BDJ Oral Medicine Themed Issue PRACTICE

Orofacial pain – an update on diagnosis and

management
S. Ghurye1 and R. McMillan*2

In brief
Provides a comprehensive overview of common Provides guidance with regards to diagnosis, Highlights the importance of adopting a
non-dental facial pain which will be of interest to management and when to refer facial pain patients. biopsychosocial approach to facial pain management
non-specialist dentists.

The diagnosis and management of orofacial pain may be challenging due to complex histories, pathophysiology and
associated psychosocial co-morbidities such as depression and anxiety. Neuropathic facial pain conditions such as burning
mouth syndrome (BMS), persistent idiopathic facial pain (PIFP), atypical odontalgia (AO) and trigeminal neuralgia (TN) require
early recognition by primary care clinicians and referral to secondary care. Acute pain-related temporomandibular disorder
(TMD) may be managed in the primary care setting, with identification of those at risk of developing chronic TMD receiving
an early referral to secondary care. Adopting a biopsychosocial approach, consisting of physical therapies, pharmacotherapy
and psychological support can lead to effective management and may limit the negative impact of facial pain upon quality
of life and daily functioning.

Introduction reported a facial pain prevalence of 1.9% in management of adults with chronic  pain.14
the UK, of this 48% were reported as being These principles follow a biopsychosocial
The term ‘orofacial pain’ is used to describe chronic. These findings are significant, as it has approach and consist of three domains:
pain arising from the regions of the face and been well documented that chronic orofacial physical exercise/relaxation, pharmacotherapy
mouth. These pains may occur due to diseases pain may be accompanied by distress, physical and clinical psychology.15
of regional structures, nervous system dys- disability and negative psychosocial impact.5–7 Adopting this approach of early diagnosis
function, or as a result of referral from distant Moreover, there are economic implications for and a holistic approach to management is
sources.1 Orofacial pain of greater than three managing chronic pain, with patients often central to limiting the negative psychosocial
months duration may be described as being utilising greater healthcare resources, through impact of orofacial pain,9,15,16 whilst ensuring
chronic.2 assessment by multiple clinicians, and inves- care remains effective and efficient.9
Macfarlane et al.3 conducted a cross-sectional tigations which may not be of benefit to the The aim of this paper is to summarise the
population-based survey in the UK, in which patient.8–11 Durham et al.12 have conducted a diagnostic classifications, epidemiology,
26% of participants reported orofacial pain. study into the costs associated with persistent pathophysiology and management of the key
At the four year follow up, 54% continued to orofacial pain. The authors used the graded orofacial pain conditions – burning mouth
report orofacial pain, highlighting the potential chronic pain scale (GCPS), which takes into syndrome, persistent idiopathic facial pain,
for chronicity of orofacial pain.3 Furthermore, account pain intensity and pain-related disabil- atypical odontalgia, pain-related temporo-
a more recent study by Macfarlane et  al.4 ity.12,13 Healthcare costs were found to increase mandibular disorder (TMD) and trigeminal
by an average of £366 when moving from a neuralgia.
low to a high GCPS status; highlighting the
1
Specialist Registrar in Oral Surgery, Department of Oral & biopsychosocial impact of orofacial pain and
Maxillofacial Surgery, Queen Alexandra Hospital, Southwick Burning mouth syndrome (BMS)
Hill Road, Portsmouth, PO6 3LY; 2Consultant and Honorary the associated economic impact.12
Clinical Teaching Fellow in Oral Medicine and Facial Pain, Thus, it is important that patients with Classification and diagnosis
Eastman Dental Hospital, 256 Gray’s Inn Road, London,
WC1X 8LD, UK orofacial pain receive an early diagnosis with Burning mouth syndrome (BMS) is a condition
*Correspondence to: Roddy McMillan instigation of appropriate management.9 The characterised by burning sensation or dis-
Email: roddymcmillan@nhs.net
overall management strategy for orofacial comfort affecting the mouth, occurring in the
Refereed Paper. Accepted 31 July 2017 pain may be extrapolated from the guidelines presence of clinically healthy oral mucosa.17–19
DOI: 10.1038/sj.bdj.2017.879
produced by the British Pain Society for the BMS commonly affects the tongue, however,

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patients may also report more extensive BMS more commonly affects women (with a Management
discomfort affecting other areas of the oral varying ratio between five and ten females to BMS is a chronic, often long-term pain
cavity.17,19,20 Patients may alternatively report every male).17,18,24,26,27 It has been documented condition and thus an important aspect of
sensations such a tingling or numbness;21 while in the literature that BMS peaks between the management is providing reassurance, hope,
additional symptoms of xerostomia and taste fifth and seventh decades.17 educating patients about their condition,6 and
disturbance may also be encountered. BMS is a chronic condition which usually facilitating self-management.33 Bonathan et al.6
Scala et al.20 have described that ‘primary’ persists for many years, occasionally with have demonstrated that provision of informa-
BMS occurs when organic causes for oral episodes of remission.22 Sardella et al.28 reported tion regarding chronic facial pain conditions,
burning cannot be identified; whereas 3% of patients experienced complete remission delivered in a sensitive manner, can aid in
‘secondary’ BMS may arise as a result of local or after five years of onset of the condition. alleviating patients’ feelings of helplessness
systemic pathology. Therefore, the diagnosis of towards their condition. Moreover, this
burning mouth syndrome is made following a Pathophysiology educational approach can facilitate self-
comprehensive pain history, with the exclusion Recent studies have suggested that several management.6,34 Consequently, patients with
of medical, dental and drug-related causes for neuropathic mechanisms act at different BMS should be encouraged to develop self-
the symptoms.19,20 Clinical examination is levels of the nervous system to contribute management strategies involving physical
important, in order to exclude local factors to the pathophysiology of BMS.19 It has also activities, relaxation and distraction.34
which may lead to oral burning sensation.20,22 been suggested that BMS is multifactorial A recently published Cochrane review19 on
Oral mucosal conditions such as lichen planus, in origin, occurring as a result of a complex the management of BMS suggested that there
candidosis and geographic tongue may also interaction between local, systemic and psy- is currently a dearth of high quality evidence
give rise to oral burning sensations.20 Allergic chosocial factors.26 Further supporting the to support, or refute any specific treatments
reactions to dental materials and food may lead proposals for neuropathic mechanisms in for BMS. The review concludes that further
to an oral burning sensation, thus patch testing BMS, an elegant hypothesis promulgated by clinical trials should be conducted, looking at
may be indicated for patients with a history and Woda and colleagues suggests that a significant medications used in other neuropathic pain
presentation in keeping with a type I hypersen- proportion of BMS may be attributed to neuro- conditions and psychological therapies. In light
sitivity (allergic response), or presenting with pathic changes secondary to perimenopausal of the association of BMS with depression and
a suspected type IV hypersensitivity reaction hormonal dysregulation.18 Moreover, a study anxiety19,30,31 it has been suggested that antide-
(such as a lichenoid lesion).22,23 Assessment by Lauria et al.17 found that tongue biopsies pressants may be beneficial in the management
of saliva flow may also be performed in cases from BMS patients demonstrated a lower of BMS.19 The blockade of the central nervous
where xerostomia is suspected as being the density of epithelial nerve fibres in comparison system (CNS) receptors by antidepressants
underlying cause of discomfort.18,20 to the control group. Morphological changes may result in increased activity of descending
In order to investigate systemic causes of affecting epithelial and subpapillary nerve inhibitory pain pathways.19 Tricyclic antide-
BMS, patients should receive haematologi- fibres were noted, suggesting that BMS may pressants (TCAs) such as amitriptyline may be
cal and biochemical investigations to exclude be due to small fibre trigeminal sensory neu- of benefit in managing BMS.19,35 However, there
anaemia and haematinic deficiency (low folate, ropathy. Similarly, studies have demonstrated is limited evidence to support, or refute the
B12 or iron) which may result in oral burning involvement of the central nervous system in use of antidepressants for the management of
sensation.16,24 Testing of serum zinc levels has also the development of BMS,18,26 with positron BMS. Similar findings have also been reported
been advocated.16 One study has demonstrated emission tomography (PET) scanning of for the use of anticonvulsants such as gabapen-
low serum zinc levels in patients with BMS;25 BMS patients demonstrating decreased levels tin, and the use of benzodiazepines.19 Although
however, it was concluded that there is limited of dopamine in the putamen.29 robust evidence for the medical management
evidence to suggest that this is a causative factor Additionally, understanding the impact of BMS is lacking, there is evidence for the
in the development of BMS. Random blood of psychosocial factors in the development use of antidepressants and anticonvulsants
glucose and HbA1c may be required to help of BMS is of paramount importance.20,30 in the management of neuropathic pains in
exclude diabetic neuropathy.16 In patients where Lamey et al.30 reported that BMS patients may general – amitriptyline, duloxetine, gabapentin
connective tissue disorders, or other autoim- demonstrate a higher incidence of adverse and pregabalin are considered appropriate first
mune conditions such as Sjögren’s syndrome are early life experiences and chronic fatigue. line medical therapies for neuropathic pains
suspected, immunological investigations such as Moreover, it has been documented that BMS according to the National Institute for Health
autoantibody screens may be performed.16 patients may exhibit higher levels of depression and Care Excellence (NICE).36 In view of the
In summary, the diagnosis of BMS is based and anxiety.30,31 Further to this, brain dopamine evidence supporting BMS as a neuropathic
upon pain history, normal clinical examination hypofunction is shared between BMS and psy- pain, it would be reasonable to consider such
and laboratory investigations.19,20 chiatric comorbidity – suggesting that patients neuropathic pain medications in the manage-
with BMS are more likely to develop anxiety ment of BMS.
Epidemiology and depression, and vice versa.31 Psychological therapies such as cognitive
BMS is reported to affect 0.7–15% of the Burning mouth syndrome is a chronic behavioural therapy (CBT) have been seen to
population.26 The variability in the preva- neuropathic pain condition that can have a reduce pain intensity in patients with BMS.37
lence is suggested to be due to the differing significant negative impact on quality of life. A combined approach with medical and psy-
criteria used in the diagnosis of BMS, with Several studies have shown reduced quality of chological therapy, with an emphasis on self-
some studies also including secondary BMS.26 life in BMS patients compared to controls.24,32 management may help to limit the negative

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psychosocial impact of BMS and improve occur prior to the development of PIFP and Epidemiology
quality of life.19,20 may similarly run a chronic course.31 Further AO may affect a younger age group and dem-
supporting these associations, some studies onstrate less variation in incidence between
Persistent idiopathic facial pain have identified brain dopaminergic hypofunc- genders.38
tion in PIFP patients, in a similar way to other A study by Pigg et al.42 examining the long
Classification and diagnosis chronic pain conditions.41 term prognosis of patients with AO, reported
Persistent idiopathic facial pain, previ- that a third of patients demonstrated improve-
ously termed ‘atypical facial pain’,16 has been Management ment in their symptoms over time; however
described by the International Classification Early diagnosis of PIFP, in conjunction with the majority of patients continued to experi-
of Headache Disorders (ICHD)38 as being patient education is central to the manage- ence long term discomfort.
‘Persistent facial and/or oral pain, with varying ment of PIFP.39 This approach is of paramount The prevalence of persistent pain after suc-
presentations, but recurring daily for more importance, as invasive procedures may result cessful root canal treatment has been reported
than 2 hours per day over more than 3 months, in traumatic neuropathy and worsening of to be 12%.45
in the absence of clinical neurological deficit.’ symptoms40.
PIFP commonly presents unilaterally and Medications may be considered to manage Pathophysiology
may initially be limited to one side of the face, the symptoms associated with PIFP.39,40 In view The pathophysiology of AO is suggested to
commonly affecting the maxillary region, of the overtly neuropathic nature of PIFP, one be of neuropathic origin.39,42,46 This is further
though it may spread to involve a larger area.39 could consider consulting the NICE guide- supported by studies which identify AO devel-
The pain is normally poorly localised, not lines for neuropathic pain36 – which suggest oping following dental treatment.43,44
following the distribution of a peripheral nerve first line management with either: amitrip- A study by Baad-Hansen et  al.46 found
and is often of dull and aching character,39 tyline, duloxetine, gabapentin or pregabalin. changes in intraoral somatosensory function in
though sharp exacerbations may also occur.38 If sufficient benefit is not achieved, then it is patients with AO – with a higher frequency of
The ICHD diagnostic classification for PIFP suggested that patients may change to one of hypersensitivity to intraoral stimuli in patients
includes the features described previously, with the alternative medications, or take a combina- with AO, in comparison to healthy controls.
the addition of normal clinical neurological tion therapy. Moreover, one may also include Some have suggested that PIFP and painful
examination and exclusion of a dental cause.38 the intermittent use of tramadol (an opioid) post-traumatic trigeminal neuropathy (such
The diagnosis of PIFP is primarily based for breakthrough pain. However, solely using as pain resulting from a neuropathic injury for
upon pain history and clinical examination.8 medications may be insufficient for managing example, lower third molar surgery)47 share
Radiographic examination should also be PIFP.39,42 many characteristics, and can be considered
carried out to exclude dental causes.8 As described previously, patients with PIFP part of the same continuum.40,41,48
may also present with significant distress, psy-
Epidemiology chiatric co-morbidities, and impaired quality Management
The reported estimated incidence of PIFP is of life.6,31,39 Although these issues may be partly Similar to the other neuropathic pain condi-
given as 1 per 100,000, though this may not be addressed by using the previously described tions described in this paper, early diagnosis
representative of the true incidence due to dif- medications, it is important to consider a and patient education is important in the
ficulty in applying the classification criteria.39 holistic approach, incorporating patient management of AO.39,42 Accurate and timely
The incidence of PIFP is higher in women than education and psychological therapies such as diagnosis of AO is crucial to avoiding
in men8,39 and most often occurs between the CBT to facilitate self-management.10 futile and unnecessary dental and surgical
ages of 30–50 years old.39 interventions.39
There is a lack of data with regards to Atypical odontalgia Management of AO is largely similar to
remission rates for PIFP; however, it may be other neuropathic facial pain conditions.39 As
inferred that this condition follows a similar Classification and diagnosis described previously, medical management
natural history as other chronic orofacial pain AO has been reported as being a subform following the NICE guidelines for neuro-
conditions, with long-term pain symptoms.10 of  PIFP. 38,39 However, as AO may occur pathic pain36 may be implemented. Similarly,
following trauma, it may also be classified as AO may be also be associated with significant
Pathophysiology a form of painful post-traumatic trigeminal levels of depression and anxiety, thus psychol-
PIFP is reported as being a neuropathic pain neuropathy.38 ogy therapies in conjunction with medical
condition.39,40 This is supported by publications AO is suggested as being continuous dull management may be required.10,39,42
that report these symptoms often develop pain, affecting the teeth, or commonly at the
following dental treatment, suggesting under- site of a previous dental extraction.39,42 These Pain-related TMD
lying neuropathic pathology.39,40 Moreover, it is symptoms occur in the absence of clinical
suggested that there is involvement of central and radiographic findings.39,42 It has been Classification and diagnosis
sensitisation pain mechanisms.40 reported that these symptoms may develop TMDs refer to conditions affecting the tempo-
Patients with PIFP may demonstrate greater following dental treatment.39,43,44 The pain romandibular joint (TMJ), and/or the muscles
incidence of psychiatric co-morbidities such remains persistent despite dental treatments, of mastication.49
as depression and obsessive-compulsive per- including extraction, and may even migrate to The original research diagnostic criteria
sonality characteristics.31 These conditions may adjacent teeth.39 for TMD (RDC/TMD)50 classified TMD into

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disability in TMD patients. The hospital Moreover, it has been reported that TMD
Table 1 Classification of TMD50
anxiety and depression scale (HAD) may be may arise due to both central and peripheral
Myofascial pain (affecting muscles of mastication) used to screen for anxiety and depression.54 sensitisation mechanisms.64 Unlike the other
With limited opening
Special investigations, such as imaging, may facial pain conditions, TMD is not consid-
also be performed when diagnosing TMD. ered to be a neuropathic pain, rather it is
Without limited opening Panoramic radiographs may enable detection best described as a ‘central sensitisation’ pain
TMJ disc displacement of dental pathology.51 A study by Crow et al.55 syndrome; whereby, peripheral nociceptor
reported that condylar changes and degenera- inputs produce a reversible, but prolonged and
With reduction of the disk (with clicking)
tion were also detected on panoramic radio- increased activity in the central nociceptive
Without reduction of the disk, with limited opening graphs of healthy controls. Thus, it is has been pathways – resulting in pain hypersensitivity
Without reduction of the disk, without limited opening suggested that imaging should be conducted and hyperalgesia.65
only following assessment of the clinical
TMJ arthritides
findings.51,56 Magnetic resonance imaging Management
TMJ osteoarthritis (MRI) may be used to assess disc position, The majority of patients presenting with TMD
TMJ osteoarthrosis osteoarthrosis and inflammatory changes.57 can be effectively diagnosed and managed in
Computed tomography (CT) and cone beam the primary care setting;15,51 however, those
TMJ arthralgia
CT may enable detection of osseous changes.57 presenting with chronic TMD, significant
However, there is limited evidence with psychosocial risk factors and other chronic
three diagnostic groups which are detailed in regards to the benefit of CT or MRI in TMD.57 pain-related co-morbidities, may benefit from
Table 1. Therefore, it is important that consideration is early referral to secondary care.9,15,51
The RDC/TMD classification has since been given to the overall impact that imaging will Initial management of TMD should focus
superseded by the more recent diagnostic have upon the management of each individual upon patient education to encourage the
criteria for temporomandibular disorders (DC/ TMD case.55–57 development of self-management strategies.33,66
TMD).22 In summary, the DC/TMD suggests These self-management strategies include
that pain-related TMD is: pain involving the Epidemiology physical exercises and relaxation, for example,
TMJ; muscles of mastication, which are tender The reported prevalence for TMD is that yoga,15,67 which has been shown to benefit
to palpation; pain is evoked by function; and it may affect up to a third of the population patients with other chronic pain conditions
the pain is not attributed to another pain during their lives.58 Current literature reports with a musculoskeletal component, such as
diagnosis. that TMD is one of the three most common fibromyalgia.68 Educating patients about their
The diagnosis of TMD follows a thorough chronic pain conditions, along with headache condition is vital in facilitating self-manage-
history and examination. The history should and back pain.58 The prevalence of TMD is ment – one study demonstrated the benefits of
include pain character, precipitating/exac- seen to be higher in women;58 the incidence education over splint therapy in the manage-
erbating factors and previous  trauma. 51 of TMD peaking in the second and third ment of TMD.69 Similarly, physiotherapy may
Moreover, a comprehensive medical history decades.59 Moreover, TMD may also be classi- enable muscle relaxation and improvement in
is required, in order to ensure that conditions fied as acute or chronic.60 Acute TMD is often function.70
that may give rise to TMD symptoms, such attributable to an identifiable cause, such as Psychological therapies, such as cognitive
as rheumatoid arthritis and Ehlers-Danlos prolonged dental treatment, and the symptoms behavioural therapy may also facilitate self-
syndrome are detected.15 are normally short-lived and self-limiting.51 management, through the development
Clinical examination should include The recently published prospective cohort of techniques to manage pain associated
palpation of the TMJ and assessment for series, ‘Orofacial Pain: Prospective Evaluation with TMD.8,51
joint  noises.51 The muscles of mastication and Risk Assessment’ (OPPERA), suggested A Cochrane review has demonstrated a
should also be palpated, in order to assess for that the annual incidence of new onset TMD lack of high quality evidence with regards to
tenderness or hypertrophy. In patients aged symptoms in a cohort of 18–44-year-olds was the role of medications in the management
over 50 with new onset TMD symptoms, the 3.9% per annum.61 In chronic TMD, the pain is of TMD.71 Acute TMD exacerbations may be
temporal pulses should be checked,51 and one of a longer duration, exceeding three months;51 managed effectively with simple analgesia,
could consider conducting an erythrocyte sed- which is reported to occur in approximately such as a non-steroidal anti-inflammatory
imentation rate (ESR) and C-reactive protein 20% of TMD patients.62 These prolonged drug (NSAID).51 Similarly, benzodiazepines
(CRP),52 to help exclude a possible diagnosis of symptoms may lead to depression and chronic may be used to manage acute TMD accompa-
giant cell arteritis (temporal arteritis). A dental pain-related disability.53 nied with limited opening, though in light of
assessment should also be performed in order the potential for dependency, a short course
to rule out dental pathology.15 Pathophysiology of treatment is recommended.72 TCAs such as
It has also been suggested that psychological The pathophysiology of TMD is multifacto- amitriptyline or nortriptyline may be effective
assessment is required, due to the impact that rial, arising from a complex interplay between in managing chronic TMD which is refractory
chronic TMD may have upon quality of life various anatomical, physiological and psycho- to conservative measures;51,72 the benefit may
and the development of chronic pain-related logical factors.15,49,53,63 be seen even in the absence of depression.72
disability.53 The graded chronic pain scale Table 2 summarises the pathophysiological Occlusal splints have been widely used in
(GCPS),13 may be used to assess pain-related factors associated with pain-related TMD.15,63 the management of  TMD.15,51 A systematic

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and functional problems which are refractory

Table 2 Pathophysiological factors associated with pain related TMD15,63
to conservative measures.51 Surgical inter-
Level of evidence ventions should be avoided in patients with
Factor chronic TMD without significant functional
Strong Moderate Low No association
impairment, as such interventions are unlikely
Endogenous pain to yield benefits and may exacerbate their
modulation Autonomic nervous
Nervous system Neurodegenerative symptoms.51 Minimally invasive interventions,
Peripheral/central system
such as arthrocentesis may be performed,79
sensitisation
alternatively arthroscopy which carries the
Dental interventions benefit of fibreoptic guidance for lavage of
Trauma Cervical (debatable)
Facial macro trauma the joint space may be considered to improve
symptoms and function in some patients.80
Demographics Gender Age Ethnicity
TMJ replacement surgery is only considered
Stress for those with severe degenerative disease.49,51
Socioeconomic NICE have produced guidelines with regards
Psychological Catastrophising Depression Personality disorders
(debatable) to case selection and provision of TMJ replace-
Childhood events ment surgery.81
Dento-skeletal Occlusion
Trigeminal neuralgia
Functional Parafunction (daytime)
Orthodontics
Nutrition
Classification and diagnosis
Lifestyle Trigeminal neuralgia (TN) is a neuropathic
Smoking condition affecting one or more branches of
Sleep Sleep disorders Sleep bruxism the trigeminal nerve.82,83 The pain is episodic
and of brief duration, occurring unilaterally,
Genetics Genotypic Inheritable
with abrupt onset and termination. The pain
Headache is often excruciating and may be described as
stabbing, or like an electric shock, and may
Lower back pain
Co-morbidities/ Secondary gain occur spontaneously, or be triggered by mild
Fibromyalgia Infection
secondary Irritable bowel syndrome (debatable) stimuli such as touch, eating or wind.82,83
The International Headache Society (IHS)84
Chronic widespread pain
have previously classified TN into two categories
– classical TN and symptomatic TN. Classical
review and meta-analysis conducted by and splint therapy may lead to hypervigilance TN is described as occurring secondary to
Fricton et al.,73 reported that hard splints have and propagation of parafunction.51 Therefore, neuroavascular compression, commonly of the
some weak evidence to support their use in the splint therapy should not be used in isolation, superior cerebellar pontine artery. Symptomatic
management of TMD pain and the prevention and could be considered along with other self- TN refers to TN indistinguishable from classical
of tooth wear. However, these modest benefits management strategies.15,73 TN, other than it arises as a result of a struc-
were not any greater than other management There is no evidence base for the role tural lesion other than a vascular compression,
strategies for example, self-management, of occlusal adjustment in managing such as multiple sclerosis (MS) or a space
medications and acupuncture. Moreover, chronic TMD.75 Similarly, a recent Cochrane occupying  lesion.84 A more recent working
hard occlusal splints are expensive to produce review did not find any evidence for the role group has suggested maintaining the classical
and require complex adjustments,74 and hence of orthodontics in the management of TMD.76 and symptomatic sub-classifications, and has
soft splints may be considered for patients Botulinum toxin type A (‘Botox’) has also added a third diagnostic category for TN –
at low risk of periodontal disease and tooth be used in the management of chronic TMD.51 ‘idiopathic’ TN (whereby no compression, or
wear secondary to parafunction.74 Anterior However, with regards to the management of pathology is identified).85
bite plane devices, such as the nociceptive pain-related TMD, there is a lack of evidence TN may have a significant impact upon
trigeminal inhibition device (NTI), demon- as to the effectiveness of botox.77 Moreover, a quality of life, with a significant impact upon
strate similar efficacy in comparison to full randomised controlled trial has suggested no the ability to perform daily tasks and negative
coverage splints,51 and also carry a significant difference between botox and placebo in the effects upon health status related to the pain
risk of occlusal changes (such as anterior management of pain-related TMD.78 severity.82 Studies have reported that patients
open bite) if worn for a prolonged period of The first line management for pain-related may experience social isolation due to the
time.51,73 Therefore, anterior bite plane devices TMD normally consists of conservative severity of pain and even loss of employment.86
are not recommended according to current measures as previously described.15,49 Surgical Similarly, patients may also demonstrate depres-
national guidelines.51 Furthermore, it has been interventions may be considered for patients sion and anxiety as a result of their TN.82,83
suggested that the benefits derived from splint demonstrating disc displacement, or degen- The diagnosis of TN is primarily based
therapy may be secondary to placebo effect,73 erative joint pathology associated with pain upon the history, as there are no objective

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Table 3 TN medications87,88,92

Medicine Daily dose range Side effects Recommendations Comments

Contraindicated with unpaced AV

conduction abnormalities Adverse drug interactions
eg, warfarin
Carbamazepine Begin with small doses,
Neurological side effects (dose related) depending on tolerability;
Evidence rating A: Effective/ 200–1600 mg
increase and decrease
Should be used Hyponatraemia/blood disorders - monitor slowly HLA‑B*1502 allele in individuals
bloods at regular intervals of Han Chinese or Thai origin –
increased risk of SJS/TEN
Rarely SJS/TENS
Neurological side effects
Oxcarbazepine Hyponatraemia with higher doses Use on a four times a day
Evidence rating B: Probably 300–1200 mg Generally better tolerated than CBZ
Very rarely blood disorders basis
effective/Should be considered
SJS/TEN

Baclofen
Being slowly, divided Withdraw drug to avoid side effects
Evidence rating C: Possibly 50–80 mg Neurological side effects
doses Useful in patients with MS
effective/May be considered

Neurological side effects Initially very slow

Lamotrigine
escalation. Cutaneous reactions common if
Evidence rating C: Possibly 200–400 mg Blood disorders
Can use in conjunction increase dose too quickly
effective/May be considered
Rarely SJS/TENS with CBZ

1800‑3600 mg Use of ropivacaine reduced dose of

Gabapentin with ropivacaine
(RCT utilised up to Ropivacaine injected gabapentin required.
Evidence rating C – Possibly Neurological side effects
900 mg) + 2 ml of weekly into trigger spots (Small RCT with newly diagnosed
effective/may be considered)
mg/ml ropivacaine patients likely to go into remission)

Medicines not evaluated in randomised controlled trials

Neurological side effects

Can use with CBZ.
>300 mg can lead to severe side
Phenytoin 200–300 mg Blood disorders HLA‑B*1502 cross effects
reactivity with CBZ
Rarely SJS/TEN

Neurological side effects

Monitor liver function
Sodium valproate 600–1200 mg Blood disorders, Often used by neurologists
for first six months
Rarely hepatic dysfunction

Neurological side effects – dose dependent Use twice daily, avoid Long-term cohort study shows
Pregabalin 150–600 mg
abrupt withdrawal promise
Peripheral oedema with higher doses
HLA-B*1502 – Human Leukocyte Antigen-B*1502.
AV – Atrioventricular
SJS/TEN – Stevens Johnson syndrome/toxic epidermal necrolysis

investigations or tests that can confirm the Epidemiology ineffective, were recently refuted by a cohort
diagnosis.83,87 A full dental examination with A primary care based study has reported an study of classical TN patients on medication.90
dental radiographs should also be performed incidence of 27  per 100,000  for  TN.89 The
to exclude dental pathology.86,87 incidence is seen to be higher for females Pathophysiology
MRI should be conducted for patients pre- across all age groups, with a peak incidence The pathophysiology of TN is reported as being
senting with symptoms consistent with TN, to between 45 to 59 years.89 neuropathic in origin.83 Devor et al.91 described
assess for possible underlying pathology such The disease progression of TN is relatively the ‘ignition hypothesis’ – whereby the develop-
as MS plaques and tumours.88 MRI may also unknown, due to a lack of published cohort ment of TN occurs as result of damage to the
demonstrate the presence of neurovascular data regarding the long term behaviour of TN.87 trigeminal axons in the nerve root or ganglion;
compression of the trigeminal nerve in the The common notions that TN pain worsens which frequently occurs due to vascular com-
posterior cranial fossa.86 over time, and medications gradually become pression of the nerve in the root entry zone. The

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Table 4 TN surgery87,88,92

Pain relief duration

Procedure Mortality Morbidity Comments
(Kaplan-Meier estimate)
Peripheral that is, cryotherapy,
neurectomy, laser ablation, Localised sensory loss, Can be performed under local
acupuncture,thermocoagulation, anaesthetic
injections of alcohol/phenol 50% at 12 months Nil haematoma formation,
Suitable for medically unfit (for general
(Evidence rating U – data inadequate/ infection anaesthetic (GA)
treatmentunproven)
Sensory loss >50%,
Gasserian ganglion that is, dysaesthesia <6%, Can be performed under heavy
radiofrequency thermocoagulation, sedation, or short GA
anaesthesia dolorosa 4%,
glycerol rhizolysis, balloon Often suitable alternative for patients
compression 50% at six years Very low eye complications 4%, unfit for MVD
(Evidence rating C – Possibly effective/ meningitis 0.2%, Glycerol rhizolysis provides shortest
may be considered up to 50% have masticatory deficit pain relief duration
following balloon compression
Gamma knife Problematic sensory loss 6–13% often The only non-invasive technique.
(Evidence rating C – Possibly effective/ 52% at 3 years Nil six months later Pain relief can be delayed up to six
may be considered Anaesthesia dolorosa very rarely months

Microvascular Major post-operative morbidity 4%,

Decompression 10% ipsilateral hearing loss,
73% at five years 0.2–0.5% Highest improvement in quality of life
(Evidence rating C – Possibly effective/ transient diplopia,
may be considered sensory loss 7%

sequelae results in hyperexcitable neurones that may provide TN patients with pain relief and high quality comparative studies involving the
demonstrate a phenomenon described as ‘after fewer side effects when compared to existing, different surgical techniques.87
discharge’, which occur secondary to external centrally active anticonvulsants.94,95 Difficulties faced in the management of
stimuli and continue after the stimulus has Patients who have been newly established TN patients include – delays in diagnosis,
ceased. This ‘after discharge’ triggers adjacent on systemic medication and are experiencing side-effects from medication, and a lack of
neurones, resulting in the symptoms of electric an acute exacerbation of TN, may benefit from psychological support.98 Classically, TN has
shock type pain. The resultant refractory period local anaesthetic blocks into trigger points – to tended to be managed using a very biomedi-
that follows is due to potassium influx hyper- provide short term analgesia while awaiting cal model – with medications and surgery.
polarisation, resulting in the neurone being oral medications to take effect.87 Current thinking suggests that it is important
refractory to further stimuli. Although the majority of TN patients are to enhance the care of TN patients by using
managed using medications, reduced drug a biopsychosocial approach and multidisci-
Management efficacy and side effects may lead to the medical plinary team working.98 There is a significant
TN is generally managed medically, with management of TN being unsuccessful.96–98 negative psychosocial impact associated
carbamazepine being the first-line medica- Table 3 describes the medications that may with TN – with 45% of TN patients having a
tion.88,92 Stevens-Johnson syndrome (SJS) and be considered for managing TN.87,88,92 negative impact on activities of daily living,
toxic epidermal necrolysis (TEN) may occur Surgery may also be considered in the over 30% being depressed, and over 50%
as a result of treatment with carbamazepine, management of TN, though a review by having anxiety.100 This evidence supports the
with patients of Asian and Oriental ethnicity Gronseth et al.92 stated that there is insufficient suggestion that there is a significant role for
being at greater risk.93 The HLA B*15:02 and evidence to determine when surgery should be pain management psychology in the treatment
HLA  A*31:01 alleles are linked to these offered. A study on patient decision-making in of TN patients.101 Additionally, it has been
reactions and it is suggested that at risk patients the management of TN reported that patients shown that patients may benefit from attending
should undergo genetic testing if carbamaz- may opt for surgery over medication.99 TN-focused patient support groups.102
epine is being considered.93 Oxcarbazepine is The surgical management of TN may be
considered to be the second line medication categorised into three groups according to Conclusion
in TN management,88,92 and is normally con- site: peripheral; Gasserian ganglion level;
sidered to have fewer side effects and potential and posterior fossa root entry zone.87 Table 4 Orofacial pain conditions occur due to
drug interactions than carbamazepine.83 Novel describes the surgical management options complex pathophysiology, often associated
TN medication research is being undertaken available for TN. with psychological co-morbidities. Chronic
regarding the use of the selective sodium Microvascular decompression is con- orofacial pain may have a significant impact
channel blocker BIIB07494 (an as yet unnamed sidered to provide the longest duration of upon quality of life and daily functioning.
drug that was previously known as raxatrig- pain  relief.88,92 However, though it has been Early diagnosis and referral to secondary
ine).95 Due to its selective action on peripheral documented in the literature that TN may be care is of paramount importance to ensure
neural receptors, it is suggested that BIIB074 managed effectively surgically, there is a lack of evidence-based management is instigated. A

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l
o
f
t
h
e
B
r
i
t
i
s
h
D
e
n
t
a
l
A
s
s
o
c
i
a
t
i
o
n
.