Forgetting rates in neuropsychiatric disorders
- Neuropsychiatry and Memory Disorders Clinic, Division of Psychiatry and Psychology, United Medical and Dental Schools of Guy’s and St Thomas’s Hospital, St Thomas’s Campus, London, UK
- Dr M D Kopelman, Academic Unit of Psychiatry, United Medical and Dental Schools of Guy’s and St Thomas’s Hospital, St Thomas’s Campus, Lambeth Palace Road, London SE1 7EH, UK.
- Received 6 October 1997
- Revised 28 May 1998
- Accepted 15 June 1998
Abstract
OBJECTIVE Previous studies have attributed accelerated forgetting rates on recognition memory tasks to temporal lobe pathology, but findings in some patient 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 confusional states (post-elecroconvulsive therapy (post-ECT), delirium), with those obtained in schizophrenic patients (with putative temporal lobe pathology), 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 forgetting 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 between 10 minutes and 2 hours compared with healthy controls, associated with a rapid decline in “hit rate”. This was not attributable to differential changes 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 post-traumatic amnesia” patients with head injury) show accelerated forgetting on a recognition memory task and, in this, they contrast with patients who have focal structural lesions or widespread cortical atrophy. Accelerated forgetting may reflect the effect of disrupted cerebral metabolism on either “consolidation” or memory “binding” processes.
