA, chest radiograph, and CT or MRI scan. Other tests based on likely causes include drug levels, EEG (20% of all elderly have an abnormal EEG), LP (rarely), arteriography, HIV, and heavy metal screen, etc. The EEG is useful for identifying pathology in the usually silent CNS areas (frontal and temporal lobes)—investigate further if the dementia is mild, but the EEG is grossly abnormal.

These can (a) help identify a focal lesion, (b) provide a baseline, (c) help with the diagnosis, and (d) identify strengths to be used in planning treatment. Useful tests include the WAIS, Bender-Gestalt Test, the Luria test, and the Halstead and Reitan Batteries (very time consuming; do not use routinely). A brief but useful screening test is the Mini-Mental State Exam (2); numerous others exist. Patients with even mild dementia often will show impaired constructional ability; thus have them draw simple figures (e.g., a diamond, a cross, and a cube or the face of a clock set at a certain time—can be done on initial interview). Repeated drawings can be used to track the illness over time (3).

Approximately 50%⁺ of all dementias (5% to 10% of people older than 65; 50% of those older than 85), but usually it is a diagnosis by exclusion. AD is the “classic cortical dementia.” It is frequently overdiagnosed. Typically begins insidiously in the 50s (early onset, familial, presenile form—2% of cases) or later in the 60s to 80s (much more common late-onset form) and progresses to death in 6 to 10 years (4). Look initially for impaired recent memory, language problems, mild mood and personality changes, impaired problem solving. These all worsen over the next several years, becomes severe in 5⁺ years. Ceaseless pacing and a shuffling gait are common; social responses become simplistic but often remain intact until very late. Look for cortical atrophy and enlarged ventricles by MRI. The EEG is often normal for age early on but is a good screening test because it is often abnormal with reversible causes of dementia [except for general paresis and normal-pressure hydrocephalus (NPH)]. Histologically, senile plaques (degenerated nerve terminals surrounding a neurotoxic β-amyloid core), neurofibrillary tangles, and neuronal granulovacuolar degeneration are found. Recent evidence implicates primary degeneration of cholinergic neurons of the basal forebrain, particularly the nucleus basalis (although serotonergic and other neurons are increasingly being implicated—very heterogeneous).