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

Walter Schmitt, D.C, D.I.B.A.K


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.


  1. Postural Analysis
  2. TS Line Analysis
  3. Test Muscles - Find Weak Muscle(s)
    1. Measure, Measure, Measure (ROM, Pain, etc.)
  4. Does Autogenic Facilitation Strengthen?
    1. No: Use IRT - Rubbing over Area(s) of Injury will Strengthen Weak Muscle
    2. Yes: Use NSB and/or Set Point Technique for Recent Injury Use Origin/Insertion Technique for Muscle or Ligament Injury

Summary: Identify a weak / inhibited muscle first, then fix injuries to restore normal function of the ipsilateral cerebellum, the contralateral cortex, and the descending muscle spindle cell control mechanisms necessary for muscular and postural control. These corrections normalize autonomic, endocrine, and immune responses that are secondary to nociception.

Many AK procedures can be performed using either a strong or weak muscle to determine what procedures are optimal. It is most useful, however, to begin with an inhibited muscle if possible, and then work to identify the source of inhibition. Sometimes, this is difficult or impossible, so we may use a strong indicator muscle and observe for changes due to the effects of sensory challenges.

If a muscle is over facilitated, AI will not weaken the muscle, and this muscle should not be used as an indicator muscle. There are times when all muscles are over facilitated (referred to as “all muscles strong”) and then we must address some systemic source of over facilitation such as an over firing sympathetic nervous system in a fight or flee response. Further discussion of this concept will be left for another time.

The point is that our initial procedures are best served if we can identify an inhibited muscle(s). Postural analysis and temporosphenoidal line (T.S. Line) analysis are great time savers in this effort. Further, reassessment of postural analysis during and at the conclusion of the treatment provides objective feedback for the clinician as to the progress and effectiveness of the treatment session. The first goal, then, is to identify a weak (inhibited) muscle or muscles and then work from there.

Neurological patterns related to injuries creating a need for Injury Recall Technique (IRT) must first be considered first when encountering an inhibited muscle. The theory of IRT was discussed in a previous paper. 8 Simply put, IRT is thought to be an adaptation to an injury that is maintained by an ipsilateral cerebellar and a contralateral cortical response to the muscle (flexor reflex afferent) pattern created by the injury. Some injuries will result in an IRT pattern (an IRT injury) and others will not. An IRT injury on the right side, for example, will cause muscle response that will create a right cerebellar adaptation that will carry this message (via the dentatorubrothalamocortical tract) to the opposite cortex. The cortex will send messages back through the corticopontocerebellar pathway and this cerebellar-cortical-cerebellar loop then becomes active and maintains the muscular and postural adaptation to the injury. The net effect alters (probably by cerebellar effects of descending brainstem pathways – vestibulospinal and/or reticulospinal) muscle spindle control maintaining the adaptation.

The essentiality of optimal muscle spindle cell control cannot be over emphasized. This may be determined by using manual manipulation of the muscle spindle feedback loop to create a facilitating effect to the inhibited muscle, or AF. If AF does not create a temporary strengthening of the weak muscle, this means that the most powerful reflex – and arguably the most important reflex, the only monosynaptic reflex in the body – is being over shadowed by some other source of inhibition, presumably from descending pathways in adaptation to the injury. IRT injuries must be corrected to restore this muscle spindle control system. Correction of an IRT injury will restore normal AF response to the weak muscle, or oftentimes, the muscle will return to a normal testing response following IRT correction.

Mechanoreceptor (MR) stimulation blocks the effects of nociceptors (NOC) at the spinal cord level, and at higher levels also. Rubbing the skin over the area of any IRT injury that needs treatment will strengthen the weak muscle due to MR stimulation. Rubbing will temporarily negate the effects of inhibition somewhere along the associated pathway (just as we instinctively rub an area we have just injured) even if the injury is ancient. Rubbing the skin over the suspected IRT injury is a quick and efficient way to identify the location that requires IRT.

There are two common IRT injuries that should be addressed at this point, but that may elude the AF screening process. Iliolumbar ligament IRT patterns will often not be seen unless the patient is weight-bearing. It is possible to directly challenge for the IL ligament at this point with the patient recumbent, and this is often a good idea. The other pattern is the hiatal hernia / GERD challenge. Once again, this is often an IRT problem that will not show up unless directly challenged. Although both of these problems will be identified at a later point in the protocol, since they are IRT injuries, the appropriate time to check for and correct them is at this juncture. The history should be your guide here. In the presence of hiatal hernia / GERD, the initial correction (inferiorly directed manipulation of the stomach) and the IRT should be performed at this time. Other associated traditional hiatal hernia / GERD corrections (e.g., dorsolumbar fixation, psoas imbalance) should be deferred until later in the protocol and only be corrected if they are not resolved by other procedures.

The importance of correcting IRT injuries first must be considered in the light of the cerebellar-cortical-cerebellar adaptation loop as well as their muscle spindle cell control consequences. Adaptations to injuries maintained by this loop impact both the cerebellum and the cortex in a significant way. Cerebellar tests such as finger-to-finger, one foot standing, Romberg, hypermetria, etc. will often be seen to move towards normal following IRT correction. Similar tests of cortical activity as well as those using muscle testing and right brain – left brain activity will often be normalized by IRT correction.

This implies (and in fact it is the recommended clinical procedure) that any cortical or cerebellar testing should be performed after (as well as before) IRT corrections in order to obtain a clear view of neurological function. Many neurological signs throughout the body are significantly changed towards normal by IRT corrections; so many in fact, that an initial neurological examination prior to IRT correction can often create misleading information as to the location of the primary area of lesion. Correction of IRT will allow the primary area of neurological involvement to be identified more clearly.

Asymmetrical cortical over stimulation from an injury becomes ingrained in the patient’s nervous system and is often mistaken as the commonly found chiropractic neurology pattern referred to as hemisphericity. It might better be labeled as a decreased hemisphericity. Hemisphericity (or decreased hemisphericity) denotes an imbalance between the right and left halves of the cerebral cortex. For example, a right hemisphericity (or right decreased hemisphericity) means involvement of the right cerebral hemisphere.

When one cerebral hemisphere fires, there are three important patterns of muscle activity:

  1. Ten percent of cerebral neurons fire via the corticospinal tract, corticoreticulospinal tract, and corticorubrospinal tract to muscles on the contralateral side of the body for meaningful, purposeful movement. The other ninety percent of cerebral neurons fire into the ipsilateral brainstem creating two additional patterns:
  2. a general increase in muscle tone on that side of 5 the body, and
  3. an ipsilateral increase in muscle tone of posterior (extensor) muscles above T-6 and an increase in muscle tone of anterior muscles below T-6. (Recall that in the embryological development of humans, anterior lower limb muscles are extensors as they have migrated from the posterior location where they would be found in lower animals.)

This third pattern originates in the pontomedullary reticular formation (PMRF) which is excited from above by the ipsilateral cortex. The reticulospinal tract that originates in the PMRF inhibits ipsilateral anterior muscles above T-6 (allowing for the increase in posterior muscle tone above T-6), and it inhibits ipsilateral posterior muscles below T-6 (allowing for the increase in anterior muscle tone below T-6.) For example, when the right cortex fires into the right PMRF, one might find weakness of the right biceps brachii along with increased triceps tone. Similarly, in the lower extremity, one might find a weakness of the foot plantar flexors tone with an increase in the dorsiflexors tone.

Decreased frequency of firing of the neurons in this pathway (as would occur in a decreased hemisphericity) has been observed to result in an increased tone of the anterior muscles above T-6, and an increased tone in the posterior muscles below T-6 on the ipsilateral side. This increased facilitation yields increased inhibition of the antagonistic muscles.

The observed pattern is very similar to stroke antalgia, and also resembles the normal gait pattern. As a result, some or all of the ipsilateral upper limb extensors (and abductors) and ipsilateral lower limb flexors (and adductors) may be inhibited, and unable to meet the demands of manual testing. Hence, with a decreased right cortex and decreased right PMRF, one might find increased biceps brachii tone and increased finger flexor tone accompanied by weakness of the right triceps and right finger extensors. In the lower extremity, this might be seen as increased tone of the right plantar flexors with weakness of the right dorsiflexors of the foot. (This has been called a “pyramidal distribution of weakness”, but it is actually an inhibition of the other descending motor pathways that have lost the ability to perform inhibitory functions that modulate pyramidal influences.) 1

In summary, when one cortex fires, it causes

  1. meaningful, purposeful movement on the opposite side of the body,
  2. general increased muscle tone on the same side of the body, and
  3. increased ipsilateral muscle tone of posterior (extensor) muscles above T-6 and increased ipsilateral muscle tone of anterior muscles below T-6.

The third phenomenon creates a gait-like distribution of muscle facilitation and inhibition.

The first pattern of meaningful movement (on the opposite side of the body from cortical firing) requires the second and third patterns to create stability (on the same side of the body as cortical firing) and allow the movement to happen. For example, consider lifting a heavy ball with the left hand. The right cortex fires to initiate the left-sided activity, but without the right cortex also firing down to create stabilizing muscle activity on the right side of the body, the person would fall over toward the left side rather than be able to lift the ball.

Correcting IRT injuries will often resolve imbalanced afferentation to the opposite hemisphere and signs of a hemisphericity lesion disappear. Often, there is a history of multiple IRT injuries on both sides of the body. This can cause confusing clinical presentations and complicates the diagnosis of hemisphericity lesions. Although there are cases where correcting a hemisphericity pattern will correct an IRT, the IRT should be corrected first and then the patient should be evaluated for hemisphericity patterns. As will be discussed under gait patterns below, there are common mechanical and chemical presentations that also create a gait pattern of muscle imbalance. These, too, may be mistakenly diagnosed as a hemisphericity lesion.

Applications of therapies and rehabilitation procedures aimed at a hemisphericity pattern are often employed by the chiropractic neurologist with remarkable success. However, when the apparent hemisphericity lesion is actually secondary to an IRT injury (or other pattern mentioned later), such treatment is less effective, and even inappropriate in some cases.

Ignoring the IRT pattern will cause the clinician to “paint over rust” with further corrections. Adaptations will be treated rather than primary causes. AK techniques like reactive muscles and strain-counterstrain, that depend on manipulation of muscle spindle cells, become obsolete in light of the IRT correction. Restoring central muscle spindle control mechanisms eliminates the source of the problem identified and treated with these techniques.

In a similar fashion, acute injuries must be dealt with as a priority. (Acute injuries as used here means within approximately one week of the injury, sometimes longer for major fractures or surgeries.) Similar, but different neurological patterns will be maintained in adaptation to acute injuries. Nociceptor Stimulation-Blocking technique (NSB) is the preferred approach when dealing with acute injuries. (Other approaches such as cold laser treatment have been reported to be effective, but we have not seen any neurological comparison between these treatments and NSB. Whether both approaches fully normalize the same pathways is not known.)

When there is a need for IRT or NSB techniques, the interference with normal neurological function is of utmost significance. The presence of either pattern disrupts normal neuromuscular control mechanisms (flexor reflex afferent patterns), autonomic patterns (both locally at the IML and via ascending spinothalamohypothalamic connections to systemic autonomic control areas of the hypothalamus), endocrine patterns (via the same spinothalamohypothalamic connections), and cognitive activity. Any attempt to treat the patient with other therapies in the presence of these underlying disturbances will, at best, be treating adaptations, and is often useless in making any significant changes.

Nociceptor driven spinothalamohypothalamic pathways can create or obscure patterns of hypothalamic-pituitary-endocrine effects and their parallel neuromuscular effects via hypothalamoreticulospinal pathways. The hypothalamus (HPT) interacts with the immune system such that each affects the function of the other: immune system problems alter HPT function, and changes in HPT activity impact the immune response. In a similar fashion to nociception impacting endocrine effects, nociception changes immune system responses. Evaluation of the immune system and endocrine system must be deferred until correction of IRT injuries and other sources of nociception (such as those addressed by NSB or SP techniques) is completed.

There is a nociceptive driven reflex loop from the spinal cord synapse of nociceptors via the spinoreticular tract up to the caudal reticular formation. The large nuclei located in this lower brainstem area (nucleus gigantocellularis, nucleus raphe magnus, etc.) send descending axons back to the spinal cord area of nociceptor synapse and counteract the three effects of nociceptors in the spinal cord. That is, the reticulospinal tracts from these caudal reticular nuclei inhibit incoming nociception, restore muscle balance at the anterior horn motorneurons, and inhibit local IML sympathetic activity. The theoretical basis for NSB technique involves enhancing this pathway by tapping acupuncture head points (mechanoreceptors) in the presence of a nociceptive stimulation in order to restore spinal cord nociceptor transmission, neuromuscular balance, and IML autonomic activity to pre-injury status.

It is important to correct IRT and/or NSB prior to any nutritional testing (with one exception.) In the presence of the need for IRT or NSB, nutritional test results will be obscured by the effects of nociception on various areas. This includes effects in the brain stem (where oral nutrient testing stimuli impact gustatory centers in the nucleus of the tractus solitarius), the hypothalamus (where gustatory messages also synapse and can have autonomic and likely, endocrine effects), the cerebral cortex (where perception is distorted by nociception), and even the spinal cord’s neuromuscular response.

The one exception that allows nutrient testing prior to performing IRT or NSB is to do nutrient testing to see if any nutrient negates an IRT or NSB challenge. This can be a valuable tool in identifying which nutrient(s) will be most effective at reducing the pain and inflammation related to the injury and to speed the healing of the injured area. Other systemic nutritional testing should be postponed until later in the protocol as indicated.

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