I recall Joel's statement so clearly andwondered about the many implications of that statement. At the time, I had completed my first of two years studying Neuropsychological Assessment and I understood there to be a class of impairments called ├ éČ┼"Disconnection Syndromes├ éČ Ł. Although there are many types and subtypes of aphasia, depending on where a problem occurs, Dr. Lubar was discussing one that involved Neurofeedback remediation in a pathway of fibers called the ├ éČ┼"arcuate fasciculus├ éČ Ł which links Broca's area to Wernicke's area.
Damage from a lesion or infarct to the arcuate fasciculus yields a disconnection syndrome called ├ éČ┼"conduction aphasia├ éČ Ł. It presents itself,
for example, as a patient knowing the meaning of a word but unable to
pronounce it correctly or the inability to articulate words they hear.
The pervasive belief at that time, which continues to the present time, was that this and other types of aphasia have no known cure.
Lubar's discovery began the evolution of protocol developments to
better document improved functioning utilizing Neurofeedback. He also
initiated the articulation of a theoretical foundation for
Neurofeedback applications in rehabilitation of disconnection
syndromes. Due to the dedication and cooperation of many individuals
who walk in the shoes of pioneers like Dr. Barry Sterman and Dr. Joel
Lubar,and Dr. Joe Kamiya studies with very little funding have continued to show efficacy through qEEG guided Neurofeedback therapy. Aided by the development of better diagnostic tools, more precise amplifiers, and continuing refinement of the qEEG, research is supporting powerful and exciting applications of Neurofeedback to treat disconnection-type disorders.
To date, preliminary studies consistently indicate improvement in functioning in diseases with known etiologies arising from disconnection syndromes. Furthermore, improvements are not limited to one type of etiology; rather they include disconnection syndromes resulting from inherited disorders (ex., Dyslexia and Auditory Processing Disorders), those induced by trauma (ex., Traumatic Brain Injury), and those disorders arising from developmental exposure to toxins or disease (ex., Autism, Stroke, or Multiple Sclerosis).
years of study of the human brain, we remain at the beginning of our
understanding of the intricate relationship between the areas of the
brain known as the grey and white matter. The fact that we still call
these by the color they appear to the human eye and that we call it
├ éČ┼"matter├ éČ Ł is indicative of the elementary level of our understanding.
Neuroscientists once accepted as fact that higher cortical functions were exclusively the domain of the brain's grey matter.
In the late 19th century as we better understood multiple sclerosis, this understanding was replaced by the belief that it was the white matter that mediated and determined the degree of competency in a wide range of brain functions. As we proceeded into the 20th century, the consensus was that the most pervasive disorders affecting cognitive performance and emotional stability were associated with disturbance in the heavily myelinated outer 3 mm of the brain called ├ éČ┼"white matter├ éČ Ł.
It was not until the 1980's when brain imaging such as MRI and, more recently, qEEG technology developed, that a more integrated and complex understanding emerged. Contemporary thinking is that the grey matter mediates and coordinates (├ éČ┼"gates├ éČ Ł) linkages of neuronal ensembles between regions of the brain's white matter as well as the deeper brain structures to produce in a kind of coordinated symphony of behavior. Today we understand that many impairments in human behavior, cognition, and emotion stem from electrical or blood flow disturbances and/or disconnection patterns (lesions) in the grey or white matter as well as deeper brain structures such as the basal ganglia, amygdala, thalamus, and even the brain stem and cerebellum.
One thing is clear, myelinated ├ éČ┼"white matter├ éČ Ł connects cortical and subcortical regions as well as lateral interhemispheric regions via distributed networks that gate electrical brain activity in a way that supports higher cortical function. Impairments in specific areas of the brain that are critical to a particular ability (expressive speech, decoding, social prosody) or a breakdown or sheering in the critical pathways connecting these areas will show up as a problem. Either of these can be a sources of impairment affecting the degree of competency (fluency in speech, proficiency in reading, ability to make friends).
One cannot write about the disconnection syndrome without giving proper credit to Norman Geschwind (1926-1984). A Harvard Medical School graduate, Professor of Neurology, and Director of Research at the Boston University Aphasia ResearchCenter, he is considered the father of contemporary behavioral neurology. His seminal work titled ├ éČ┼"Disconnexion syndromes in animals and man├ éČ Ł was published in the journal Brain in 1965. He explained how disconnection syndromes are involved in disorders such as aphasia, dyslexia, cerebral asymmetries and explored the control of seizures by severing neural pathways that facilitate kindling. His discoveries and those of his students influenced much of what we have come to accept as fact in terms of the importance of connectivity in the brain.
Perhaps of interest to the readers, Dr. Geschwind was a huge proponent of interdisciplinary research including speech and language experts, evolutionists, and cognitive and behavioral psychologists. Also, much of his work was accepted based on single case studies, an approach to research that today is dismissed by the academic establishment as having any scientific merit.
Dr. Geschwind defined the disconnection syndrome as higher function deficits that resulted from white matter lesions or lesions of the association cortices, the latter acting as relay stations between primary motor, sensory and limbic areas.Although challenged, his theories have substantially remained foundational to the understanding of neural impairments. Of course, some of his statements have been discovered to lack a level of sophistication gained through further research and the development of better tools. Yet, much of what he taught has been verified and expanded upon . He was truly a man who deserves credit for so clearly demonstrating and teaching a fundamental principle of the brain: disconnection yields dysfunction.
An important development since Geschwind's foundational work related to Neurofeedback was the discovery of disorders related to hyperconnectivity. Today we understand that lack of proper differentiation of a brain area or problems during the development of important intracranial pathways are both sources of impairment. Hyperconnectivity can be thought of as a kind of immaturity wherein areas meant to specialize and take on specific tasks and abilities do not. It is accepted by most experts in our field and related fields that hyperconnectivity can yield at least as serious of an impairment, if not greater, as disconnection syndromes. The commonly accepted nomenclature in our field is that we call disconnection syndromes ├ éČ┼"hypoconnectivity├ éČ Ł and areas that are undifferentiated or overly connected ├ éČ┼"hyperconnectivity├ éČ Ł.
The Neurofeedback tool utilized to remediate these problems and thereby normalize brain function is coherence or comodulation training. Unfortunately, nowhere in our field is our diversity more evident than in our lack of agreement as to a definition of coherence. We also lack agreement as to how it is best measured and its clinical significance. I view this as a temporary but confusing issue especially to people new to the field. As many of us have come to accept, our field is one that is evolving and we should remain confident that these issues, like others in the past, will be resolved.
I would never, nor do I recommend anyone, engage in coherence
Neurofeedback training without a qEEG to guide you. Also, once a qEEG
is done and indicates that hyper or hypo coherence problems exist, it
is important to know if the instrument you are utilizingwill train
coherence in the same way the qEEG measured it and found it to be
abnormal. This problem will hopefully be cleared up as experts in our
field agree on definitions and measurements of coherence and build
these into our equipment as defaults. I can not emphasize enough the
importance of being educated with respect to what it is you are doing
and to apply this technique with great caution. Coherence training is
many times more powerful than amplitude training and therapists must
exercise caution in its application.Although Z-Score training claims to manage many concerns especially that of over or under training, this assertion has yet to be scientifically demonstrated to my satisfaction.
It may be good to remember that any Z-Score training application can be no more reliable than the qEEG database upon which it is derived. At the present time, I do not believe there is a highly reliable qEEG database available to us. By standards typically used by Neuropsychologists to evaluate the validity and reliability of tests (called psychometrics), all the U.S.-based qEEG databases fall short in many areas.This is particularly true for children whose brains develop capacities quickly with differing competencies coming on-line for them within genetically programmed timeframes that differ from family to family. In keeping with what I stated earlier, many of these issues will likely disappear as the science of this application evolves, our databases become more robust, and our instruments train in accordance with the qEEG metric that indicated impairment.