The brain is a hyperconnected system. It contains on the order of 10 billion neurons, each of which can have hundreds or thousands of connections to other neurons. The brain depends on dynamically managing trillions of connections, to regulate the interactions between all of its parts (Calvin 1995, Sejnowski 2004) How are all of these connections managed toward useful ends? The key lies in the ability of the network to selectively enable or disable connections, based upon a simple model of excitation and inhibition.
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Connectivity refers to the mechanism by which parts of a system work together, via communication and control. Connectivity results when information is shared between parts, and used in a coherent manner to produce sensation, perception, decision-making, and behavior.
One of the most important functions in the brain is that of inhibition This is true on the microscopic level, and also on the macroscopic level. Early sensory experiences have profound effects on the fine structural and functional organization of the brain. . (e.g. Jiao 2006). A great deal of this adaptation takes the form of creating and shaping connections between neuronal assemblies, mediated by the dynamic balance of excitatory and inhibitory connections in the network. In the words of Sir Charles Sherrington (1933), The dictum that life's aim is an act not a thought must be modified to admit that, often, to refrain from an act is no less an act than to commit one, because inhibition is coequally with excitation a nervous activity.
When we examine the synaptic inputs a typical pyramidal cells in the cortex or even in the thalamus, we see that in excess of 90% of the inputs to a particular cell may be inhibitory. Only a small fraction are typically excitatory, inasmuch as most neurons are inherently excitable by virtue of their membrane properties, and need to be "sedated," more than they need to be even more excited.
A great deal of inhibition is in the form of collateral inhibition. This takes place when collateral fibers in a pathway inhibit each other whenever information is being sent. As a result of this inhibition, neuronal bundles and tracts are able to transmit information with sharpness, fidelity, and high resolution. As an example of the power of this fidelity, consider that the auditory nerve can respond with action potentials to a deflection in the basilar membrane of no more than 1 Angstrom, which is the diameter of a hydrogen atom. This reveals unimaginable acuity in the physiological and neuronal mechanisms at work. Similarly, the eye is capable of seeing a candle light at 12 miles, which corresponds to a stimulus rate of one photon per second. If neuronal signals were allowed to mix and scramble, such acuity and precision would not be possible. Without inhibition at a cellular level, brain activity would degenerate into pure chaos including seizure activity, devoid of purposeful control or meaning.
At the larger systems level, inhibition is an important component to brain function. Jeffrey Carmen has observed that the reaction of a chicken to having its head removed is to flap its wings, run about, and attempt to squawk, before finally expiring. The function of the chicken's brain is more to inhibit automatic mechanisms than to instigate specific behaviors. I the same way, Carmen refers to the frontal lobes of the human brain as the "chicken's brain" of the entire brain. That is, the frontal lobes spend the majority of their activity inhibiting activities, including behaviors, that the rest of the brain is all too ready to undertake. This explains why dysfunction of the frontal lobes often results in disorders characterized by a lack of inhibition of thoughts or behaviors that are detrimental to the individual.
When EEG training is performed at the level of brain connectivity and communication, it becomes possible to address directly the relative excitation and inhibition, but particularly the inhibition, of neuronal pathways and conjoint functioning. Thus, whereas conventional EEG amplitude training addresses synchrony at a local level, connectivity training addresses synchrony at a global level, and in a manner specifically targeted at neuronal assemblies and their interaction.
When we examine the thalamocortical relay circuits and their role in generating EEG brain rhythms, it is evident that measurable brain signals are produced when existing circuits are disinhibited (relaxed), allowing the cortical cells to participate in a volley of activity. There are inhibitory connections at both the thalamic and at the cortical levels, that hold these rhythmic circuits at bay, so that the brain can process information, perform corticocortical interactions, and generally be involved with higher-frequency, beta-like activity.
In other words, relaxation at the level of individual neurons and neuronal connections, is one primary mechanism that is addressed when the brain is challenged to modify its EEG activity through training. Whereas amplitude training addresses neuronal synchrony at the local level, connectivity training addresses neuronal synchrony at a nonlocal level. And one mechanism that the brain uses to alter nonlocal synchrony is to dynamically reconfigure connections, and this is accomplished largely by modulating inhibitory influences on participating cortical pathways.
This can all be related back to the core issues of stress, relaxation, flexibility, and appropriateness of brain state. A considerable degree of ills can be ascribed to disregulation in the central nervous system, predominantly the form of disturbances of normal rhythms and patterns of excitation (concentration) and relaxation. In the same way that a chronic stone in a shoe can cause one to throw a hip out of joint, chronic misadjustments in neuronal circuits can lead to long-term patterns of dysfunction with myriads of clinical manifestations.
Healthy brain function depends upon the continual operation and maintenance of dozens of major pathways that connect functional areas together to accomplish complex tasks. Researchers at Brown University, for example, have shown that Alzheimer's patients exhibit an inability to bind information from dorsal and ventral visual streams, as revealed in a global motion coherence task. This neocortical disconnectivity is manifest in deficits in sensory integration and attention.
Through EEG connectivity training, we address these types of issues in a form that appeals to relaxation, normalization, and restoration of normal levels of communication and control. If, for example, we use 4 brain sites, for example F3, F4, P3, and P4, we are able to train amplitudes at 4 locations, but also to train connections along all 6 paths. This provides a level of information that is not accessible with methods based solely on amplitudes, or on simple coherence or synchrony targets. The monitoring and feedback of complex information relating to brain connectivity is made tractable by methods such as live Z-score feedback. This makes it possible to address the complex interplay of brain activity with an eye toward appropriateness of brain connectivity, in addition to working with the basic elements of local excitation and relaxation.
Through a cohesive approach to path-specific relaxation training, we open the door to teaching the brain complex interactions that are much more akin to real-world tasks. To use a physical analogy, we can move from simply lifting weights to doing the mental equivalents of walking, riding a bicycle, or even doing yoga. This will allow us to work more directly with neural coherence and assess its importance whenever learning, memory, attention, language, or other complex mechanisms are disregulated.
Sherrington, Sir Charles (1933), Brain and its Mechanisms; Cambridge University Press. Calvin, W.H. (1995), "Cortical Columns, modules, and Hebbian cell assemblies", Handbook of Brain Theory and Neural Networks, M.A. Arbib (ed), MIT Press Sejnowski, T. (2004) "Communication in Brain Systems," Cold Spring Harbor Laboratory report, May, 2004. Festa, E.K., Insler, R.Z., Salmon, D.P., Paxton, J., Hamilton, J.M., & Heindel, W.C. (2005) Neocortical disconnectivity disrupts sensory integration in Alzheimer's disease, Neuropsychology, 19(6), 728-738. Y. Jiao (2006) "Major effects of sensory experiences on the neocortical inhibitory circuits, Journal of Neuroscience, August 2006."
