Respiratory Assist: New Concepts on Old Observations

Back in the early 70’s, as a student leaning this new technique, at the time, called Goodheart technique, I was awed by the knowledge and skill of a certain Dr. Goodheart. (Looking back, I know now that it was not only his command of the human body that impressed me, but it was his passion with which he delivered his skills). I was frantic to know where to start when I find a weak muscle. His answer would always be, without fail, “have them take a deep breath”. As all of you who practice AK technique know, inspiration or expiration facilitating a weak muscle has certain implications. These implications at first were thought to be a feature of cranial bone movement and the flow of cerebral spinal fluid. Later the respiratory implications were extended to include the treatment of, and the detection of “hidden” neurolymphatic’s, acupuncture points, ICV, and the list goes on and on. In other words, having the patient breath in or out changes muscle strength and treatment options in a variety of clinical situations.

So, precisely what happens in the central nervous system when a patient breathes? All of the central integration, including all the pathways, both the afferent and the efferent, can be considered to clarify why we observer these changes in such a wide range of circumstances. Many things happen centrally, in addition to crainal bone movement and CSF flow.  Refining our understanding of neurophysiology and using it to explain our exceptional results is advantageous for many reasons.

So what happens centrally in the neuraxis, when you breathe?

I won’t bore you with all the details, but it does make for an excellent review, and I highly recommend it. I will highlight a couple of clinical applications, and hopefully provide you with food for thought for additional discoveries and research, ultimately leading to better service of our patients.

Let’s start with inspiration. The act of telling a person to take a deep breath as we do daily in our AK practices engages cortical centers in the brain. The patient volitionally inhales with a cortical awareness. This voluntary inspiration uses different sets of neuronal circuitry then the circuits that allow us to breath while we sleep or throughout the day without thinking about it.  For our AK purpose let us take the volitional route through the brain because that is the one we use when we ask the patient to breath in. (Actually we do test muscles in all phases of the respiratory cycle, including breath holding. This not only has value as a diagnostic and therapeutic tool, but also has potential to cause a flaw in reproducibility. The fact that the patient may be in different phases of breathing when we test muscles has a probability of changing our observations regarding strong or weak muscles from observer to observer. The afferent information to the brain, the central integration, and hence the output from the brain is entirely different in different phases of respiration). When you ask the patient to breath-in many things have to happen, all of which should be considered when testing muscles. First of all, the patient has to be motivated to do what you ask. One could devote a lifetime of study to the understanding of what motivates human behavior, and is beyond the scope of this article. Suffice it to say that it is complex, involving the neocortex the limbic system, the basal ganglia, the cerebellum, brain stem and the spinal cord. The point being, that an altered central integrated state in any one of these areas can change muscle-testing results.  For example asking an autistic child or an adult with Alzheimer’s to breath-in will yield different motivational states than the average patient.  The central integration of any one of the above structures may be aberrant and varied even from “normal patient” to “normal patient”.  For instance, there may be a lesion in the right hemisphere in one patient, the basal ganglia in another or cerebellum in still another. The list of possible functional lesions sites is daunting. These central changes will cause the output to the motor neurons of the diaphragm and the intercostals to be at very different resting states from patient to patient.  If there are such fundamental differences in the underlying neurophysiology of patients, then when we test muscles, we are essentially asking different questions of the nervous system. It is merely the words “take a deep breathe” that are the same, but the actual question we are asking of the neurophysiological system is completely different.   This is good to know because it helps us understand and explain why respiration is linked to so many AK findings. It also helps us realize how difficult it is to devise a research model using AK techniques. Let us assume that for our purposes here that the motivational states are “normal”.

Let us begin with inspiration from the medulla. The neurons of the caudal solitary nucleus (NTS) in the dorsal respiratory group (DRG) are mainly responsible for inspiration. This same part of the caudal NTS receives sensory input from mechanoreceptors and chemoreceptors for control or respiration. From there the signal travels to the C3-C5 ventral horn cells of the phrenic nerve and ventral horn cells in the thoracic cord to fire the intercostal muscles.

(So you can appreciate the above statement regarding the fundamental differences in the underlying neurophysiology, let’s take just one system and briefly review.  Recall just some of the inputs to the NTS. In the rostral end, taste from VII, IX, and X. In the caudal end chemoreceptors, baroreceptors, respiratory reflexes, reflexes to the heart, reflexes regulating motility and secretions throughout the gut. The outputs of the NTS are to the amygdala, hypothalamus, and the visceral motor and respiratory centers. The point being; the NTS is a wondrous and busy place. Do you see how respiration could be linked to so many AK techniques? Basically we are functionally testing a component of the NTS. Have you ever tried having a patient inhale or exhale while tasting a nutrient? Try it, and let me know what you find. When you consider the enormity of integration at the NTS, it’s a wonder that it all works.   I suspect that the NTS is at a very different central integrated state in most of our patients, based on the fact that so many of our patients have symptoms that involve the NTS.   Thus, skewing results including the tasting of nutrients, from examiner to examiner and making it almost impossible to proceed with research when the fundamental question is flawed.

Sleep apnea in most cases is a lesion of the NTS the DRG or the VRG.

Patients with this condition experience considerable discomfort; first and foremost with the condition of sleep deprivation and all of its ramifications. Secondly, with the arcane treatment.

It is a tremendous service to your fellow man to fix cause of the problem in the brainstem and allow the patient to receive all of the exponential benefits.

There are four neurons that make up the Ventral Respiratory Group (VRG), the rostral nucleus retrofacialis, caudal nucleus retroambiguus, nucleus para-ambiguus, and the pre-Botzinger complex.  The VRG is responsible for mainly expiration, but also shows some activity during inspiration.

The pneumotaxic center in the pons or the pontine respiratory group (PRG) inhibit the ventral horn cells of the phrenic nerve to limit inspiration, to prevent damage from over inflation.

The apneustic center excites the Dorsal Respiratory Group (DRG), to assist in inspiration, but it is antagonized by the PRG.

The DRG is responsible for inspiration and is hard-wired to the posterior semicircular canals.  The posterior semicircular canals are hard wired to the depressor muscles of the eyes. To say it another way the DRG, inspiration and depressor eye muscles (the inferior rectus and the superior oblique) are hard-wired together.  The VRG that is responsible for expiration is hardwired to the anterior semicircular canals. The anterior semicircular canals are hard-wired to the elevator eye muscles (the superior rectus and the inferior oblique). To say it another way, the VRG, expiration and elevator eye muscles are hard-wired together. (Dr. Goodheart said many times that if A=B, and B=C than C=A) by this logic, one could extrapolate that depressing the eyes is similar to inspiration, and elevating the eyes is similar to expiration. The big difference is that moving the eyes should have no effect on respiratory crainal bone, or CSF movement.

Try this the next time you have a patient that strengthens on inspiration. Have the patient activate the depressor eye muscles by looking toward their toes in a supine position. Make sure they are in a neutral phase of respiration, or have them cease respiration altogether. If the patient strengthens with depressor eye movements, I suggest that their lesion may be in the NTS, the apneustic center, the pons (PRG), or the DRG neurons and not in crainal bone or CSF movement (possibly the reason why inspiration assist strengthens more times than expiration assist) You have effectually ruled out crainal bone movement with this challenge. The fact that the patient hasn’t breathed by definition rules out crainal/CSF movement.

If the patient strengthens on expiration have them activate the elevator muscles by looking up toward their forehead. If this strengthens a muscle by having them look up in a neutral phase of respiration, then I suggest that the lesion is in the VRG, the anterior semicircular canals, or the muscles that elevate the eyes.

These new ways to think about diagnosis will help us differentiate and isolate lesion sites and enable us to better develop treatment options for patients. It also explains why respiration is involved in so many AK findings. It also allows us to develop better research protocols, based on isolated functional lesions in the patient’s neuraxis.