Editor's Note: Part 1 of this series ran in the March 25 issue.
I have received numerous e-mails and calls regarding my previous article "Pain in the Brain," where the concepts of a low-firing and high-firing brain in relation to pain perception were discussed. My replies were stunted, at best, because the neurological processes related to these concepts, specifically transneural degeneration and hemisphericity, are in themselves theories that might each consume a full 15 hours of a neurology seminar to flesh out and make sense of. Regardless, due to the interest and confusion these ideas have inspired, I will try to explain some aspects of each and hope that at least a working knowledge of both concepts can be applied to your patient population immediately.
When a brain is too "high firing," and thus pain perception (and all sensations, for that matter) may be increased, there is the possibility we are dealing with cortical transneural degeneration (TND). I say "possibility" because other conditions might produce this same state of hypersensitivity: infection, pH disorders, toxicities and compression from tumors or other sources, among other things, may all mimic TND. Conversely, TND may very well mimic all these other diagnoses, which means we must properly differentially diagnose for the sake of the patient. A neuron, when sickened or injured, actually will fire faster and easier. The reasons for this are many, but the bottom line is there will be the tendency to have a breakdown of the Na+/K+ pumps when the energetic systems of the cell are compromised, and the internal state of the cell will go from a negative state to a more positive state.
As the cell polarization changes to a more positive state, the neuron will fire from lesser stimuli than a normally healthy cell. Based on this phenomenon, we can understand how cells that should not normally be firing (such as an olfactory neuron in the temporal lobe or a visual neuron in the occipital lobe during the prodrome stage of a migraine attack) will produce a real central event in the absence of outside receptor stimulation. Cells undergoing TND will be at a higher central integrative state; they will be more apt to fire and thus more likely to produce a central realization of sensation or motor function. The implications of this are understandably profound. Spasm, pain, hearing, visual disturbance, vertigo - all these conditions can be explained and addressed when we are treating a TND brain.
Due to the fact a TND cortex is firing higher, the worst thing we can do to these patients is to overly stimulate those neurons. A TND cell that has failed in its Na+/K+ pump system and is thus more sensitive will not have the capacity to reset to a stable state following stimulus, and thus the cell actually might undergo calcium ion free-radical oxidation and cell death. Overstimulate a muscle cell and it breaks down and comes back stronger. Overstimulate a TND neuron and we have the great possibility of injuring that cell. This, of course, means it is imperative we know what we are dealing with when we assess a patient.
Perhaps a patient's pain is due to a localized injury and the normal physiological process of reflexogenic cord responses or just maybe that nonresponsive patient is due to a TND brain and the more we treat, the worse they seem to get. These patients must be treated within the limits of their physiology. Some of these patients can only tolerate acupuncture, initially. Some of these patients can only tolerate low-force adjustments to begin with. Some, even though their pain might be headaches, can only tolerate lower extremity stimuli or adjusting. The trick is doing something to improve that sensitive neuronal state, but not so much that we perpetuate the degradation of the cells.
Clinical skills and evaluation become imperative at this point. Skin color, pupil dilation, pulse rates and respiration all become paramount in your clinical assessment. In my practice, I use kinesiology to assess when a treatment will be positive or overly stimulatory for a patient, always assessing every other parameter. The point is to bring the system to a level of stability such that the patient not only improves, but also can then tolerate stronger and more aggressive stimuli, such as full-spine adjusting. As in many things in life, sometimes "less is more," initially. Clinically, a TND neuron, due to its immediate physiology, will fire faster, but also will fatigue faster.
Thus, a patient who has very fast pupil constriction, but whose pupil then immediately dilates even with continued stimulus would be highly suspect for TND. The vertigo patient that has a severe spinning to one side, and then finds they begin to spin in the opposite direction, also would be highly suspect for TND. That pain patient that feels more pain and spasm following a very good adjustment might be undergoing TND, and may just not be capable of tolerating even the best of adjustments. I know for most of you, this gives very little in the way of actual clinical value and actually might confuse the heck out of the majority of you, but remember we, as neurology diplomates, spend many hours going over these concepts in the courses. At the very least, this might start some of you on the road to questioning your approach to patients whose conditions seem hopelessly resistant to treatment.
Hemisphericity is the term we use to describe those neurons that are the exact opposite physiologically. They are further from their normal central integrative state and thus not firing as they should. This can have many implications and many etiologies. The most likely cause we have found is simply a lack of excitatory impulses into the neuron, leading to a sluggish response when the excitation finally occurs. The most common scenario is an area of the neurological system with great central ramifications being shut down and/or inhibited. This can happen with the loss of a limb, and the related interesting phenomenon of "phantom pain." With the loss of a major source of afferentation, the brain will suffer a chain of reactions such that a whole series of neurons will not be firing up to their potential, and thus a plethora of clinical presentations can surface from sensory issues to motor issues to visceral issues.
Using an example I give to my patients - for all intents and purposes, there is no practical difference between a light bulb that is broken and a light bulb that is off. There is, in the end, no light. Functionally, there is no practical difference between a neuron that is dead and a neuron that is asleep: in the end, we have no function. How do we perform a differential diagnosis? Stimulate the nerve. If you see a clinical response where previously there was none, the greater likelihood is we were dealing with a hemispheric brain and thus a brain that needed stimuli. Another common reason we may see this lack of afferentation is, of course, because of subluxations. The greater the properly coupled relationship of the spinal joints, the greater the amount of central afferent barrage that enters the cortex, and thus the greater likelihood central responses will occur.
When we do have a subluxation, we are neurophysiologically decreasing afferent input and thus, having substantial central ramifications. The higher in the neuraxis we go, the greater the afferent barrage, so, centrally at least, a cervical adjustment is going to have greater neurological consequences than a lumbar adjustment. For this reason, as well as many others, we better make darn sure the brain is ready to submit to a cervical adjustment when we give it. On the other hand, when we do have a hemisphericity that is causing central changes, sometimes only a properly delivered cervical adjustment to the proper side will have the desired affect.
Every one of us knows a good adjustment can do miracles for chronic pain patients, and sometimes in ways neurology and anatomy just cannot explain: "Well, Mr. Jones, we truly do not understand how your foot pain improved from a neck adjustment, but the innate intelligence of the body knows what to do with the healing forces we have released." I'm being facetious here, of course, but you get the idea. In neurology, everything has an explanation, and knowledge is power. Perhaps what was truly addressed were central affects related to hemisphericity, of which an understanding of clinical signs and symptoms would minimize the guesswork (and thus maximize the successes) in our treatments.
Hemisphericity is defined as neurons that are not firing at their appropriate rate and strength. Thus, symptoms will be related to nonfiring systems: sluggish reflexes, muscle weakness patterns, sensory imbalances, even emotional issues and of course, chronic pain can all be related to a hemispheric cortex. Treatment is directed to the opposite side, such that a hemispheric right-cortex patient would only be adjusted on the left side and vice versa. Based on the area of the dysfunction, sound and light therapies become important, as well as certain exercises that may be needed to stimulate the brain on a more consistent basis.
I have only briefly covered some of these neurology concepts, and in so doing have probably raised more questions than I have answered. That would not necessarily be a bad thing if it motivates us to learn more and apply our considerable skills at a higher level.
