1995 issue 4


Volume 11, issue 4


Zastosowanie metody farmakoelektroencefalograffii (farmako-EEG) w monitorowaniu terapii depresji

Michał Skalski1, Waldemar Szelenherger1, Maria Radziwon-Zaleska1, Halina Matsumoto1
1. I Klinika Psychiatryczna Akademii Medycznej w Warszawie
Farmakoterapia w Psychiatrii i Neurologii, 1995, 4, 60-69


Drugs, which change human behavior, modify neurons' metabolism and bioelectric activity. This was the first notion that led to developing of pharmaco-eeg. Main objects of this method are: description of changes caused by various drugs, objective classification of psychotropic medications, foreseeing possible effect of new drugs on CNS and helping in therapy. Parietal and occipital leads are most frequently used in pharmaco-eeg studies.
Fifteen patients -10 female, 5 male (mean age 52 years, 27-78 years), all meeting DSM-III-R criteria of major depression were included into this study. For one week before the study patients did not receive any antidepressive drugs. EEG recordings were made seven times during the study: before medication, 3 and 24 hours after the first dose and after 2, 4, 6, 8 weeks of therapy. Bach patient was evaluated clinically according to the following scales: Hamilton Depression Rating Scale (HDRS), Hamilton Anxiety Rating Scale (HARS), Global Impression Scale (GIS) and authors' own Side Effects Scale (SE). Blood levels of TCA's and theirs metabolites were measured by means of FPIA method IDx Abott. In part of the patients hydroxylation phenotype was established before the study, using debrysoquine as a model drug. EEG was recorded from P3-01 and P4-02 for about ten minutes. Artifacts were eliminated visually. Relative Power spectra were obtained by Fast Fourier Transform (FFT) and were calculated for EEG bands. Final profiles were calculated as changes between relative power for each EEG rhythm in each recording in comparison with recording made prior to the study.
Following results were found: significant relationship between therapeutic blood level of TCA and antidepressive EEG profile (chi 2 = 15.8, p=0.00007); significant correlation between an increase in beta 2 power and therapeutic blood level of TCA (for P4-02: Pearson r = 0.43, p < 0.001; for P3-01: Pearson r = 0.38, p <0.001); significant correlation between beta 2 power and TCA's blood level (for P4-02: Pearson r = 0.33, p < 0.01; for P3-01: Pearson r = 0.42, p < 0.00l); antidepressive profile of EEG correlated significantly negatively with scores in clinical scales; scores in HDRS and GIS scales correlated negatively with power spectra in beta 2 band in P4-02 (HDRS Pearson r = 0.31, p < 0.0l; GIS r = 0.31, p < 0.01). There was no significant correlation between beta 2 power and HARS and SE scores. Analysis of individual cases revealed that 2 patients, which did not improve during treatment, despite therapeutic blood levels of TCA, did not show antidepressive profile of EEG.
Pharmaco-eeg is helpful in answering the question if the dose is relevant, and the drug is being well absorbed and metabolised and if it has any influence on the CNS. Results from patients are not as unequivocal as data from a healthy population. This may be due to more pronounced group heterogeneity, commonly occurring polypragmatic drug use and adaptation to pharmaceutic agents. Despite such restrains pharmaco-eeg is the most sensitive physiological method of evaluating course and efficacy of psychotropic medication. Our results let us hope that in the near future it may be a very helpful method in forecasting individual clinical outcome.