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.