This is an article I wrote as an Osteopathic student for a writing competition.......

The Neurophysiological Basis of Somatic Dysfunctions

A Detailed Model


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


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


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~


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


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


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


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


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.


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


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


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


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


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


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.


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


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.


Both the positive feedback loop and the cerebellar comparator

models for the maintenance of somatic dysfunction would account :


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).


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*


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


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


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


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


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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Low back pain

Low back pain is very common, 50% of Americans will have some in their lifetimes. It is one of the more common reasons patients seek my care or that of other Osteopaths. Although there are a number of causes of low back pain, most is considered by conventional medicine to be nonspecific or “Mechanical” low back pain. I like to call this “Garden Variety” low back pain. In Osteopathic Medicine we consider the cause most often to be Somatic dysfunction, which I explain on my Website “About Osteopathic Manipulation”. This type of pain is the most likely to benefit from Osteopathic manipulation. Pain associated with other cases sometimes can be helped as well, but less predictably. Somatic dysfunction is where the muscles are made to contract by a hyperactive reflex arc between the muscle stretch receptor and the spinal cord, which then sends a signal to the muscle to contract. A constantly contracting muscle becomes painful, and sometimes if intense enough would be a “spasm”.  Exactly why the pain can be so intense, and why it can come on suddenly isn’t completely clear, but is typical. We all have some Somatic dysfunction, even without pain, but if it becomes more severe it goes above a threshold which then causes pain. This reflex may be “tweaked” by a minor motion, sometimes resulting in severe pain from seemingly minor motion. There was a more significant injury earlier which set up the pattern, which may or may not have resulted in pain at the time, but a quick, minor move may be enough to bring it over the threshold even years later. It is very common to have self-limited episodes of back pain, where the back seems as if it “goes out” suddenly, and often will resolve without any specific treatment. Some people live all of the time above the threshold, with chronic daily pain. The goal of manipulation is to quiet down he reflex circuit to well enough below the threshold to have a buffer against future episodes. 


There are other causes of back pain, although more often there may be coincidental anatomic changes which are not actually causing pain, but are attributed as the case often by non-osteopathic practitioners. 


There are very serious and potentially life-threatening causes of back pain, but thankfully these are quite uncommon compared to the myofascial pain of Somatic dysfunction or other benign causes. Generally cancer, infection and fracture are the serious cases to consider. I adults most “bone cancer” has spread from other cancers, although the patient may not have yet been diagnosed. Generally this pain is gradual in onset, as opposed to the “going out” scenario, and isn’t very specifically related to movement as is garden variety pain, where it may be painful to bend over but not arch back, twist one way but not the other, etc. There are often other symptoms of fatigue, unexpected weight loss. Infection in the back is another serious and urgent cause of back pain, but is rare outside of injection drug users who have bacterial spread in the blood. Compression fractures are usually in older adults associated with osteoporosis, and are sudden in onset, generally due to a minor fall or other injury.


There can be other benign causes of pain with a specific anatomic point source pain generator, although as I say many people may have “abnormalities” on X-ray or MRI and have no pain, so in patients with pain this may or may not be the cause. “Arthritis” of the spine or disc related problems may be specific sources of pain. It can be difficult to know based on clinical symptoms, examination findings or even imaging studies. I had sudden onset of low back pain 35 years ago building a deck, and visualizing the location in my mind’s eye, and knowing the anatomy, I would have placed it right at the L5-S1 disc, the lowest. But it was not coming from the disc because I could resolve the pain by curling myself up like a pretzel, utilizing the Strain-Counterstain Osteopathic technique on myself. The pain was primarily muscular, and since the muscles operated across L5-S1, the brain’s simplistic representation was “L5-S1”.    


Spinal disc herniations are generally not a cause of pain, although they can cause limb pain by compressing nearby nerves. When I was in Osteopathic Medical School, the teaching was that there was no pain because anatomists couldn’t find any pain receptors in the disc. Much later it was felt that there could be “discogenic” pain. This would be defined by an interventional procedure called a “provocative discogram”, in which a needle would be placed into the disc, and if while injecting contrast dye under pressure, the dye leaks from the disc and the patient’s pain goes up with the pressure, that defines discogenic pain. This approach has largely fallen out of favor in the Pain field, in part because nearby discs can be injected also causing pain, and basically the only treatment available would be disc replacement or spinal fusion surgery. There are a lot of terms used in describing disc disease. The intervertebral disc is made up of the central, jelly-like “nucleus pulposus” and is held in place around the margins of the vertebra by a tough fibrous tissue called the “annulus fibrosus"   There is “degenerative disc disease”, largely age-related changes, where the disc loses water content, shrinks down and narrows the disc space between the 2 adjacent vertebra. There can be disc “bulges” where the edge of the disc, the annulus, goes beyond where it normally should be, but not beyond the edge of the vertebra. Generally this doesn't cause a problem compressing the nerve unless there are other contributors to narrowing the space around the nerve, such as bone spurs from disc degeneration or arthritis of the little facet joints, discussed below. Beyond bulges are “protrusions”, where the disc goes out beyond the edge of the vertebra. Although somewhat more likely to cause problems, in one study of MRI in patients who have never had back or sciatic type pain, 40% have disc bulges and 10% have disc protrusions. One man even had a disc “extrusion” where a piece of the inner nucleus was squeezed out and floating free in the spinal column, but was not pushing on a nerve so didn’t cause pain. A disc “herniation” can result in a bulge, protrusion or extrusion. This is where there is a tear in the fibers of the annulus, and some of the nucleus pushes out. There terms can be very confusing to patients, especially when they may not have anything to do with the cause of the pain and could lead to unnecessary interventions including surgery. 


Disc herniations can and do cause pain if they compress the nerves as they exit the spinal column. Although the problem is in the spine, it is a characteristic of nerve compression pain that it feels as if it is coming from along the nerve. It is like the phantom pain of the amputee, were the missing part of the leg is where the pain feels like it is. “Sciatica” is a term often used for nerve compression pain emanating from the low back, although in my experience patients complaining of sciatica often do not have this pattern. Classic sciatica begins in the buttock, generally not in the midline of the back itself, and seems to travel down the back of the thigh, calf and then wraps around the inner ankle bone into the foot. The 4th and 5th toes my have burning or tingling. Because the lowest level of the low back, L5-S1 where the lowest vertebral bone rests on the sacrum, a bone formed of a number of fused vertebra which form a triangular bone which sits between the two iliac bones “hip bones”. This level is the most common to cause nerve pain, and so most nerve compression pain is classic sciatica, but if higher up nerves are compressed, the location of the pain changes, in a pattern which can be helpful diagnostically. 


In the development of the fetus, we start out as a long tube made up of vitally similar segments. Some segments merge and become very specialized, as in or brain and head, some into the arms or legs. The spine retains the segmental pattern, so a “segment” is made up of the vertebral bone, the disc, and a pair, right and left, of spinal nerve “roots”. A compressed or pinched nerve, if it causes pain we call that “radicular” since the latin word for root is “radicle”. Things getlittle more complicated in the low back because the spinal cord, from which all the nerves peel off at their segment, is shorter than the bony spinal column. The end of the cord is about L1 or L2 more near the top of the low back. So the nerves need to travel past a couple of disc levels before exiting at the level associated with the nerve. Commonly the nerve is compressed in the canal,called the foramen, as it exits the spine. A foramen is just a hole or tunnel. This may be narrowed in several ways. A common way, especially in younger persons who aren’t likely to have the other problems, is a protruding disc. The edge of the disc runs all along the edge of the adjacent vertebral bones, but herniations in some locations aren’t really a problem. Since the spinal canal is behind the main vertebral body, enclosed in the parts of the protective arch, herniations in the front bulge into the fat and muscle in the front, and aren’t big enough to cause a problem. If the bulge is to the rear, and especially if off to one side or the other, it can compress the nerve as it is in or just outside of the canal. Typically this will be one or the other side and not both at the same time, because if both sides are bulging then so is the center, and that tends to cause other problems, spinal stenosis or the cauda equina syndrome by compressing the bundle of nerves coming from the end of the spinal cord. The spinal cord and the nerve roots don’t like to be touched. They float in the thin fluid enclosed inside the spinal canal, called cerebrospinal fluid. There is normally plenty of fluid around the nerve root until it is outside if bony column when the “dura mater” the thick membrane surrounding the brain and spinal cord merges with the nerve now nestled in muscle and fat. The foramen that the root passes is dynamic in its size and capacity, because the bony part of the canal is formed by a notch in the arch of the upper and of the lower vertebra. When we move, these bones come closer together and father apart. When they come closer, and if other problems are contributing to the narrowing, there might be pain only in certain positions. Typically if compressed in the foramen, backward bending of the spine will worsen the compression so positions in which this happens, including standing or walking, tend to aggravate. In addition to the disc, the canal may be encroached upon by bone spurs, which occur as a result of disc degeneration, coming from the edges of the vertebral body. If these protrude backwards and outward they can narrow the foramen. There is a bony arch coming from each vertebral body, to protect the spinal cord and nerves. To allow smooth movement and to coordinate the arches at adjacent levels, there are little joints on each side from one arch to the next. This are cartilage joints and can develop osteoarthritis like the knuckles and the knees. Bone spurs, technical term “osteophytes” also occur as a result of Osteoarthritis, and if they go backward and inward can narrow the foramen. Sometimes other things can contribute to the narrowing (technical term stenosis) including thickened ligaments and sometimes a forward or backward slippage of on vertebra on the other known as a “listhesis”. The nerve root can also be compressed at a level or sometimes 2 levels above where it exits. As it nears it’s exit point it lies farther to the side, and can be compressed in the “lateral recess”. So a single nerve root, which may have a characteristic pattern of pain, might be compressed at one of 2 or even 3 levels. Stenosis or narrowing in the foramen, the lateral recess or the main canal can be of varying severity. Usually symptoms aren’t associated with narrowing less than “severe” or “moderately severe” on MRI reports (the nerves can’t be seen on X-ray), and these narrowing are also common in patients with no back or limb pain. Stenosis of the main canal can cause a pain pattern of “neurogenic claudication” Claudication can occur with narrowed arteries limiting blood flow into the buttocks or legs, but neurogenic claudication causes a somewhat similar pattern, in which the pain comes on the longer and more vigorous a person walks, and to relieve the pain they can’t just stop but must sit or bend forward. So disc problems are common, may or may not cause pain but if they do it is radiating limb pain one not typically back pain.


Back pain, midline or at least symmetrical (although can be right or left) canbe caused by pain arthritis of the little facet joints, although many many of us as we age develop this arthritis and do not have pain. Some features can be helpful. The pain is usually pretty close to the midline of the spine, at the level of the painful joint, although may travel down and out some, sometimes at L5-S1 down the back of the thighs, but not beyond the knee like radiculopathy. Because the axis of bending of the spine is through the middle of the vertebral body, bending forward opens up or gaps the facets, and generally is more comfortable, and bending backwards puts more pressure on the joints and is painful. This can be useful diagnostically, although myofascial pain can have the same pattern depending on the nature of the original injury. 


Since painless arthritis is common, finding changes of facet arthritis on X-ray or MRI does not at all prove that the joint is the source of pain. If suspicious based on features noted above, and if disabling, diagnosis can be determined or refuted by specialized injections which are done under fluoroscopy or video X-ray. There are 2 approaches, one is to inject a local anesthetic directly into the joint. If the pain is received for the duration of the anesthetic, from 2-18 hours depending on which anesthetic was used, that is considered diagnostic of acetogenic pain. Usually a cortisone type steroid is injected as well. This can be helpful for a few months, although it has been hard to prove there is general benefit in randomized trials comparing to a sham injection. A more useful therapeutic approach is to block the small nerve that goes to the joint, called the median branch, which sends signals of pain to the spinal cord and brain. This nerve can be “ablated” or “burned” by a catheter which emanates radiofrequency waves, and heats up the tissue. This blocks the pain transmission. This can also cause a small area of numbness of the skin in the area, and weakness a small area of muscle, but usually these are not significant. The nerve does regrow, and pain may reoccur in 3-18 months, although the procedure can be repeated. To see if the procedure might be effective, diagnostic injections with local anesthetic are done to see if the pain is temporarily resolved. These diagnostic injections are called “median branch blocks”, and the radiofrequency procedure is called RFA, radiofrequency ablation, median branch radiofrequency rhizotomy and other names, most commonly “RFA”. 


Non-interventional approaches to back pain include physical therapy. One approach, developed at New England Baptist Hospital, is called “Functional restoration” or often “Back boot camp”. This involves vigorous exercise aimed at strengthening the back muscles, recognizing that there will be pain involved in doing the exercises for a few months, but physical therapists are trained to coach people through this. I have generally recommended strengthening exercises in between episodes of pain, or after the pain has been reduced or resolved with my approach to manipulation.