The first important argument is that EEG is a direct measure of neuronal activity, whereas the blood oxygenation-dependent (BOLD) signal is not. Modeling the relationship between BOLD signal and neural activity hinges on a number of assumptions, the validity of which may be unclear in particular cases. The exact nature of neural activity reflected by BOLD signal is also poorly understood. Although it has been established that the BOLD signal is associated with gradual postsynaptic potentials, rather than action potentials of the neurons, the relative contribution of inhibitory (IPSP) and excitatory (EPSP) postsynaptic potentials to the BOLD signal remains to be determined. An increase in the BOLD signal is commonly interpreted as “activation”, however, if IPSPs make a substantial contribution to the increase in BOLD signal, the validity of this straightforward interpretation may be challenged. Furthermore, it cannot be excluded apriori that functionally meaningful changes in neuronal activity may occur without significant changes in local metabolism, for example when some neurons reduce while others increase their activity within the same region, or when synchronization of activity changes without the change
