Forgetting rates in neuropsychiatric disorders

Citation
P. Lewis et Md. Kopelman, Forgetting rates in neuropsychiatric disorders, J NE NE PSY, 65(6), 1998, pp. 890-898
Citations number
41
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY
ISSN journal
00223050 → ACNP
Volume
65
Issue
6
Year of publication
1998
Pages
890 - 898
Database
ISI
SICI code
0022-3050(199812)65:6<890:FRIND>2.0.ZU;2-T
Abstract
Objective-Previous studies have attributed accelerated forgetting rates on recognition memory tasks to temporal lobe pathology, but findings in some p atient groups may have been attributable to metabolic disruption. Findings in psychiatric disorders such as schizophrenia are conflicting. The purpose of the present study was to compare forgetting rates in patients with conf usional states (post-elecroconvulsive therapy (post-ECT), delirium), with t hose obtained in schizophrenic patients (with putative temporal lobe pathol ogy), non-ECT depressed patients, and healthy controls. The findings could also be compared with previous reports in patients with head injury, focal structural lesions, and Alzheimer's dementia. Methods-Two studies employed a picture recognition task to examine forgetti ng rates, the first between delays of 1 minute, 15 minutes, and 30 minutes, and the second between delays of 10 minutes, 2 hours, and 24 hours. Results-There were no significant differences in forgetting rates between 1 minute and 30 minutes, but the ECT group showed accelerated forgetting bet ween 10 minutes and 2 hours compared with healthy controls, associated with a rapid decline in "hit rate". This was not attributable to differential c hanges in either depression or severity of memory impairment. There were no differences in forgetting rates across the other subject groups. Conclusion-Post-ECT confusional state patients (similarly to "within posttr aumatic amnesia" patients with head injury) show accelerated forgetting on a recognition memory task and, in this, they contrast with patients who hav e focal structural lesions or widespread cortical atrophy. Accelerated forg etting may reflect the effect of disrupted cerebral metabolism on either "c onsolidation" or memory "binding" processes.