16
Section 4 Multidisciplinary aspects of endodontic management
The orofacial pain–endo interface
DEFINITION OF PAIN
Pain is defined as an unpleasant sensory and emotional experience associ­
ated with actual or potential tissue damage. Pain has a strong motivational
input to behaviour, yet the link between tissue damage, pain and behaviour
is not always proportionate or direct. Pain from an accidental burn, such
as a hot iron, elicits sharp, transient pain causing a withdrawal reflex; this
is acute pain, which is protective in its behavioural drive. A stimulus that
is potentially damaging to tissues is considered noxious. The endodontic
equivalent of acute pain is that of dentinal, pulpal or periapical origin. Pain
that lasts for a few days or a few weeks can follow musculoskeletal or
sports injuries; this is prolonged pain, which can also be protective in its
behavioural drive. In a proportion of cases, the prolonged pain becomes
persistent or chronic, lasting beyond the period of injury and its healing;
this no longer has a protective value but it may continue to affect behav­
iour. The endodontic equivalent is neurogenic pain or pain from other
structures that appears to arise from teeth and its associated structures.
Although there are relatively few conditions to diagnose for the endo­
dontist, their overlapping presentation and innate subtleties complicate
straightforward identification (see Chapter 4). The problem is similar and
even more complicated when considering the overlapping presentation of
pain from other orofacial structures.
Orofacial pain may arise from or be associated with teeth, periodontium,
oral mucosa, temporomandibular joints (TMJ) and associated musculature,
cervical spine and associated musculature, maxillary sinuses, nose, eyes,
throat, salivary glands, nerve supply, vascular supply, and confounding
with headaches. Pain from these different structures and sources may have
distinctive characteristics, which aids their identification through knowl­
edge, practice and experience.
OROFACIAL PAIN PREVALENCE
It is difficult to determine accurately the true prevalence and incidence of
pain, both in general and in the orofacial region. Nevertheless, it is esti­
mated that a quarter of the adult population have suffered from orofacial
pain (MacFarlane et al., 2001). In children, toothache is the most common
orofacial pain, 12% experiencing an episode before the age of 5 and 32%
by the age of 12. Meanwhile, two recent UK studies of adults showed
12–19% of the population reported orofacial pain within the previous
month (Drangsholt & LeResche, 2009).
The prevalence of chronic pain is reputed to be 35.5% in the general
population (Raferty et al., 2011). In another large scale survey of 15 Euro­
pean countries, 19% of adults reported suffering from chronic pain, which
seriously affected the quality of their lives (Breivik et al., 2006). Further­
more, the overall incidence of chronic orofacial pain has been given as
38.7 per 100 000 per year (Koopman et al., 2009). In referred endodontic
patients, about 12% may have some form of chronic pain, either as a result
of endodontic treatment or because of initial misdiagnosis (Polycarpou
et al., 2005).
NEUROPHYSIOLOGICAL BASIS OF OROFACIAL PAIN
The sensory transmission of orofacial pain is conveyed predominantly by
Aδ and C fibres of the trigeminal nerve, which project to the nucleus
caudalis in the medulla. The latter is sometimes referred to as the
© 2014 Elsevier Ltd. All rights reserved.
R Leeson, K Gulabivala, Y-L Ng  
medullary dorsal horn as it is the functional equivalent of the spinal dorsal
horn. Pain input is modulated at this site in the brain stem before fibres
then project via the spinothalamic tract to the thalamus and thence to the
cerebral cortex. The sensory-discriminative component of pain and activa­
tion of the endogenous analgesic system are believed to originate within
the cortex. A schematic diagram illustrating the trigeminal pain pathway
is presented in Figure 16.1.
Convergence, inflammation and development of central sensitization
may collectively serve to intensify and confuse the pain experienced.
Convergence to the nucleus caudalis accounts for poor localization, spread
and referral of pain as seen in deep pain conditions involving the dental
pulp, the TMJ and associated musculature. Deep tissues have fewer noci­
ceptive nerve endings than cutaneous or mucosal tissues, which are more
clearly recognized as the source.
Sensitization and neuroplasticity may develop, first peripherally then
centrally, when persistent nociceptive facilitation exceeds inhibition. It
involves enlargement of the receptive field, decreased activation threshold,
wind-up with increased transmission of stimuli perceived as pain, altered
gene expression leading to prolonged functional change and, finally, per­
sistent pain and central sensitization. Allodynia and/or hyperalgesia are
common clinical presentations. Allodynia represents pain elicited by a
normally innocuous stimulus, while hyperalgesia represents pain of an
increased or prolonged nature, due to a noxious stimulus. Allodynia may
be observed when carefully examining a patient using a wisp of cotton
wool on the gingivae and discovering this initiates severe pain. Similarly
for hypersensitivity, gentle application of pressure to the apical area can
be perceived as intense pain.
Blocking peripheral inflammatory mechanisms by anti-inflammatory
drugs or blocking the conduction of nerve impulses with local anaesthetics
can reduce nociceptive input and potentially prevent the development of
central sensitization.
CLASSIFICATION OF OROFACIAL PAIN
Orofacial pain (OFP) is defined as pain whose origin is below the orbito-
meatal line, above the neck and anterior to the ears, including pain within
the mouth (Zakrzewska & Hamlyn, 1999).
Chronic OFP can be defined as pain in the face, mouth or jaws that has
been present intermittently or continuously for 3 months or longer. In
addition, chronic orofacial pain has also been defined by a persistence of
pain combined with signs of “chronification”, such as a strong association
with psychosocial problems, frequent changes of physicians, and multiple
further areas of pain.
Numerous classification systems based on the structures, symptoms or
treatment (Table 16.1) have been proposed for the orofacial region, the
more detailed assigning individuals to multiple categories, which ideally
incorporate both the physical component and the psychological impact of
pain. The number of classifications reflects the fact that the discipline is
still developing and there is still uncertainty about aetiopathogenesis, in
turn reflected in a rich field of research.
DIAGNOSIS OF OROFACIAL PAIN
A careful history is obtained to determine the characteristics of the orofa­
cial pain, as well as any history of other generalized chronic pain condi­
tions. Information on co-morbid anxiety, depression, sleep problems,
 370  The orofacial pain–endo interface

Fig. 16.2  The

associations and  
Vascular Neuropathic
overlap of various pain
Dura Convergence of primary Cerebral cortex categories

Eyes
Thalamus
Sinus Idiopathic

Muscle Spinal tract nucleus of

the Trigeminal nerve
Tooth
Inflammatory Musculoskeletal
Trigeminal
thalamic tract
Temporomandibular
joint Trigeminal ganglion

Nucleus caudalis Table 16.2  Factors determining the characteristics of orofacial pain
"Medullary dorsal horn"
Characteristics of orofacial pain
Duration and frequency – Acute/chronic
Anatomical location – Source/site
Trigeminal nerve
Symptoms and signs
Aetiology and pathophysiology
Aggravating and relieving factors
Fig. 16.1  A schematic diagram illustrating the trigeminal pain pathway
Mechanisms of pain

Table 16.1  Origin of some classification systems

Some of the classification systems available for orofacial pain

Table 16.3  Character and associated features of various types of
RDC/TMD (Research Diagnostic Criteria for Temporomandibular Disorders) 1992 orofacial pain
IASP (International Association for the Study of Pain) 1994
AAOP (American Academy of Orofacial Pain) 2008 Character of pain – an aid to orofacial pain differential diagnosis
ICHD (International Classification of Headache Disorders) 2nd edn 2004 Pain categories Character Associated features
Inflammatory Dull, aching, throbbing, Redness, swelling, heat, loss of
pounding, burning, function, hyperalgesia,
pressure, sharp, stabbing allodynia
social and family history should all be recorded. Pre-consultation question­ Musculoskeletal Dull, aching, pressure, Can be referred pain, often
naires may be useful when managing chronic pain to assess the behav­ occasionally sharp worse on function,
hyperalgesia, allodynia
ioural impact of pain and in establishing the patient’s goals and expectations. Neuropathic Continuous burning, Hyperalgesia, allodynia,
Clinical examination, together with special tests if required, is used to episodic electric shock, numbness, paraesthesia,
confirm diagnosis. The differential diagnoses of orofacial pain constitute stabbing. dysaesthesia
a vast list but a broad assessment is essential to exclude rare presentations (Neuro)Vascular Throbbing, pounding, Worse on increased intracranial
pulsating, sometimes pressure: head movement,
of intra- or extracranial malignant neoplasia, severe infective inflammatory stabbing physical activity, Valsalva
conditions before considering the more commonly encountered presenta­ manoeuvre, light and sound
tions of pain. The main causes of chronic orofacial pain are then often sensitivity, nausea, vomiting
classified into inflammatory, vascular, musculoskeletal, neuropathic and Idiopathic Range of character, often Anatomical distribution may not
dull aching with sharp be consistent with sensory
idiopathic (Fig. 16.2). episodes nerve distribution, may be
alleviated by eating, drinking
and distraction
CHARACTERISTICS OF OROFACIAL PAIN

The characteristics of the pain may assist in differentiating pain categories

but is not necessarily diagnostic (Table 16.2). There is much variation and
overlap in the presentation of pain (Fig. 16.2) and the clinician must
always rely on integration of history and examination findings to establish
the correct diagnosis (Table 16.3).
The anatomical location can sometimes be difficult to ascertain since
the source may not correspond to the site of pain. In addition, the pain
may be diffuse and difficult to localize. This is particularly evident
when there is convergence of nociceptive input to the caudal nucleus.
Descriptive terms for the character of pain vary considerably and include
the terms, sharp, dull, aching, burning, and throbbing. Together with fre­
quency (continuous, intermittent or paroxysmal), they may provide clues
as to the pathophysiology. Lancinating, electric shock-like, paroxysmal
pain is often used to describe trigeminal neuralgia, while a constant burning
sensation may be used to describe neuropathic pain.
Assessment of signs and symptoms, aggravating and relieving factors
are another important step in establishing a diagnosis. Acute inflammatory
conditions of non-odontogenic origin may commonly include sinusitis,
characterized as blockage, obstruction, congestion or nasal discharge with
or without loss or reduction in sense of smell causing pain in maxillary
teeth and face particularly on head movement. Sialadenitis or blockage of
salivary glands can cause swelling or pain on swallowing or salivation on
the thought of food. Temporomandibular joint disorder pain is often dull
 The orofacial pain–endo interface  371

Table 16.4  Characteristics of some commonly encountered orofacial pain conditions

Tension-type Migraine without or Trigeminal

Characteristics Atypical odontagia TMD/myofacial pain headache with aura Cluster headache neuralgia
Frequency Continuous Continuous or Episodic or chronic Intermittent Episodic or chronic Intermittent
intermittent
Duration Months or years Variable 30 minutes to 72 4–72 hours 15–180 minutes Brief; seconds
hours
Location Unilateral/bilateral; Unilateral/bilateral; Bilateral; Unilateral; Unilateral; Unilateral;
poorly localized around TMJ jaw occipital, parietal, frontal, temporal orbital, one or more
around a tooth/teeth musculature temporal, frontal supraorbital, divisions of the
often undergone temporal trigeminal nerve
multiple procedures
Quality of pain Dull, aching, Dull, aching, throbbing, Dull, non-pulsing, Pulsating, throbbing Hot searing, Electric shock-like,
throbbing, burning occasional sharp pain tightness, pricking, drilling lancinating
pressure, soreness
Intensity of pain Mild to moderate Mild to moderate Mild to moderate Moderate to severe Severe Severe
Aggravating Spontaneous or history Stress, mechanical jaw Stress, posture and Stress, routine physical Smoking, alcohol Washing, light
factors of trauma or movements muscle strain, activities, food, touch, shaving,
deafferentation missed meals, odour, loud noise, smoking, talking,
(pulpectomy/ weather changes, bright light, missed tooth brushing
extraction) menstruation, meals, alcohol,
fatigue menstruation, fatigue
Relieving factors Topical lidocaine, Systemic medication, Systemic Systemic medications, Systemic Systemic medication
systemic medication hot/cold pack, jaw medication, supine in a dark medication
exercises, hard/soft exercise, room, sleep
occlusal splint, stretching, fresh
acupuncture air
Associated May develop atypical Sense of fullness, May report neck, Nausea, photophobia, Conjunctival Severly debilitating.
symptoms facial pain buzzing or popping shoulder and phonophobia infection, Many patients
in the ears, limitation TMD pain Aura may occur prior to lacrimation, unable to eat,
in mouth opening or headache onset with nasal congestion, drink, clean the
restricted jaw visual disturbance, rhinorrhea, teeth, wash or
movment, noise on paraesthesia of forehead & shave the face
jaw movement hand,arm,face and facial sweating, due to pain
dysphasia miosis, ptosis,
eyelid oedema

Table 16.5  Four primary types of pain OROFACIAL PAIN AND ENDODONTICS

Nociceptive Transient pain Endodontic patients often present because of pain, which may or may not
In response to a noxious stimulus
be associated with previous treatment interventions. The topic of endodon­
Inflammatory Spontaneous pain and hypersensitivity
In response to tissue damage and inflammation
tic pain prior to any treatment intervention has been covered in Chapters
Neuropathic Spontaneous pain and hypersensitivity 4 (Diagnosis of endodontic problems) and 10 (Management of emergen­
In association with damage to or a lesion of the cies and traumatic injuries). Persistent pain associated with teeth after
nervous system non-surgical or surgical endodontic treatment has been used as an indicator
Functional Hypersensitivity to pain of treatment failure. However, pain may be experienced in a tooth or
Resulting from abnormal central processing of
normal input adjacent site in the absence of clinical or radiographic signs of dental
disease. Such diagnostic dilemmas in decision making during treatment
Woolf, 2004 planning were highlighted by Hunter as early as 1778. Failure to detect
pathological change on periapical radiographs may reflect limitations of
the diagnostic method rather than an absence of an osteolytic lesion.
Superimposition of adjacent anatomical structures over the suspect tooth
may further obscure the view. Conversely, residual periapical disease may
with sharp episodes; there may be pain on jaw movement originating either be truly absent and the pain may be non-odontogenic.
from the joints or muscles (masseter, temporalis, pterygoids and anterior Pain in a tooth site of neurogenic origin has been reported in the litera­
digastric), which can be referred to the maxillary molars. Conversely, ture but only a few published studies have investigated the occurrence
muscular pain may arise from painful dental conditions and can then of neuropathic pain after dental treatment. Evidence of the association
persist as an independent entity. Characteristics of some common chronic between dental treatment and chronic neuropathic pain has been presented
non-odontogenic orofacial pain problems are presented in Table 16.4. by Marbach (1978), Schnurr & Broke (1992) and Vicker et al. (1998), who
A mechanism-based approach to pain diagnosis can be useful when reported that most patients diagnosed with atypical odontalgia related the
considering appropriate treatments. The four primary types of pain (Table onset of the pain to dental treatment, dental infection or dental trauma.
16.5) are often considered to be the acute nociceptive and inflammatory Only four epidemiological studies (Marbach et al., 1982; Campbell
pains as opposed to the maladaptive neuropathic and functional pains et al., 1990; Berge, 2002; Oshima et al., 2009) have investigated the preva­
(Woolf, 2004). lence of chronic neuropathic pain after dental treatment. The study by
 372  The orofacial pain–endo interface
Marbach et al. (1982) was conducted by a single endodontist, who mailed
questionnaires to patients one month following non-surgical endodontic
treatment. Only female patients were included in their analyses because
the male sample was considered too small. Out of the 256 female patients
assessed, 20 (9%) reported persistent pain during the period of survey but
only 11 female patients attended for clinical and radiographic examination
to exclude an odontogenic cause of pain. Out of the 11 patients, 8 (3% of
256 female patients) were diagnosed with “phantom toothache”. Campbell
et al. (1990) carried out a similar survey of patients who had undergone
surgical endodontic treatment 2 years previously and found that 59 (50%)
of the 118 patients suffered from chronic pain that divided equally into
two groups; post-traumatic stress dysaesthesia (absence of pain preopera­
tively) (PTD) and phantom tooth pain (PTP) (presence of pain preopera­
tively). Oshima et al. (2009) reported 5.9% of 271 patients who had
chronic persistent pain that did not respond to previous endodontic proce­
dures were diagnosed with neuropathic tooth pain. In contrast, Berge
(2002) found none of the 1035 patients in their survey suffered from
chronic neuropathic pain following surgical removal of third molars 5–6
years previously. None of these studies extended their investigation to
include risk factors affecting prevalence of persistent pain after dental
treatment.
CASE HISTORIES OF TYPICAL OROFACIAL/ENDODONTIC
PAIN DILLEMAS
Scenario 1 
A 69-year-old male presents with a severe toothache in the maxillary left
canine, for which he requests endodontic treatment.
The pain is described as stabbing in character, “like an electric shock”,
lasting seconds in duration. He is unable to shave or wash the face on the
left or even to clean the teeth, eat, drink or allow cold air to touch this area
without triggering pain. However, pain does not disturb the patient from
sleep at night. Clinically, the canine is heavily restored and there are
extensive plaque deposits and inflammation of the gingivae in the upper
and lower dental arches.
• Question: What non-odontogenic condition may the patient be suffering
from?
• Answer: Trigeminal neuralgia. (Maxillary division V2).
• Question: What investigations would you consider?
• Answer: Radiograph to exclude endodontic problems with the canine.
Baseline blood tests prior to commencing medication. MRI to assess
trigeminal nerve.
• Question: What treatment might you consider and to whom would you
refer?
• Answer: Carbamezapine medication, referral to their General Medical
Practionner, an Orofacial Specialist or Neurologist.
Scenario 2 
A 49-year-old female presents with a dull, burning, continuous pain in the
upper right first premolar, with signs of allodynia and hypersensitivity in
the maxillary right maxilla. The tooth was restored then root-canal treated
6 months ago but the pain never subsided. Clinically and radiographically
the tooth in question appears to have an excellent non-surgical root-canal
treatment with good apical seal. However, the patient is adamant that the
tooth should be extracted.
Previously, a similar pain was present in the maxillary right second
premolar tooth which was restored, root-canal treated and subsequently
extracted. Unfortunately, maxillary right first and second molars underwent
a similar fate of restoration, root-canal treatment and extraction.
• Question: What is your advice to the patient with regards to the
extraction?
• Answer: Advise against extraction.
• Question: What is the most likely condition?
• Answer: Neuropathic pain (atypical odontalgia).
Scenario 3 
A 32-year-old male smoker presents with a 3-month history of a toothache
in the left maxilla possibly from a molar tooth, which wakes the patient
from sleep. On questioning, the pain occurs regularly at night, 1–2 hours
after falling asleep. When the patient awakes, he is experiencing an intense
pain which lasts from half an hour to 2 hours. He is unable to lie in bed but
agitation causes him to pace the room and seek distraction. Pain is located
in the eye, supraorbital and temporal region with associated features,
including ipsilateral conjunctival injection and lacrimation, rhinorrhea, nasal
blockage and ptosis.
• Question: What is the most probable non-odontogenic diagnosis?
• Answer: Cluster headache (Migranous neuralgia).
CONCLUDING REMARKS
If endodontic pain diagnosis is challenging, diagnosis of orofacial pain
mimicking endodontic pain is even more complex. It requires a systematic
gathering of relevant information and its appropriate processing through a
surgical sieve to identify likely causes. The responsibility lies with the
endodontist to exclude pain of dental and endodontic origin and then to
refer appropriately to specialists with the relevant knowledge and skills.
Depending on the country of residence, the relevant speciality may include
orofacial pain or oral medicine.
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