Lisanne E M Breuer1, Antoine Bernas2, Paul Boon2,3,4, René M H Besseling2, Evelien C B Carrette4, Anton de Louw, Albert P Aldenkamp1,2,4. 1. Academic Centre for Epilepsy Kempenhaeghe/MUMC+, Department of Behavioral Sciences, Heeze, the Netherlands. 2. University of Technology Eindhoven, Department of Electrical Engineering, Eindhoven, the Netherlands. 3. Ghent University Hospital, Laboratory for Clinical and Experimental Neurophysiology, Neurobiology and Neuropsychology, Ghent, Belgium. 4. Academic Centre for Epilepsy Kempenhaeghe/MUMC+, Department of Neurology, Heeze, the Netherlands.
Abstract
OBJECTIVE: Shed light on cognitive deterioration in Accelerated Cognitive Ageing (ACA) in epilepsy from a neuropsychological point of view in order to improve clinical diagnostics. METHODS: We compared the IQ-profile including GAI, OPIE IV-premorbid IQ and deterioration-scores of 21 epilepsy patients with ACA with 21 matched epilepsy patients without ACA (Epilepsy Controls) and 16 age- and education-matched Healthy Controls. Memory was also evaluated. RESULTS: Premorbid IQs were equal in all groups. Deterioration was apparent in the ACA-group in the WAIS-IV FSIQ and PRI, whereas no deterioration was found in the two control groups. PSI was impaired in both epilepsy groups, though with more impairment seen in the ACA-group. The VCI remained unimpaired. The FSIQ-GAI discrepancy was equal in both patient groups and significantly larger than in the Healthy Controls. WMS-IV memory indices were of average level in all groups. Memory impairment in ACA was not statistically different from the Epilepsy Controls. 85.7% of ACA-patients could be correctly classified through factors DET_FSIQ and PSI. CONCLUSIONS: Cognitive deterioration in ACA is characterized by an average drop of 19 IQ-points in FSIQ and PRI. Verbal abilities remain unimpaired. Impairments in fluid functions compromise cognitive abilities in epilepsy, but only partially contribute to cognitive deterioration in ACA. PSI proved to have some diagnostic value in differentiating epilepsy patients from healthy controls, but fails to differentiate between ACA and Epilepsy Controls. A comparison made between OPIE-IV equations and obtained IQs leads to a significant better detection of cognitive deterioration in epilepsy than the use of GAI-FSIQ discrepancies alone.
OBJECTIVE: Shed light on cognitive deterioration in Accelerated Cognitive Ageing (ACA) in epilepsy from a neuropsychological point of view in order to improve clinical diagnostics. METHODS: We compared the IQ-profile including GAI, OPIE IV-premorbid IQ and deterioration-scores of 21 epilepsypatients with ACA with 21 matched epilepsypatients without ACA (Epilepsy Controls) and 16 age- and education-matched Healthy Controls. Memory was also evaluated. RESULTS: Premorbid IQs were equal in all groups. Deterioration was apparent in the ACA-group in the WAIS-IV FSIQ and PRI, whereas no deterioration was found in the two control groups. PSI was impaired in both epilepsy groups, though with more impairment seen in the ACA-group. The VCI remained unimpaired. The FSIQ-GAI discrepancy was equal in both patient groups and significantly larger than in the Healthy Controls. WMS-IV memory indices were of average level in all groups. Memory impairment in ACA was not statistically different from the Epilepsy Controls. 85.7% of ACA-patients could be correctly classified through factors DET_FSIQ and PSI. CONCLUSIONS:Cognitive deterioration in ACA is characterized by an average drop of 19 IQ-points in FSIQ and PRI. Verbal abilities remain unimpaired. Impairments in fluid functions compromise cognitive abilities in epilepsy, but only partially contribute to cognitive deterioration in ACA. PSI proved to have some diagnostic value in differentiating epilepsypatients from healthy controls, but fails to differentiate between ACA and Epilepsy Controls. A comparison made between OPIE-IV equations and obtained IQs leads to a significant better detection of cognitive deterioration in epilepsy than the use of GAI-FSIQ discrepancies alone.