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.

Extraocular Muscle Imbalance: A Cause of Crainal Faults?

Persistent and/or recurrent crainal faults can be a riddle in any AK practice. It is straightforward to recognize crainal faults that have origins in trauma. The less recognizable causes are more difficult to pinpoint. We all want to assign the correct answer to our patients’ question, “why does this keep going out? As AK doc’s we pride ourselves in treating the underlying cause of dysfunction and dis-ease. We don’t want to treat the same thing over and over. Dr Goodheart said if you have to do the same thing over and over you have to be missing something.

Muscle imbalance causing changes in bony alignment is a hallmark concept in AK. I have heard Dr. Goodheart state on many occasions: bones don’t move muscles, muscles move bones.

Eye movements and eye positions have been a considerable and constructive part of AK technique. Many of our ingenious members, as well as many others have discovered the value and clinical efficacy of various eye positions on clinical outcomes, for example, eyes into and out of distortion, Eye Movement Desensitization Reprocessing (EMDR), NET, etc.

Functional neurology has an explanation for these recurring crainal faults inclusive of the previous observations, but developing an enhanced model based on a neurological principle. This model, based in neurophysiology is an excellent bridge to patient and intra-professional understanding of what we do, and how it really works.

The four recti muscles arise from the annulus of Zinn, (which in turn is attached to the inferior root of the lesser wing of the sphenoid), and inserts into the sclera. The superior oblique also arises from the sphenoid and inserts into the sclera. The inferior oblique arises from the maxilla and inserts into the sclera. The sclera is continuous with the cornea, which is continuous with the dura. Since muscles move bones, any imbalance in extraocular muscles will cause dural tension and crainal faults. The possibility also exists that extraocular muscle imbalance and the consequences in the dural system, could transfer tension anywhere in the meningeal system.

Think of the pupil like a joint, and as with all joints, the direction of the movement of the pupil is determined by the line of pull of the extraocular muscles. {The superior and medial recti are more closely attached to the dura of the optic nerve, most likely causing the pain with eye movements in optic neuritis.

The position of the pupil is determined by the ambient tone of agonist /antagonist muscles. In other words, when the patient is looking straight ahead (in the primary position) there should be no deviation in ocular alignment. When the patient is examined in the cardinal fields of gaze there should also be no weakness or deviation.  The patient should be evaluated for fatigability in all positions of gaze. Fatigability can be measured by having the patient repeatedly look horizontally from right to left and from left to right, carefully observe for slight torsion, elevation or depression of the eye.

Recall that the extraocular muscles have a primary, secondary, and tertiary movement. In the case of horizontal movements, you are testing the primary movements of medial and lateral rectus only. If the medial or lateral rectus fails and a secondary muscle takes over, its action will cause the eye to tort, elevate or depress. (If the secondary muscle has to take over, you have a weakness in either the medial or lateral rectus.) Simple recruitment like we see in any muscle dysfunction. Here is where it gets a bit more interesting; the medial rectus is crainal nerve III and is driven from the mesencephalon. The lateral rectus is crainal nerve VI and driven from the pons. The horizontal eye movements are also hard wired to the horizontal canals and indirectly to the cerebellum. The right cerebellum drives the eyes to the left and the left cerebellum drives the eyes to right.  Now, superimpose all the other extraocular muscles with their central connections and you have a magnificent window to the brain. For example, if a patient is activating the left cerebellum by looking from left to right, and you observe elevation of the adducted eye. You know that the left cerebellum is hard wired to the left superior oblique that should cause depression of the adducted eye when activated. If the eye elevates, ever so slightly after a few passes you now have an excellent window into the fatigability of the left cerebellum.

(Below is an example of left head turning activating the left horizontal canal the left medial rectus and the right lateral rectus driving the eyes to the right. This is also linked to, and activates the left cerebellum that would also excite the superior oblique and superior rectus on the ipsilateral or the left side.)

Another way to observe for fatigue is have the patient converge. Usually after 4 or 5 times you will observe the eyes converge and then one will break loose and deviate laterally. You will need practice to observe this, for it is subtle. The patient should be examined without the ability to fixate their gaze, as with an infrared camera or frenzel goggles. Because, when the patient fixates she overrides the background muscle tone and substitutes with neocortical activation.  To view this without high-tech equipment, the cover and uncover test, or an ophthalmoscope with an occluder is a excellent bedside test to bring out ocular distortions. This type of exam will very nearly always yield some type of aberrancy in extraocular muscle function, such as a tropia, a phoria, or a skew deviation, especially when challenged to fatigue. Also, head tilts and rotations are compensatory to eye muscle imbalance. Eye position can also be a compensation for head posture, the point being, eye position and head posture are intimate and can never be separated without great discomfort to the patient.

Now when you contemplate the central integration of the cerebellum, the labyrinth, the brain stem, and the neocortex and all the possible inter-relationships to eye muscle function it becomes clear why so many clinicians have stumbled on this concept of eye positions causing changes in muscle strength. It also explains why the results vary from doctor to doctor and patient to patient. Patients with the same symptoms may have completely different parts of the brain involved.  For example, a patient with a right cerebellar lesion will have a different outcome then a patient with a left cerebellar lesion when asked to move her eyes to the left. For instance a patient with a teres minor weakness on right causing a rotator cuff  dysfunction will have a greater probability of getting stronger while looking to the left because looking left activates the right cerebellum and the right cerebellum excites the all the extensor muscles on the ispilateral or right side in this case. Unless, that same patient has a left cerebellar lesion causing a right cortical diaschisis producing too much flexor tone on the right thereby inhibiting the extensors or the right teres in this case. Same diagnosis, but different eye positions will cause different results. This is a very simple and clear-cut neurological model, that is reproducible and predictable. Therefore it is necessary to test eye muscles by observation, otherwise you miss an important piece of the puzzle that could lead you to mediocre results.

Due to the origin and the insertion of the extraocular muscles and their relationship with the dura it is easy to see how aberrancy in function would influence crainal bone function. It should also be obvious that there is a very high probability of imbalance of the eye muscles. If we accept the premise that muscles move bones than we must become experts at evaluating eye muscles. As AK doc’s we are better than anyone else at manual muscle testing. In fact, we can observe subtleties of muscle function in patients that elude other physicians. Although we cannot manually test the extraocular muscles, we can become better at observation. The correction of altered eye muscle function once mastered, gives added benefit to your clinical skills. It corrects altered head posture and persistent crainal faults. It also gives one a clinical advantage it treating brain dysfunction with all the concomitants. Extraocular muscle imbalance is a window to brain and in most cases will lead you to the primary lesion.

Supersegmental Control of Spinal Cord Reflexes: When Good Care is Made Superior!

As Chiropractors, and especially as Chiropractors with AK practices, the understanding of the spinal cord reflexes is paramount in gaining improved clinical skills. A working knowledge of functional neurology will provide access to new and innovative treatments for your patients. These “thoughts” are meant to be of a functional nature, and hopefully you will find new ways to apply them to your patients. This is not verbatim neurology, which you can look up in any text.

This knowledge is more apropos in an AK practice for the purpose that the patient visit is to facilitate muscles, or to make muscles “strong”. The basic premise of AK is to make muscles strong to benefit the patient. Thus, facilitating the muscles does many things for the patient, both centrally and locally including joint and posture stabilization, and improved feedback to the brain. In fact, Llinas states in I of the Vortex that thought is the internalization of movement. Consequently, our movement is an expression of our humanism. (I will limit the contents of this article to the neurological consequences in the cord and the brain, not the ramifications of weak or inhibited muscles in the AK context).

So what happens in the cord when a muscle is facilitated? First of all, what has taken place neurophysiologically at the muscle spindle?

Let’s take the spindle first. There are two components of the muscle spindle. There is a sensory portion (afferent limb) and a motor portion (efferent limb). Something had to change in both the sensory and motor portions of the spindle for a muscle to modify its tone, or get strong.

When a muscle is stretched (or loaded) the firing rate of the primary afferents increases thereby monosynaptically increasing the tone of the agonist and synergist muscle: termed the simple stretch reflex. Consequently, the antagonist is inhibited disynaptically (reciprocal inhibition).  The cross cord reflexes are polysynaptic and work as follows.

Anterior compartment muscles (think flexors) above T6 inhibit posterior compartment muscles (think extensors) above T6 ipsilaterally.

Anterior compartment muscles above T6 inhibit the contralateral anterior compartment muscles above T6.

Anterior compartment muscles, above T6 inhibit anterior compartment muscles below T6 ipsilaterally.

Anterior compartment muscles above T6 inhibit posterior compartment muscles below T6 contralaterally.

For example, the cross cord reflexes work as follows; when you excite a posterior compartment muscle above T6 you also excite the contralateral flexors above T6. You also excite ipsilateral flexors below T6 and the contralateral extensors below T6. Using the above as a template, you could take a few moments to work though all the possibilities for the mono, di, and polysynaptic reflexes.

(An essential qualification to bear in mind clinically is that the distal quadriceps is an extensor, but the proximal quad is a flexor, and that the distal hamstring is a flexor, but the proximal portion is an extensor. The reason for this is that the neurologic delineation between the anterior and posterior divisions is not so clear-cut in the lower extremity).

There are supersegmental influences on motor neurons that set the sensitivity and gain of the muscle spindle, much of it through the gamma motor neuron system. These are mainly reflexogenic and are mediated through mostly cerebellar feedback loops. There are also additional descending motor systems that modulate the spinal cord reflexes as well, such as the cortex, the subcortical motor nuclei, and the brainstem. This is where we can get into trouble with iatrogenic muscle weakness. If the brains output is aberrant on one side to the motor nuclei in the ventral horn of the cord, then there is a probability that when you facilitate a muscle there will be an unwanted inhibition in the reciprocal muscle.

Here is my clinical observation and food for thought.

A typical clinical case scenario would be as follows.

A patient presents with a liver problem and has the concomitant weakness of, in this case the right PMS. They also happen to have a left hemisphericity with a decreased output of the left ponto-medullary reticular formation (PMRF). One of the things that the PMRF does is to inhibit the flexors above T6 and extensors below T6 ipsilaterally. Therefore if you decrease the output of the PMRF you get less inhibition of the flexors above T6 on the same side. In other words, the flexors get more tone and the extensors get more inhibited. Now keep in mind that this scenario is involving a right PMS (a flexor) so when you strengthen it, it will in turn inhibit the contralateral PMS, which in this case, (with a left hemisphericity) is too excited. All well and good, end of story, and you are home free! (The reason why the left PMS was not weak in the first place is because of the increased tone do to the left hemisphericity) This, in my opinion, is why we frequently see muscles weak on only one side of the body with systemic issues that are really ubiquitous in nature.

Now consider an alternate scenario where an almost identical patient presents with a liver problem and a weak PMS on the right side.  However, this patient has left cerebellar demise with right hemisphere diaschisis (almost the reverse of the above brain pattern, but a different way to say it). You go ahead and strengthen the right PMS as you did in the first case. Now, the left PMS weakens because of the lack of supersegmental influence.  You have also increased the feedback to the right cerebellum, the side that is already too active. In this scenario you have not only caused iatrogenic muscle weakness of the contralateral PMS, you are also perpetuating the brain lesion. (This patient is not likely to respond in a positive fashion to your treatments, whereas the previous example is likely to get a more desirable result).

Discussion: When I cause facilitation of a flexor muscle in the upper extremity: for example, I make the pectorals major sternal  (PMS) strong (a flexor), that activation should not weaken another muscle. That is to say, if the cord reflexes are working normally and there is equal and bilateral supersegmental innervation, there will be no change in muscle strength, monosynaptically, disynaptically, or polysynaptically. The PMS turning “on” should not inhibit the teres minor, but the point is that many times it does.  The PMS turning on should not inhibit the ipsilateral proximal quad, but many times it does. Even though under normal circumstances there are inhibitory postsynaptic potentials (IPSP’s) arriving at those motor neurons, and under normal circumstances it should not be sufficient to fire the inhibitory alpha motor neurons, bringing them to threshold, and turning “off” the antagonist, or reciprocal muscle. That is, unless there is an abnormality in the Gamma system, the cerebellum, or some other aberrant supersegmental influence causing a modification in the gain and sensitivity of the muscle spindle. If there is supersegmental involvement, then you will see weakness in the antagonist or reciprocal muscle, and that weakness will persist.  In my experience it does not respond in any way like a reactive muscle, nor does it respond to direct muscle spindle activity.

Example:

1. You facilitate the PMS and the ipsilateral proximal quad goes weak and stays weak.
2. You facilitate the bicep and the previously strong contralateral bicep goes weak.
3. You facilitate the teres minor and the PMS is inhibited, and so on, in any combination of the cord reflex pattern.
4. Any possible combination of disynaptic of polysynaptic muscle patters.

Discussion: In my opinion these are iatrogenic inhibited muscles. This inhibition leads to further breakdown in the feedback loops, and promotes added brain demise. There is a remedy for this, but it is complex and varies from patient to patient. Some patients have cerebellar involvement, some have neocortical, and some have sub cortical or striatal involvement. If you do find this situation as frequently in your patients, as I do, let me know. If you have any questions or comments feel free to blog me. I would love to hear from you.