Electroencephalography. Fig. 8. Pharmaco-EEG profile of scopolamine: inferential non-parametric testing (N =12) of differences has been carried out on an electrode-by-electrode basis with decreases in several bands at frequencies >8 Hz, and increases in delta, compared to placebo. Note that overall, a slowing in EEG can be deduced; the biomarker can be used to test reversal by (new) antidementia drugs and hence a single Phase I trial in a co-administration design, known as scopolamine model, predicts efficacy at an early stage.

EEG as Biomarker in Clinical Studies

In addition to being a diagnostic tool, EEG may be useful in assessing the effectiveness of particular therapies. EEG modifications in the diseased state are likely to reflect deficits in one or several neurotransmitter systems and conversely, pharmacotherapy should ideally normalize such deficits. For example,

Acetylcholinesterase inhibitors as cognitive enhancers have been shown to reverse EEG abnormalities in patients with Alzheimer's disease, even after short-term treatment (rivastigmine; Brassen and Adler 2003). Similarly, EEG can be useful to assess directly and objectively the effectiveness of new hypnotics in sleep disorders and of anticonvulsants for epilepsy in patients. EEG

Electroencephalography. Table 1. Summary of EEG profiles for members of various classes of psychotropic drugs, separated in (a) increases in EEG variables, and (b) decreases in EEG variables compared to placebo (consensus from Mucci A, Volpe U, Merlotti E, Bucci P, Galderisi S (2006) Clin EEG Neurosci 37:81-98; Saletu B, Anderer P, Saletu-Zyhlarz, Arnold O, Pascual-Marqui RD (2002) Methods Find Exp Clin Pharmacol 24(suppl C):97-120 for the new generations of drugs like clozapine and citalopram, respectively, in the first two lines in (a) and (b), third and fourth line according to Boeijinga PH, Calvi-Gries F, Demazieeres A, Luthringer R (2002) Planning of pharmacodynamic trials: specificities and possible solutions and interpretation of drug effects on EEG. Methods Find Exp Clin Pharmacol 24(suppl C):17-26).

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