Journal of Back and Musculoskeletal Rehabilitation 25 (2012) 103––107 103

DOI 10.3233/BMR-2012-0317
IOS Press

A note to the musculoskeletal physiotherapist

Max Zusman
Department of Health Science, Curtin University of Technology, School of Physiotherapy, GPO Box U1987, Perth,
WA 6845, Australia
Tel.: +61 8 9266 4644; Fax: +61 8 9266 3699; E-mail: M.Zusman@curtin.edu.au

Abstract. Musculoskeletal (formerly manipulative) physiotherapy is widely used for the rehabilitation of patients with common
musculoskeletal pain and related disability. As part of its progress from largely empirical beginnings to becoming basic sciences
informed this sub-specialty of the physiotherapy profession has developed a profound interest in pain mechanisms, causal and
therapeutic. It is of some concern, however, that the use of pain terminology and classication among the fraternity has tended to
be typically idiosyncratic and at times inaccurate. This is not only confusing to followers of the wider medical science literature.
It also compromises clear communication between the physiotherapist and fellow orthodox health care professionals. This ‘‘note’’
restates the acknowledged pain terminology and its applicability to recognised pain categories.

Keywords: Musculoskeletal physiotherapy, pain terminology, pain pathology

1. Introduction such modalities as warmth, cold, TENS, short-wave

The musculoskeletal physiotherapist (MPT) may be
described as an orthodox ancillary health care profes-
sional who ‘‘gets people moving’’. Indeed, for optimal
rehabilitation of common (and even some less com-
mon) musculoskeletal pain patients there is no better
trained, therefore potentially skilful, clinician than the
modern-day MPT.
The key clinical aim with such patients is to restore
everyday functional activity. This has always been seen
by the physiotherapy profession to require the rational
use of therapeutic active movement, broadly termed
‘‘exercise’’. However, because of the aversive effects
of pain on movement, patients are often reluctant to
engage in active exercise. In order to help mitigate
this problem MPT’’s may elect to draw on a range of
‘‘passive’’ treatments.
2. Passive treatments
Traditionally these are predominantly a variety of in-
and-out-of-favour thermoelectrotherapeutic modalities
that have in common the stimulation of peripheral nerve
endings. This confers on them the clinically desirable
potential for creating pain inhibition in the central ner-
vous system [1]. Over the years they have included
diathermy, microwave, interferential therapy and ultra-
sound. Massage and stretching also have stimulato-
ry/inhibitory capabilities. While some modalities may
have additional benecial physiological consequences,
the denitive objective of these passive physical treat-
ments appears to be pain palliation (see Hurley and
Bearne [2]). Reduction in pain provides MPT’’s with
a window of opportunity in which to introduce, and
progress, the necessary active treatment.
Importantly, the passive modalities are intended to
facilitate voluntary movement. As stand-alone treat-
ments it has been difcult to justify either their clini-
cal or cost effectiveness [2]. Moreover used unwisely
some may encourage dependency along with a tenden-
cy to absolve musculoskeletal pain patients from tak-
ing a necessarily active role in their own rehabilitation.
These unintended but nonetheless detrimental conse-
quences were highlighted by the cost-explosive 20th
century health care ‘‘disaster’’,low back pain [3]. Forced
to abandon long-held structure-based causes of pain for
the overwhelming majority of cases (‘‘non-specic’’),
it became apparent to all from the evidence that pro-
longed rest and passive intervention were not particu-
larly helpful [4]. While it remans appropriate to avoid
unnecessary movement during the early acute stage of
a bout of back pain, it is now recognised that graduated
resumption of everyday activity, even if mildly painful,

ISSN 1053-8127/12/$27.50 ” 2012 –– IOS Press and the authors. All rights reserved
104 M. Zusman / A note to the musculoskeletal physiotherapist
was not ‘‘dangerous’’ and constituted an ultimately more
sound rehabilitative path. Along with other issues this
turnabout in our understanding and the optimal man-
agement of low back pain now appears in clinical best
practice guidelines globally [5].
2.1. Manually delivered passive movement
In an attempt to get beyond simple thermoelec-
trotherapeutic palliation, the implication that manually
delivered therapeutic passive movement, the mainstay
of the MPT, could directly facilitate the resumption of
pain-free active movement seemed reasonable [6]. In
other words, passive (and assisted active) movement
would act as precursor to everyday mobility and func-
tional recovery. Unfortunately ensuing research has re-
vealed that there is little convincing evidence for any
lasting alteration in tissue length, position, shape or
content following passive movement (see refs in [7]).
Hence, a direct movement-facilitated effect has yet to
be convincingly demonstrated. However, since its de-
livery entails subjecting patients to graduated exposure
to mechanical stimuli it would be useful if therapeutic
passive movement also constituted a means of mechan-
ical stimulus-induced pain inhibition [1,8]. To this end
research has shown that manually delivered TPM does
indeed have distinct pain inhibitory capabilities [9––11],
for review see Vicenzino and Wright [12]. Thus in ad-
dition to a possible direct inuence on tissue repair [13,
14], manually delivered passive movement would be a
further means of temporarily decreasing pain and as-
sisting with nervous system ‘‘desensitisation’’.
2.2. MPT and pain mechanisms
To a MPT world long accustomed to viewing clin-
ical musculoskeletal pain in structural-biomechanical
terms, the relatively recent move into neurological
events in the central nervous system has inevitably
been somewhat fragmented and independent. On the
one hand there is the reluctance to fully abandon orig-
inal clinical reasoning associated with various ‘‘con-
cepts’’ of passive movement (see for example Daykin
and Richardson [15]. On the upside it has aroused a
profound interest in pain mechanisms right down to
the molecular level –– something deemed largely unnec-
essary in the past [16,17]. Perhaps not unexpectedly
certain issues have arisen in endeavouring to meld the
two. In some instances there appears to have been at-
tempts to ‘‘adapt’’ pain mechanisms to t with the clin-
ical ‘‘technique’’/procedure (instead of the other way
around). The present issue however is with a tendency
by some to misuse and thereby create misunderstanding
of recognised pain terminology.
3. Nociception
Of course MPT’’s are at liberty to adopt and use id-
iosyncratically whatever terminology they choose, for
example Smart et al. [18]. However, doing so imme-
diately compromises enlightened communication with
most medical colleagues. In this eld it would seem
wise for several reasons to remain consistent with ter-
minology used and understood by the bulk of orthodox
medicine.
Thus it is generally recognised that the term noci-
ception refers to everyday mechanically and thermal-
ly evoked pain that falls short of actual tissue dam-
age [19]. Nociceptive pain is therefore always evoked
(not spontaneous), localised (doesn’’t spread), is tem-
porary (doesn’’t linger) and requires a suprathreshold
stimulus (doesn’’t sensitise). It may be superimposed,
deliberately or unintentionally, upon existing inam-
matory or neuropathic pain. However, it is not a patho-
logical clinical entity in its own rite and should not be
used in this regard.
4. Inammatory pain
This is by far the most common of two major types
of pain seen clinically in which there is or has been
adequate tissue damage. It is characterised by chem-
ical sensitisation of peripheral nociceptors (peripheral
sensitisation) and varying degrees and duration of cen-
tral sensitisation. With inammatory pain peripheral
thresholds for thermal or mechanical evoked pain are
dramatically lowered. Pain with suprathreshold stim-
uli is greatly magnied. Importantly pain may be pro-
duced by normally inadequate (subthreshold) periph-
eral stimuli. Pain also occurs spontaneously and may
persist in the absence of any additional peripheral stim-
ulus. It has a tendency to spread (be perceived) beyond
the area of actual tissue damage. Obviously all of the
above makes tissue damage pain quite different from
nociception [19].
It should be noted that varying degrees and dura-
tion of central sensitisation for inammatory pain oc-
cur more or less routinely at segmental and possibly
adjacent levels of input. Central sensitisation has the
effect of magnifying, spreading and (sometimes) main-
taining peripherally perceived pain [20]. It may, but
does not invariably become widespread systemically
(this tends to occur more often where there are signi-
cant psychosocial factors contributing to the [chronic]
pain syndrome). Widespread systemic central sensiti-
 M. Zusman / A note to the musculoskeletal physiotherapist
sation, without any identiable peripheral pathology is
also seen with so-called ‘‘functional’’ pain (see below).
Central sensitisation is not synonymous with ‘‘central
pain’’; this refers to pain-producing pathology of the
central nervous system, for instance stroke, spinal cord
damage, multiple sclerosis [21].
5. Neuropathic pain
Now often termed ‘‘true’’ neuropathic pain due to past
confusion as to its nature, neuropathic pain is current-
ly dened as ““pain arising as a direct consequence of
a lesion or disease affecting the somatosensory sys-
tem”” [22]. Thus with peripheral neuropathic pain it
is necessary for there to be adequate peripheral axon-
al/fascicular damage.
At least initially, peripheral ‘‘sensitisation’’ with neu-
ropathic pain consists of the creation of neuronal sites
of ectopic nerve impulse generation [23]. Such sites
may occur at various locations on both damaged and
undamaged large as well as small diameter peripheral
afferents. They discharge spontaneously, and are also
susceptible to the full range of naturally occurring me-
chanical, thermal and pathological chemical/immune
system stimuli [24,25].
Impulses so produced enter the central nervous sys-
tem and initiate central sensitisation in much the same
way as with inammatory pain. This probably also
involves a signicant contribution from glia [26,27].
There is however an additional critical clinically signif-
icant entity with respect to central sensitisation for neu-
ropathic pain that should be noted by the MPT. This is
a lasting concerted disablement of certain components
of in-built pain inhibitory systems [24,28]. Physiolog-
ical and anatomical changes affecting mechanisms of
endogenous pain inhibition following peripheral nerve
damage render many common methods for the induc-
tion of pain relief only partially effective/ineffective.
Thus even with the best available science-based re-
sources the current management of the symptoms (let
alone the pathology) of true neuropathic pain is less
than satisfactory [29,30]. At the present time, from
the basic sciences (and clinical) evidence it is difcult
to see how true neuropathic pain might be effectively
reduced by additional mechanical stimuli.
5.1. Diagnosis of neuropathic pain
Given that there may be some degree of overlap,
discriminating between predominantly neuropathic and
105
inammatory pain presentations at the clinical level has
proved more difcult than expected [31]. This is a
matter of concern not just to the MPT but universally.
Sufce it to say that denitive criteria have yet to be
fully agreed upon [32––35].
Probably the best the MPT can do at this time is
to determine rstly whether the history is indicative
of nerve damage –– for example trauma (knife wound,
surgery), vascular (diabetes), viral (post-herpetic), neo-
plastic (disease, treatment). Then determine that the
pain and (any) sensory decits are more or less con-
ned to the innervation territory of the lesioned nerve
or nerve root using ‘‘bedside’’ sensory testing, and ques-
tionnaire [31,32,36,37].
Allowing for the occasional innervation territory
overlap (due for instance to anatomical aberration or
central sensitisation), all in all the two together can be
thought to be reasonably supportive of a positive di-
agnosis. Ideally were this to also be backed by neu-
roimaging or neurophysiological investigations such as
nerve conduction studies, laser-evoked potentials or
nerve biopsy examination then the conclusion would
then be much more denitive [21].
6. Functional pain
This title refers to a group of widespread and also
regional chronic pain conditions for which currently no
initiating peripheral pathology can be detected [19,38].
Logical treatment therefore is mainly directed towards
the central nervous system.
The list includes bromyalgia, temporomandibu-
lar joint disorder, tension-type headache, non-cardiac
chest pain, the pain of chronic fatigue and irritable bow-
el syndromes, ‘‘functional’’ abdominal pain, interstitial
cystitis and vulvodynia [19,38]. The role of the MPT
with such syndromes is not clear. While the mainstay
treatment is frequently cognitive behavioural therapy,
some of these patients may benet from physical treat-
ments, including an active ‘‘exercise’’ component, in a
multidisciplinary pain management setting. Whether
pain is widespread or regional what seems to be evident
with such cases is their rather generalised hypersensi-
tivity to various evoked stimuli, sometimes referred to
as (indicative of) ‘‘central sensitisation’’.
6.1. Central sensitisation
Central sensitisation –– at least in the experimen-
tal setting –– denotes a peripheral nociceptive activity-
106 M. Zusman / A note to the musculoskeletal physiotherapist
initiated increase in the excitability of spinal dorsal
horn neurones [39]. The peripheral activity- (and later
transcription-) dependent increases in the excitability
of dorsal horn neurones results in their expanding their
receptive elds, and responding to subsequent stim-
uli/incoming information in an exaggerated and ‘‘ab-
normal’’ manner. Clinically this manifests as patients
heightened perception of peripheral mechanical stim-
uli applied to normal tissue surrounding the patho-
logical site. Specically, there is increased pain to a
suprathreshold ‘‘punctate’’ mechanical stimulus known
as secondary hyperalgesia, and the detection as painful
of a normally innocuous moving mechanical stimulus
known as allodynia [19,39]. It is the latter in particular
that distresses and disables patients (individuals in pain
tend to avoid suprathreshold environmental, or for that
matter therapeutic, stimuli).
It is important to appreciate that varying degrees
and duration of central sensitisation is probably quite
common following clinically relevant peripheral tissue
damage [40]. Indeed, Woolf [41] lists a wide variety of
pain conditions whose amplication and maintenance
can be largely down to central sensitisation. These in-
clude osteoarthritis; neuropathic, dental, visceral and
post-surgical pain; complex regional pain syndrome
type 1 (CRPS-1); and a range of ‘‘miscellaneous mus-
culoskeletal disorders’’ such as low back pain, shoul-
der impingement, post-whiplash pain and epicondylal-
gia [41].
What distinguishes the ‘‘functional’’ pain category is
the absence of any obvious peripheral pathology. This
raises the question as to the nature of any peripheral
input likely to maintain both central sensitisation and
its ‘‘extension’’ generalised systemic hypersensitivity. It
is suspected that not only with functional pain, in some
cases there may be little or even no (post-healing) on-
going peripheral nociceptive afferent activity [41]. In-
stead low-threshold normally innocuous everyday me-
chanically evoked large diameter afferent input may be
adequate, particularly with susceptible individuals [41,
42]. In any case, if the problem is found to lie mainly or
wholly in the central nervous system it is here that any
worthwhile treatment would need to have its effects.
In this regard, evidence to date that the major thera-
peutic mechanism of (passive) movement-based thera-
pies is largely neurological (activation of endogenous
inhibition) rather than ‘‘mechanical’’, is encouraging [7,
12].
In conclusion MPT’’s are urged to understand and
use pain terminology in conventional terms. They are
also asked to appreciate the pathological realities of
clinical pain presentation and its attempted classica-
tion particularly in relation to ‘‘manual diagnosis’’. It is
hoped that together these will help inform MPT’’s clini-
cal reasoning and decision-making process and smooth
the way for mutual understanding with fellow orthodox
health care professionals.
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