Pain
CHAPTER CONTENTS
Definition of pain . . . . . . . . . . . . . . . . . . . . . . . 3
Perception and modulation of pain . . . . . . . . . . . . . 3
Peripheral nociceptive system . . . . . . . . . . . . . 4
Afferent nociceptive system . . . . . . . . . . . . . . 4
Pain modulation systems . . . . . . . . . . . . . . . . 5
Referred pain . . . . . . . . . . . . . . . . . . . . . . . . . 6
Introduction . . . . . . . . . . . . . . . . . . . . . . . 6
Possible mechanisms . . . . . . . . . . . . . . . . . . 6
Clinical consequences . . . . . . . . . . . . . . . . . 7
Rules of referred pain . . . . . . . . . . . . . . . . . . 7
Dermatomes . . . . . . . . . . . . . . . . . . . . . . . 9
Discrepancies between dermatomes and
myotomes . . . . . . . . . . . . . . . . . . . . . . . 14
Referred pain in visceral diseases . . . . . . . . . . . 15
Referred pain is felt deeply and distally in the
dermatome . . . . . . . . . . . . . . . . . . . . . . . 15
Segmentally referred pain does not cross
the midline . . . . . . . . . . . . . . . . . . . . . . . 16
Dura mater an ‘exception’ to segmental
reference . . . . . . . . . . . . . . . . . . . . . . . . 16
Referred tenderness . . . . . . . . . . . . . . . . . . 16
Factors determining reference of pain . . . . . . . . 18
1
although no peripheral tissue damage exists, the pain is just as
distressing as somatic pain2 (see Section 16).
The taxonomy committee of the International Association
for the Study of Pain defined pain as: ‘an unpleasant sensory
and emotional experience associated with actual or potential
tissue damage, or described in terms of such damage’.3 Pain is
thus not a ‘primary sensation’ in the sense that smell, taste,
touch, vision and hearing are, but is an ‘emotional state’, like
sorrow, love or hate. The consequence is that it is extremely
difficult to explain one’s pain to another person. This is
reflected in the numerous words that patients use to describe
intensity and quality of pain: twinge, ache, distress, discomfort,
soreness, cramp, suffering, misery, agony, torment, anguish.4
The fact that pain is always a subjective experience provides
the first difficulty in its use in diagnosis. The language used is
not always easy to understand, and the examiner usually needs
a high level of competence and understanding to translate
patients’ subjective descriptions into more objective and useful
statements.
However, unlike the other affective states, pain is always
felt in some particular part of the body. Having said this, the
localization of the pain very often lacks precision, and it is often
experienced at some distance from its source – ‘referred pain’.
This constitutes the second problem in using the symptom of
pain as a diagnostic aid.
Perception and modulation of pain
Definition of pain
Pain is the presenting symptom in almost every orthopaedic
patient. A complaint of pain is always indicative of some variety
or degree of dysfunction1 and results from a combination of
physical and psychological causes, although sometimes one or
the other predominates. All pain must be regarded as real. Pain
entirely devoid of somatic cause is labelled ‘psychogenic pain’:
© Copyright 2013 Elsevier, Ltd. All rights reserved.
The intensity of pain does not depend only on the intensity of
irritation of the peripheral nociceptive system (receptors and
their afferents). Centripetal transmission of peripheral noci­
ceptive stimulation is subject to varying degrees of facilitatory
and inhibitory modulation at different synapses during its
course to the cerebral cortex. An important modulation site,
of major concern to the orthopaedic physician, is the gateway
synapse in the basal spinal nucleus, but there are also
General Principles
modulation systems in the spinal grey matter, in the thalamus
and in the cerebral cortex itself.5
II
I
Peripheral nociceptive system
Nociceptive receptors are defined as nerve endings that are
sensitive to noxious or potentially noxious (mechanical and
chemical) stimuli. The perceptual aspect of the nociceptive
system consists of unmyelinated free nerve endings, distrib­
uted three dimensionally throughout skin, subcutaneous and
adipose tissue, fasciae, aponeuroses, ligaments, tendons,
muscles, periosteum and bone.6,7 Clinically, three distinct areas
of pain perception may be considered: the skin (superficial
somatic pain); the locomotor system (deep somatic pain); and
the viscera (visceral pain). Of these, only the skin is adapted
to localize pain exactly in the region of injury. Deep somatic
and visceral pain are often felt in unusual locations (see
Referred pain, p. 6).
In normal circumstances, this nociceptive receptor system
remains largely inactive. The unmyelinated free nerve endings
are depolarized only by the application of mechanical forces
sufficient to deform or damage the tissue that contains them
or after exposure to sufficient concentrations of irritating
chemical substances (lactic acid, serotonin, prostaglandins and
histamine), released from local inflammatory cells and from
the peripheral terminals of the primary afferent fibres
themselves.8–10
Another important influence on nociceptor sensitivity is the
pH of the tissue. High local concentrations of protons are
known to occur in inflammation and the consequent reduction
in pH contributes to the sensitization of nociceptors.11,12
Afferent nociceptive system
Nerve impulses generated at the nociceptive receptor system
are delivered into the spinal cord by small myelinated and
unmyelinated nerve fibres (5 µm or less in diameter), that
mainly belong to the Ad and C groups of afferent nerve fibres
(Fig. 1.1). Their cell bodies are located in the dorsal root
ganglia of the spinal nerves. The very small diameter of the C
nerves explains their slow conduction velocity (1 m/s), and
their extreme sensitivity to blockade by local anaesthetic drugs.
The myelinated Ad fibres are slightly larger and have a faster
conduction velocity (10 m/s).13
The nociceptive afferents enter the spinal cord, where they
divide into short ascending and descending branches, before
they terminate at synapses on various groups of relay neurones
in the dorsal horn of the spinal grey matter. Most of the con­
nections are to the neurones in the basal spinal nucleus (at the
base of the dorsal horn).14,15
The efferents of these cross the cord obliquely to turn
upwards on the contralateral side and form the anterolateral
spinal tract, which connects the basal spinal nucleus with the
thalamic nuclei and has therefore traditionally been called the
‘spinothalamic tract’. Most of the fibres in this tract, however,
do not directly ascend to the thalamus without interruption,
but instead synapse with neurones in the brainstem reticular
system, while others re-enter the spinal grey matter to synapse
4
C
III
B
A
Fig 1.1 • The afferent nociceptive systems. Projection areas: I,
perceptual area; II, emotional area; III, memory storage. Three levels
of sensory neurone: A, primary sensory neurone; B, dorsal horn cell
(gateway synapse); C, thalamic relay.
with internuncial neurones.16 However, the majority of the
ascending nociceptive inputs terminate (sometimes after cross­
ing several synapses) in the thalamic nuclear relay sites.17 It
should be emphasized that not only do the neurones in the
thalamic centres respond to peripheral noxious stimulation
but they can also be activated by mechanoreceptor peripheral
stimulation (see Pain modulation systems below).
The axons of the thalamic nuclei then ascend to the neu­
rones of the cerebral cortex. Three thalamocortical projections
can be defined: those responsible for perception; those related
to the emotional experience; and those responsible for
memory.18
The first project to the superior paracentral region of the
cerebral cortex and seem to contribute to the so-called
‘perceptual component’ of pain – the patient’s ability to perceive
whereabouts (in which segment of his body) the pain is
localized.19
The activation of the second thalamocortical projection
system, projections that pass from the medial and anterior
thalamic nuclei to the frontal lobes, evokes the emotional disturbances related with pain.20 Thus, a stimulus ‘hurts’ only
when the nociceptive afferent projections arrive at the frontal
cortex.
Pain
A third thalamocortical projection system links some of the
medial thalamic nuclei to the cortex of the ipsilateral temporal
lobe. Here the recent and long-term memory storage systems
of the brain are located.21,22
A fourth projection system exists which relates some tha­
lamic nuclei to subjacent hypothalamic nuclei in the ventral
diencephalon. It is very probable that this thalamohypotha­
lamic system provides the means whereby nociceptive afferent
activity entering the brain evokes the complex of visceral reflex
(cardiovascular and gastrointestinal) effects and hormonal
changes that are so often associated with the experience
of pain.23
In conclusion, activity of nociceptive receptors distributes
pain into four different projecting systems in the brain, each
contributing to a specific component of the global experience
‘pain’. However, the projection of pain from a peripheral
receptor to the brain is not via a straight-line system. The
intensity of pain is not only determined by the intensity of
peripheral stimulation but also depends largely on peripheral
and central modulation systems at the various synaptic stages
in the course of the afferent pathway within the central nervous
system. These modulation systems account for the large vari­
ation in the intensity of pain experienced. Patients with appar­
ently comparable pathological lesions undergo widely different
degrees of suffering; even in an individual patient, the intensity
of experience of pain varies widely with the prevailing emo­
tional mood, with concentration on the problem or with sug­
gestions from others.
Pain modulation systems
There are both peripheral and central pain modulation systems.
Peripheral modulation of pain
One of the most important sites at which a synaptic modula­
tion operates from both the peripheral and central sources
is at the synapses in the basal spinal nucleus. In 1965,
Melzack and Wall,24 basing their theory mainly on the work of
Noordenbos,25 published an article entitled: ‘Pain mechanism:
a new theory’. They called their concept of peripheral pain
modulation the gate control theory (Fig. 1.2), which is based
on three premises:
• Afferent nerves contain two types of fibres: small fibres
(P), as described above, and large-diameter afferents (M),
which are derived from the various mechanoreceptors in
the articular capsule, ligaments and muscle spindles.
These fibres produce information about static joint
position, pressure changes in the joints, joint movement
and stresses that develop in the joint at the extremes of
movement. The fibres of mechanoreceptor transmission
have a lower stimulation threshold and a faster conduction
velocity than the smaller and mostly unmyelinated fibres
of the nociceptive system.
• In the substantia gelatinosa (SG) of the dorsal horn, both
afferent systems converge and interrelate, with the overall
effect that the large-diameter afferents have an inhibitory
effect on the relay neurones located in the basal spinal
CHAPTER 1
M
DM
SG
TR
P
Fig 1.2 • Gate control theory (after Melzack and Wall24): P, small
nociceptive fibres (pain); M, large mechanoreceptive fibres; TR,
transmission cells (relay neurones in the basal spinal nucleus); DM,
descending modulation; SG, substantia gelatinosa; +, excitatory
effect; –, inhibitory effect.
nucleus. This inhibition is presynaptic and is reduced only
when there is a massive input from the small nociceptive
afferent fibres. The latter thus facilitates central
transmission of pain. The interaction between both
systems is gate control: impulses travelling along the larger
fibres close the gate, and those in the small fibres open
the gate so that impulses to thalamus and cortex can pass
through.
• The activity of the gate is not only modulated by impulses
from nociceptive and mechanoreceptor systems but also
receives a descending and regulating feedback from the
reticular system, the thalamus and the cerebral cortex.
This peripheral modulation of pain has considerable clinical
importance. It indicates that centripetal projection into the
central nervous system of afferent activity from the nocicep­
tive receptor systems is not passed straight to any ‘pain centre’
in the brain but receives constant modulation at its synaptic
portal of entry into the neural axis at the level of the basal
spinal nucleus. The modulation stems from the concurrent
activity of the mechanoreceptors located in the same tissues,
and from feedback through projection systems descending
from the brainstem and cerebral cortex. This effect is one of
the reasons why movement and selective stimulation of mecha­
noreceptors can cause inhibition of pain.
Central modulation of pain
Awareness of pain is also modulated at the central projection
systems.
At the reticular formation
A modulation system at the reticular formation in the brain­
stem exerts a continuous inhibitory effect on the projection
neurones in the spinal nucleus ganglion via the reticulospinal
tract, which is discharging continuously at varying frequencies
throughout life.26 The inhibitory effect on nociceptive afferent
transmission is augmented when the attention of the patient
is distracted from the site of pain. This is what occurs when
5
General Principles
another painful site elsewhere in the body is stimulated
(counter-irritation), when the patient concentrates on work or
other activities or when hypnosis is induced.27 The inhibitory
effect of this reticular system also increases when the blood
concentration of catecholamines is very high, as can be the case
in states of great emotional tension.28 Also some drugs (chlor­
promazine, diazepam and morphine) may selectively increase
the activity of the reticular neurones that operate this inhibi­
tory system.29
Inhibitory reticular activity is depressed and pain is enhanced
when attention is concentrated on the painful site, or following
the administration of barbiturates, caffeine or theophylline.30
The cerebral cortex
The cerebral cortex, especially the sectors located in the frontal
and paracentral regions, in turn regulates the activity of the
reticular formation. Reticular activity is increased, and percep­
tion of pain thus inhibited during rest and sleep and after the
ingestion of alcohol. Conversely, depression of reticular activity
is seen during increasing cortical activity, for example with
anxiety, uncertainty and fear.
Referred pain
Introduction
When the skin is pricked with a pin, the patient can exactly
pinpoint the injury. This ability to localize the pain is limited
to skin and does not apply when the source of the pain is in
deep tissue. Deep somatic pain and visceral pain are often felt
far from their point of source. In consequence, the examiner
needs to know the patterns of pain reference so as not to be
misled about where to search for the seat of the trouble. Diag­
nosis of orthopaedic lesions often rests entirely on history and
clinical examination and is therefore almost impossible if the
rules and conditions relevant to referred pain are not clearly
understood.
Those who originally studied pain reference soon noted that
although it appeared erroneous and anarchic, some rules of
presentation did exist. For instance, pain from specific struc­
tures is always referred to the same parts of the body: colic
from a ureteral stone to groin and testicle, diaphragmatic dis­
orders typically to the shoulder, angina pectoris to one or both
arms, and the pain caused by arthritis of a hip very often to
the ipsilateral knee. Also pain is, in the main, referred distally
and its localization depends in a certain way on the severity of
the lesion.
In 1905, Sir Henry Head described referred pain in the
abdominal wall caused by a visceral disease.31 Using the der­
matological appearances in herpes zoster, he constructed
schemes of segmental innervation of the skin.32 He also
described dermatomic zones that became painful in the event
of provocation of a related visceral structure. His theory of
pain reference was built on the concept of the segmental
organization of the human body and its nociceptive system.
Further experiments in this sphere were conducted by Sir
Thomas Lewis in 1936.33 In 1938 and 1939, Kellgren published
6
the results of a systematic examination of the phenomena of
referred pain, demonstrating segmental radiation and failure to
cross the midline.34,35
His experiments were confirmed by others.36–38 Later, the
concept of segmental reference of pain was refined39,40 and
exact borders of the different dermatomes mapped out.41–44
Possible mechanisms
The fact that referred pain is an error in perception was first
pointed out by John Hunter in 1835 (cited by Cyriax).45 It was
obvious that if pain is felt elsewhere than at its true site, the
nociceptive mechanism is reacting inappropriately. However,
since there seems to be logical consistency in the way the errors
are made (pain from specific lesions is always referred to the
same areas), there must also be a logical explanation for ‘fail­
ures’. (If a machine always makes the same mistake, a struc­
tural or functional disorder must exist.) The basis for the
inadequacy must therefore be sought in a miscalculation in the
pain mechanism. Theoretically, the defect can lie anywhere
along the afferent pathway, from the peripheral receptors to
the synapses in the spinal cord and the reticular area and pro­
jection zones in the sensory cortex.
During the last century, numerous investigators have studied
referred pain. Two main hypotheses have been put forward:
• Error at the level of the spinal cord. Most authors have
opted for this hypothesis. Mackenzie described an
‘irritable focus’ in the grey matter of the spinal cord as
being responsible for the phenomenon.46 Also Livingston47
placed the basis of the error at synapses in the dorsal
horns. Wedell et al48,49 and Pomeranz50 accepted a double
origin for the sensitive neurone – afferent fibres of a
somatic structure, and those coming from a related
visceral structure synapse with the same spinal ganglion.
Taylor et al51 and Wells et al52 also made a plea for the
spinal explanation of referred pain. Their view is that
separate peripheral sensory nerves (deep somatic, skin and
visceral) converge on to the same cell in the dorsal horn
of the spinal cord (Fig. 1.3).
• Failure at the sensory cortex. A number of authors have
proposed that the misinterpretation is at the projection
area of the sensory cortex rather than at the spinal
level.33,53,54 The concept was clinically elaborated by
Cyriax who based his theory on a number of premises:
Referred pain is a pain experience felt elsewhere than
at its true site of origin.
 Skin is an organ adapted to localize the pain accurately.
 Pain is experienced in the sensory cortex, which is
organized dermatome by dermatome.
 The skin is represented accurately in the sensory
cortex.
 A memory storage system is located in the sensory
cortex. This is fed by constant input from the skin.
Input from deeper somatic structures is very rare in a
normal and healthy individual.
As pointed out previously, pain is experienced at three differ­
ent locations in the cerebral cortex. Perception – of the site of

CHAPTER 1
Pain
Fig 1.3 • Separate peripheral sensory nerves
converge onto the same cell in the dorsal horn
of the spinal cord.
Superficial somatic pain
Deep somatic pain
Sympathetic ganglion
Visceral pain
Sympathetic nerve
pain – is located in the superior paracentral cortex. The frontal
lobes evoke the emotional disturbances related to pain, and the
memory store is in the temporal lobes.
The ability to localize pain in the region of injury is limited
to skin and does not apply when the source of the pain is in
deep tissue. In due course, a certain pain memory is built
up in the temporal lobes, and achieves a high degree of ana­
tomical precision. The efficacy of the long-term memory
storage system is not simply a function of the intensity of the
painful experience but also relates to the length of time a
painful experience lasts or to the frequency with which it is
repeated.55,56 Since the frequency of painful stimuli coming
from the skin is much higher than the frequency of stimuli
coming from deeper structures, it will be obvious that pain
memory will centre around painful experiences from the skin.
When the same cortical cells receive a painful message arriving
from a deep-seated structure, the memory will interpret it on
the basis of past experience; in that the sensory cortex is
arranged segmentally, the pain will be ascribed to the correct
segment but the system will fail to localize it accurately at the
site of the lesion. The brain therefore ‘places’ it in the tissue
it has a reference for – the skin. Pain is thus felt under the
surface area connected with the particular cells that belong to
the same segment as the tissue from which the nociceptive
afferents originate. The pain is felt deep to the skin of the
relevant dermatome and not accurately in the skin.
Clinical consequences
The concept of referred pain is extremely important to the
orthopaedic physician, who has to deal daily with the problem.
If the principles of erroneous localization by the cortex are
clearly understood, the examiner can turn a misleading phe­
nomenon to diagnostic advantage. In the Cyriax concept,
referred pain obeys certain rules. The inadequacy in the sensory
cortex is structural and therefore can easily be accommodated.
To a certain degree, referred pain can be compared with the
refraction of light when it falls on a water surface. The observer
does not see objects under the water surface at their exact
localization. However, since the error of perception is struc­
tural and obeys particular physical rules and laws, it is easy to
correct what is seen (provided the observer knows the correc­
tion formula) and so locate the object accurately. The same
applies to referred pain. The examiner must constantly ask if
the localization of the pain is also the exact localization of the
disorder and, if the answer is negative, what corrections must
be made to arrive at the exact localization.
Before this discussion of referred pain is continued, it should
be stressed that root pain reference does not necessarily mean
that a nerve is involved. The false idea that wide radiation of
pain is evidence of involvement of nerves is still strongly held
by some and is usually the most important obstacle to a logical
understanding of referred pain. To approach the problem of
referred pain with an open mind, the reader must constantly
remember that referred pain is an error of perception. Although
the nerve supply to these peripheral structures is distributed
on a segmental basis, it does not indicate that referred pain
‘runs down’ a somatic nerve. For instance, pain at the anterior
aspect of the leg does not necessarily mean that a nerve struc­
ture (L3, femoral nerve or peripheral branches of the femoral
nerve) is involved. Although inflammation of the dural sleeve
of the L3 nerve root does of course lead to pain extending in
the L3 dermatome, the same pain can be provoked by a lesion
in any other tissue belonging to the L3 segment (e.g. hip joint
or psoas bursa). There will not be any difference in the nature
and extent of the pain. The only distinction between pain as
the result of a compressed and inflamed nerve root and pain
originating from trauma to other structures is the appearance
of paraesthesia (see Pressure on nerves, Ch. 2).
Rules of referred pain
(Box 1.1)
The first rule – reference of pain within the borders of the skin
area that belongs to the same segment as the tissue lesion that
causes pain – follows directly from the premise that the noci­
ceptive mechanism is organized on a segmental basis. Nocicep­
tors, afferent fibres and the sensory cortex are all arranged
segmentally. Afferents from skin, deep somatic structures and
visceral organs from the same segment relay on the same dorsal
neurones and project to the same area in the sensory cortex.
Pain reference is therefore confined to, and remains within, the
borders of the cutaneous area (or dermatome) that belongs
7
General Principles
embryologically to the same segment as the tissue from which
the pain is arising.
To understand the segmental organization of the nocicep­
tive mechanism, it is necessary to reconsider embryogenesis
(Fig. 1.4).
Embryogenesis
Primitive body
When a fetus is between 4 and 6 weeks old, 42 pairs of somites
develop: four occipital, eight cervical, 12 thoracic, four to six
lumbar, five sacral and eight to 10 coccygeal.57 The first two
and the last seven or eight pairs disappear early in develop­
ment. The ventral aspect of each somite differentiates into the
sclerotome which, together with the chorda around the neural
tube, forms the origin of the axial skeleton. The other part of
the somite becomes the myotome, covered by the dermatome.
Each pair of somites develops its own segmental innervation
Box 1.1
Rules of referred pain
•
•
•
•
The pain radiates segmentally and does not cross the midline
The pain is usually felt deeply
The pain is referred distally within the dermatome
The pain does not necessarily cover the area of the causative
lesion
• The pain is felt anywhere in the dermatome but not necessarily
in the whole dermatome
1
which later leads to the development of the spinal ganglion and
spinal nerve.
In due course, the dermatome differentiates into skin and
subcutaneous tissue, the myotome into muscles, tendons, liga­
ments, capsules and bursae, and the sclerotome into bone and
fibrous septa. Although the original form of most segments is
modified as the limbs are formed, their segmental innervation
remains constant throughout life. The projection area in the
cerebral cortex also remains segmentally organized.
Limb formation
After the first month of intra-uterine life, two pairs of buds
originate at the lateral sides of the fetus. The proximal papules
appear first at the base of the neck, followed by the formation
of two distal buds in the caudal area. These extensions gradu­
ally project from the cylindrical fetal segments from which
they originate. As the limbs grow further and further laterally,
some dermatomes become totally disconnected from the trunk
(Fig. 1.5).
For the upper limb, the dermatomes C5, C6, C7, C8 and
T1 leave the trunk completely to form the covering of the arm.
T2, although also present at the inner aspect of the upper arm,
connects with the trunk again, and borders with C4.
In the lower limb, parts of L2, L3 and the whole der­
matomes L4–L5 and S1 withdraw from the trunk to form the
lower limb. S2 is present partly in the limb and partly in the
buttock, where it borders with L3.
During limb formation, some muscles undergo centripetal
migration and others centrifugal. As a rule, however, der­
matomes distally project further than myotomes, and some­
times a muscle becomes completely dissociated from the
covering dermatome. An example of dermatome migration is
10
4
8
6
III IV
I II
7
9
11
2
13
3
9
12
5
Fig 1.4 • Embryogenesis: 1, neural tube; 2, aorta; 3, intestine; 4, myotome; 5, dermatome; 6, primitive spinal ganglion and spinal nerves;
7, myoseptum between the segments; 8, horizontal septum; 9, frontal knob; 10, maxillar knob; 11, cranial limb bud; 12, caudal limb bud;
13, umbilical cord; I–IV, gill arches.
8
Pain
CHAPTER 1
Fig 1.5 • Limb formation. As the limbs grow
further and further laterally, some dermatomes
become anatomically disconnected from the
trunk.
4
5
4
6
5
6
7
T2 T1
2
3
S2 S1
the C5 segment in the upper limb: the myotome does not
extend beyond the elbow, but the fifth cervical dermatome
descends to the radial styloid. An example of centrifugal dis­
sociation between a muscle and its relevant dermatome is the
diaphragm, which has a C4 origin: the C4 dermatome ends at
the scapular spine and under the clavicle, and is therefore
completely separated from the thoracic localization of the
muscle. Another instance of muscle migration is the latissimus
dorsi muscle (C7–C8) which shifts its origin to the iliac crest.
The dermatomes of the seventh and eighth cervical segment,
however, do not occupy the trunk, so dissociating the muscle
almost completely from its corresponding dermatomes.
Because of these muscle migrations, with overlaps and dis­
continuous areas, it is very difficult to draw accurate maps of
the myotomes. However, in the appropriate chapters of this
book, we will indicate to which segment each of the structures
under discussion belongs.
Dermatomes
The cutaneous area supplied by one spinal nerve is a der­
matome. The first clinicians to draw dermatomic maps were
Head and Campbell.58 Their diagrams are the basis for the
classical drawings in standard neurological textbooks. However,
they did not take into consideration the significant degree of
variability and overlap in dermatomic borders.57,58 Later inves­
tigators such as Keegan and Garrett, and Fukui et al59,60 have
demonstrated that dermatomes of adjacent spinal nerves
overlap markedly.
An example of this is pain at the anterior aspect of the thigh,
which can be of second or third lumbar origin. The second
lumbar dermatome spreads from the groin, down the front
of the thigh, to the patella. Pain of third lumbar origin
again spreads along the anterior aspect of the thigh and the
patella but it can continue down the anterior aspect of the leg,
to just above the ankle. Pain at the anterior aspect of the thigh
therefore can be of second or third lumbar origin but if it
spreads further down below the patella then its origin is
third lumbar.
Another example of overlap between dermatomes is referred
pain in the hand and fingers: C6 pain refers to the dorsal aspect
of the hand, the thumb and the index finger, whereas C7 refers
8
4
5
7
8
T2 T1
2 3
4
5
S2
S1
also to the dorsum of the hand and the index finger, as well as
to the long and ring fingers. In a patient complaining of pain
at the back of the forearm or at the dorsum of the hand and
the index finger, it is difficult to decide whether the pain is of
sixth or seventh cervical origin.
We use the charts drawn by Foerster41 in 1933 and corrected
by Cyriax in 1982,45 in order to give the broadest possible
information about the area to which pain from a particular
segment may refer. The extreme importance of accurate locali­
zation of pain in orthopaedic medicine requires the physician
to use a map of dermatomes that is as close as possible to
clinical reality. The figures showing the dermatomes are based
on Foerster,41 Cole et al,61 Cyriax,45 Conesa,62 Wakasugi,63 and
Mitta.64
Cervical and thoracic dermatomes
C1 to C4 occupy the scalp (C1), the back of the neck and
the temporal area, the upper half of the ear and the upper half
of the face (C2), the neck, lower mandibular area and chin
(C3), and the lower half of the neck, shoulder area, front of
the upper chest and the area above the spina scapulae (C4)
(Fig. 1.6).
C5 to T2 are projected from the trunk to form the covering
of the upper limb (Figs 1.7 and 1.8).
C5 covers the deltoid area and the outer aspect of the arm
up to the base of the thumb.
C6 is the anterolateral aspect of the arm, the thenar emi­
nence, thumb, dorsum of hand and index finger.
C7 comprises the back of the arm and hand, together with
index, long and ring fingers.
C8 is the inner aspect of the forearms, the hypothenar area
and palm, together with the three ulnar fingers.
T1 includes the inner aspect of the forearm as far as the
hypothenar eminence.
T2 is Y-shaped and overlies the inner aspect of the upper
arm and the axilla, where it divides into an anterior and a
posterior component. This latter part of the dermatome
borders with the inferior aspect of the C4 dermatome.
If the upper limb is held outstretched horizontally with the
thumb pointing upwards, the original position of the embryo­
logical bud is recreated, and one can reconstruct the way the
dermatomes project from the trunk. This is a good way to
9
General Principles
C1
C2
C3
C4
Fig 1.6 • C1 to C4 dermatomes.
Fig 1.7 • C5 to C8 dermatomes.
10
C5
C6
C7
C8
Pain
T1
CHAPTER 1
T2
Fig 1.8 • T1 and T2 dermatomes.
C5
C6
C7
C8
T1
T2
T4
Fig 1.9 • Outstretched arm with arrows showing the dermatomes.
T7
memorize the position of the separate dermatomes in the
upper limb (see Fig. 1.9).
From T4 to T12, the dermatomes encircle the trunk, more
or less following the original segmental construction of the
embryo (Fig. 1.10).
T4 constitutes the axilla and a patch on the front of the
chest.
T4 encircles the trunk at the level of the nipple.
T7 reaches the lower costal margin and covers the xiphoid
process.
T10 is level with the umbilicus, and T12 reaches to the
groin, and probably also the area between the femoral tro­
chanter and iliac crest.
Lumbar and sacral dermatomes
L1 is also more or less circular (Fig. 1.11). It comprises the
lumbar region from the second to the fourth lumbar vertebrae,
and runs along the upper aspect of the buttock and the iliac
crest to the lower abdomen and the groin.
L2 and L3 are two discontinuous areas, one in the lower
lumbar region and upper buttock, and one in the leg (Fig.
1.12). The areas in the buttock largely overlap. Also, in the leg,
there is considerable overlap between L2 and L3: L2 involves
the whole front of the thigh, from the groin to the patella. L3
also takes in the anterior aspect of the thigh, but spreads
further down, as far as the anterior and medial aspects of the
ankle.
L4, L5 and S1 are completely disconnected from the trunk,
overlying the surface of the leg and foot (Figs 1.13 and 1.14).64
T10
T12
Fig 1.10 • T4, T7, T10 and T12 dermatomes.
In consequence, the third lumbar dermatome lies adjacent to
the upper border of the second sacral dermatome at the lower
buttock.
L4 occupies the lateral aspect of the thigh, crosses the leg
above the ankle, and ends at the medial malleolus, the inner
border of the foot and the big toe.
L5 consists of the outer aspect of the leg and crosses the
ankle above the lateral malleolus, to end on the dorsum of
the foot. L5 also comprises the big, second and third toes,
and the inner half of the sole.
S1 includes the calf, the heel, the lateral malleolus and foot,
the two outer toes and the whole sole of the foot (Fig. 1.15).
Sicard and Leca65 demonstrated that the fifth lumbar and first
sacral dermatomes also comprise a small vertical band at the
11
General Principles
L1
Fig 1.11 • L1 dermatome.
L2
Fig 1.12 • L2 and L3 dermatomes.
12
posterior aspect of the thigh, which could account for the thigh
pain commonly described by patients suffering from L5 or S1
sciatica.
S2 is large and comprises the plantar aspect of the heel, the
calf, the back of the whole thigh and the lower buttock. In the
buttock, it borders with the lumbar part of L3 (Fig. 1.15).
S3 is a narrow zone at the inner side of the thigh, where it
borders with L2 anteriorly and S2 posteriorly (Fig. 1.16). The
tip ends just proximal to the knee. The upper extent reaches
the inguinal ligament where it adjoins the 12th thoracic and
first and second lumbar dermatomes. It follows that the groin
is a confluence of dermatomes, and pain, apart from that of
local origin, may be referred from a 12th thoracic, a first or
second lumbar, or a third sacral origin. The groin is also a
common site for extrasegmental dural pain reference.
S4 comprises the saddle area, anus, perineum, and scrotum
and penis or labia and vagina.
S5 is the coccyx.
As in the upper limb, the original position of the distal
embryological bud can be reconstructed by abducting the thigh
to 90°, and by lateral rotation until the big toe points upwards.
This position demonstrates the way the dermatomes were
projected from the trunk and also constitutes a good way of
memorizing the position of the various dermatomes in the
lower limb (Fig. 1.17). Proximally to distally and then turning
proximally again, the following are encountered: L2 at the
L3
Pain
L4
CHAPTER 1
L5
Fig 1.13 • L4 and L5 dermatomes.
(a)
L4
L5
S1
S1
(b)
L5
S1
S2
S2
Fig 1.14 • Dermatomes of the foot, (a) dorsum (b) sole.
Fig 1.15 • S1 and S2 dermatomes.
13
General Principles
S3
anterior thigh, L3 at thigh and leg, L4 at the lateral aspect of
the leg, anterior aspect of ankle and inner border of foot up to
the big toe, L5 at the dorsum of the foot and the three inner
toes, S1 at the lateral aspect of the foot, outer malleolus and
calf, S2 at the posterior aspect of the leg; turning back to the
trunk in the gluteal area, the boundary zone in the perineum,
between leg and trunk is comprised of S3 and S4.
S4
Discrepancies between dermatomes
and myotomes
We have mentioned already that, as the outcome of embryo­
logical development, dermatomes do not always precisely
cover the underlying myotomes. Cyriax described eight areas
in the human body where the skin and the structure it covers
have completely different embryological derivations (Cyriax45).
These are the head, scapular and pectoral region, hand,
intrathoracic and intra-abdominal region, buttock and scrotum.
Head
S3–S5
The skull, head and face are derived from the two remaining
occipital somites, originally situated at the back of the neck.
During development, a pair of frontal knobs and two mandibu­
lar arches form and fold forwards to create the skeleton and
soft tissues around the buccal cavity. The skin of the head and
face, however, are formed from the upper two cervical
segments.
S4
Scapular region
The growth of the protuberances that are to become the upper
limbs draws some segments out from the cylindrical cervical
and thoracic structures. At the same time, the scapula and its
muscles, together with the latissimus dorsi (C5–C7) move
centripetally between the skin of the thorax (circularly arranged
thoracic dermatomes) and the underlying ribs and intercostal
muscles (circularly arranged thoracic sclerotomes and myo­
tomes). Therefore, pain in the scapular area can have both
scapular (cervical) and thoracic origins.
S3
S5
Fig 1.16 • S3 to S5 dermatomes.
Pectoral region
During the growth of the upper limb bud, the same phenom­
enon as occurs in the scapular region takes place at the pectoral
region. The pectoral muscles, derived from cervical segments
(C6–C7) move centripetally between the thoracic dermatomes
and their myotomes.
L2
S1
S2
L3
L5
L4
The hand
The thenar muscles form part of the eight cervical and first
thoracic myotomes, but the skin is formed from the fifth and
sixth cervical dermatomes. The interosseus muscles are C8 and
T1, but the skin of the dorsum of the hand, except at the ulnar
border which is also C8, is derived from the C6 and C7
segments.
Intrathoracic region
Fig 1.17 • Outstretched and rotated leg, with arrows showing the
dermatomes.
14
It is obvious that there are numerous discrepancies in origin
between the thoracic cage and its content. The diaphragm, for
instance, is derived from the third and fourth cervical segments
Pain
and thereafter descends. Hence a lesion of the diaphragm may
cause pain felt in the neck and at the upper scapular and pec­
toral region, even though it lies at the lower thoracic level. The
heart is derived from C8 to T4. Therefore myocardial pain may
radiate to the chest, the shoulder and the inner aspect of the
arm, as far as the ulnar border of the hand. It is presumed that
a small part of the myocardium, probably the auricles, has a
third cervical origin, which could explain the well-known clini­
cal fact that the pain of angina often radiates to the neck
anteriorly. The oesophagus is T4–T6 and the lungs have a
T2–T5 origin.
L1
CHAPTER 1
L2
L3
S2
Intra-abdominal region
The abdominal wall has a more or less circular construction,
from T7 at the xiphoid process, over T10 at the umbilicus, to
L1 at the iliac crest, inguinal ligament and groin. In the abdomi­
nal wall, the dermatomes exactly overlie the myotomes.
Most of the intra-abdominal content also has a mid- and
lower thoracic origin. The embryological derivation of the
stomach and duodenum (T6–T10), liver (T7–T9 right), gall
bladder (T6–T10 right),66 pancreas (T7–T8) and small intes­
tine (T9–T10), fit very well with their actual localization in the
abdominal cavity, and therefore pain derived from these organs
approximates with their surface representation. Structures of
lower thoracic, lumbar or even sacral origin, however, show a
more complicated pattern of referred pain. The kidney and
ureter, for instance, have a T11–L1 derivation and, although
they are localized high up in the abdomen, referred pain can
reach the inguinal fossa and the groin (T12–L1). The colonic
flexure is from L2 to L3, which allows the pain not only to
radiate to the lower back but also to the front of the thigh.
The sigmoid colon and rectum have S3–S5 origin. Hence, in
diseases of the sigmoid and the rectum, pain can be felt in the
iliac fossa, perineum, penis, vulva and inner aspect of the thigh.
The buttock
The skin of the lower lumbar area and the outer buttock is
derived from L1. At the upper buttock, there is considerable
overlap with the lumbar patches of the L2 and L3 segments
(Fig. 1.18). The skin of the lower buttock is derived from S2.
The gluteal muscles forming the buttocks are derived from
the fourth lumbar to the first sacral segments. Consequently,
the dermatomes descend further distally than the myotomes
they cover.
Scrotum
The testicles are derived from T11–T12 and L1. The epidi­
dymis has a T10 origin. The scrotum, however, belongs to the
S4 dermatome. A trauma to the testicle therefore may cause
not only local pain but also pain spreading along the iliac crest
posteriorly and up to the lower thoracic region. Testicular
disease frequently produces pain in one or the other iliac fossa.
Referred pain in visceral diseases
It is important to emphasize that referred pain is not a phe­
nomenon of orthopaedic medicine only. As described earlier,
many visceral diseases also cause referred pain. For the con­
venience of practitioners often faced with thoracic or
Fig 1.18 • Overlap of the dermatomes at the back and the buttock.
Box 1.2
Referred pain in visceral diseases
Heart (auricles?)
Lungs
Oesophagus
Diaphragm
Stomach and duodenum
Liver and gall bladder
Spleen
Pancreas
Small intestine
Appendix
Kidney
Ureter
Suprarenal glands
Ovary and testis
Epididymis
Colon: ascending
flexure
sigmoid
Rectum
C8–T4 (C3?)
T2–T5
T4–T6
C3–C4
T6–T10
T7–T9 right
T7–T10 left
T8
T9–T10
T10–L1
T10–T12 (L1)
T11–T12
T11–L1
T11–T12 (L1)
T10
T10–L1
L2–L3
S3–S5
S3–S5
abdominal pain, a list of the segmental derivations of the
viscera, based on the work of Cyriax45 (see his p. 30), William
and Warwick,67 Lindsay et al68 and Guyton (cited by Van
Cranenburgh69 is given in Box 1.2).
Referred pain is felt deeply and distally
in the dermatome
An important difference between local pain and referred pain
is that in the latter the pain is felt deeply and vaguely. The
15
General Principles
patient thus does not point to a localized and precise area, but
outlines an approximate one and tends to describe it as ‘deep’.
That pain – with some exceptions – is always referred dis­
tally, remains a purely empirical clinical observation and has
hitherto not been explained on neurophysiological grounds.
The fact that pain that arises from the proximal part of a
segment can be felt distally in the dermatome but a distal
lesion is not referred proximally within this same segment,
remains an inconsistency that is hard to rationalize. However,
this clinical observation is very important to the clinician con­
fronted with referred pain, for the lesion must never be sought
in a structure that is localized distally of the painful area. Pain
at the distal aspect of the L3 dermatome (knee and lower limb)
can have a proximal origin (spine, hip), but pain only in the
hip or the groin, cannot be caused by a lesion at the knee or
the thigh.
Segmentally referred pain does not cross
the midline
The segments in the body are arranged in pairs, each of which
has its own segmental innervation and its own projection area
in the cerebrum. Hence it is obvious that the cerebral cortex
will easily differentiate between a left-side or a right-side pain,
and no one will question that a C5 pain on the left side has a
left-side origin and vice versa. The fact that pain stemming
from a unilateral structure does not cross the midline, becomes
important in the interpretation of more or less centrally local­
ized pain, for instance in aches in the neck or back. It is evident
that a lesion of a unilateral facet joint will not cause pain radiat­
ing all over the lower back. Only centrally localized structures
(vertebral body, longitudinal ligaments, intra- and supraspinal
ligaments and dura mater) can theoretically be responsible for
a bilaterally radiating pain at both sides of the midline. A pain
felt centrally or bilaterally must originate from a central struc­
ture, or from two bilateral structures (two facet joints or two
sacroiliac joints) but it can never be the result of a lesion in a
unilateral structure.
Dura mater an ‘exception’ to
segmental reference
Pain originating from the dura mater has a rather peculiar
behaviour. First, in that the dura is a midline structure, it is
innervated from both sides, so that pain refers bilaterally.
Second, pain stemming from the dura has a very broad refer­
ence and seems to cover several consecutive dermatomes. For
instance, pressure of a lumbar disc on the dura at the L5 level
can cause pain in the back which radiates to the abdomen and
groins, down to the anterior and posterior aspect of both thighs
and legs, and upwards to the back of the lower chest. This
type of pain reference is inexplicable in terms of segments.
We therefore call it ‘extrasegmental reference’ of pain. Because
in orthopaedic medicine, the dura is the exclusive source
of this type of pain radiation, it is also called dural reference.
Pain of this nature can be very difficult to interpret if it
is felt in a part or parts of the possible reference area. As in
16
purely segmental reference, dural reference can be to only
a part of the respective dermatomes. Thus, instead of the
broad radiation to the whole back, both glutei and both legs,
dural pain sometimes only affects a small part, for instance one
groin, or one buttock or the whole posterior aspect of the
thigh. The differential diagnosis from a more segmental pain,
for instance as the result of a nerve root compression, is then
difficult.
A common clinical finding in a cervical disc protrusion that
impacts on the dura is unilateral interscapular pain or pain in
the trapezius or pectoral area. In the latter instance, suspicion
of angina pectoris may then easily arise. Also the removal
of an appendix for dural pain of lumbar origin referred
extrasegmentally into the iliac fossa and groin is not at all
exceptional.
A possible explanation for the misleading pain reference of
the dura may lie in its multisegmental origin, which is reflected
in the great overlap between the fibres of the consecutive
sinuvertebral nerves innervating its anterior aspect.70–73 More
recent researchers describe division of the nerves into ascend­
ing and descending branches which ramify variously, to give off
longitudinally and transversely orientated branches.74,75 In a
recent study that used the very sensitive acetylcholinesterase
method, more ramifications between the nerve branches were
demonstrated (Fig. 1.19).76 Ascending branches up to four
segments cranial to the level of entry into the dural nerve
plexus and also descending branches extending up to four seg­
ments caudally were observed. In addition, many vertical and
horizontal interconnections between the various ascending and
descending branches were seen. The conclusion is that dural
nerves may spread over eight segments and that a great overlap
exists between adjacent and contralateral dural nerves.
These findings may form an anatomical explanation for the
clinical observations of Cyriax on the limits of extrasegmental
reference of dural pain.77 Upwards, pain originating in the
lower cervical part of the dura may spread to the occiput, skull
and forehead (Fig. 1.20). Downwards it can descend to T7
which corresponds with the lower angles of the scapulae.
Anteriorly the pain can occupy the whole pectoral area.
Extrasegmental pain does not extend beyond the upper half of
the arms.
A middle thoracic disc lesion can cause dural extrasegmental
pain that may radiate to the base of the neck, and downwards
to the whole abdomen and to the upper lumbar region
(Fig. 1.21).
Dural extrasegmental reference from a low lumbar level
may reach the lower thorax posteriorly, the lower abdomen
deep to the umbilicus, the groins, the buttocks, and the sacrum
and coccyx (Fig. 1.22). Unlike the cervical dura – which does
not radiate far into the arms – extrasegmental reference from
a lumbar origin may also involve the legs, both the anterior and
the posterior aspects, and descend to the ankles.
Referred tenderness
There seems to be more to referred pain than just mislocation
by the patient. Within or near the area of referred pain, it is
often possible to find small trigger points which are exquisitely
Pain
CHAPTER 1
Fig 1.20 • Limits of dural multisegmental pain of cervical origin.
sensitive. Pressure on one of these immediately produces a
deep and radiating tenderness which is identified by most
patients as the source of their symptoms. Classic localizations
of these tender spots are:
• In cervical dural compression, the upper border of the
trapezius, the scapular muscles or the base of the neck.
• In lower lumbar dural involvement, the sacroiliac region
and the upper part of the buttocks.
Fig 1.19 • The nerve plexus of the lumbosacral posterior
longitudinal ligament (L1 to S4). Dorsal view after complete
laminectomy and after removal of the spinal cord and the ventral
dura. *, cut pedicle of a ventral arch; cv, vertebral body; di,
intervertebral disc; drg, spinal ganglion; rval, ventral ramus of the
spinal branch of the lumbar artery; small arrows, sinuvertebral
nerves entering the vertebral canal; open arrows, crossing
sinuvertebral nerves. Reproduced with permission from Groen GJ. Nerves
and nerve plexuses of the human vertebral column. Am J Anat 1990;188:282–96.
If the tender area is palpated without the prior conduct of a
proper functional examination of the neck or lumbar spine, the
tenderness is regarded as the primary lesion, the more so
because the patient insists that it is the apparent origin of the
pain. It is no wonder then that ‘fibrositis’, ‘myofibrositis’ or
‘myofascial pain’ syndromes have long been regarded as primary
lesions. The ‘fibrositis’ concept has been used to explain the
cause of lumbago.78 Lewis33 was the first to recognize that
trigger points and myalgic spots were not primary lesions and
that the painful area, although tender to the touch, did not
contain a focus.
Cyriax considered that the localized tender area is a
secondary effect of pressure on the dura mater.79,80 He
derived his theory from the simple clinical observation that
the tender spot shifted from place to place over a few seconds
after a successful manipulation and that, when a full and
painless range of motion had been restored, the tenderness
disappeared.
17
General Principles
Fig 1.21 • Limits of dural multisegmental pain of thoracic origin.
However, referred tenderness has also been demonstrated
in muscular and fibrous tissue lesions,81 in visceral lesions such
as ischaemic heart attacks82 and in pathological viscera. The
phenomena are not completely understood as yet but it is
reasonable to assume that trigger points are caused by summa­
tion mechanisms which can be understood in terms of gatecontrol mechanisms.79
Summation – the excitatory effect of converging inputs – is
an important pain mechanism. Pain may be triggered by two
sources of nerve impulses: a major one from the lesion; and a
minor one from normal skin which add together. If one source
is removed, it becomes more difficult for the other to trigger
the feeling of pain.83
Factors determining reference of pain
Referred pain is a faulty perception of the origin of a pain. In
orthopaedic medicine it is common to see marked differences
in the extent of reference between segments, between distinct
affected tissues and between different degrees of the same
condition.
The degree of reference – that is the distance between the
localization of the perception and the site of the lesion –
depends on four different factors (Box 1.3). Some can be
explained on the basis of the known pathways, others remain
unexplained and result purely from clinical observations.
18
Fig 1.22 • Limits of multisegmental pain of lumbar origin.
Box 1.3
Factors favouring reference of pain
Strength of the stimulus:
• The stronger the stimulus, the more reference of pain
Position of the affected tissue:
• The more central the lesion, the more reference of pain
• The more distal the lesion, the less reference of pain
Depth of the affected structure:
• More reference from deep-seated structures
• Less reference from superficial structures
Nature of the affected tissue:
• Little reference: bone and periosteum
• More reference: muscle
• Much reference: capsule, ligament, bursa, tendon, dura, dural
sleeve and perineurium
The strength of the stimulus
The greater the stimulus, the more extensive the reference of
pain. In other words, intense stimulation radiates the pain
widely and slight irritation localizes the pain closer to its origin.
This phenomenon is used in orthopaedic medicine to
estimate the degree of irritation or to evaluate treatment. A
Pain
classic example is the C5 pain that results from shoulder
arthritis. In this disorder there is a typical development of pain
which gradually increases. At first, pain is felt only in the
deltoid area, close to the shoulder. During the following months
it gradually spreads to the arm, first above the elbow but later
also to the forearm. At its worst, the pain can even be felt at
the distal end of the radius and the base of the thumb. If treat­
ment is successful or the condition regresses, the pain gradually
leaves the forearm and moves upwards until it is only at the
shoulder area. That the area of reference of pain becomes
smaller indicates that the strength of the stimulus is decreasing
and inflammation improves. Serious sacroiliac arthritis can
provoke pain in the whole of the S1 and S2 dermatomes, with
pain at the back of the thigh and the leg, down to the heel and
the sole. If the condition improves, pain first leaves the heel
and the calf. Further regression of the arthritis will probably
result in localized pain in only the neighbourhood of the sacro­
iliac joint, with some reference to the buttock.
The mechanism of this phenomenon is probably based on
the fact that the more the peripheral sensory nerve fibres are
stimulated, the more there is cerebral cortical activity.84
The position of the affected structure
Pain seems to refer distally only; this being so, the closer to
the midline the affected structure lies, the greater the possibil­
ity of extensive reference of pain. The further the lesion lies
from the midline, the more accurate will be the localization of
the lesion by the pain it provokes. As a rule, a lesion in the
wrist or in the ankle does not give rise to diffuse pain and the
patient usually knows quite well where the source is. Lesions
in the hand or foot can therefore be precisely indicated. Also
lesions in the elbow and knee cause quite well-defined pain
that does not radiate enough to confuse either the patient or
the examiner. Lesions that involve the shoulder, the hip, the
sacroiliac joints and the spine usually provoke extensive pain
reference. The segments to which the shoulder, hip and sacro­
iliac joints belong (C5, L3 and S1–S2) have the longest der­
matomes of the body; as a consequence, pain can be referred
a long way distally – calf pain in sacroiliac arthritis or knee pain
in arthritis of the hip.
CHAPTER 1
depth from the surface. This was confirmed later by other
studies.38,44
Pain originating from a superficial lesion is usually pin­
pointed correctly by the patient but deep lesions can cause
wide reference. This follows immediately from the way
referred pain originates. We have seen that referred pain is an
error of perception and that pain memory is based upon the
experience gathered by recurrent stimuli through the skin,
which is adapted correctly to localize pain. It follows that the
deeper structures lie from the skin, the less the chance that
they will be stimulated by external factors. When internal
(pathological) factors activate the nociceptors in these deeply
situated structures, the memory mechanism is inadequate and
places the pain within the affected segment.
The nature of the structure
There are many discrepancies in our knowledge of pain referral
and further research is required to clarify why some structures
give more pain reference than others. For example, pain origi­
nating in bone or periosteum, although usually located deeply,
hardly radiates at all. This does not mean that bone pain cannot
be very severe, but it seldom gives extensive reference. This
phenomenon is of great value in clinical diagnosis. Serious but
localized pain always points to the possibility of a lesion of the
bone. For example, an intense but localized pain in the lumbar
spine is typical of a bony lesion, such as fracture, infection or
new growth at a vertebra. Also intense, deep, but very localized
pain in a limb draws attention to bone disease. In addition,
severe but localized pain at the shoulder, precisely felt at the
true site, is always an indication of a bony lesion.
Pain stemming from a lesion in a joint capsule, bursa, liga­
ment or tendon is referred in an uncharacteristic way – the
degree of pain reference is not determined by the type of tissue
involved. Pain originating in a muscle seems to cause less refer­
ence than pain stemming from the tendon or the tenoperiosteal
insertion.
Intense pain reference can also result from pressure on the
different parts of the peripheral nervous system. Depending
on the localization of the compression, the reference will be
segmental or extrasegmental (see earlier).
The depth of the affected structure
As early as 1939, Kellgren35, and Lewis and Kellgren85 stated
that the localizing ability of a structure depended largely on its
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19
Pain
CHAPTER 1
References
1. Bonica JJ, Albe Fessard D. Advances in
Pain Research and Therapy. New York:
Raven Press; 1976.
2. Elton D, Stuart GV, Burrows GD.
Self-esteem and chronic pain. J Psychosom
Res 1978;22:25.
3. Merskey H. Pain terms: a list with
definitions and notes on usage.
Recommended by the IASP Subcommittee
on Taxonomy. Pain 1979;6:249.
4. Melzack R, Torgerson WS. On the
language of pain. Anaesthesiology
1971;35:50.
5. Wyke BD. Neurological mechanisms in the
experience of pain. Acupunct Electrother
Res J 1979;4:27.
6. Ralston HJ, Miller MR, Kasahara M. Nerve
endings in human fasciae, tendons,
ligaments, periosteum and joint synovial
membrane. Anat Rec 1960;136:137.
7. Besson JM, Guilbaud G, Abdelmoumene
M, Chaouch A. Physiologie de la
nociception. J Physiol (Paris) 1982;78:7–
107.
8. Iggo A. The case for ‘pain’ receptors, In:
Janzen R, Keidel WD, Herz A, Steichele C,
editors. Pain: Basic Principles,
Pharmacology, Therapy. Stuttgart: Thieme;
1972. p. 60.
9. Van Hees J, Gybels JM. Pain related to
single afferent C fibres from human skin.
Brain Res 1972;48:397.
10. Sarkin LS, Wallace MS. Acute pain
mechanisms. Surg Clin North Am
1999;79(2):213–29.
11. Dray A. Inflammatory mediators of pain. Br
J Anaesth 1995;75:125–31.
12. Reeh PW, Steen KH. Tissue acidosis in
nociception and pain. In: Kunasawa T,
Kruger C, Ulisumara K, editors. Progress in
Brain Research, vol. 13. Amsterdam:
Elsevier Science; 1996. p. 143–51.
13. Wall PD, McMahon SB.
Microneuronography and its relation to
perceived sensation. Pain 1985;21:209.
14. Nathan PW. The gate-control theory of pain:
a critical review. Brain 1976;99:123.
15. Price DD, Dubner R. Neurons that
subserve the the sensory-discriminative
aspects of pain. Pain 1977;3:307.
16. Wyke BD. The neurology of low back pain.
In: Jayson MIV, editor. The Lumbar Spine
and Back Pain. 2nd ed. Bath: Pitman
Medical; 1980. p. 265–339.
17. Yaksh TL. Spinal Afferent Processing. New
York: Plenum; 1986.
18. Melzack R, Casey KL. Sensory, motivational
and central control determinants of pain: a
new conceptual model. In: Kenshalo D,
editor. The Skin Senses. Springfield:
Thomas; 1968. p. 923–93.
19. Hand PJ, Morrison AR. Thalamocortical
projections from the ventrobasal complex
to somatic sensory area I and II. Exp
Neurol 1970;27:291.
20. Desijaru T, Purpura DP. Organisation of
specific–nonspecific thalamic internuclear
synaptic pathways. Brain Res 1970;21:169.
© Copyright 2013 Elsevier, Ltd. All rights reserved.
21. Penfield W. The role of the temporal cortex
in recall of past experience and
interpretation of the present. In:
Wolstenholme GEW, O’Connor CM,
editors. The Neurological Basis of
Behaviour. London: Churchill; 1958.
p. 149.
22. Newcombe F. Memory. In: Critchley M,
O’Leary JL, Jennett B, editors. Scientific
Foundations of Neurology. London:
Heinemann; 1972. p. 205.
23. Black P. Physiological Correlates of Emotion.
New York: Academic Press; 1970.
24. Melzack R, Wall PD. Pain mechanism: a
new theory. Science 1965;150:971–9.
25. Noordenbos W. Pain. Problems Pertaining to
the Transmission of Nerve Impulses Which
Give Rise to Pain. Amsterdam: Elsevier;
1959.
26. Mayer DJ, Price D. Central nervous system
of analgesia. Pain 1976;2:379.
27. Tan S-Y. Cognitive and behavioural methods
for pain control: a selective review. Pain
1982;12:201–28.
28. Langen D. Psychosomatic aspects in the
treatment of pain. In: Janzen R, Keidel
WD, Herz A, Steichele C, editors. Pain:
Basic Principles, Pharmacology, Therapy.
Stuttgart: Thieme; 1972. p. 164.
29. Chapman CR, Feather BW. Effects of
diazepam on human pain tolerance and pain
sensitivity. Psychosom Med 1973;35:330.
30. Fields HL, Henricher MH. Anatomy and
physiology of a nociceptive modulatory
system. Phil Trans Roy Soc B
1985;308:361–79.
31. Head H. The afferent nervous system from
a new aspect. Brain 1905;28:99.
32. Head H, Campbell AW. The pathology of
herpes zoster and its bearing on sensory
location. Brain 1900;23:353–523.
33. Lewis T. Pain. New York: MacMillan; 1942.
34. Kellgren JH. Observations of referred pain
arising from muscle. Clin Sci 1938;3:175.
35. Kellgren JH. On the distribution of pain
from deep somatic structures. Clin Sci
1939;4:35.
36. Inman VT, Saunders JB de CM. Referred
pain from skeletal structures. J Nerv Ment
Dis 1944;99:660.
37. Travell J, Berry C, Bigelow N. Effects of
referred somatic pain on structures in the
reference zone. Fed Proc 1944;3:49.
38. McCall IW, Park WM, O’Brien JP. Induced
pain referred from posterior elements in
normal subjects. Spine 1979;4:441.
39. Hansen K, Schliack H. Segmental
Innervation. Stuttgart: Thieme; 1962.
40. Kunert W. Wirbelsäule and Innere Medizin.
Stuttgart: F. Enke; 1975.
41. Foerster O. Dermatomes in man. Brain
1933;56:1.
42. Lewis T, Kellgren JH. Observations relating
to referred pain. Visceromotor reflexes and
other associated phenomena. Clin Sci
1939;4:47.
43. Keegan JJ, Garett FD. The segmental
distribution of the cutaneous nerves in the
limbs of man. Anat Rec 1948;102:409.
44. Hockaday JM, Whitty CWM. Patterns of
referred pain in the normal subject. Brain
1967;90(3):481–96.
45. Cyriax JH. Textbook of Orthopaedic
Medicine, vol. 1. 8th ed. London: Baillière
Tindall; 1982. p. 22, 35.
46. MacKenzie J. Krankheitszeichen und ihre
Auslegung 3. Translated by J Müller,
Würzburg: Kabitsch; 1917.
47. Livingston WK. Pain Mechanisms. New
York: Macmillan; 1944.
48. Wedell G, Sinclair DG, Feindel WH.
Anatomical basis for alterations in quality
of pain sensibility. J Neurophys 1948;11:99.
49. Wedell G. Referred pain in relation to the
mechanism of common sensibility. Proc Roy
Soc Med 1957;50:581.
50. Pomeranz B, Wall PD, Weber WV. Cord
cells responding to fine myelinated
afferents from viscera, muscle and skin.
J Physiol 1968;199:511–32.
51. Taylor DCM, Pierau FR-K, Mizutain M.
Possible bases for referred pain. In: Holden
AV, Winslow W, editors. The Neurobiology
of Pain. Manchester: Manchester University
Press; 1984. p. 143.
52. Wells PE, Frampton V, Bowsher D. Pain
Management by Physiotherapy. 2nd ed.
Oxford: Butterworth-Heinemann; 1994.
53. Cyriax JH. Massage, Manipulation and
Local Anaesthesia. London: Hamilton;
1941.
54. Ruch TC. Visceral sensation and referred
pain. In: Fulton JF, editor. Howell’s
Textbook of Physiology. Philadelphia: WB
Saunders; 1946.
55. Merskey H, Spear FG. Pain: Psychological
and Psychiatric Aspects. London: Baillière
Tindall and Cassell; 1967.
56. Neurological aspects of the diagnosis and
treatment of facial pain. In: Cohen B,
Kramer I, editors. Scientific Foundations of
Dentistry. London: Heinemann; 1974. p.
278.
57. Patten BM. Human Embryology. New York:
McGraw-Hill; 1968.
58. Head H, Campbell AW. The pathology of
herpes zoster and its bearing on sensory
location. Brain 1900;23:353–523.
59. Keegan JJ, Garrett ED. The segmental
distribution of the cutaneous nerves in the
limbs of man. Anat Rec 1949;101:409.
60. Fukui S, Ohseto K, et al. Distribution of
referred pain from the zygapophyseal joints
and dorsal rami. Clin J Pain
1997;13(4):303–7.
61. Cole JP, Lesswing AL, Cole JR. Analysis of
lumbosacral dermatomes in man. Clin
Orthop 1968;61:241.
62. Conesa SH, Argote ML. A Visual Aid to
the Examination of Nerve Roots. London:
Baillière Tindall; 1976.
63. Wakasugi B. Dermatomes of the body and
the extremeties. Surg Treatment
1982;132:270.
64. Mitta H. Study on dermatomes by means
of selective lumbar spinal nerve block.
Spine 1993;18:1782–6.
19.e1
General Principles
65. Sicard A, Leca A. Place de rachiotomie
dans le traitement chirurgical des
sciatiques. Press Med 1954;62:1737.
66. Doran FSA. The sites to which pain is
referred from the common bile duct in
man and its implication for the theory of
referred pain. Br J Surg 1967;54:599–606.
67. Williams PL, Warwick R. Gray’s Anatomy.
Edinburgh: Churchill Livingstone; 1980.
68. Lindsay KW, Bone I, Callander R.
Neurology and Neurosurgery Illustrated.
2nd ed. Edinburgh: Churchill Livingstone;
1991.
69. Van Cranenburgh B. Segmentale
verschijnselen. Utrecht: Bohn, Scheltema
and Holkema; 1985.
70. Pedersen HE, Conrad FJ, Blunck MD,
Gartner E. The anatomy of lumbosacral
posterior rami and meningeal branches of
spinal nerves (sinu-vertebral nerves). J Bone
Joint Surg 1956;38A(2):377–91.
19.e2
71. Stillwell DL. The nerve supply of the
vertebral column and its associated
structures in the monkey. Anat Rec
1956;125(2):139–62.
72. Kimmel DL. Innervation of spinal dura
mater, and dura mater of the posterior
cranial fossa. Neurology 1961;11:800–9.
73. Edghar MA, Nundy S. Innervation of the
spinal dura mater. J Neurol Neurosurg
Psychiatr 1966;29:530–4.
74. Jackson HC, Winkelmann RK, Bickel WH.
Nerve endings in the human lumbar spinal
column and related structures. J Bone Joint
Surg 1966;48A:1272–81.
75. Edgar MA, Ghadially JA. Innervation of the
lumbar spine. Clin Orthop Rel Res
1976;115:35–41.
76. Groen GJ, Baljet B, Drukker J. The
innervation of the spinal dura mater:
anatomy and clinical implications. Acta
Neurochir 1988;92:39–46.
77. Cyriax JH. Dural pain. Lancet 1978;1:919–
21.
78. Gowers W. Lumbago. BMJ 1904;i:117,
79. Travell JG, Simons DG. Myofascial Pain
and Dysfunction. Baltimore: Williams and
Wilkins; 1983.
80. Cyriax JH. Fibrositis. BMJ 1948;ii:251.
81. Simons DG. Muscle pain syndromes, part
II. Am J Phys Med 1976;55:15–42.
82. Kennard MA, Haugen FP. The relation of
subcutaneous focal sensitivity to referred
pain of cardiac origin. Anaesthesiology
1955;16:297–311.
83. Melzack R, Wall P. The Challenge of Pain.
London: Penguin; 1991.
84. Woolsey CN, Marshall WH, Bard P.
Observations on cortical somatic sensory
mechanism of cat and monkey. J
Neurophysiol 1941;4:1.
85. Lewis T, Kellgren JH. Observations relating
referred pain, visceromotor reflexes and
other associated phenomena. Clin Sci
1939;4:47.
© Copyright 2013 Elsevier, Ltd. All rights reserved.