doi:

International Journal of Osteopathic Medicine 8 (2005) 39e40

www.elsevier.com/locate/ijosm

Editorial

What is the significance of somatic dysfunctionin a multicausal model of aetiology?

The early developers of osteopathy borrowed heavilyfrom mechanistic materialism, inasmuch as the philoso-phy of mechanistic materialism is the basis of thephilosophy of osteopathy.1 One of the characteristics ofthe framework of mechanistic materialism is that forevery cause there has to be an effect, and for everysingular effect, there has to be a single cause. Put simply,an event ‘A’ occurs, and as a result of ‘A’ occurring,another event ‘B’ occurs; therefore ‘A’ caused ‘B’. This issimple reasoning. We use it in our daily lives to explainthe phenomena that surround us because it is uncompli-cated and quickly turns our observations into mind-orientated knowledge.

For example, in the event of a motor vehicle accident,we might say that one car failed to stop at an intersectionand impacted into another vehicle. Therefore, failing tostop at an intersection caused the accident (A caused B).This is very convenient.However, closer inspection revealsthat it explains little about what really happened. Whatwas the real reason or reasons why the car failed to stop atthe intersection?Did thebrakes fail andwas this the cause?Did the traffic signals fail and was this the cause?

So, what was it that caused the accident e the failedbrakes, or the failed traffic lights? One can see that theprevention of future accidents depends upon the answerto this question.However, what if bothwere true?What ifthe traffic signals were not working and, just at the criticalmoment when the brakes were needed, they too failed?What about driver concentration? Perhaps the driver fellasleep momentarily. In this case we might say that thesleeping driver caused the accident. But what if all threewere true? Asleep for a few seconds, the driver wakes tofind himself entering into a road with oncoming traffic.The traffic signals had failed to work and as the brakeswere applied, they too failed and the accident ensued.

In this last scenario, it appears that we have threepotential causes. However, there aremore. The driver wassleeping because the medication he had been prescribedfor an illness had made him drowsy. So, enter themedication into the mix of causal factors. The practi-

10.1016/j.ijosm.2005.04.003

tioner who had prescribed this medication had failed toinform the driver that it might make him drowsy. So,enter the practitioner’s lack of communication into themix of causal factors.

What really caused this accident?Well, isn’t it obvious,anyone can see that the car entered an intersection intooncoming traffic and caused an accident. However, thisanswer is superficial and, from a scientific point of view,unacceptable. It is a mere description of observed eventsand tells nothing about why the event occurred.

Wemust be careful not to use such simplistic reasoningas the basis for our understanding of osteopathy, somaticdysfunction, and health. Yet, unfortunately, this typeof thinking is rather widespread. In the language ofepidemiologists,2 the idea that somatic dysfunction cancause symptomatic effects would be that somaticdysfunction is both necessary and sufficient to cause theeffect. In other words, the effect cannot occur in theabsence of somatic dysfunction (it is necessary), andsomatic dysfunction, in and of itself, can cause the effect(it is sufficient). However, since in human biologyintermediate steps are virtually always present in anycausal process, the concept that somatic dysfunction isboth necessary and sufficient to cause symptoms orpathology is likely to be false.

Perhaps the culture for this thinking is derived, at leastin part, from the famous quote of Still: ‘‘find it, fix it andleave it alone’’. This statement implies and encouragesthe concept of monocausality, a concept prevalent inStills era, that there is only one thing causing the effectand if you can find and correct ‘it’, then removal of thiscause will remove the effect. This idea is manifest in theconcept of the ‘primary’ somatic dysfunction. ‘‘If wecould just find the primary, and correct it, then all thesecondary dysfunctions and symptoms would be re-solved.’’ This concept places considerable pressure on theosteopath to find the primary dysfunction, yet findingthe primary dysfunction with any accuracy relies uponthe existence of a method for detection that has provenreliability and validity.

40 Editorial / International Journal of Osteopathic Medicine 8 (2005) 39e40

An alternative to thinking about somatic dysfunctionas monocausal (being both necessary and sufficient tocause symptoms), is to consider that somatic dysfunctionmay be necessary, but not sufficient. That is, somaticdysfunction has to be present in order for symptoms toarise, but that the presence of somatic dysfunction aloneis not sufficient to cause symptoms, and that the presenceof some other factors are required before the symptoms(effect) occurs.

Alternatively, somatic dysfunction might be sufficient,in and of itself, to cause symptoms, but not necessary;meaning that some other factor may also produce thesame symptoms in the absence of somatic dysfunction.Such factors should be identified when present andmanaged appropriately.

The final scenario provides for the possibility thatsomatic dysfunction may be neither necessary norsufficient to produce symptoms; and this possibilityshould be given serious consideration in regards to ourunderstanding of the osteopathic approach to health care.

At first glance, this statement may be unacceptable, asit challenges the validity of a fundamental concept ofosteopathy. Another illustrative example may help tofurther explain this statement. Nociception is oftenconsidered to be the basis of pain and has been presentedthis way in textbooks for many years. In fact, one mightconsider that nociception causes pain. This is a simple ‘A’causes ‘B’ hypothesis where ‘A’ is necessary and sufficientto cause ‘B’. However, this concept has been invalidatedby modern studies of the human pain experience over thelast few decades, and now nociception is known to beneither necessary nor sufficient to cause pain. Firstly,nociception is not sufficient to cause pain, and there aremany examples of nociceptive information being trans-mitted in peripheral neurons, but which does not lead tothe experience of pain. Explanations for this phenomenoninclude the gate theory of pain control at the dorsal horn,and also endogenous pain inhibition pathways arising inthe rostral medulla and periaqueductal grey matter of thebrainstem. Also, pain can be experienced in the absence ofnociception (e.g. in some thalamic stroke syndromes,brainstem lesions and in deafferentation pain), meaningthat nociception is not necessary for pain to be experienced.

Nociception is, of course, still physiologically impor-tant; however, any monocausal relationships that wepostulate about nociception are simplistic. Like nocicep-tion, somatic dysfunction might not be as significant incausation as it is often reputed to be. If this were so, itwould help to explain why clinically relevant somaticdysfunction is difficult to measure objectively. Further,it may help to explain why studies investigating osteo-pathic manipulative treatment fail to show convincingand compelling results when the treatment in such studiesare based on a diagnosis of somatic dysfunction.3

For example, if the study population consisted ofthose with lumbar spinal pain (LSP) of unknown origin,then this group might have representatives fromdifferent sub-groups, such as:

(1) LSP, but no somatic dysfunction;(2) LSP with somatic dysfunction, but that this somatic

dysfunction is not clinically relevant; or(3) LSP with somatic dysfunction that is clinically

relevant.

In any randomised controlled trial investigating theefficacy of osteopathic manipulative medicine in treatingpatients with LSP, an inability to accurately differentiatebetween those with, and without clinically relevantsomatic dysfunction, would mean that patients in theOMT group would include those without clinicallyrelevant somatic dysfunction (for which OMT wouldnot typically be indicated). This represents non-differ-ential bias and typically has the effect of diluting theresults in favour of finding no effect for the treatment.

At present, there are no definitive prospective studiesdemonstrating that somatic dysfunction increases therisk of symptoms, such as LSP. Using the logic ofclinical reasoning, a treatment should be recommendedon the basis of a valid diagnosis, and the predictivevalidity of a diagnosis provides a rationale for treatmentbecause it addresses the pathophysiology described bythe diagnosis. Therefore, an urgent area of research forour profession is to determine the significance of somaticdysfunction in a multicausal model of aetiology.

References

1. Ferrell D. Osteopathy’s relationship to allopathy through the

perspective of the history and philosophy of science. Part II.

Australas Osteopath Med Rev 1998;2:60–70.

2. Gordis L. Epidemiology. Philadelphia: WB Saunders; 1996.

3. Licciardone JC, Stoll ST, Fulda KG, Russo DP, Siu J, Winn W,

et al. Osteopathic manipulative treatment for chronic low back

pain: a randomized controlled trial. Spine 2003;28:1355–62.

Nicholas Lucas*School of Exercise & Health Sciences,

University of Western Sydney,Sydney, Australia

E-mail address: n.p.lucas@uws.edu.au

Robert MoranSchool of Health & Community Studies,

Unitec New Zealand,Auckland, New Zealand

E-mail address: rmoran@unitec.ac.nz

*Corresponding author.