The Neurological Rationale for a Comprehensive Clinical Protocol Using Applied Kinesiology Techniques

Walter H. Schmitt, DC, DIBAK, DABCN

ABSTRACT

A procedural protocol for the application of applied kinesiology techniques is presented. It is based on neurological and biochemical principles and thirty years of clinical observations of comparative applications of techniques. Short summaries of each section are included prior to the section to enable a brief review of the information.


INTRODUCTION

Applied kinesiology (AK) techniques can be interpreted in light of their effects on neurological function.1 In this model a change in manual muscle testing response is ultimately due to changes in facilitation/excitation and inhibition at the anterior horn motorneurons (AHMNs) of the muscle in question.

Fundamentally, AK is all about excitation and inhibition of neural pathways. AK is a series of sensory receptor based diagnostic challenges followed by monitoring of manual muscle testing outcomes. All AK techniques are about creating sensory receptor stimulation that results in a net effect of excitation and inhibition leading to more optimal neurological function. These positive changes can be observed through somatic windows by changes toward normal in muscle facilitation and inhibition (muscle balance, range of motion, deep tendon reflexes) and through various autonomic windows that can also be monitored (pupil light response, blood pressure, heart rate, etc.) The changes in muscle testing responses are termed conditional facilitation and conditional inhibition dependent on the conditions present at the instant of the muscle test. In this paper, we will simply use the terms facilitation (or excitation) and inhibition. We will also use the terms strong and weak to denote muscle testing responses which represent AHMN facilitation/excitation and inhibition, respectively.

Many neurological pathways lead to AHMNs and impact the ability of the associated muscle(s) to respond to the demands of the manual muscle test. Through thirty years of observing both somatic and autonomic windows as well as symptom responses of patients, a step-by step clinical protocol for AK emerged. This protocol presents the most optimal application of AK techniques considering the neurological hierarchy of pathways that influence the AHMNs. The clinical application of the protocol is presented in a new reference manual that is coauthored by Kerry McCord, DC, DIBAK and this author. 2 McCord has also authored a paper presenting four diverse case histories each treated by following the same protocol. 3

One of AK’s most important and attractive features is that it is an open system. That is, AK allows for evaluation of the impact on a patient’s nervous system of virtually any modality or therapy. This protocol is no exception to the openness of the AK approach. The hierarchy presented here is comprehensive, but the therapies listed are not all-inclusive. For example, evaluation and treatment of food allergies is presented at a certain point in the protocol as identification of the existence of a food allergy response is imperative for optimal progression through patient assessment and treatment. Yet any additional allergy diagnostic activity may be added and, although one particular allergy treatment procedure is included, any effective allergy treatment procedures may be used. The key is when to employ various diagnostic and therapeutic steps. This protocol is open to the clinician’s choice of techniques as it is based on fundamentally sound principles of the basic sciences of neurology and biochemistry.

Similarly, at the point in the protocol for emotional recall assessment, there are many emotional treatment procedures available to the practitioner. Choose the emotional technique that you have found to be the most effective, but employ it at the designated time in the protocol for optimal effects.

Richard Belli introduced the terms autogenic facilitation (AF) 4 and autogenic inhibition (AI) 5 to represent manual manipulation of muscle spindle cells or Golgi tendon organs to cause a net facilitating or inhibiting effect, respectively, at the anterior horn. Manipulating muscle spindle cells in the belly of the muscle to create a net facilitation can be used to help determine the status of a muscle’s AHMNs.

The resulting net effect of facilitation and inhibition on a neuron at any given moment has been called the central integrated state of that neuron. Clinically speaking, we see three possible states for a particular muscle’s AHMNs that can be reflected by muscle testing:

  1. inhibited AHMNs (muscle tests weak)
  2. normally facilitated AHMNs (muscle tests strong and AI weakens)
  3. over facilitated AHMNs (muscle tests strong and AI doesn’t weaken)

Each of these three states represents the central integrated state of the AHMNs and is a sum of the net effects of all pathways to those neurons. Hence, there are various combinations of excitation and inhibition arriving at the anterior horn that are derived from either direct sensory input (more or less segmental in nature) or from a distant pool of neurons, hence ascending and descending pathways including suprasegmental pathways. Suboptimal muscle function as seen in AK can be interpreted as a neuron pool somewhere that is:

  1. inhibited and in need of facilitation (or increased afferentation)
  2. over facilitated and in need of inhibiting

All of the above assumes neuron metabolism within normal ranges of function. Deranged neuronal metabolic function results in transneural degeneration (TND) 6, 7 The presence of TND would suggest an approach designed to address the metabolic function of the neurons as the primary goal rather than the typical AK approach that primarily addresses facilitation and inhibition. Although the clinical approach to TND (which is at the core of the chiropractic neurology approach) is the stuff of another paper, the concepts may be summarized here for contrast with the AK approach that is focus of this paper.

  1. TND neurons may be too close to firing threshold (cells in danger of over stimulation and death by apoptosis) and these cells need to be stimulated with inhibitory activity to drive them away from firing threshold.
  2. TND neurons may be in need of stimulation by excitation to increase their metabolic rate and make more intracellular protein (for its negative charge) to drive the cell away from threshold, but the level of stimulation must not be so close to threshold that stimulation will kill them.

AK procedures may be combined with the awareness derived from observing of autonomic windows on neurological function to address these issues, but as mentioned, that discussion is for another paper. However, in either approach, AK (the facilitation – inhibition approach) or chiropractic neurology (the neuron metabolic state approach), muscle testing can be seen as a somatic window on neurological function and is a valuable tool in assessing the patient and directing therapy to the most optimal outcome. In fact, all of our therapies, and each and every therapy of any discipline can be seen as having their clinical influence by affecting one or more of the above states of neural activity.