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Facilitated Segments

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The passage critically reviews the concept of facilitated segments which has dominated osteopathic neurophysiology. It aims to reexamine the original studies and reinterpret the findings in light of current neurophysiology knowledge.

The passage notes several criticisms of the facilitated segment model. It does not account for descending influences from higher centers, anatomical specificity is lost within the spinal cord, and it creates a biological paradox not supported by research or clinical observations.

The text lists three specific problems with the model: 1) it does not include descending influences, 2) segmental specificity is lost within the spinal cord, and 3) it creates a biological paradox not supported by research.

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FacilitatedSegments

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FacilitatedSegments:acriticalreview
Keywords:Facilitatedsegments,manualtherapy,osteopathy
The concept of spinal facilitated segments has dominated osteopathic neurophysiology for
over half this century. This concept has been at the heart of osteopathic teachings and is
oftenusedbothinclinicaldiagnosisandaspartoftherationaleoftreatingdifferentmusculo
skeletal and visceral conditions. Surprisingly, such an important subject has never been
criticised: the existence of facilitated segments and their relevance to manual therapy or
osteopathic medicine has never been questioned. This article reexamines the original
studiesofKorr,Denslowandtheircoworkers,aimtoidentifywhathasbeendemonstrated
in these studies and to reinterpret their findings in the light of current knowledge of
neurophysiology.
Thespinalfacilitationconcept
Inprinciple,thefacilitatedsegmentwasdescribedasaspecificareaofthespinalcordthat
wascapableoforganisingdiseaseprocesses.Itwasaverysimplisticmodel:ithadtwoinput
and two output routes. The input routes were sensory from musculoskeletal and viscera.
Theoutputrouteswerethemotorefferentstomuscleandautonomicmotortosweatglands,
bloodvesselsandviscera.Insidethespinalcorditwassuggestedthatabnormalactivityin
oneareaofthespinalcordcouldspreadtoadjacentareas.Thefacilitationprocesswouldbe
initiatedwhenaberrantsensoryinformationfromanareaofdamageorpathology(muscleor
viscera) was conveyed via the afferents to the spinal cord. This would alter the neuronal
activityatthesamesegmentallevelandmightspreadtoadjacentareasofthespinalcord
affecting spinal centres not directly related to the original injury. For example, a
musculoskeletal injury could reach the spinal cord through its afferent connection causing
spinal facilitation or sensitisation to take place. Because of the anatomical proximity of the
motorandautonomicspinalcentres,thisspreadofexcitationwouldeventuallyinvolvethese
lateralcentres.Thisinturnwouldalterthesegmentalautonomicactivityleadingtochanges
in vasomotor, sudomotor and visceral activity. The reverse could happen too: through the
sameneurologicalmechanismsapathologicalconditioninthevisceracouldendupaffecting
skeletalmuscleactivity.
Even before examining the original research, we can see that there are several problems
withthefacilitatedsegmentmodel:
a.Thedescendinginfluencesfromhighercentreswerenotincludedinthemodel,although
theyhaveprofoundsegmentalinfluences.Thisomissionisunrealisticthespinalcentresdo
not work in isolation from the higher centres. Both movement and autonomic activity are
heavilyorganisedfromabovethespinalcord(Sherrington,1906Folkow,1956Bard,1960
Brown,1968Ganong,1981Schmidt,1991).
b. Outside the spinal cord afferent and efferent connections are, anatomically, highly
segmental. However once in the spinal cord all anatomical specificity is lost (Luscher &
Clamann, 1992). Motoneurons of several muscles are intermingled within the ventral horn
anddistributedoverseveralsegmentsupordownfromthepointofexit(efferentperipheral
nerve).Similarlyafferentsfromoneareaormuscle,onceinthespinalcord,tendtodiverge
up and down over several segments terminating on many different motoneurons and
interneurons (Luscher & Clamann, 1992). For example, spindle afferents from one muscle
connectwithmotoneuronsofothermusclegroups(Ecclesetal,1957Eccles&Lundberg,
1958). This implies that if lateral spread of sensitisation does take place, it will not
necessarilybesegmentallyspecific.
c. The facilitation model creates a biological paradox which is not supported either by
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research or by clinical observations. If damage in muscle caused spinal facilitation and


consequentlyvisceraldysfunction,itwouldmeanthateachtimewedamageourmusclesit
wouldautomaticallyresultinsomevisceraldysfunction.Inthisscenariocommonconditions,
suchasdelayedonsetmusclesorenesswhichisassociatedwithmuscledamage(Bobbetet
al, 1986 Ebbeling & Clarckson, 1989), would inevitably lead to visceral dysfunction. Yet,
'viscerally' speaking, most sports people are fairly healthy. They do not seem to develop
visceraldysfunctioninresponsetoacuteorchronicmusculoskeletalconditions.
Theoriginalresearch
Korr, Denslow and their coworkers were the first to describe the facilitated segments in
osteopathicmedicine.Theoriginalresearchconsistedofseveralstudieswhichwerecarried
outonalargenumberofnormalhealthysubjects.Theyuseddifferentexperimentalsetups
andwereabletodemonstratethefollowingfindings:
1.Varyingmotorthresholdspressureoverthespinousprocessesproducedreflexmuscle
contractionatandclosetothesegment.Insomesegmentsthisresponsewasexaggerated
(Denslowetal,1947).Everypersonhadanindividualpatternofresponse.
2.Varyinglevelsofskinconductivitythereweredifferencesinthesweatingpatternofthe
backs of all normal individuals (Korr et al, 1958). This suggests increased activity of the
sweatgland,implyingalteredsympatheticactivity.
3.Varyinglevelsofvasomotoractivityusingtemperatureandlightsensorstheywereable
todemonstratethatallnormalsubjectshaveindividualvasomotoractivitywhichischanged
indifferentpartsoftheback(Wrightetal,1960).
4.Viscerosomaticchangessometimes,knownvisceralpathologiesmanifestedsegmentally
asincreasedskinconductivity(Korretal,1964).
5.Eachindividualhadauniquethermalpatternwithsomecommonpatternssharedbyall
normalsubjects(Wright&Korr,1965).
Contrarytocommonlyheldbelief,theydidnotdemonstratethefollowing:
1.Theydidnotshowfacilitationmostofthestudieswerecarriedoutonnormalhealthy
subjects. In all subjects they found varying levels of neurological activity at different
segmentallevels.Thisisacomplexsituationtobeginwith:ifthesubjectswerehealthyhow
cometheyalldisplayedasupposedlyneuropathologicalstateoffacilitation?Ifthebiological
normisthathealthysubjectsallshowsignsoffacilitation,itimpliesthattheregionalchanges
observedprobablyrepresentthenormalvariabilityofahighlycomplexsystemratherthana
facilitation phenomenon. Such variability can be demonstrated anywhere in the body. For
example, if you prod different parts of your own leg, you will find some areas are more
tender, with the muscles feeling stiffer, and if you press hard enough you may make the
muscle contract to evade pain and discomfort. When this procedure was applied to the
spine,asDenslowetal(1947)did,itwasveryattractivetoviewitassegmentalfacilitation.
Spinal facilitation does occur and can be seen following musculoskeletal injuries. It is well
established that inflammation produces both peripheral sensitisation of the afferents (such
asfreenerveendings)andcentralsensitisationwithinthespinalcord(Dunbar&Ruda1992,
Hyldenetal1989,Cooketal1987,Woolf&Walters1991).Thissensitisationmeansthatthe
threshold of different neurons is reduced, so they respond to mechanical stimuli to which
they were impervious before injury. This process tends to spread laterally in the spinal
cord but in a selective way not all neurons are sensitised. The selectivity of the spread
seems to be functional in character supporting the process in some way. For example,
lateralsensitisationhasbeenshowntospreadtothemotoneuronswhichsupplythemuscles
intheaffectedarea(Heetal,1988).Thismayhaveafunctionalroleinthemuscleguarding
often observed at the site of damage. It is very difficult to imagine what would be the
functionalroleofalateralspreadtoautonomicvisceralcentresinmusculoskeletaldamage.
It should also be noted that the sensitisation process seems only to take place when
nociceptorsareexcitedbypainorinflammationandnotwhenproprioceptorsarestimulated,
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suchasduringamanualtreatment.
A similar sensitisation phenomenon was demonstrated by Korr and his coworkers (1962),
by introducing chemical insults to different spinal structures. They demonstrated that this
lateral spread could alter sympathetic activity to the segmental sweat glands. This change
only took place when pain was inflicted. However, the spread was not always 'neatly'
segmental some of the changes were general or remote from the segmental distribution.
This finding is not surprising in the light of what has been discussed about afferent
divergencewithinthespinalcord.Thesechangesinsympatheticactivitymaynotnecessarily
have been due to facilitation. They may arise as a secondary functional physiological
process,e.g.tosupportchangesinmuscleactivityortheinflammationprocessatthesiteof
damage. Furthermore, such sympathetic changes in sudomotor activity have no clinical
relevance to osteopathic practice. More important clinically are changes in motoneuron
thresholdbyspinalsensitisationasdescribedbyHeetal(1988).
WhenKorretal(1962)introducedposturalinsults,suchasheelliftsononeside,orhaving
the subjects sit on a tilted chair, they observed changes in the pattern of sweating. The
changes were general but sometimes more noticeable as an exaggeration of the pattern
observed before the insult. Again, they concluded that these changes were due to
facilitation. However this is also doubtful: the changes were probably due to whole body
adjustmentstochangesinpostureratherthanalocallyorganisedchangeinthespinalcord.
Heretoothelegcanbeusedasanexample.Ifyouaskasubjecttostandononelegthere
willbeconsiderabledifferencesinthemuscleactivitiesofthetwolegs.Naturallytheblood
supply and sweat gland activity will also vary considerably between the two legs with an
increase in activity in the balancing leg. These are whole body postural adjustments
incorporatingcomplexpatternsofneuromuscularandsupportiveautonomicchanges.These
patternsofrecruitmentareorganisedwithinthewholesystemratherthensegmentallybythe
limitedandlocalprocessesoffacilitation.
All the changes that were demonstrated were during separate studies on different
individuals: one study showed that in normal subjects there may be a variable pattern of
muscleresponsetopressure(Denslow,1947).Anothershowedchangesinskinconductivity
(Price&Korr,1957),andathirdshowedvariabilityofvasomotortone(Wright&Korr,1960).
Theynevertookthelogicalstepofexaminingallthreephenomenaoffacilitationinthesame
group of subjects! This is equivalent to seeing three different patients, one with joint pain,
onewithconjunctivitisandanotherwithurethritis,anddiagnosingthemallashavingReiter's
Syndrome!Eventuallytheydidexaminethethreemanifestationsoffacilitationinagroupof
subjectswithmusculoskeletalinjuries.However,forsomereasonnotallsubjectshadthefull
testprocedure,e.g.somehadskinconductivitybutnotEMGexamination.Inthisstudythey
claimed that "frequently" the exaggerated patterns were segmentally related to the site of
injury.Thissuggeststhatthenervoussystemdoesnotrespondinastereotypicmannerto
injury. Unfortunately no statistical analysis was carried out on the data and their use of
terminologysuchas"frequently"isnotveryhelpfuldoesitmean10%or90%ofsubjects?
Furthermore they never compared the findings of this study (subjects with musculoskeletal
injuries) to the extensive control group of the previous studies (normal subjects).
Interestingly,whenonecomparesthephotographsofskinconductivityofsubjectswithinjury
(Korretal,1964,pages6870)tothoseofnormalsubjects(Korretal,1958,pages3537),
theydon'tseemtobedifferent.Theresultsinthisstudycouldbeinterpretedliketheresults
oftheirotherstudiestheydemonstratedindividualvariabilityratherthanfacilitation.Overall,
given that the studies did not exclud the influences of higher centres and made no direct
recordingsfromthespinalcorditcanbearguedthatallthechangesobservedinthestudies
werenotduetolocalsegmentalfacilitationbutwereinfactorganisedbythetotalnervous
system(withtheprominentroleofsupraspinalcentres).
2.TheydidnotdemonstratesomatovisceralreflexesTheseearlystudiesdidnotshow
thatabnormalmuscleactivityorskeletalabnormalitieswillspreadtoaffecttheviscerabythe
process of facilitation. This is a very important point: they assumed (along with many
generationsofosteopaths)thatsympatheticchangestosweatglandsoftheskinmeanthat
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thewholesegmentalautonomicsystemhasbeenaffectedincludingtheautonomiccentres
controlling visceral activity (Korr, 1948 Korr et al, 1962 Korr 1978). This conclusion is a
fantastic hypothetical leap, one which was never demonstrated in humans with intact
nervous systems. Furthermore, they did not show that stimulation of mechanoreceptors
(proprioceptors)wouldcauseachangeinvisceralactivity.Theysimplyobservedthetriadof
muscle tone, local tenderness and local sympathetic changes (skin conductivity and
vasomotor). The generally held belief that stimulation of different groups of proprioceptors
canaltervisceralactivitywasneverdemonstratedinthesestudies.Theyhavedemonstrated
the reverse: that sometimes, known visceral pathologies manifested segmentally as
increased skin conductivity. However, that does not mean that the reverse is true, i.e. that
stimulation of the soma will alter the activity in the viscera. This would be comparable to
suggestingthatsincewereflexivelycloseoureyesduringsneezing,wewouldsneezeeach
timewecloseoureyes.
3. They failed to demonstrate relevance to osteopathic manual therapy Another
interesting point is that there is no mention in all these studies of which form of manual
techniquecouldbringaboutautonomicchanges.Thelogicalnextstepofthesestudieswas
never taken and was totally sidestepped in the articles, i.e., testing the effect of different
formsofmanualtechniquesonspinalfacilitation.Withoutdiscussingtechniques,theconcept
offacilitatedsegmenthasnomeaningtoanosteopath.Theosteopathneedstoknowhowto
change the activity of the facilitated segment. So many generations of osteopaths have
assumedthathighvelocitythrusts(HVT)arethemostappropriateformofmanipulationfor
normalisingorresettingthefacilitatedsegment.
Recentstudiesintotheeffectsofmanualtechniquesonneuromuscularactivityhavestrongly
suggestedthatpassivemanualtechniquesareunlikelytoaffectthissystem(Sullivanetal,
1991 Kukulka et al, 1986 Leone & Kukulka 1988 Belanger et al, 1989 Goldberg, 1992
Sullivan et al, 1993 Lederman, 1997 Newham & Lederman, 1997). They only produce a
transient artefact event that has no permanent influence on, or ability to bring about
functional changes in overall motor processes. Even if one accepts the possibility of
facilitated segments as described by Korr, Denslow and their coworkers, it is extremely
doubtful that passive stimulation of the soma would result in the resetting of neurological
activity (Lederman, 1997). All neuromuscular activity is organised centrally to spread
centrifugally to the periphery (Schmidt, 1991). The peripheral receptors (proprioceptors /
mechanoreceptors)providefeedbackratherthancontrolthemotorsystem.
Fascinatingsegments
Thecriticisminthisarticleisnotaboutthequalityoftheresearchbuttheinterpretationsof
theresultsandthefarreachingconclusionsthatweredrawn.Overallintheirstudies,Korr,
Denslowandtheircoworkersdidnotdemonstratethefacilitationphenomenon.Inthelight
ofourcurrentunderstandingofneurophysiologyitisdoubtfulwhetherthefacilitatedsegment
model as described by Korr, Denslow and their coworkers has any neurological basis or
clinicalapplication.
Aninterestingquestionarises:whatwasandstillissoattractiveintheconceptoffacilitated
segments? The answer I believe lies in the high velocity thrust (HVT) and segmental
adjustments.Theconceptofthefacilitatedsegmentprovidesthejustificationforperforming
averyaccurateHVTonparticularsegments.ItgivestheHVTaphysiologicaldepthbeyond
thebiomechanicalstructuralfixingofthespine.Theosteopathisnowabletoreachdeepinto
the interior of the patient to affect visceral pathologies. This was done at a great cost to
osteopathy osteopathic understanding of neurophysiology has starts and ended at the
facilitated segment. In my view, the principle of the facilitated segment has stifled the
developmentofosteopathicneurophysiologyforthelast50years.Importantissuessuchas
neuromuscular rehabilitation following musculoskeletal injuries, central nervous damage,
posture and movement guidance, the psychodynamics of touch and psychophysiological
processes and pain management have never been addressed in depth. Some of these
issuesandtheirrelevancetoosteopathyandmanualtherapyhavebeendiscussedindetail
byLederman(1997).
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Thewayforward
Thereisaneedinosteopathytodevelopabetterunderstandingofneurophysiologytosee
thewiderpictureratherthanconcentrateonasinglefractionofthetotalsystem/person.
Therealsoneedstobeabetterunderstandingofhowosteopathicmanualapproachescan
be developed to become effective therapeutic processes for treating the nervous system.
This is essential for working with a wide range of clinical conditions which have a
neurophysiological element in them. Some of these are common clinical conditions that
osteopaths see in daily practice such as postural and movement changes, neuromuscular
changesfollowingmusculoskeletalinjuriesandtheneurophysiologicalaspectsofpain.
In order to influence the nervous system treatment should imitate natural processes that
bringaboutchangesinthenervoussystem.Mostimportantistheuseofcognition,volition
and repetition and avoiding the use of reflexive type treatments that have been
demonstrated to have no long term effects (Lederman 97, Newham & Lederman 97).
Lederman (1997), has discussed in detail how these elements of neurophysiology can be
incorporatedintoandexpandosteopathicpracticeenablingthetreatmentofawiderrangeof
conditions.Someofthesepointswillbediscussedinfuturearticles.
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