Premorbid cognitive leisure independently contributes to cognitive reserve in multiple sclerosis.
Summary of "Premorbid cognitive leisure independently contributes to cognitive reserve in multiple sclerosis."
OBJECTIVE:
Consistent with the cognitive reserve hypothesis, higher education and vocabulary help persons with Alzheimer disease (AD) and multiple sclerosis (MS) better withstand neuropathology before developing cognitive impairment. Also, premorbid cognitive leisure (e.g., reading, hobbies) is an independent source of cognitive reserve for elders with AD, but there is no research on the contribution of leisure activity to cognition in MS. We investigated whether premorbid cognitive leisure protects patients with MS from cognitive impairment.
METHODS:
Premorbid cognitive leisure was surveyed in 36 patients with MS. Neurologic disease severity was estimated with brain atrophy, measured as third ventricle width on high-resolution MRI. Cognitive status was measured with a composite score of processing speed and memory.
RESULTS:
Controlling for brain atrophy, premorbid cognitive leisure was positively associated with current cognitive status (r(p) = 0.49, p < 0.01), even when controlling for vocabulary (r(p) = 0.39, p < 0.05) and education (r(p) = 0.47, p < 0.01). Also, premorbid cognitive leisure was unrelated to brain atrophy (r = 0.03, p > 0.5), but a positive partial correlation between leisure and atrophy emerged when controlling for cognitive status (r(p) = 0.37, p < 0.05), which remained when also controlling for vocabulary (r(p) = 0.34, p < 0.05) and education (r(p) = 0.35, p < 0.05).
CONCLUSIONS:
Premorbid cognitive leisure contributes to cognitive status in patients with MS independently of vocabulary and education. Also, patients with MS who engaged in more cognitive leisure were able to withstand more severe brain atrophy at a given cognitive status. Premorbid cognitive leisure is supported as an independent source of cognitive reserve in patients with MS.
Affiliation
Neuropsychology & Neuroscience Laboratory, Kessler Foundation Research Center, 300 Executive Drive, Suite 10, West Orange, NJ 07052 jsumowski@kesslerfoundation.org.
Journal Details
This article was published in the following journal.
Name: Neurology
ISSN: 1526-632X
Pages: 1428-31
Links
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/20956787
- DOI: http://dx.doi.org/10.1212/WNL.0b013e3181f881a6
Medical and Biotech [MESH] Definitions
Delirium, Dementia, Amnestic, Cognitive Disorders
Cognitive disorders including delirium, dementia, and other cognitive disorders. These may be the result of substance use, trauma, or other causes.
Cognitive Reserve
Capacity that enables an individual to cope with and/or recover from the impact of a neural injury or a psychotic episode.
Executive Function
A set of cognitive functions that controls complex, goal-directed thought and behavior. Executive function involves multiple domains, such as CONCEPT FORMATION, goal management, cognitive flexibility, INHIBITION control, and WORKING MEMORY. Impaired executive function is seen in a range of disorders, e.g., SCHIZOPHRENIA; and ADHD.
Cognitive Therapy
A direct form of psychotherapy based on the interpretation of situations (cognitive structure of experiences) that determine how an individual feels and behaves. It is based on the premise that cognition, the process of acquiring knowledge and forming beliefs, is a primary determinant of mood and behavior. The therapy uses behavioral and verbal techniques to identify and correct negative thinking that is at the root of the aberrant behavior.
Aphasia, Primary Progressive
A progressive form of dementia characterized by the global loss of language abilities and initial preservation of other cognitive functions. Fluent and nonfluent subtypes have been described. Eventually a pattern of global cognitive dysfunction, similar to ALZHEIMER DISEASE, emerges. Pathologically, there are no Alzheimer or PICK DISEASE like changes, however, spongiform changes of cortical layers II and III are present in the TEMPORAL LOBE and FRONTAL LOBE. (From Brain 1998 Jan;121(Pt 1):115-26)
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