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* Please Note: The following article is provided by Body Mechanics for the sole purpose of
educating and informing our current and future patients.
THE EFFECT OF MANIPULATIVE TECHNIQUES ON THE CENTRAL NERVOUS SYSTEM AND MUSCLE TONE
BY EDWARD R. ISAACS, MD FAAN
As a neurologist, I have tried to understand the interplay between manipulation and the central nervous system. It seemed reasonable to consider the gamma motor system and in particular, the silent period or reduced type IA afferent input after muscle spindles were unloaded as an important factor in the development of post isometric muscle contraction relaxation. Over time, a concept developed that if the nervous system could be viewed as an advanced computer and that the standard neurological examination was simply testing the "hardware" of that computer. The postural mechanisms and the motion characteristics of any musculoskeletal system would then reflect the operations, of either an inherent, or learned "program". Dysfunctions of the musculoskeletal system could then be viewed as altered programs causing faulty performance, which would persist as long as the altered program was in place. Since the nervous system functions mostly as a reflex system, that responds to input, information received from altered mechanoreceptors and proprioceptors could perpetuate this program. This would be analogous to the computer jargon for "garbage in- means garbage out". If there is a way to change input, to get rid of the "garbage", then the computer should be able to be reprogrammed back to a better operating version.
An overview about current understanding of central and peripheral nervous system physiology and the effect on muscle tone was written by R. A Davidoff, M.D.' This presentation of basic neuroscience might appear to have little practical value to the neurologist, practicing standard neurology. However, it has tremendous practical value when one considers manipulation as a means to reprogram the nervous system.
Considering the end point, of treatment as a modification of muscle tone, the responsible mechanisms or "hardwiring" must influence the output from the alpha motoneuron to its muscle fibers. The final common path to the initiation of the nerve action potential is the result of the sum of all of the postsynaptic inhibitory and excitatory potentials delivered to the alpha motoneuron at any given instant.
Mechanically activated peripheral sensory receptors:
Muscle spindles
1. Primary spindle endings on bags, bag2 and chain fibers which respond to static stretch and very sensitive to changes in the rate of stretching, and give rise to group la afferents.
2. Secondary spindle endings on bag2 and chain primarily affected by slow or prolonged static stretch and give rise to group II afferents.
Muscle spindles are innervated by gamma motoneurons and as many as 70% may also be directly innervated by collateral axons from certain alpha motoneurons called beta axons (Figure 2). Dynamic fusimotor fibers enhance spindle sensitivity for
small rapid changes in length. Static fusimotor fibers shorten intrafusal muscle fibers maintaining sensitivity during unloading by contraction of extrafusal fibers. There is independent supra spinal control for the dynamic and static fusimotor systems.
There is no significant fusimotor background drive to relaxed muscles.
Golgi tendon organs
Golgi tendon organs (GTOs) are receptors lie in series with the muscle fibers and tendon and are located at the myotendinous junction (Figure 3). Each GTO is activated by 10 to 20 extrafusal muscles fibers that insert through the tendinous fascicle and represent portions of different motor units. It is difficult to fire a GTO by passive stretch alone because the force must be generated first through surrounding connective tissue. Yet, it may be possible for one muscle fiber contracting in series, to fire its GTO. The GTO gives rise to group lb afferents.
Intemeurons
Renshaw cells; (Figure 4) excited by recurrent collaterals from alphamotoneuron and input from complex descending and other afferents. Renshaw cells generate inhibitory postsynaptic potentials (IPSPs) to:
1) Homonymous and synergistic alpha motoneurons
2) Gamma motoneurons
3) la inhibitory interneurons
4) Other Renshaw cell la inhibitory intemeurons are responsible for reciprocal inhibition to antagonist muscles and their synergistic cohorts and receive excitatory postsynaptic potentials from la afferents from the directly stimulated muscles and their synergists. This interneuron also generates an IPSP in other alpha motoneurons to muscles that are not antagonists and other types of interneurons. The la interneuron receives additional afferents from:
1) High threshold afferents from skin, muscle and joints
2) Axons from Renshaw cells
3) Descending fibers from vestibular and red nuclei
4) Descending fibers from sensorimotor cortex
Intemeurons mediating group I nonreciprocal inhibition are excited by lb afferents and also in a parallel fashion by la afferents and receive additional input from:
1) Cortico-, rubro- and reticulospinal tracts
2) Other than group I peripheral afferents
All three types of interneurons receive additional converging afferents from supra spinal systems, so that transmission through any intemeuron is gated by the summation of IPSPS and EPSP derived from these central and peripheral sources.
Presynaptic inhibition
Primary afferent depolarization is a means for inhibition that appears to occur between, lb and la afferents and thereby a GTO can have an inhibitory effect on a muscle spindle by presynaptic inhibition. There also appears to be a way in which supra spinal effects can be mediated to bias whether muscle spindle or GTO feedback is critical.
Long latency responses
Muscle spindle afferents project to the sensorimotor cortex causing cortical motoneurons to discharge and generate late muscle responses or possibly programmed patterns of activity triggered by external cues.
Alpha-Motoneurons
The alpha-motoneuron is the final common path that responds to heterogeneous synaptic input from afferent and descending pathways. The force developed by a muscle is determined by the number of alpha motoneurons recruited and the frequency of the discharge rate from them.
Synaptic contacts include the following:
1) Group la afferents- Fifteen percent of input from homonymous muscle
may have multiple synapses with their inhibitory interneurons and along
with those la afferents from synergistic muscles generate excitatory
postsynaptic potentials (EPSP).
2) Group II afferents also derive from homonymous muscle and their synergists and synapse with the alpha-motoneuron, generating EPSPs.
3) Descending reticulo-, vestibulo-, rubro- and cortico spinal fibers- extensive
excitatory connections. Reticulospinal fibers from the pons and medulla
and vestibulo spinal tracts influence alpha motoneurons that innervate
proximal and axial musculature concerned with the control of posture.
Presynaptic inhibition
Primary afferent depolarization is a means for inhibition that appears to occur between, lb and la afferents and thereby a GTO can have an inhibitory effect on a muscle spindle by presynaptic inhibition. There also appears to be a way in which supra spinal effects can be mediated to bias whether muscle spindle or GTO feedback is critical.
Long latency responses
Muscle spindle afferents project to the sensorimotor cortex causing cortical motoneurons to discharge and generate late muscle responses or possibly programmed patterns of activity triggered by external cues.
Alpha-Motoneurons
descending vestibulo-spinal pathways and from proprioceptive responses from neck, trunk, or both, along with visual inputs and voluntary responses.
Reprogramming the central nervous system by various manipulative techniques
Barriers that limit joint motion are, at least in part, due to abnormally increased muscle tone in a muscle or muscles directly affecting joint function and abnormally decreased muscle tone in the antagonistic muscles and their synergists. The increase in the resting muscle tone results in muscle fiber shortening which, over time will alter the associated intrinsic and extrinsic connective tissues of the muscles, tendons, fascia and joint capsules. One inherent "program" that takes priority, especially in predatory animals (like us), is to maintain a posture that maintains a head position that keeps the eyes and ears level. The drive to maintain this posture, with the least expenditure of energy, will encourage adaptations of the vertebral axis and the extremities to accommodate positional changes or dysfunctions that can alter a balanced system. Any factor which can change the discharge frequency of the alpha motoneuron not only affects muscle stiffness locally at the local barrier, but can also affect the adaptations, which may have generated other barriers for free motion elsewhere.
In summary, those factors, which can reduce the discharge frequency of an alpha motoneuron, include the following:
1) Reflex inhibition by:
a) reciprocal inhibition by muscle spindles
b) inhibition mediated by Golgi tendon organs
c) presynaptic inhibition
d) Renshaw cell inhibition of alpha and gamma motoneurons
2) Postural long latency reflexes mediated by the vestibulo-spinal and rubrospinal pathways, especially to the axial musculature by considering; a) adaptive postures
b) position of patient during treatment
c) mechanical loads
d) changes in posture following treatment
3) The inhibitory effect of contact with skin and pressure over joints and fascia by either the treating hand or the palpating, monitoring hand.
4) Cortico-spinal effects initiated by voluntary muscle control to inadvertently assist the operator while adding the influence of a patterned controlled movement.
5) Cortico-spinal effects on learned behaviors and motor responses, which may be influenced by the expectations of the patient.
6) Controlling level of patient effort to focus on either smaller or larger muscles.
These factors may be emphasized or predisposed by various techniques. Muscle energy techniques probably use most of these including, (1) unloading of the spindle for post-contraction relaxation; (2) the effects of reciprocal inhibition; (3) inhibition from the Golgi tendon organ and Renshaw cells; and (4) long latency reflexes from the cortex and brainstem, while emphasizing the changes associated with static stretch of the
muscle. Certainly the functional techniques utilize reflex changes and long latency responses plus skin and joint contact. Impulse techniques emphasize reflex responses from joint, fascia, and skin, along with dynamic stretch responses from the muscles. Myofascial techniques rely heavily on contact and long latency postural reflexes and then on segmental reflexes. Counterstrain would seem to be reliant upon postural changes and segmental reflexes.
Appropriate exercises following treatment would reinforce proper retraining of weakened muscles by techniques, which include disinhibition, proprioceptive neuromuscular facilitation, and by increasing stimulation through postural and corticospinal mechanisms.
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