Brain, Vol. 125, No. 12, 2750-2765,
December 2002
© 2002 Oxford University Press
Suppression of false recognition in Alzheimer’s disease and in patients with frontal lobe lesions
1 Division of Cognitive and Behavioral Neurology, Department of Neurology and 2 Department of Neurosurgery, Brigham and Women’s Hospital, 3 Harvard Medical School, Boston, 4 Smith College, Northampton and 5 Department of Psychology, Harvard University, Cambridge, MA, USA
Correspondence to: Andrew E. Budson, MD, Division of Cognitive and Behavioral Neurology, Department of Neurology, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115, USA E-mail: abudson{at}partners.org
Previous research has shown that patients with Alzheimer’s disease show increasing levels of false recognition across five repeated study–test trials of semantic associates. The present study tested the hypotheses that (i) the increasing false recognition was partly due to the frontal lobe dysfunction of patients with Alzheimer’s disease, and (ii) a failure of source monitoring was the central mechanism by which frontal lobe dysfunction led to increasing false recognition across trials. In Experiment 1, patients with frontal lobe lesions and controls were examined in the same repeated trials paradigm as that used previously in patients with Alzheimer’s disease. Although controls were able to reduce their false recognition across trials, the patients with frontal lobe lesions were not, and instead showed a constant level of elevated false recognition across the study–test trials. In Experiment 2, two groups of patients with Alzheimer’s disease and healthy older adult controls were studied: the first group was given a single study session followed by a recognition test, the second group was given five study sessions followed by a single recognition test. Older adults who were exposed to five study lists demonstrated lower levels of false relative to true recognition, whereas patients with Alzheimer’s disease in this condition exhibited levels of false recognition elevated to that of their true recognition, even with the source memory confusion of intervening tests eliminated. The authors suggest that impairment in aspects of frontal lobe function, such as verification–inhibition mechanisms, probably contributes to the inability of patients with Alzheimer’s disease to suppress their false recognition across repeated trials. Lastly, it is speculated that one way in which the frontal lobes enable normal episodic memory function is by facilitating the suppression of false recognition and other distortions of memory.
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