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Speaking at the recent U.S. Psychiatric & Mental Health Congress, Wilfred G. Van Gorp, Ph.D., associate professor and director of the neuropsychology program at Cornell University, offered some guidelines. He began by reviewing the neuropsychological changes associated with normal aging. Crystallized intelligence-those verbal abilities that deal with long-held knowledge-tends to be resistant to change following any kind of brain perturbation or central nervous system (CNS) stressor, he said. This remains relatively stable until a person reaches their mid-60s. In contrast, fluid intelligence-psychomotor speed and nonverbal, often visuospatial tasks-is more susceptible to CNS changes. These nonverbal abilities, typically those that are timed and involve psychomotor speed, have a more precipitous decline, beginning after age 40. The fragility of certain cognitive tasks, as measured by the timed performance subtests on IQ tests, has been called the classic aging pattern, Van Gorp said.
He presented study data showing that changes in the frontal part of the brain and the subcortical structures are likely responsible for this cognitive decline of aging. To further explore this pattern, he and his colleagues compared normal elderly individuals to patients with AIDS dementia complex. They reported a remarkable similarity of both pattern and level of performance on every neuropsychological test. The normal elderly, who had an average age of around 75, resembled, in both level and pattern of cognitive functioning, the 35- and 40-year-old patients with HIV dementia.
What does this mean? When evaluating an elderly patient, the clinician first has to determine whether the symptoms are caused by normal aging. This means embarking upon a battery of neuropsychological tests with norms to compare with other people in the same age group. The clinician experienced in working with older adults can also give a mental exam and compare to see if it is a deviation from normal aging or not.
Before surveying the literature about the cognitive manifestations of depression and comparing these manifestations to dementia symptoms, Van Gorp stressed the difficulty of interpreting that literature. The majority of the cognition and depression studies conducted around the world have looked at depressed patients who have neurologic illnesses, such as Parkinson's disease, stroke or progressive supranuclear palsy, any of which may have caused the depression. Ruling those out leaves only 13 qualified studies that focus solely on cognition and depression.
Van Gorp pointed out three other issues to consider when reviewing the literature:
The first is the severity of the illness (dementia and depression). Severity of depression tended to be a key factor in whether or not a study found that a major depressive disorder had a significant impact upon cognition. Studies in which the subjects were inpatients almost always found significant neurocognitive deficits, whereas studies in which subjects were outpatients often failed to find an effect.