1040
DISCUSSION
In our previous study, local and referred head
pain was reproduced during manual pressure over the
atlas or C2 in 95% of migraineurs.3 Similarly, in the
present study, head pain was reproduced during this
procedure in all 15 participants. Thus, referral of
head pain from upper cervical structures could be
an important but underrecognized characteristic of
migraine. Furthermore, after repeated application
of manual pressure, local and referred head pain
decreased in parallel with decreases in the trigeminal
nBR (ie, a decrease in the AUC and increase in
latency of the ipsilateral R2 waveform). To our
knowledge, this is the first time a manual cervical
examination technique has been shown to influence
trigeminal nociceptive neurotransmission.
Spinal mobilization is typically applied when dys-
functional areas of the vertebral column are found.
Clinicians utilizing manual therapy identify spinal dys-
function based on various features; among these are
the ability to reproduce local and referred pain, and
restrictions in spinal joint motion.30,31 The clinician’s
objective in applying manual techniques is to restore
normal motion and normalize afferent input from the
neuromusculoskeletal system.29 Despite clinical evi-
dence for the benefits of spinal mobilization, the bio-
logical mechanisms underlying the effects of spinal
mobilization are not known.32-34 One of the principal
rationales for manual therapy intervention is that an
ongoing barrage of noxious sensory input from bio-
mechanical spinal dysfunction increases the excitabil-
ity of neurons or circuits in the spinal cord.35-37
Mechanoreceptors including proprioceptors (muscle
spindles, both primary and secondary endings and
Golgi tendon organs), low- and high-threshold mecha-
noreceptors, high-threshold mechano-nociceptors,
and high-threshold polymodal nociceptors38 within
deep paraspinal tissues react to mechanical defor-
mation of these tissues.39 A significant effect of this
“biomechanical remodeling” could be restoration of
zygapophyseal joint mobility and joint “play,”40 pre-
cisely the intention of the techniques used in this study.
Thus, biomechanical remodeling resulting from mobi-
lization may have physiological ramifications, ulti-
mately reducing nociceptive input from receptive
nerve endings in innervated paraspinal tissues.35,36,39
June 2014
Our findings of decreased AUC and increased
latency of R2 during the cervical intervention are sup-
ported by a functional magnetic resonance imaging
study in which manual therapy was administered to the
ankle joints of rats following capsaicin injection. Subse-
quent to mobilization,there was decreased activation of
the dorsal horn.41 By analogy, upper cervical afferents
may have an excitatory influence on trigeminal circuits
in migraine sufferers that can be reduced by reproduc-
tion and lessening of usual head pain.
The reduction in the nBR during spinal mobiliza-
tion is consistent with previous studies demonstrating
a functional connectivity between the cervical and the
trigeminal system in the trigeminocervical complex of
the brainstem.9-12,42-44 This inhibitory effect may be due
to a general reduction of afferent cervical nociceptive/
excitatory input in the trigeminocervical complex as
result of biomechanical remodeling, perhaps restoring
joint mobility and joint play,40 as inhibition of R2 was
more significant than during the arm intervention.
Therefore, the highly significant reduction in head
pain referral during the cervical intervention could be
a clinical correlate of lessening central sensitization
of the TCN. In particular, it is conceivable that palpa-
tion and stretch of dysfunctional cervical paraspinal
tissues elicits tenderness that lessens as remodeling
occurs.35,36,39 This could explain why tenderness ratings
decreased during the cervical intervention and not the
arm for, presumably, participants’ arm tissues were not
dysfunctional and subject to remodeling.
However, the perception of pain is not only deter-
mined by the intensity of the afferent pain signal
(nociception).45 Nociceptive inputs to the dorsal horn
of the spinal cord are also influenced by potent
endogenous descending inhibitory and facilitatory
processes from supraspinal regions. This bidirec-
tional, central control incorporates a frontal, limbic,
brainstem, and spinal cord neuronexus46-49 that is
driven primarily by noxious inputs and associated
emotional responses. Importantly, this includes spinal
cord activity because the spinally mediated nocicep-
tive flexion reflex is influenced by central pain modu-
lation processes.50 While the exact mechanisms
responsible for emotional modulation of pain are
not fully understood, heightened anxiety appears to
increase sensitivity to pain (hyperalgesia),51-68 while
Headache
moderate fear inhibits pain (hypoalgesia).51,69-77 This
suggests that anticipation of an unpredictable, threat-
ening intervention could result in enhanced pain,
while hypoalgesia results from exposure to a predict-
able, threatening event (fear).51
As we did not assess the participants’ psychologi-
cal state, we are unsure whether this changed over
the course of the experiment. Nevertheless, it seems
unlikely that psychological factors had a major influ-
ence on our findings for the following reasons. First,
participants were included only if usual head pain
could be produced when stressing either the AO or
C2-3 segments – the “inclusion/exclusion” session. In
the case of head pain referral, both segments were
examined (prior to the experimental sessions) to
ascertain which segment reproduced usual head pain
most clearly.Thus, participants experienced reproduc-
tion of their usual head pain, which ceased immedi-
ately on cessation of the technique (ie, essentially,
participants were “cued” to believe that the proce-
dures were not threatening). Second, participants,
armed with the knowledge that they could terminate
the experimental session at any time, were in control,
further lessening the role of psychological factors.78-83
Third, pain ratings to the supraorbital stimuli were
comparable for the cervical and arm interventions,
and remained unchanged across the trials. This disso-
ciation between pain perception and R2 activity sup-
ports the possibility that the reductions in referred
head pain, cervical tenderness, and inhibition of R2
were due to a specific “cervical,” neurophysiological
effect, rather than psychological influences.
Another possible mechanism for the inhibitory
effect on pain demonstrated in our study is that of
placebo. Previous work has shown that the prospect
of reduced pain can reduce the pain reported in
response to a noxious stimulus.84-88 The “inclusion/
exclusion” session provided an expectation that head
pain would increase during the interventions and
cease immediately after cessation of the technique.
However, participants had no prior expectation of the
likely course of referred head pain as the technique
was sustained. Accordingly, we considered that any
placebo effect was minimal.
An additional potential inhibitory mechanism is
diffuse noxious inhibitory controls (DNICs).The DNIC
1041
process involves inhibition of neurons in the dorsal
horn of the spinal cord in response to nociceptive
stimuli applied to any part of the body, unconnected to
their facilitatory fields.89-91 However, if DNICs were
operational, we would have expected identical effects
on the nBR during the arm and cervical interventions as
mean ratings of local tenderness were the same.
Limitations.—Although standardization of pressure
clearly is important, for it to be achieved during appli-
cation of techniques used in this study and in a PAIVM
examination, pressure algometers would need to be
devised, which are not only attach to the thumb but are
sufficiently fine to allow for skilled palpation and per-
ception of mobility.The absence of such a device in our
study could be regarded as a shortcoming. The sample
size could also be considered a limitation; nevertheless,
effects of the cervical intervention were strong enough
to be detected even in our small sample. Perception
and self-reporting of pain clearly involve psychological
influences such as anxiety and fear. These influences
need to be investigated in future studies.
CONCLUSIONS
To our knowledge, this is the first time cervical
manual examination techniques have been shown to
influence trigeminal nociceptive neurotransmission.
Our results suggest that cervical spinal input contrib-
uted to lessening of referred head pain and cervical
tenderness, and inhibition of R2. These findings
support the concept that noxious cervical afferent
inputs contribute to headache in migraine sufferers.
They corroborate previous results related to anatomi-
cal and functional convergence of trigeminal and
cervical afferent pathways in animals and humans,
and suggest that manual modulation of the cervical
pathway is of potential benefit in migraine.
STATEMENT OF AUTHORSHIP
Category 1
(a) Conception and Design
Peter D. Drummond; Dean H. Watson
(b) Acquisition of Data
Dean H. Watson
(c) Analysis and Interpretation of Data
Peter D. Drummond; Dean H. Watson
1042
Category 2
(a) Drafting the Manuscript
Dean H. Watson; Peter D. Drummond
(b) Revising It for Intellectual Content
Dean H. Watson; Peter D. Drummond
Category 3
(a) Final Approval of the Completed Manuscript
Peter D. Drummond; Dean H. Watson
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