The Neurophysiological Basis of Somatic Dysfunctions
A Detailed Model
by
Craig Redfern
Submitted to the Osteouathic Medicine Student
Writing Competition
May 1980
I shudder to think that my osteopathic principles professor,
John Harakal, might read this article. We are continually
reminded in class that the etiology and maintenance of somatic
dysfunction is multifactorial and variously interdependent.
This reminds me of the first lecture in a certain undergraduate
ecology class at Cornell University. The professor spent the
first hour warning us of the pitfalls of what he called 'one
factor ecology*. At the end of the lecture he apologetically
announced that the material in the rest of the course would look
very much like 'one-factor ecologye# such is the state of the
art and to some extent the nature of science. So here I make
the same plea. All physiological processes are multifactorial,
especially one which has eluded detailed understanding for over
one hundred years. Nevertheless I will present here a model,
a plausibility argument, for the development and maintenance
of somatic dysfunction, using only what might be called a *functional
somatic motor system* approach. This plausibility argument
draws in considerable detail from the literature of 'motor control*
and I will unfortunately only be able to mention in passing how
this model might interface with the various other factors involved
i n the actual clinical entity, somatic dysfunction.
This paper, appearing as a bachelor's thesis, was first
inspired by the 1975 article by Irvin Korr, "Proprioceptors and
Somatic Dysfunction". This article presented in broad terms an
'idea*. Being somewhat tangential to Dr. Korr's main research
efforts, it was presented without a thorough review of the relevant
literature. My purpose, then, was to investigate in more detail
the mechanisms by which the somatic motor system, the musclespindle/
gamma motor sytem in particular, might account for
various salient features of somatic dysfunction. For these
purposesaomatic dysfunction is seen primarily as a local,
functional derangement of the tonic control of input to the
somatic motoneurons. As such the mechanisms proposed will involve
such things as alterations of gain in reflex pathways, that is,
quantitative, functional differences from normal operation of
the system. Perhaps more important than a detailed mechanistic
proposal will be a section discussing means by which some of
these ideas might be tested clinically.
Motor System Im~licatea Osteomthi~ View a
Somatic Dysfunctioq
I have never found the term somatic dysfunction completely
satisfying as a descriptor of the clinical entity to which the
profession of osteopathic medicine historically owes much of its
exixtence. The term reflects two things. One is the wide-ranging,
multifactorial nature of the problem as alluded to above. To
me it also reflects the lack of a consistent view of the nature
of the problem. This second factor is the motivation behind the
present paper. There seem to be large portions of the osteopathic
profession who have found this lack of specificity incompatable
with the remainder of their practice, which appears to be more
directly supported by scientific knowledge. Even in these fields
I'm sure that it would be admitted by most clinicians that the
gap between the science and the practice is still vast. And
while I wish that the osteopathic profession-.had put more emphasis
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on the scientific elucidation of the process so intimate to the
profession, this lack of success must be viewed in light of the
state of the relevant field in basic science. While Z speculate
here on some mechanisms which sight be involved in the subtle
and complex process called somatic dysfunction, it is readily
apparent from the motor control literature that there is no
basic understanding of the real function of these mechanisms
under normal circumstances. For example, contrary to the classic
presentation in physiology class, a dim memory for most, it is
not known what real functions the muscle spindle subserves.
Nevertheless, the osteopathic profession cannot wait for the basic
scientists to clear up these matters in order to proceed investigating
a process of both clinical, and as we may see here,
potentially significant intrinsic scientific interest.
Descriptions of somatic dysfunction differ, quite naturally,
among clinicians according to their particular experience. These
vary from a sentence in the Mitchell-Pruzzo manual (taken here
out of context to illustrate the point): 'In this sense an
osteopathic lesion can be considered to be simply a stiff:jointo,
to a full-blown description of the Vacilitated segmente.
In view of the observation that somatic dysfunction is
readily reversible, I think the primary descriptor of the phenomenon
might be 'functional'. This contrasts somatic dysfunction
from much of disease process, which might be called eorganic*.
The rapidity of the reversal, in addition to other points discussed
below, implicate the nervous system in its basis.
A parameter which a long been considered to be a major part
of somatic dysfunction is bony derangement. Until recently
this was probably considered to be primary in the etiology of
somatic dysfunction. The bones were actually thought to be
*hung upg on their articulations (Korr 1975). In this paper,
though, bonymalposition is seen as neither necessary nor
sufficient for somatic dysfunction. If a bone is out of place,
it is simply because a muscle is pulling it out of place, but
too close adherence to this criterion might result in the
overlooking of more anatomically well compensated dysfunction
(I,. H. Jones, pers. comm.). Even though anatomical malpositioning
is not seen to be necessary here, the classic osteopathic
relationship between structure and function is still important.
It -inrs in the anatomy that may result in, and is in turn
limited by somatic dysfunction.
Palpable muscular hypertonicity is surely one of the
hallmarks of somatic dysfunction. It is widely becoming accepted
that this is primary at least to any bony derangement, and it
is the proposal here that it is in most cases primary to the
dysfunction syndrome in general. It is proposed here that the
hypertonicity is due to reflex incongruities arising in loops
with muscle receptors as their afferent limbs (although see
of joint afferents
the transfer characteristics~Clark and Burgess 1975) and their
re2lexes (Grigg 1975). Sympathetic nervous involvement and
the aspect of associated pain are two very important parameters
of somatic dysfunction, but unfortunately cannot be considered
here. The interface of these aspects and the present somatic
motor model would be of considerable interest. It is simply that
these mechanisms do notpossess the *cybernetice qualities necessary
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to account for the production and maintenance of a purely
functional chronic alteration such as is somatic dysfunction.
It will be argued below, that the muscle spindle afferents,
with their reflex effects and their particular motor innervation,
are the most likely transducers of this functional problem.
I have attempted to both motivate and excuse the present,
limited approach to the modeling of the mechanisms of somatic
dysfunction. I will next review the relevant parameters of
somatic dysfunction as determined by clinical and experimental
means, and will follow this by a detailed examination of
neurophysiological mechanisms which might serve to explain the
basis of these parameters.
-T-h e Clinicians and the Kirksville Physiolo~iste
The muscular hypertonicity of somatic dysfunction is
notably localized, often restricted to one joint or closely
related joints. What is also noteworthy is that the palpable
tension, the electromyographic hyperactivity and the restriction
of range of motion is decidedly unilateral, in most if not all
cases. In severe cases this unilateral tension is sufficient
to alter the resting position of the joint, although the more
evoluntary' guarding from pain can be involved here as well.
There is both active and passive motion loss. The restriction
of motion can be considerable when compared to the physiological
range. It is often observed that motion in the opposite
direction seems to be facilitated, both in terms of the release
of tension and the comfort gained (Jones 1964; Johnston 1972).
It is well known that for each painful joint there is
a specific direction of position that greatly aggrevates
the pain and stiffness. Movement of the joint in this
direction results in immediate reflex and voluntary
muscular resistance, to the point of rigidity. The converse
ia alae true: for each painful joint there is a specific
direction of position that greatly relieves the pain and
muscle tension. Movement of the joint in this direction
results in immediate and progressive reflex and voluntary
muscular relaxation, to the point of complete relaxation
and comfort. (Jones 1973).
What is remarkable about eomatic dysfunction, from the
point of view of the study of motor control, is that the
muscular hypertonicity is chronic, i.e. it may be maintaihed
for long periods of time, with or without pain (the widely
observed *subclinical lesion* ). Since the hypertonicity is
surely maintained by mechanisms *below8 the level of consciousness,
the tendency is to relegate the phenomenon th the level of
reflex. This is the basic approach of the present paper, but
it may be noted from the outset that these mechanisms are by
no means limited to the spinal cord. As mentioned above the
gamma motoneuron/ muscle spindle system with the numerous
spinal and supraspinal inputs is the ideal candidate.
The only extant electrophysiological investigations of
somatic dysfunction is the early work of Denslow and Korr.
Unfortunately for the purposes here is that the main inquiry
of these investigators was involved in the autonomic mechanisms
involved. Some EMG experiments were performed which shed some
light on the matter. In this work it was determined clearly that
the palpable muscular tension was due in part if not completely
due to measurable EMG activity over and above normal. Pressure
on tender spinous processes at the level of somatic dysfunction
elicited EMG responses in these muscles well over and above the
normal segments. That this was due to increased sensitivity
in the alpha motoneurons and not the sensory receptor on the
spinous process was amply demonstrated by the fact that the
response would spread the hyperactive muscle from pressure
on adjacent spinous processes but not fro4 the sap. of the
lesioned segment. It may be noted as well, in connection with
the notion of Jones presented above regarding the position of
reflex relaxation, that these investigators often found somatic
dysfunction with resting EMG a c t i v i t y that could be silenced by
positioning (Denslow 1947).
ptiolom a Somatk &&function: Frecedena Osteomthi~
Literature
Although-it is well known that the causative factors in
somatic dysfunction may be visceral (so-called secondary somatic
dysfunction), or postural (i.e. tonic), it is widely recognized
that the most effective causative agent may be some kind of
mechanical @traumae (a phasic etiology). This l a s t possibility
w i l l be considered to be the *classicale etiology. Most descriptions
of classical conditions in the l i t e r a t u r e are similar in several
respects. A few variations w i l l be outlined below.
The first to be mentioned is that developed in the a r t i c l e
by Dr. Korr mentioned above. The salient features of t h i s model
include @ 1) a strong, centrally ordered contraction during a
moment when the muscular attatchments (for example two vertebrae)
have been closely and abruptly approximated by facto r&ns
centrally orderede ( ~ o r 1r9 75). i e an external force or the
unanticipated yielding of a load. "In the suddenly slackened
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state the spindles would be silenced equally suddenly. In .
calling, or continuing to call on the silent, slackened muscle
the CNS on receiving no feedback, would greatly increase the
gamma discharges to the intrafusal fibers until the spindles
resumed their reporting.' Subsequent stretch is seen to
further increase the spindle activity, resulting in reflex
tonic effects on the alpha motoneurons.
Another proposed etiological circumstance involves the
inappropriate anticipatory @setm to a particular activity,
such as attempting to lift a walght which is unexpectedly heavy
(Grainger 1969). Another example, common to Dr. Korres model,
would be the unexpected yielding of a load. Grainger also
considers that it would be the shortened rather than the stretched
muscle which would respond with hypertonicity.
The etiological model which, in the course of the present
work has proved to be most useful in being able to develop a
plausibility argument around, is that of L. H. Jones (19641
pers. corm.). This model can serve to include the above proposals
and may account for @posturalN etiologies as well. What is
seen as important is the development (either posturally or phasically)
of a position wherein the muscle in question is at its
physiologically shortest length. This position is seen to result
in somatic dysfunction if and only if superimposed upon it is
the ra~i.4c ontraction of the antagonist muscle, serving to
ra~idlv stretch the shortened muscle. The rapidity of initiation
of this movement, as opposed to the final amplitude, is deemed
important. A *panic8 response, triggered either by the initial
traumatic shortening of the *to-be-lesioned* muscle or by an
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unrelated event, would be most effective.
The Jones model was developed anecdotally, based upon many
clinical examples. Below it is examined in detail regarding the
physiological mechanisms which would be brought into play at
each step and could result conceivably in the generation of
an inappropriate activity in the motor 'reflex' pathways. The
mechanisms invoked are vast, and there is no way here of knowing
if these mechanisms, studied under certain proscribed conditions,
might behave in the ways proposed during the circumstances just
described. The model in a sense can be seen as a self-fulfilling
prophecy, but the real value in producing such a model is that
it may point to potentially fruitful lines of investigation.
It is hoped that it may aid in the elucidation of a phenomenon
which has remained refractory for over 100 years, and that these
subsequent investigations may even shed some light on the normal
functioning of the systems in question.
A Brief Review Motor Neuro~hysiolo~
The neurophysiological sub-field known as 'motor control'
is quite complicated- especially since it is at this point rather
riddled with controversy. Nevertheless I feel it important to
give this more than a cursory glance here, since, after all, it
was a detailed investigation of this literature which motivated
this article and will hopefully make it unique* The results
of this investigation indicate that no single phenomenon or
'reflex* can adequately explain the development and maintenance
of such a local, chronic hypertonicity. Rather a series of
phenomena, temporally associated as in the 'classical' etiology,
might serve to explain the condition. Certain of these mechanisms
will only be mentioned in passing, for example those on the
level of the microphysiology of the muscle spindle itself.
The phenomena which have proved to have the most potential
explanatory value are those inolving supraspinal levels, often
studied indirectly in 'humans. I hope this brief review might
be of general value to the clinician as well. I will avoid
reviewing the very basic properties of the system, and if the
reader wishes to refresh the memory, I refer perhaps to the
article of Dr. Korr, or anyphysiology text.
In medical school physiology courses the muscle spindle is
regarded in passing as a length transducer involved in a
spinal monosynaptic reflex serving to oppose the effects of
unintentional perturbation of muscle length. Its gamma motor
system is seen to modify the mismatch between intrafusal and
extrafusal fiber length so that the corrective mechanism may
be effective over a wide range of muscle length. As such the
system was regarded as a length regulating servo-mechanism.
Although the actual functions are not clear it is obvious that
the system is rather uneffective as a length correction mechanism,
and the real effects are not nearly this simple.
First of all, there are two gamma systems. Static gamma
motoneurons increase the spindle discharge for any resting muscle
length. Dynamic gammas have no effect upon resting discharge
but rather heighten the phasic response of the spindle la afferents,
noted for the increased discharge with movement, related to
velocity-of stretch. The dynamic gamma system (at first sight
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paradoxically) probably subserves the function of helping to
regulate postural disturbances. The static system, on the other
hand, seems to help regulate some parameters of voluntary
movement, including perturbations occuring at this time. This
latter function is due to the fact of alpha-gamma coactvation,
indicating that nearly every input to the alpha motoneurons
reaches the homonymous gammas:as-well. These common inputs
include descending pyramidal pathways, extrapyramidal inputs
(but see below), nociceptive flexor reflexes, disynaptic inhibition
by antagonist las, and recurrent inhibition by alpha excited
Renshaw cells (RCs). The only exception known of input to alphas
which do not reach the gammas is the monosynaptic reflex (MSR).
Each of these connections mentioned is important in the present
argument.
The significance of alpha-gamma coactivation is made
particularly clear in the pioneering work of Vallbo and Hagbarth
(references below), using direct percutaneous recording of
spindle afferents during well described voluntary movements.
From this work it is clear that in normal humans the la and I1
afferents fire at higher frequencies during contraction than
during rest. The response is of course greater for isometric
or lengthing contractions (due to load) than for shortening
contractions, but even the latter may be considerably higher than
the greatest discharge during passive stretch (Hagbarth and Young
1979). '^he discharge is strongly related to effort, that is,
resistive load during movement, and for strong contractions there
is little relation of discharge to muscle length.
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The load compensatory properties and the effects of length
and load perturbations on the motor systems is obviously important
in the present context. These phenomena have been studied in
various ways. A few generalizations as to the results might
be made here. The MSR, familiar as the tendon jerk, is never
strong enough during rather severe postural perturbations to
produce an EMG burst (Nashner 1977.). A response at this latency
may be found during certain perturbations with voluntary movements
(e.g. Marsden et. al. 1972, 1973, 1974). With purely postural
perturbations the earliest EMG response occurs at a much longer
latency (e.g. 100-120ms vs. &Oms for MSR in crural muscles).
The direction of the response is in the same direction as the
MSR but may be gated in successive trials if the result is
inappropriate in the experimental situation to maintain posture.
The magnitude of the response is not nearly enough to correct
for the disturbance (Nashner 1977;Melville et. al. 1971).
During voluntary contraction perturbation will produce as many
as three EMG waves of latency longer than the MSR, each in the
same direction. Two appear, from correlations with animal
studies, to be *transcortical@, traveling via lemniscal pathways,
(VI and V2) and the last a cerebella-cortical path (V3). It is
this latter "reflex* that appears during the postural disturbances.
These are considered in humans to constitute @functional stretch
reflexesa (FSR), although as mentioned they do not serve to '
offer much correctiveforce. The earliest effective response
is considered gvoluntary@ and occurs at a latency of about 500ms.
Various theories have been proposed to account for the real function
of these early responses, ranging from the linearizing of muscle
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properties (Hasan and Houk 1975). to a notion, interesting
for the present purposes, of Allum (1975). He suggests that
the reflex response represents a 'pulse test information signale,
designed to inform the CNS of the current conditions of the
muscle and load. This is especially interesting in relation to
the 'cerebellar comparator' theory of Oscarsson (1970). The
cerebellum performs several functions, including vestibular and
postural effects, and the control of ballistic movements. The
mechanism of action in these cases may result from a @computatione
and comparison of the higher order signal to the conditions in
the periphery, the spinal reflex paths which serve as descending
paths as well.
The output parameters of the cerebellum, which may relate
to the comparator notion and to the V3 response, are indicated
by a recent study of Thach (1979). The temporal pattern of
neuronal activities during voluntary movement in monkeys
indicate a pathway as follows: dentate (receiving input from
associational cortex), motor cortex, interpositus (comparable
to n. globosus and embolliforis in humans) and finally muscles.
Although this is not direct evidence for a causal relationship,
the results are significant in the present context. The interposed
nucleus is known to involve the maintenance of muscular
tone, and is well known to respond dynamically to muscular
stretch (Oscarsson 1970). What is interesting in the present
context is the response of interpositus neurons to various
conditions. Muscle and motor cortical cells behave-similarly
during the holding of position against load, during directed
movement, and during perturbation. The-cortkctcl neurons which
are active during, for example, positions of holding in which
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the extensors are active will increase discharge during
extensor directed movements and during perturbation which
stretches the extensor muscle. In contrast, interpositus nuclear
cells active during holding decrease activity during movement
directed by the same muscle and during perturbat~on which
stretches the muscle. It is nevertheless thought that these
neurons project to the motoneurons of the holding-linked
muscle, and the paradoxical output of these neurons is involved
in the function of holding and of stopping movements, rather
than in the initiation of movements, a-function subserved
by the dentate and motor cortex. The output parameters of these
interpositus neurons is of especial interest as contributing
to the inception and maintenance of somatic dysfunction.
A Mechanistic Model for soma ti^ D~sfuncti.011
The *classica etiology of somatic dysfunction described
above may be broken down for this discussion into various parts.
Broadly the mechanisms involved may be considered as those
leading to'.the hypersensitivitv of the muscle spindles, hyper-
-a~ tivitvi n the spindle afferents, and the paintenance of the
activity the the apprpriate 'reflex* pathways. Temporally these
functions may be associated with the sequence of eventsin the
traumatic etiology. Mechanisms which might confer hypersensitivity
would be acting during the period of initial agonist (from here
on out refering to the to-be-lesioned muscle) contraction and
during the rapid shortening of the muscle with unloading or
by external force. Since the effects of various mechanisms would
be additive, it is not necessary that, for example, the agonist
be actively contracting during the shortening, it is just that
this sequence seems the optimal condition to maximize the addition
of various effects. The second temporal event is the panic
contraction of the (now stretched) antagonist and the resultant
rapid stretch of the agonist. Lastly to be considered would be
mechanisms by which a temporary, inappropriately high spindle
activity might be chronically maintained.
During the initial strong agonist contraction the gamma
motoneurons would be strongly coactivated with the alphas.
In one form of the @classice etiology this muscle becomes
unloaded, implying that the initial contraction is at least
partially isometric* From the studies of Vallbo*~ group
(esp. Burke et a1 1979) it could be presumed that the spindle
afferents would be highly active. The dynamic sensitivity
of the spindles increases with increasing load (Burke et a1 1978)
indicating a coactivation of dynamic gammas (or a separate but
parellel activation: see From and Noth 1976, and Thach 1979
for cortical neurons perhaps gamma-d specific.). In cat
preparations there are known to be aftereffects of (especially
dynamic) gamma activity on the spindle afferents, causing a
relative increase in la activity for a period of at least
500ms (Durkovic 1976)e This aftereffect would surely overlap
into the period of subsequent stretch, heightening the effect
of stretch* In addition there is evidence in humans for the
continued supraspinal input-to gamma motoneurons after
unloading (Struppler 1975).
A6 the muscle is rapidly unloaded and shortens, several
phenomenamight be expected to occur. In classic unloading experiments
there occurs what is known as the 'silent period*
and *rebounde in-the EMG record (Alston et a1 1967). The
silent period is due to the discontinuation of the
voluntary descending input and to the shortening of the
spindle afferents. The rebound occurs at a latency of about
Â
70ms (in the forearm). It is thought that this represents continued
fusimotor input (Alston et a1 1967). This EMG activity
is indeed concurrent with rebound activity in the shortened
spindles as recorded directly (Struppler and Erbel 1975).
Crago et a1 (1976) somewhat tangentially observed that in many
of their subjects the EMG burst in response to shortening was
considerably greater than the response to stretch during active
contraction. This result is especially interesting in the present
context. Unfortunately this result was not germane to their
main inquiry, but it almost seems to account for the initial
high spindle activity considered to be involved in the inception
of somatic dysfunction. Marsden et a1 (1979) also noted that
the EMG response to shotening during active contraction, normally
a reduction, could increase at a *transcorticaltlatency if the
nature of the task is altered so as to make the response
appropriate (see also Marsden et a1 19790).
It is speculated here that these *anomalous* results might
be related to input from the neurons in the n. globosus and
embolliformis (the interpositus neurons of ~ k c h(1 979)) ,
perhaps through a path from the red nucleus known to produce
specific dynamic gamma effects (Jeneskog 1974). K. rubra is known
to be connected with interpositus. As mentioned above, interposed
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neurons active during holding against a load in a certain
direction, i.e. an isometric contraction as was the case with
the initial agonist contraction, .increase firing in response
to perturbation which shortens the muscle involved in holding.
This would probably then result in an increase in activity
to the agonistfusiaO'torneuron8 following the dramatic shortening
invoked in the present model. Â
There is also some evidence for a negative cortical feedback
effect, as speculated in the etiology of Korr mentioned above.
This is seemingly in opposition to the stretch reflex effects
of Marsden et a1 (above) but it is noted in the work of Thach
(1979) that there appear to be three classes of motor cortical
neurons associated with a hold and move task, and the negative
feedback loop could be subserved by the set which is closely
correlated with joint position. MacLeh and Porter (1974)
found an increase in activity in cortical neurons after level
1 procainization, indicating a possible negative feedback loop
with the la afferents.
In addition to these direct inputs to the gamma motoneurons
there are several other mechanisms which would tend to disinhibit
the gammas and alphas, increasing the actual effects of the
facilitory influences. As the agonist is unloaded and the
voluntary descending input to the alpha motoneurons is discontinued
the Renshaw Cell inhibition of the gamma motoneurons
would also stop (Fromm et a1 1975; Ellaway 1974). It is also
known that the antagonist las reciprocally inhibit agonist
gammas as well as alphas (Hultborn et a1 1976). While this
would tend to inhibit the agonist motoneurons during stretch of
antagonist, there are several factors which might tend to
obviate this effect and even reverse it under the conditions
of the traumatic etiology presented here. Immediately after
stretch of muscle there has been found to be a marked negative
adaptation of the spindle afferents, lasting up to 500ras
(Cheney and Preston 1976). This reduction in activity would
transiently disinhibit the agonist gammas. It is not known
whether the reciprocal facilitation from the lb afferents
project to gammas as well as alphas, but it may likely be the
case considering the widespread nature of alpha-gamma linkage.
If this were the case the rather severe stretch of the antagonist
during the trauiaatic-shortening of the agonist might be expected
to facilitate the gammas from a spinal level. .
Thus it can be seen that several factors will overlap
during the period of rapid muscle shortening which will tend
to produce a higher gamma/spindle activity than would be expected
in the position which otherwise would be relaxed and shortened,
reducing spindle activity.
The second part of the traumatic etiology is of course the
*panice contraction of the antagonist, and the resultant rapid
stretching of the agonist. Each of these processes can be
examined separately as to the mechanisms involved. The *panice
contraction will be viewed as a triggered ballistic movement.
with the distintive qualities of this class of movements. This
type of movement will have direct ramifications on the activity
in the agonist spindle afferents, in addition to the effects
of stretch on the agonist. The combination will be seen to
result in a condition wherein the activity of the spindle afferents
is much greater than would normally be the case for the muscle
length and velocity of stretch.
The trigger for the ballistic contraction of the antagonist
muscle is the source which produces the unloading of the agonist
contraction. The minimum latency of such a voluntary response
would be about 500ms (Nashner 1976: Allum 1975). This contraction
would occur during a moment when the effects considered in the
previous section would be active.
Ballistic movements, preprogrammed by the cerebellum and
dentate nucleus, have several distinctive properties. The
classical sequence of EMG activity during these movements involves
an initial agonist (in our case the @antagoniste) burst to
initiate the movement, a second burst of activity which is present
in the antagonist, to begin retarding the movement to bring it
to completion, and a final burst in the agonist to complete the
movement to achieve the desired result. Only the latter two
bursts are sensitive in magnitude to perturbation during the
movement (Marsden et a1 1979). The cerebellum serves to time
the duration of the movement and hence the distance traveled.
If the output is indeed dependent upon a comparator function,
it may be surmised that the condition of the reflex arcs/descending
pathways would be considerably different at the moment the
movement was triggered, i.e. the unloading of the @agonista, than
when the descending volley would reach the cord nearly 500ms
later. Indeed afferent input may actually be inhibited duriu
ballistic movement (Ghez and Pisa 1972) and the true conditions
in the cord would not be available for sampling.
Nevertheless the three part pattern of b a l l i s t i c movements
may vary quantitatively depending upon the conditions. Hallett
and Marsden (1979) found that perturbations unloading a muscle
during b a l l i s t i c movementcaused a l a r g e r antagonist EKG burst.
Although there is no i n i t i a l load during the contraction of our
@antagonist8 it might behave as if there were, due to the @panice
nature of the contraction and the f a c t that the muscle is contracting
from its position of greatest length, with conaiderable i n e r t i a l
load. This would tend to depolarize the gammas ( i n linkage)
during the period of antagonist contraction i n our model.
Additionally Delwaide (1976) found i n studying reciprocal
inhibition during movement i n humans that there is a transient
reciprocal f a c i l i t a t i o n , l a s t i n g up to 300ms, at the onset
of b a l l i s t i c movement. This is probably due to the R.C. inhibition
of the l a inhibitory interneuron ( l a 1 ~ )(H ultborn e t al. 1971).
In our present consideration, the 'panic' contraction of the
antagonist would surely a c t i v a t e t h e larger alphas which seem
to preferentially excite the RCs (Ellaway 1976).
Thus it seems that several mechanisms might operate during
the antagonist contraction to cause a disharge i n the spindle
afferents much larger than appropriate f o r the length of the
muscle and the velocity of stretch. The rapidity of the stretch
would i n i t s e l f of course produce considerable discharge. This
a c t i v i t y might then be further amplified, at a short spinal
latency, by excitatory autogenetic reflexes from the las onto
the gammas. Fronun and Noth (1976) and Trott (1976) have both
demonstrated the existence of excitatory polysynaptic reflexes.
The dynamic gammas recieve the strongest input but even the s t a t i c
fibers may receive considerable excitation. The reasan that
this effect had not been discovered earlier is that in the
decerebrate cat, where the extensor alpha motoneurons are strongly
active, the R.C. inhibition onto the gammas occludes the excitatory
effect. But in normal circumstances, when the spindle discharge
has much less direct effect on the alphas, the input to the
gammas might be expected to be quite strongly positive, especially
if the spindle activity is transiently very high. (It may be
noted that positive feedback loops, such as is constituted by
this system, are considered to produce instability. Under
normal conditions this positive loop is of course linked to
the negative loop of the spindle as a length transducer. But
if this reflex is indeed involved in the inception of somatic
dysfunction, then it may be considered to be a source of
*instability8.)
The characteristics of the interpositus neurons dicussed
above in relation to their response to perturbation, also might
come into play during this latter part of the etiology of
somatic dysfunction. As mentioned above, neurons active during
*holdinga wherein one muscle is active, will increase discharge
during movern~nts directed by the antagonist, in the present case
further exciting the agonist gammas. This property may be
related to the antagonist burst during ballistic movement, but
during the present situation the output of the cerebellar
comparator might be expected to be anomolous. This notion
may be considered in relation to the notion of Allum (1975) that
aspects of the FSR may serve as a pulse test information signal.
-22-
Although it is assumed above that the earlier transcortical
reflex might contribute to the excitation of the agonist gammas,
Marsden et al(1974) report that this response may be gated in
certain instances. If the early response acted as a pulse test
signal for the cerebellar comparator and perhaps for the V3
burst, the smaller return from the pulse test might result in
a greater V3 input to be produced. This inordinately large
response might also be reflected in the interpositus 'holdingg
neurons, as will be considered below.
The transient production of an inappropriately high activity
in the spindle loops is not hard to support with the various
mechanisms described above. What becomes more difficult due
to the lack of precedent in the literature is how to understand
how the hyperactivity might be maintained chronically. As stated
in the introduction, this lack of precedent is probably not due
the lack of mechanisms per se but rather to the lack of suitable
inquiry. The mechanisms which might be proposed for this final,
part of the inception of somatic dysfunction must not only account
for the properties of the maintained dysfunction, but also for
the therapeutic means by which it is found to be alleviated.
Here the hypertonicity and hyperreflexia of somatic dysfunction
is seen to be @functional', that is, it involves inappropriate
activity in normal neural pathways. It is proposed here that
this hyperactivity might be maintained by one of two ways, or
by a combination of the two. The first involves a continuation
of activity in positive feedback loop reflexes, made possible by
some manner of sensitization occuring in these pathways. me
second possibility involves the functional, quantitative alteration
-23-
in the tonic, postural output to the agonist and antagonist,
probably the result of the comparator function.
The positive feedback loops which might be invoked in the
present argument would of course be the autogenetic polysynaptic
spinal pathway (Fromm and Noth 1976) and the three supraspinal
reflexes. The V3 response may be considered a part of the
cerebellar model below. But the maintenance of chronic hypertonicity
must rely on more than mere circuit analysis. Activity
could only be maintained if there were never an even transient
reduction in the activity of the loop. This is unlikely since
the muscle spindles, even though hyperactive, will still decrease
the discharge somewhat with shortening. As will be discussed
below, the Joneas technique seems to be effective by just this
means of shortening the muscle, but it is clear that in this case
the muscle must be held in this position for about 90 seconds.
This sort of a time lag cannot be explained by circuit analysis,
but requires some sort of plasticity in the reflex paths. Two
phenomena will be discussed which may offer some precedent for
such a process.
Although humans normally do not display a tonic stretch
reflex, there is a phenomenon called the tonic vibration reflex.
Very low amplitude vibration from the tendon is known from
animal studies to selectively activate the la spindle afferents.
The reflex contraction resulting from the application of such
vibration is unusual in that it persists for many seconds after
the cessation of the stimulus, even though the spindle afferents
themselves are silenced at this time (Hagbarth 1973). The
TVR pathway is known to be polysynaptic and it is assumed that
the slow decay is due to residual activity in this path (Delwaide 1976)
M. M. Patterson, a physiologist familiar to the osteopathic
profession, has shown that spinal FRA reflexes may be sensitized I
by a classical stimulus paradigm, and has indeed discussed
this in relation to the maintenance of somatic dysfunction
(Patterson 1976). The FRA pathways are thought to also serve
as descending interneuronal paths (Oscarsson 1970) and might
as such be involved in the descending @reflexe inputs considered
here. Thus there are at least hints in the literature that
such reflex pathway sensitization and plasticity might be
invoked to span the time lags and allow the hypertonicity
to be maintained with hyperactivity in reflex paths despite
transient reductions in activity.
The notion that maintained, local hyperactivity might
be explained by the response of a corebellar comparator to
inappropriate input is not exclusive of the above explanation
in that the descending activity resulting from cerebellar
output would also traverse these spinal pathways. It is
not known exactly how such a comparator might function. Tine
input from the periphery is compared to the descending command
and an output generated which will serve to result in the
desired position, either postural or as the result of movement,
depending of the portion of hemisphere involved. In this case
the periphery would, after the stretch of the agonist, be sending
information appropriate to a much longer length, and the
lessened activity in the antagonist spindles would be appropriate
for a much shorter length. The maintenace of a postural midline
would then call for contraction on the part of the agonist, even
though it is actually already shortened. This is effectively
a viscious cycle, leading in theory to greater and greater tension.
-25-
Both the positive feedback loop and the cerebellar comparator
models for the maintenance of somatic dysfunction would account :
I
for the observed properties. There is some evidence, based on
on the use of spinal depressant muscle relaxants in the treatment
that the dysfunction involves a polysynaptic spinal pat
of dysfunction,È(Greenwoo 1970) based on the known pharmacological
effects of these drugs (Gesler et a1 1968). but as stated,
this might be the case for either model. The muscle spindles
would be hyperactive in both cases. The increase in tension
with stretch could be seen as a local tonic stretch reflex, due
to the overactivity in the spindles.
La Ha Jones has noted that in severe cases of somatic
dysfunction that the antagonist muscle is markedly weakened.
The antagonist weakness could be explained on the basis of
reciprocal inhibition mediated by the highly active agonist
las. Yangasawa and Tanaka (1976) have shown that selective gamma
blockade in patients with hemiplegic spasticity caused an
increase in strength of the flexors, normally weakened in this
condition. This is seen to offer a precedent for the magnitude
of such an effect.
The efficacy of the Jones* manipulative tchnique is perhaps
most easily explained by this model. If the mechanism is indeed
that of hyperactivity in reflex loops, the extreme shortening
of the dysfunctional muscle would serve to effectively silence
the spindles. The considerable stretch of the antagonist would
by means of la mediated reciprocal inhibition further silence
the gammas directly. Indeed Jones currently refers to the
technique as 'counterstrain". That the position must be maintained
for 1-2 minutes is seen as allowing time for the residual sensitivity
in the reflex pathways to become reduced. The very slow return
to the midline position which is necessary to the technique
would obviate any high dynamic la discharge which might reinstitute
the hyperactivity. The Jones* technique might also be
explained in terms of the cerebellar comparator. Bizzi et a1
(1976) have shown that it is probably the ratic of tension
and activity in paired agonist/antagonist muscle groups which
underlies the maintainence cf positional holding, a function
subserved by the cerebellum. As stated above, the cerebellar
comparator function involved in a dysfunctional muscle pair
has become *fooled8 as to the actual lengths of the muscles and
hence position. The Jones' technique, by silencing the agonist
and firing the antagonist las, would produce a pattern more
appropriate to that which would normally be the case at resting
midline. The joint is then very slowly brought back to midline,
minimizing any dynamic spindle response. Since the positional
gain of the spindle afferents is quite low (Vallbo et a1 1972)
this might be done with little disruption of the cmidline'
pattern, while actually returning the joint to the position
at which the cerebellum assumed it to be.
The muscle-energy technique of Mitchell might be similarly
explained by either of the maintenance models, although perhaps
somewhat less convincingly. In considering the first model,
the most plausible explanation might involve the Renshaw Cell
inhibition of the gamma motoneurons during the active contraction
of the hypertonic muscle. This inhibition could serve to silence
the spindle afferents, allowing the hypersensitive reflex pathways
to de-sensitize, or perhaps even to habituate (Patterson 1976).
-27-
It may be noted by the reader that the muscle in this technique
is being continually lengthened* a procedure which would presumably
increase the activi3y in the spindles, seemingly counterproductively~
One exg3anation invokes an additional.-i~ibitiobny the presumably
highly active (Hagbarth and Young 1979) lbs, which are also
presumably active in alpha-gamma linkage (W. Grimes, pers.
Interesting in relation to the mechanism of action .of M.E.
technique are two modifications* one on this technique and one
on the Jones technique* An alternate M.E. method involves
the active contraction of the antagonist* This would presumably
act by reciprocally inhibiting the agonist gammas in linkage*
D. Longsdon has modified the Jones technique by having the
patient actively contract the antagonist muscle while in the
Jones position (Jones, pers* corne )
The are phenomena in the literature which suggest that the
efficacy of M.E. technique might be more well explained by
the cerebellar comparator model* a1thoughethe details of how the
general function might work are not known. The resetting
of the comparator would still have to proceed by the inhibiting
of the gammas resulting in a lower discharge* It is noteworthy
that the delayedventralspinocerebellar pathway conveys largely
lb informationv and 'this delay has been considered important
in the timing of the comparator (Oscarsson l9?O)* The lbs would
of course be quite active in the M.E. maneuvers*
The only explanation which this model offers involving
thrusting technique would be the similar lb activation during
the rapid stretching of the agonist*
Means.& Which These Notions Mi~ht & Testea
The plausibility argument presented above is of little
use unless some of the precepts are tested* As pleaded above
the state of the art in neurophysiology is such that many of the
mechanisms cannot be investigated directly* While there might
be value in creating an animal model involving somatic dypfunction
in order to manipulate the variables and to study the fine-level
processes, what will be emphasized in this final section is the
potential use of techniques developed in the study of human
motor systems in testing some of the ideas presented above*
are infeasible,
Even some of these techniques notably and unfortunately the M
direct microneurographic recording techniques of Vallbo and
colleaguese Still various tests might be carried out in a clinical
setting with little technical sophistication, utilizing electromyography
in conjunction with tendon vibration, H-wave stimulation
and selective ischemic and pharmacological nerve blockades*
Simple EMG recording would help to eluci ate some of the
parameters of somatic dysfunctione The presence of resting
EMG activity and perhaps of a recordable tonic stretch reflex
might be expected* In particular the slope of the EMGIlength
curve should be high* In certain appendicular dysfunction
the size of the T-reflex could be noted, only it is not clear
whether it would be elevated or actually reduce the response.
The reason for this is that utivity in the polysynaptic TVR
pathway is known to presynaptically inhibit the MSR input (Delwaide
1976)e So even though the ratio of %- reflex/^-wave is classically
considered to be a measure of fusimotor input (landau and Claire
1964) this inhibition might obviate this measure*
-29-
The length at which the T- and H- reflexes first appear might
be expected to be less* given the higher activity in the spindle
afferents. The long latency supraspinal @reflexg responses to
perturbation might be expected to be increased* if for no other
reason due to the depolarization of the alpha motoneurons
themselves. It is not known whether the tonic output of the
cerebellum is connected to the phasic responses to the same .
muscles* although there is anatomical evidence for such connec~icns.
It would be of interest to deternine if the cerebello-cortical
V3 wave would be enhanced.
If the polysynaptic pathway involved in the autogenetic
excitation of gammas by la afferents (*om and Noth 1976)
is common to the TVR path (considering the widespread nature
of alpha-gamma linkage) it might be expected that the TVft
response would be facilitated. Although this might occur due
to any increase of input to the alphas* one property of the TVR
might indicate that the hyperactivity is in the TVR path itself.
In the case of the tonic rigidity of *prkinsonism the'ratio
MSR/TVR is reduced (in contrast to spasticity). Additionally
the rise time of the T W is altered (Wallin et a1 l9?3).
This might also be expected to ~e the case locally with somatic
dysfunction. It is also interesting that parkinsonian patients
display the contraction of the shortening reaction. The methodology
of TVR vibration is given in detail in Hagbarth (1973) (and
see Hoogmartens and Basmajian (1976) for use on paravertebral
muscles).
The pattern of reciprocal inhibition is seen t3 be altered
in the present model of somatic dysfunction. By applying
vibration simultaneously to the agc~ist and antagonist, a position
-30-
is found where the EMG response of each are canceled (Hagbarth
1973). In the case of somatic dysfunction the position at
which this balace would be found would be closer to the position
in which the agonist is shortened. Tanaka (1972) outlines
a methodology using reciprocal H-wave inhibition whereby
the reciprocal pattern can be studied in a different manner.
Vibration might also be used in conjunction with manipulative
treatment to help illustrate the mode of operation of the
techniques. If the techniques do indeed operate by reducing -
the output of the spindle afferents, then the application of
vibration during treatment should obviate the beneficial effects-
Another implication of the proposal that OMT operates
by lessening activity in the spindle paths is that any procedure
which lessens this activity should serve to alleviate the
observed hypertonicity. Selective blockade of either the
large las fibers or the small gammas should then produce the
effect- The larger fibers can be selectively blocked by
iscnemia (Marsden et a1 1976). , ,and the gammas by dilute
procainization (eg. Landau and Claire 1964)- While these
blokades are not recommended for therapeutic use* they are
relatively simple and may help to test the ideas presented
above.
The model above has beenpurposely developed in some
considerable detail. It is hoped that the discussion will
stimulate thinking among those active in the field* clinicians
and hopefully physiologists at the schools, but perhaps more
importantly it is hoped that it may indicate to those members
-31-
of the profession not actively involved in the treatment of
somatic dysf'unction that the phenomenon which helped to
motivate the founding of our profession is not without
physiological precedent* I hope I have shown that in some
sense it is understandable that such a subtle functional
problem has eluded under8tandi~;- gherr the facWtMt-he b@@c
scientific field of motor control is presently in so much flux*
Somatic dysfunction should indeed be considered an entity,
quite unique and worthy of consideration in its own right, and
especially as it relates to the maintename of health and
the interrelation of disease.
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