be simulated with a suitably constructed random process and all of our random

be simulated with a suitably constructed random process and all of our random number generators are deterministic. This theoretical blind alley is reminiscent of the decades lost partialing out causal attributes of nature versus nurture before knowledge of dynamical influences on nucleotide dynamics was available. It is perhaps unfortunate that for finite length real data, “house keeping requirements” (Ruelle, 1990; Rapp, 1993;1994) and “warnings on the label” with various random sequence, random phase controls (“surrogate data”) have become so intimidating to those of us in the early stages of exploring the use of these theories and methods in the brain sciences. Currently the “controls” are more relevant to abstract statistical processes and what can be said about them rather than generating and addressing new claims and the controls for them related to quantitatively oriented, experimental brain physiology. Statistical caveats have arisen to retard the emergence of potentially important and robust neurophysiologically-relevant phenomena. For example, a recent well conducted and analyzed study of the influence of low doses of ethanol in 32 normal male subjects, which honored almost all of the current analytic rituals including sequence and phase randomized surrogate data and searches for the continuity features of deterministic dynamical systems such as time asymmetry, concluded that the drug “reduced the evidence for nonlinear dynamical structure” in the brain (Ehlers et al, 1998). Though honoring the currently popular statistical rituals, what appears to be missing here are suggestions for new neurobiological or mathematical intuitions that will lead to the design of the next experiment. We now see that it is now possible to use these new ideas and methods to ask and at least partially answer more specific questions relevant to the clinically oriented neurosciences such as: whether increases in lithium-induced expansiveness and mixing in the dynamics of brain enzymes, neurons and behavior help explicate a mechanism of de-coherence in bipolar disease (Mandell et al, 1985); do these approaches to membrane conductance fluctuations suggest a new way to think about ion channel dynamics (Liebovitch, 1990); can alcohol-induced changes in statistical dynamics of the EEG predict genetic predilection in males to 249 HOUSE_OVERSIGHT_013749