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Trigger Points

Trigger Points

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Published by: rudhras22 on Jul 19, 2010
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10/25/2012

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 RESEARCH IDEAS
Trigger Points and Central Modulation—A New Hypothesis
Mark J. L. Hocking, BVSc
ABSTRACT. Objective:
A new hypothesis is proposed to explain the pathogenesis, symptoma-tology, and treatment of the trigger points [TrPs], which define the myofascial pain syndrome[MPS].
Hypothesis:
TrPs are formed due to sustained
α
-motoneuron plateau depolarization, whichis maintained by one of two different central nervous system [CNS] mechanisms. “Antecedent”TrPs are formed in withdrawal reflex agonist muscles due to central sensitization of the C fibernociceptive withdrawal reflex [NWR], visceromotor reflex [VMR], or nociceptive jaw-openingreflex [NJOR]. “Consequent” TrPs result in withdrawal reflex antagonist muscles due to compen-satory reticulospinal or reticulo-trigeminal motor facilitation. Afferent nociceptive signals arisefrom both latent and active TrPs. However, latent TrPs are not spontaneously painful, because of complete inhibition of nociceptive transmission at the spinal cord or trigeminal nucleus [SC/TN]levels. Marked SC/TN sensitization [especially with a reduced antinociceptive functional reserve]may overwhelm the brainstem antinociceptive mechanism, going beyond the MPS into the gen-eralized allodynia of the fibromyalgia syndrome [FMS]. The principal brainstem nuclei involvedin TrP sensory and motor modulation have other diverse homeostatic roles; therefore TrP-inducedbrainstem dysfunction may contribute to the pathogenesis of a variety of sensory, motor, and au-tonomic disorders. Treatment involves noxious stimulus-induced transient inhibition of the CNSmechanisms that sustain TrPs. This allows stretching of the contractured muscle fibers to resolvethe TrP local energy crisis, and to reverse muscle nociceptor and CNS sensitization.
Conclusion:
This hypothesis proposes that TrPs result in the muscles due to sustained
α
-motoneuronplateaudepolarization.DescendinginhibitionnormallyensuresthatmostTrPsremainlatent, but FMS may result if this inhibitory mechanism is overwhelmed.
KEYWORDS.
Myofascial pain syndrome, trigger points, central sensitization, ventromedialmedulla, descending modulation
 INTRODUCTION 
In this paper I propose a new hypothesis forthe pathophysiology of trigger points [TrPs]. As
Mark J. L. Hocking, BVSc, Gladesville Veterinary Hospital, Gladesville NSW, Australia.Address correspondence to: Mark J. L. Hocking, BVSc, Gladesville Veterinary Hospital, 449 Victoria Road,Gladesville NSW 2111, Australia. E-mail: mark.j.hocking@hotmail.com
a veterinarian who frequently treats the TrPs of dogs, I cannot reconcile some of my clinical ob-servations with current TrP hypotheses. Theseobservations include the following: first, the
186 
Journal of Musculoskeletal Pain, Vol. 18(2), 2010Available online at www.informaworld.com/WJMP
C
2010 Informa Healthcare USA, Inc. All rights reserved.doi: 10.3109/10582452.2010.483964
 
 Hocking 18
most clinically relevant TrPs [those that restrictstride and distort posture] are found predomi-nantly in flexor muscles. Second, after treatmentof all TrPs in a lame limb, the lameness willsometimes shift to another limb. Third, despiteit being obvious that not all canine TrPs are ac-tive [multiple TrPs are usually found in the lamelimb and TrPs are also typically found in thenon-lame limbs], it is normally impossible todetermine which TrPs in a lame limb are activeand which are latent. All TrPs feel similar, pal-pation elicits similar pain reactions, and appro-priate stimulation induces a similar local twitchresponse.I have brought together relevant informationfromnumeroussourcesinanefforttoexplainmyobservations. These sources include the humanTrPliterature[readersarereferredtoTravellandSimons(1)andMenseandSimons(2)foracom-prehensive TrP review] and published pain andotherneurophysiologicalexperimentalresearch.Myhypothesisattemptstoexplainthepathogen-esis, symptomatology, and treatment of TrPs inboth humans and other vertebrates. It may alsohelp to solve the larger puzzle of pain and pro-vide insight into the pathogenesis of a variety of other incompletely understood sensory, motor,and autonomic disorders.
 Fundamental Trigger Point Pathophysiological Mechanism
I propose that TrPs do not form due to a criti-calabnormalityofneuromuscularfunctionatthemotor endplate of an extrafusal skeletal mus-cle fiber (3), but are the result of the chronicexpression of an intrinsic
α
-motoneuron prop-erty, the plateau potential. A plateau potentialis a sustained partial depolarization of an
α
-motoneuron that may persist for at least severalseconds after synaptic excitation has reducedorceased(4).
α
-Motoneuronsmayexhibitthein-trinsic membrane property of bistability, wherethey are stable at either of two different mem-brane potentials: a less excitable, more hyper-polarized state and a more excitable, partiallydepolarizedplateaustate(5,6).Repeatedplateaupotential activation leads to
α
-motoneuronwarm-up, where there is a decreased thresholdfor, and increased duration of, plateau poten-tials (7). Sustained partial depolarization of the
α
-motoneuron increases the release of acetyl-cholinepacketsatthemotorendplate.Thisman-ifestselectricallyasendplatenoise,whichcanberecordedbyneedleelectromyogramattheactivelocus of a TrP.I propose that centrally maintained
α
-motoneuron plateau depolarization, rather thanan intrinsic disorder of the motor endplate, isthe fundamental pathophysiological mechanismwhich perpetuates the local muscle contractureassociatedwithaTrP.Warmupof 
α
-motoneuronplateau depolarization is maintained by oneof two different central nervous system [CNS]mechanisms, resulting in two essentially differ-ent types of TrPs, which I call “antecedent” and“consequent” TrPs. Antecedent TrPs are sus-tained by central sensitization of the C fiberpolysynaptic withdrawal reflexes: the NWR,the VMR, and the NJOR. Antecedent TrPs areformed in withdrawal reflex agonist muscles,which are generally, but not exclusively, flexormuscles.ConsequentTrPsaresustainedbytonicreticulospinal or reticulo-trigeminal facilitationof plateau potentials in withdrawal reflex an-tagonist
α
-motoneurons. Consequent TrPs areformed in withdrawal reflex antagonist muscles,which are generally, but not exclusively, exten-sor muscles.
 Pathophysiology of Antecedent Trigger Points
The withdrawal reflexes are complex polysy-naptic reflexes, mediated by spinal cord ortrigeminal nucleus [SC/TN] neural circuitry thatfacilitate either rapid withdrawal from a poten-tially damaging acute stimulus or ongoing im-mobilizationofaninjuredareatopreventfurtherdamage and allow healing. Activation of theNWR typically results in simultaneous contrac-tion of ipsilateral limb flexor muscles and re-ciprocal inhibition of ipsilateral limb extensormuscles to effect the withdrawal. Simultaneouscontraction of contralateral limb extensors andreciprocalinhibitionofcontralaterallimbflexorsmay also result via the interconnected crossedextensor reflex mechanism to prevent the animalfrom overbalancing. The VMR is another spinalreflex that may also cause contraction of skele-tal muscles but as a result of visceral afferent,rather than somatic or cutaneous afferent nox-ious input. The NJOR leads to contraction of  jaw opening muscles and reciprocal inhibitionof jaw closing muscles as a result of orofacialnoxious input.
   J   M  u  s  c  o  s   k  e   l  e   t  a   l   P  a   i  n   D  o  w  n   l  o  a   d  e   d   f  r  o  m   i  n   f  o  r  m  a   h  e  a   l   t   h  c  a  r  e .  c  o  m   b  y   U  n   i  v  e  r  s   i   t  y  o   f   B  r   i  s   t  o   l  o  n   0   7   /   1   9   /   1   0   F  o  r  p  e  r  s  o  n  a   l  u  s  e  o  n   l  y .
 
188 JOURNAL OF MUSCULOSKELETAL PAI
I suggest that sustained stimulation of pe-ripheral nociceptors for cutaneous, somatic, orvisceral C afferent neurons is a preconditionfor the formation of antecedent TrPs. Suchsustained noxious stimulation may result fromtraumatic injury, inflammatory disease, or sen-sitization of nociceptors in other TrPs. Onlyongoing C fiber-mediated nociceptive transmis-sion to the SC/TN leads to central sensitiza-tion of the above-mentioned withdrawal reflexmechanisms, resulting in sustained efferent
α
-motoneuron activation of agonist muscles andsimultaneous inhibition of antagonist muscles.The reflex response to C nociceptor input is alow level of muscular contraction, compared tothe reflex response to myelinated afferent inputthat is monitored with most methods of behav-ioral observation or standard electromyographicrecording (8).Central sensitization is a process that re-sults in an increase in efficiency of synaptictransmission between neurons and an increasedexcitabilityandprolongeddischarge[plateaude-polarization] of postsynaptic neurons followingcertain forms of repeated or sustained synapticexcitation. Prolonged noxious stimulation thatactivatesCafferentneuronsleadstoSC/TNcen-tral sensitization at the various synapses of theactivated polysynaptic withdrawal reflex mech-anism/s [e.g., in the SC, plateau potentials canbe evoked by primary sensory afferents in bothdorsal horn [DH] neurons and motoneurons (9)](10–12). Sustained application of an appropriatenociceptive conditioning stimulus, even at lowlevels, is sufficient to maintain DH central sen-sitization (13). Dorsal horn central sensitizationleads to an enhanced pain sensation [secondaryhyperalgesia] and reduced pain threshold [allo-dynia]. The synaptic and postsynaptic mecha-nisms of central sensitization are complex, but itis clear that they result in plateau depolarizationofthepostsynapticneuronduetoprogressiveac-tivation of L-type calcium channels (10, 12, 14).Facilitation of the C fiber withdrawal reflexesdue to SC/TN central sensitization both predis-posestoantecedentTrPformationandhelpsper-petuate these TrPs. The NWR persists duringsleep (15), so ongoing activation of the NWRmay maintain antecedent TrPs indefinitely.Lamina V wide dynamic range [WDR, con-vergent, multireceptive] SC/TN neurons arelikely to be critically involved in the pathogen-esis of antecedent TrPs. Lamina V WDR neu-rons may show graded responses to innocuousand noxious mechanical stimuli, noxious heat,noxious cold, and noxious muscle or visceralstimuli (16). They respond to repetitive C fiberactivation with a windup discharge [central sen-sitization] and are intercalated in the withdrawalreflex pathway (16, 17).I propose that warm up of 
α
-motoneuronplateau depolarization, which is maintained bycentral sensitization of the C fiber withdrawalreflexes, leads to an ongoing low-level increasein acetylcholine packet release at the motorendplates of both active and latent antecedentTrPs.Theaxonsof 
α
-motoneuronsintheplateaustate exhibit a low-level increase in electroneu-rogram activity, most visible when action poten-tials are blocked (6), which closely resemblesrecordings by needle electromyogram of end-plate noise from the active locus of a TrP. Thelow-amplitude motor endplate potentials of end-plate noise cause ongoing partial depolarizationof the postjunctional membrane and subsequentfocal sustained contractile activity of the mus-cle sarcomeres in the immediate vicinity of themotor endplate zone (18).Persistentcontractileactivityofthesesarcom-eresleadstoalocalenergycrisis,asexplainedbythe current energy crisis hypothesis. This statesthat ongoing contraction squeezes shut the cap-illaries that supply the nutritional and oxygenneeds of that region, which simultaneously hasan increased metabolic demand (19). The se-vere but local energy crisis leads to a failureof relaxation of the sarcomeres [a contracture]due to an inadequate local supply of adeno-sine triphosphate, which is required by the Ca
2
+
pump that returns calcium ions to the sarcoplas-mic reticulum to terminate contractile activity(19). Histopathologically, the localized contrac-ture of a segment of muscle fiber around the mo-tor endplate appears as a contraction knot (20).Each motoneuron controls between 300 musclefibers and 1,500 muscle fibers in postural andlimb muscles (21), so central facilitation of 
α
-motoneuron discharge would predispose to thesimultaneous formation of multiple contractionknots. If contraction knots develop in enoughmuscle fibers, a palpable nodule and restrictionin stretch range of motion of the muscle wouldresult. I propose that sustained low-level mo-toneuronal activity is sufficient to maintain theTrP local energy crisis and muscle fiber contrac-ture for an indefinite period.
   J   M  u  s  c  o  s   k  e   l  e   t  a   l   P  a   i  n   D  o  w  n   l  o  a   d  e   d   f  r  o  m   i  n   f  o  r  m  a   h  e  a   l   t   h  c  a  r  e .  c  o  m   b  y   U  n   i  v  e  r  s   i   t  y  o   f   B  r   i  s   t  o   l  o  n   0   7   /   1   9   /   1   0   F  o  r  p  e  r  s  o  n  a   l  u  s  e  o  n   l  y .

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