THE COMBINED DEXAMETHASONE/CRH TEST AS A BIOLOGICAL MARKER FOR THE DISCRIMINATION OF PATIENTS WITH EPILEPSY AND PSYCHOGENIC SEIZURE DISORDERS
Abstract number :
G.02
Submission category :
Year :
2002
Submission ID :
1445
Source :
www.aesnet.org
Presentation date :
12/7/2002 12:00:00 AM
Published date :
Dec 1, 2002, 06:00 AM
Authors :
Jörg Wellmer, Till Perrey, Astrid W. Zobel, Christian E. Elger. Dept. of Epileptology, University of Bonn, Bonn, Germany; Dept. of Psychiatry, University of Bonn, Bonn, Germany
RATIONALE: Therapeutic strategies in epilepsies differ fundamentally from those in psychogenic disorders. However, differentiation between epileptic (ES) and psychogenic seizures (PS) often proves difficult. Semiological differences may be negligible, negative long-term EEG-recordings do not exclude the presence of epileptic events. Valid biological markers are lacking. Following the observation that chronic ES influence the function of the hypothalamic-pituitary-adrenocortical system, including the secretion of steroids, we investigated if the combined dexamethasone/CRH-test (Dex/CRH-test) is a sensitive marker for the discrimination of epileptic patients from those with exclusive PS.
METHODS: Between May 2001 and April 2002, 37 patients admitted to the Department of Epileptology for either surgical or conservative treatment of chronic epilepsy or differential diagnosis of seizures were included into the study. Patients were divided into two groups: Inclusion criterion for the ES group was the validation of habitual ES by ictal EEG (n=33). Patients with successful suggestive provocation of typical events and absent ictal and interictal epileptiform activity in long term EEG monitoring under AED withdrawal were attributed to the PS group (n=4). Following an established Dex/CRH-test protocol (Heuser et al., J Psychiatr Res 1994, 28(4):341-56), after a single oral dose of 1.5mg dexamethasone at 11 PM, between 3PM and 4.15PM the following day 5 blood samples were taken from the patients to measure the basal cortisol level as well as the response to i.v.-application of 100[mu]g CRH. Results were plotted against time. In the ES group, result analysis included statistical evaluation of the effect of time since last seizure, actual seizure frequency, and interictal discharge activity.
RESULTS: In the ES group, maximum cortisol levels (mcl) and area under the cortisol response curve (auc) were significantly higher than in the PS group (ES: mcl 19.8.[plusminus] 6.2[mu]g/dl, auc 1117 [plusminus] 365; PS: mcl 5.2 [plusminus] 2.3[mu]g/dl, auc 289 [plusminus] 113, unpaired t-test: p[lt]0.001). Cut off values of 8[mu]g/dl for mcl and 450 for auc allowed good discrimination (diagnostic accuaracy: 97.3% [95%-C.I.: 92.1-102.5%, chi2: p[lt]0.001], each). No significant influence of the other clinical parameters on the cortisol response was found.
CONCLUSIONS: The combined Dex/CRH-test is a promising tool for the discrimination of patients with chronic epilepsy from those experiencing only psychogenic seizures. In the present sample, we did not find any influence of the seizure-to-test latency or the actual seizure frequency on the cortisol response. This, as shown for other steroids in chronic epilepsy, can be due to a loss of reactivity of the endocrine feedback regulation as an effect of chronic epileptic discharges. Further examinations will be necessary to show, if the test also allows discrimination between patients with newly manifested ES or oligoepilepsies and those having exclusively PS.
[Supported by: The work was funded exclusively by internal grants of the Dept. of Psychiatry, University of Bonn.]; (Disclosure: Salary - University of Bonn, Dept of Epileptology)