Curr Oral Health Rep (2015) 2:148–157

DOI 10.1007/s40496-015-0052-0

ORAL MEDICINE (T SOLLECITO, SECTION EDITOR)

Neuropathic Orofacial Pain

Janina Christoforou 1 & Ramesh Balasubramaniam 1 & Gary D. Klasser 2

Published online: 2 July 2015

# Springer International Publishing AG 2015

Abstract Dental practitioners will be exposed to patients purposes, based upon its temporal presentation, it may mani-
experiencing neuropathic pain of the orofacial region at some fest as either continuous or episodic. Continuous neuropathic
point in their careers. The pain can be distressing and affect pains are pain disorders that have their origin in neural struc-
quality of life. Therefore, an understanding of the clinical pre- tures and are manifested as a constant, ongoing, and unremit-
sentation, diagnosis, and management of neuropathic ting pain. Patients usually experience varying and fluctuating
orofacial pain is essential since some patients will convincing- intensities of pain, often without total remission. The pain is
ly express this pain to be originating from a dental source. often sensed in dental structures and has been referred to as
Neuropathic pain may be episodic such as trigeminal neural- atypical odontalgia [2] or phantom toothache [3]. Episodic
gias, or continuous, which includes peripheral painful trigem- neuropathic pain is characterized by sudden volleys of elec-
inal traumatic neuropathy, persistent idiopathic facial pain, tric-like, severe, shooting pain lasting only a few seconds to
neuritis, and burning mouth syndrome. Research has revealed several minutes and is referred to as neuralgia [4]. Often, there
that these various neuropathic pains often have specific treat- exists a perioral or intraoral trigger zone whereby
ment modalities. Hence, establishing an accurate diagnosis nontraumatic stimuli such as light touch elicit a severe parox-
and understanding the pathophysiology of the disorders are ysmal pain [4]. Unfortunately, due to the lack of recognition
critical in the management of pain as these will avoid the and understanding of these conditions, they are often treated
initiation of unnecessary dental interventions. by dental practitioners with ineffective dental interventions
[5]. Therefore, it is incumbent on dental practitioners to gain
Keywords Facial pain . Neuralgia . Trigeminal neuropathy . an understanding of the pathophysiology, diagnosis, and man-
Burning mouth syndrome . Herpes zoster . Neuritis agement of these various neuropathic conditions to avoid un-
necessary dental treatments.

Introduction
Mechanisms of Pain
Neuropathic pain is defined as Bpain caused by a lesion or
disease of the somatosensory nervous system^ [1]. For clinical Pain is BAn unpleasant sensory and emotional experience as-
sociated with actual or potential tissue damage, or described in
terms of such damage^ [1]. Noxious stimuli in the orofacial
This article is part of the Topical Collection on Oral Medicine region depolarize high threshold polymodal nociceptors com-
posed of free nerve endings described as Aδ (thinly myelinat-
* Janina Christoforou ed) and C-fibers (unmyelinated), which may further be excited
[email protected]
and sensitized by a neurochemical Bsoup^ containing such
products as prostaglandins, bradykinin, histamine, substance
1
School of Dentistry, University of Western Australia, Perth, Australia P, etc. The fibers convey nociceptive stimuli along the trigem-
2
School of Dentistry, Louisiana State University, New inal pathway to initially synapse with second-order neurons
Orleans, Louisiana, USA (wide dynamic and/or nociceptive specific) located in the
Curr Oral Health Rep (2015) 2:148–157 149

nucleus caudalis of the trigeminal spinal tract nucleus in the lead to central effects due to the hyperexcitability in the tri-
brain stem. Within the nucleus caudalis, the signal can be geminal brain stem complex and result in similar pain re-
subject to modulation (inhibition or facilitation). Second- sponses to nonnoxious as well as noxious stimuli. This corre-
order fibers then cross the midline, undergo further modulato- lates to the presence of allodynia manifested by individual
ry processes, and ascend to synapse in the thalamus, which is trigger factors such as light touch, mild wind, toothbrushing,
involved in pain perception. Finally, the noxious impulse pro- application of cosmetics, and shaving in those experiencing
jects to the somatic sensory areas of the cerebral cortex, where TN. Furthermore, a reduction in brain gray matter has been
there is discrimination and determination of the intensity of observed which correlates with greater TN duration [18], pos-
the nociceptive stimulus. The interpretation of the stimulus is sibly representing a protective effect to chronic pain.
influenced by cognitive-behavioral and affective-motivational The diagnosis of TN is based on history and examination,
factors (such as past experiences, anxiety), and hence, pain is which should include a cranial nerve examination. Also, a
recognized as a complex interaction of cognitive, affective, magnetic resonance imaging (MRI) and/or magnetic reso-
and sensory processes making it a Bpersonal experience^ [6]. nance angiography (MRA) of the brain and skull base is nec-
essary to investigate possible vascular impingement and ex-
clude intracranial pathosis.
Trigeminal Neuralgia First-line management for either form of TN is centrally
acting medications. Carbamazepine provides the most predict-
Trigeminal neuralgia (TN) is a paroxysmal pain involving one able results [19], but it has a number of side effects with
or more divisions of the trigeminal nerve distribution. potentially serious adverse consequences. Other medications
Prevalence rates for TN are 1.5 cases per 10,000 [7] and vary that have been trialed are presented in Table 1.
significantly with age. Approximately 90 % of patients with In refractory cases and where there have been no remission
symptomatic presentation are over the age of 40 years with a periods, surgical options are utilized. Microvascular decom-
typical onset between 60 and 70 years [7]. pression (MVD) is the first-line surgical option with initial
TN is classified into classical trigeminal neuralgia (parox- pain relief in 88 % of patients and stability for 9.7 years
ysmal or with associated persistent facial pain) and painful [20]. In classical TN, the vasculature, i.e., commonly the su-
trigeminal neuropathy. The precise pathogenesis of both forms perior cerebellar artery, is in close proximity to the trigeminal
is unknown, but it is suspected that both peripheral and central nerve root (mostly occurring at the entrance of the nerve root
nerve dysfunction play a role [8]. Possible etiologies include entering the pons) resulting in demyelination of the sheath and
the compression of the trigeminal nerve root, demyelinating altered neural signal propagation [21]. Teflon is placed to sep-
disorders, such as multiple sclerosis (MS) [9], neoplastic in- arate the nerve from the vessel [8].
filtration [10], and familial disorders, such as Charcot-Marie- Stereotactic strategies such as linear accelerators and gam-
Tooth disease [11], and secondary to herpetic infections [12]. ma knives are a consideration in those patients who are poor
Classical TN is considered idiopathic although it is com- candidates for surgical procedures. This is an ablative proce-
monly associated with chronic vascular compression of the dure and involves treating the trigeminal nerve with a single
trigeminal nerve at the root entry zone of the brain stem [8]. high dose of external beam radiation (70–90 Gy) delivering a
The superior cerebellar artery is most commonly involved dose to the proximal trigeminal root near the pons, resulting in
[13]. The compression results in morphological changes in focal axonal degeneration and necrosis [22].
the nerve, such as distortion, deviation, groove formation, Other ablative procedures include glycerol rhizotomy [23],
and/or atrophy of the nerve [14]. Individuals experiencing cryotherapy [24], partial rhizotomy, and radiofrequency
classical TN present with a unilateral, sharp, Belectric shock- lesioning [25]. These procedures destroy neurons or their
like^ sensation in the distribution of one or more branches of axons, thereby reducing the recruitment of ectopic neural ac-
the trigeminal nerve. Affected individuals experience refrac- tivity. They are most commonly utilized when other options
tory periods, which may last for weeks, months, or years. In have failed or in individuals with TN associated with MS. A
comparison, painful TN is due to an identifiable structural common adverse event of these procedures is a resultant par-
lesion other than vascular compression, such as multiple scle- esthesia. An additional option to be considered when other
rosis [9] and neoplastic conditions, i.e., meningioma [15] and surgical modalities have not been effective is percutaneous
amyloidoma [10]. These conditions result in similar morpho- balloon compression [26]. This involves the insertion of a
logical changes to the trigeminal nerve but are without a re- balloon into Meckel’s cave, resulting in compression of the
fractory period [16]. trigeminal ganglion once inflated. This interferes with the
The peripheral nerve morphological changes occurring in nerve’s ability to transmit signals, resulting in mild sensory
both forms of TN lead to structural changes such as focal loss.
demyelination and afferent hyperexcitability and ectopic fir- Ideal timing for surgical intervention is unknown, but a
ing, forming part of the ignition hypothesis [17]. This may long-term cohort study [27] and patient satisfaction surveys
150 Curr Oral Health Rep (2015) 2:148–157

Table 1 Medications used in the management of trigeminal neuralgia

Medication Dosage Side effects Efficacy

Carbamazepine Started at 300 mg and Leukopenia, aplastic anemia, First-line treatment. Effectiveness can be reduced
maintenance at thrombocytopenia, drowsiness, over time, i.e., initial success in 60 % of patients,
800–1600 mg/day [19] ataxia, rash, warfarin interaction, but by 5–16 years only, 22 % were still showing
abnormal liver function tests it to be effective [95].
Oxcarbazepine Started at 600 mg/day and Visual disturbance, difficulty Second-line treatment. Trials have shown similar
maintenance at walking efficacy to carbamazepine [96] but decreases
1200–1800 mg/day [19] its effectiveness over time [27].
Lamotrigine Started at 25 mg/day and Visual disturbance, nausea, Has been used in combination therapy with
maintenance at 200–400 drowsiness, serious skin carbamazepine and also as monotherapy [97]
mg/day [19] rashes, and allergies
Baclofen Started at 15 mg/day and Confusion, withdrawal symptoms, Mainly used in conjunction with other medication.
maintenance at 60–80 drowsiness, GI symptoms Increased pain relief when carbamazepine is
mg/day [19] combined with baclofen [98], but only trials
with small sample size
Gabapentin Started at 150 mg and Unsteadiness, fatigue, weight Minimal evidence. Effective first- and second-line
maintenance at 300–900 gain treatment [99]; 27 % experience complete or near
mg/day [99] complete pain relief, and 53 % experience no
relief [99].
Pregabalin Started at 150 mg and Dizziness, weight gain, Minimal evidence. Effectiveness in treatment has
maintenance at 150–600 drowsiness been shown [100].
mg/day [14]
Topiramate Started at 25 mg bid and Nephrolithiasis, mood disruption Effective in TN secondary to MS [101]
maintenance at 100 mg
bid [101]
Sumatriptan 3 mg subcutaneously [102] Hypertension, drowsiness Success in refractory TN [102]
Botulinum toxin A 25–75 units transcutaneously Headache Insufficient scientific evidence. Some success in
(7.5 units per injection site) refractory cases [104]
[103]

[28] reported that patients with poor tolerability or A computed tomography (CT) or MRI is necessary to as-
nonresponsiveness to medication and without a remission pe- sess for intracranial lesions or neurovascular compression.
riod should consider a surgical option [19]. Relapses can also First-line therapy for GPN is carbamazepine (200–1200 mg/
occur with surgical procedures, showing reduced long-term day). Alternatively, oxcarbazepine (600–1800 mg/day) may
pain relief (Table 2). be utilized [33]. Application of local anesthetic to the tonsillar
and pharyngeal wall areas may prevent attacks for a few hours
[31].
In refractory cases, MVD may be considered. Also, intra-
Glossopharyngeal Neuralgia cranial sectioning of the glossopharyngeal nerve and the upper
rootlets of the vagus nerve may be attempted [34]. Gamma
Glossopharyngeal neuralgia (GPN) is characteristically a knife surgery appears to be useful and safe for patients as
brief, unilateral, mild to moderate electric shock-like pain lo- initial therapy or for those who have failed medical and other
calized to the ear, base of the tongue, tonsillar fossa, or inferior surgical treatments [35].
to the angle of the mandible. Up to 25 % of patients may report
bilateral pain [29]. The pain is typically triggered by
swallowing, talking, coughing, or yawning. The pathophysi-
ology of GPN is unclear; however, as in TN, likely nerve Occipital Neuralgia
compression results in demyelinated axons [30]. Cardiac dys-
rhythmias and syncope may occur due to vagus nerve stimu- Occipital neuralgia (ON) is a unilateral or bilateral paroxys-
lation [31]. The incidence of GPN in the general population mal, shooting, or stabbing severe pain in the posterior part of
has been reported to be 0.2 per 100,000 persons per year [29]. the scalp, in the distribution of the greater, lesser, or third
GPN may coexist with TN in 10–12 % of cases [31, 32]. occipital nerves, sometimes accompanied by diminished sen-
Similar to TN, a significant association between GPN and sation or dysesthesia and/or allodynia in the affected area and
MS has been reported [32]. commonly associated with tenderness over the involved
Curr Oral Health Rep (2015) 2:148–157 151

Table 2 Common surgical procedures used in the management of pathophysiology of NIN is unclear; however, myelin sheath
trigeminal neuralgia
delamination is thought to play a role [41].
Procedure Success NIN is often precipitated by stimulation of an area in the
posterior wall of the auditory canal and/or periauricular re-
Microvascular First-line surgical option gion. Disorders of lacrimation, salivation, and/or taste some-
decompression Immediate pain relief in 88 % of patients with
73 % pain free with medication after 1 year
times accompany the pain associated with NIN. It is important
and stable to 9.7 years [20] to rule out local ear disorders prior to providing a diagnosis of
Balloon Considered when rejecting MVD after medical NIN. Medications used for TN may be trialed. Surgical pro-
compression [26] management. Minimal invasiveness cedures may involve sectioning of the nervus intermedius or
Initial success rate of 85 %, but from these chorda tympani nerves or MVD for pain relief [42].
patients, it reduces to 36 % after 20 months
[105].
Ablative procedures • Glycerol: Immediate pain relief but reduced
long-term success; immediate success of Superior Laryngeal Neuralgia
93 %, but after 4 years, 50 % were still pain
free [106]. Superior laryngeal neuralgia (SLN) is a rare condition with
• Cryotherapy [24]: Initial success rate of 85 %,
but at 2 years, 14.5 % are pain free [107];
severe paroxysmal pain felt in the throat, submandibular re-
can be used in demyelinating disorders. gion, or under the ear with duration of minutes to hours.
• Radiofrequency [25]: High initial pain relief Episodes of pain are precipitated by swallowing, straining
(98 %), but 15–20 % show recurrence in the voice, or head turning, and referral from an area located
12 months and 57.7 % are pain free after
on the lateral aspect of the throat overlying the hypothyroid
5 years [108].
membrane [43]. The pathophysiology for SLN is not well
Stereotactic Pain relief occurs within 3 months. Initial
radiosurgical success of 75 % and 50 % are pain free at described but thought to be related to damage to the superior
procedures 3 years [109]. laryngeal nerve from a precedent viral infection, scarring from
• Gamma knife therapy a surgical procedure such as a tonsillectomy, and chronic re-
• Linear accelerator [22]
petitive trauma to the larynx from singing, talking, or
swallowing [44].
Medications traditionally used for TN may be effective.
nerve(s). The exact pathophysiology for ON is uncertain; Surgical procedures utilizing repeated nerve blocks with high
however, the neuralgia is often a result of direct damage or doses (5–10 %) of lidocaine have shown lasting effects [45].
irritation to the occipital nerve or in its distribution due to These are administered lateral to the greater cornu of the hyoid
trauma (including flexion-extension injuries), compression to target the internal branch of the superior laryngeal nerve.
of the upper cervical roots by degenerative spine changes,
and tumors involving the second and third cervical dorsal
roots [36, 37]. Other possible mechanisms include localized Peripheral Painful Traumatic Trigeminal
infections or inflammation, gout, diabetes, and blood vessel Neuropathy
inflammation. Furthermore, it is important to distinguish ON
from occipital pain referred from the atlantoaxial or upper Peripheral painful traumatic trigeminal neuropathy (PPTTN)
zygapophyseal joints or from sources located in neck muscles is defined as a spontaneous or stimulus-dependent pain or
or their insertions [38]. Hence, imaging studies are necessary disturbed sensation, predominately affecting the receptive
to exclude underlying pathological conditions. Management field of one or more divisions of the trigeminal nerve. The
with injection of local anesthetics and corticosteroids may pain is moderate to severe in intensity and usually described
provide temporary and even long-term pain relief [39]. as burning; however, it can be stabbing [46••]. Most cases are
continuous but may be episodic (minutes to days). The pain
distribution may spread with time due to central mechanisms
but usually remains unilateral. Characteristics of the neuro-
Nervus Intermedius Neuralgia pathic pain are variable among individuals. This is due to a
combination of environmental (reduced social support) [6],
Nervus intermedius neuralgia (NIN) also known as facial psychosocial (anxious, introverted personalities) [6], and ge-
nerve or geniculate neuralgia is a rare disorder characterized netic factors (polymorphism in the gene encoding serotonin
by brief paroxysms of severe pain felt deep in the auditory transporter) [6, 46••].
canal, sometimes radiating to the parieto-occipital region. It The neuropathy typically develops within 3 months of an
may develop without apparent cause or as a complication of identifiable, traumatic event to the painful area (localized
herpes zoster (Ramsay Hunt syndrome) [40]. The pain) or relevant innervation (dermatomal pain) and is
152 Curr Oral Health Rep (2015) 2:148–157

associated with clinically evident positive (hyperalgesia, since one third of affected patients also suffer from depression
allodynia) and/or negative (hypoesthesia, hypoalgesia) signs [55]. In addition, there is currently emerging evidence of a
of trigeminal nerve dysfunction. The neuropathy may be due neurobiological origin, since differences have been shown
to major craniofacial injury or from minor oral interventions between PIFP patients and healthy controls in respect to gray
such as extractions, endodontic treatment, and implant place- matter volume in central pain processing regions (decreased in
ment [46••, 47]. The diagnosis is made after history, examina- the former) [56] and differences in neural blood flow patterns
tion, and adjunctive investigations to exclude other disorders [57]. Furthermore, increased D2 receptor density in the puta-
such as infections, neoplastic lesions, and iatrogenic nerve men was shown by positron emission tomography (PET), re-
compression. inforcing the relevance of dopaminergic neurotransmission in
Following injury to the trigeminal branches, chronic pain the modulation of pain perception in PIFP [58].
develops in about 3–5 % of patients [48]. This is due to the Establishing a diagnosis follows a process of elimination of
peripheral sensitization or activation of nociceptors from the other causes of facial pain based on information gathered
release of inflammatory mediators from tissue injury and also through patient history, clinical examination, imaging, and
increased pressure secondary to inflammation [49], which adjunctive testing, as deemed appropriate.
may then induce nerve damage resulting in neural dysfunction The goal of therapy is to manage the pain effectively while
[50]. Repeated nociceptive sensory input leads to the estab- giving rise to the fewest possible medication side effects.
lishment of central sensitization [46••]. In addition, during Optimal outcome may be achieved following a multidisciplin-
repair, there may be entrapment of a nerve in scar tissue with ary approach employing a combination of pharmacological
subsequent neuroma formation. therapy and psychological counseling involving patient educa-
Management involves the use of various medications such tion, cognitive therapy, coping strategies, relaxation techniques,
as tricyclic antidepressants (TCA), serotonin norepinephrine biofeedback, or psychotherapy [54]. Pharmacological manage-
reuptake inhibitors, and gabapentinoids [51]. These regimes ment with antidepressants and anticonvulsants, which block
can also be combined with various opioids [46••]. When the sodiumchannels, can be trialed to manage the neuropathic com-
neuropathy is episodic (rather than chronic), a combination of ponent of the pain, and also anxiolytics, analgesics, and
a corticosteroid (prednisone 60 mg daily) with pregabalin antiarrythmics may be considered [53]. Amitriptyline (25–
(150 mg twice daily) was found to be effective [52]. The 100 mg/day) is the primary choice [54]. Also, since PIFP often
efficacy of surgery remains unclear due to insufficient trials is comorbid with affective disorders, the combination of anti-
[46••]. convulsant and antidepressant medications is rational.
Gabapentin (900–1800 mg/day) and pregabalin (150–
300 mg/day) and also topical formulations, such as lidocaine
Persistent Idiopathic Facial Pain transdermal (5 %) anesthetic, may also be trialed [54].
When the pharmacological treatment lacks adequate effi-
Persistent idiopathic facial pain (PIFP) refers to persistent cacy, pulsed radiofrequency treatment of the sphenopalatine
extraoral and/or intraoral pain along the territory of the trigem- ganglion may be considered [54]. Unfortunately, pain usually
inal nerve that does not fit the classic presentation of other relapses. Available data on alternative treatments are limited;
cranial neuralgias or another disorder [53]. The pain is usually hence, it is suggested that invasive treatment should be
of long duration, lasting most of the day (if not continuous), is avoided.
unilateral, and is without sensory loss or other physical signs
[53]. It is described as a severe ache, crushing, or burning
sensation, which is poorly localized. A distinguishing feature Peripheral Neuritis
is constancy of pain and clinical characteristics usually remain
unchanged for weeks, months, or years. Most patients with Peripheral neuritis may occur with chemical poisoning, auto-
PIFP complain of other symptoms such as headache, immunity, alcohol, or nutritional deficiencies resulting in in-
neckache, backache, dermatitis, irritable bowel, and uterine flammation of the nerve. Inflammation of the nerve may be
bleeding [54]. The reported prevalence in the general popula- due to direct pressure from edema or mediator secretion typ-
tion is 0.03–1.0 % [53] and it is seen primarily in adult ically cytokines [59].
females. The most common clinical presentation is tactile allodynia
The pathophysiology of PIFP is unknown but appears to be given the dominant role of myelinated nerve fibers [50]. With
multifactorial and of heterogeneous origin. PIFP may be ini- some invasive dental procedures, transient perineural inflam-
tiated by surgery or injuries to the face or oral cavity [2] or mation may occur and is typically asymptomatic. In other
even a minor noxious event to the afferent trigeminal nerve cases, such as with periapical inflammation or a misplaced
fibers, which may result in deafferentation and long-term dental implant associated with a nerve trunk, chronic symp-
neuroplastic changes. There may be a psychogenic origin, toms may be apparent. Similarly, perineural inflammation,
Curr Oral Health Rep (2015) 2:148–157 153

pain, and other abnormal sensations can occur with temporo- Postherpetic Neuralgia
mandibular joint pathologies [60], paranasal sinusitis [61], or
early malignancies [62]. In approximately 10 % of cases [76], HZ may progress to
Treatment should focus on the resolution of the etiology of PHN. PHN may result in the loss of peripheral input from
the inflammation. Prompt administration of corticosteroids or degeneration of afferent nerves, atrophy, or scarring of the
nonsteroidal anti-inflammatory drugs may be beneficial [63]. spinal cord dorsal horn and dorsal root ganglion. This results
in the development of spontaneous discharges in the
deafferented central neurons, leading to intrinsic changes in
the CNS, and consequently, produces constant pain in addi-
Herpes Zoster tion to mechanical allodynia in the area of sensory loss [77].
There are several predictive factors resulting in the devel-
Herpes zoster (HZ) is clinically diagnosed by a painful opment of PHN after an episode of HZ. Older age may be a
vesicular rash appearing in a unilateral dermatome. It re- possible factor because afferent nerve fibers may be compro-
sults from the reactivation of varicella zoster virus (VZV), mised or have undergone degeneration of the myelin sheath
which stays latent in the spinal and cranial sensory gan- and, hence, need less viral damage to present with PHN. Other
glia after primary infection. The virus causes inflamma- factors include female gender, possibly due to the longer life
tion and neural injury, which leads to peripheral sensiti- expectancy. A more severe prodrome, a more intense acute
zation. Although herpes zoster can occur at any age, most pain, and a severe rash are also possible predictive factors,
cases occur after the age of 50 with the incidence of com- which may be due to a greater viral load and, hence, more
plications also increasing with age, i.e., the development tissue damage during the acute phase [69, 77, 78], increasing
of postherpetic neuralgia (PHN) [64]. the probability of progression to PHN.
HZ occurs when the cellular immunity is reduced after a Management is controversial as there is conflicting evidence
history of a VZV infection or vaccination. The current view is on the use of antivirals in the acute phase to prevent PHN onset
that due to the increase in vaccinations at a young age, there [77]. Anticonvulsants and antidepressants have also been utilized
are minimal exposures, and consequently, there is not a renew- for the prevention of PHN [77, 78]. Several centrally acting
al of the antibody count to VZV (herd immunity), consequent- medications have been trialed for the management of PHN.
ly reducing the cellular immunity, hence increasing the onset Amitriptyline or nortriptyline [79] and gabapentin [79] or
of HZ [65]. Increased risk for VZV, due to immunity only pregabalin [80] are considered first-line treatment options and
reaching subthreshold levels, is present in individuals with may be given solely or in conjunction with other medications.
autoimmune disease [66], cancer patients [67], transplant pa- Opioids (oxycodone, morphine, or tramadol) [81] may be
tients [68], the elderly [69], and those experiencing excessive added if there is a lack of response from the above agents.
stress [70]. It has been postulated that the vaccine for VZV Topical (transdermal) therapies may include lidocaine 5 %
decreases the morbidity associated with herpes zoster and the [79] or 8 % capsaicin patches (both FDA approved for this
incidence of PHN [69]. The vaccine contains a live attenuated condition) which has effects lasting up to 12 weeks after a
VZV, and according to the Center for Disease Control, it is single 60-min application [82]. Overall, pharmacological
recommended that patients aged 60 years and older should be management is challenging with much of the treatment not
vaccinated regardless of prior exposure to VZV [71]. being completely effective [83].
HZ has a prodrome usually lasting 2–3 days and up to a
week, which correlates to the time taken by the virus to repli-
cate and cause necrosis and inflammation in the dermatomal Burning Mouth Syndrome
skin. The pain is variable and described as throbbing or burn-
ing and characteristically increases during the day and inten- Burning mouth syndrome (BMS) has a multiplicity of nomen-
sifies when tired or stressed. clatures including stomatodynia, glossodynia, oral
When HZ is diagnosed, the duration and intensity of dysesthesia, or stomatopyrosis. It is an enigmatic pain condi-
symptoms can be reduced with antiviral therapy [72]. In tion whereby the pathophysiology is largely unknown. Data
randomized control trials, valacyclovir (1000 mg 3/day for from several experimental models support the hypothesis that
7 days) has been more effective than acyclovir (800 mg 5/ BMS is most probably neuropathic in origin [84]. The role of
day for 7–10 days) [73], and both should ideally be used the peripheral and/or central nervous system(s) is supported
within 72 h of rash onset. In ophthalmic HZ, there is risk for by studies involving quantitative sensory testing and function-
blindness, and hence, immediate referral to an ophthalmolo- al imaging methods [84]. BMS most commonly presents in
gist is necessary [74]. Supplemental medications, which can postmenopausal females with reported prevalence rates in the
aid in pain management, include TCAs, opioids, and general population varying from 0.7 to 15 % [85, 86] and
gabapentinoids [75]. being rather rare in individuals under 30 years of age [87].
154 Curr Oral Health Rep (2015) 2:148–157

For clinical purposes, BMS may be categorized into Bprimary Conclusions

BMS^ or essential/idiopathic BMS for which a neuropatho-
logical cause is likely and Bsecondary BMS^ resulting from Patients will present to their dental practitioner with the com-
local or systemic pathological conditions [88]. Primary BMS plaint of orofacial pain. In the majority of cases, the pain is
is a diagnosis of exclusion as it is not attributable to any un- likely dental in origin; however, occasionally, the pain may be
derlying systemic or local factors [89]. Furthermore, typical of a neurogenous source. Therefore, dental practitioners must
characteristics manifested by the condition are a mild to severe have a comprehensive understanding of neuropathic orofacial
burning sensation in the mucosa, dysgeusia, and xerostomia pains to avoid unnecessary dental procedures to the detriment
accompanied by a lack of clinical findings and normal results of their patients. If a patient is suspected of having neuropathic
from laboratory testing and/or imaging studies. The subjective pain, referral to a practitioner who has enhanced training and
burning is routinely observed bilaterally, most frequently in- education regarding these conditions is prudent for further
volving the anterior two thirds of the tongue, the dorsum and assessment and treatment.
lateral borders of the tongue, the anterior hard palate, and the
mucosa of the lower lip, and often presenting in more than one
oral site [90]. Typically, BMS has a spontaneous onset lasting Compliance with Ethics Guidelines
months to several years [89]. Spontaneous remission has been
Conflict of Interest Janina Christoforou, Ramesh Balasubramaniam,
reported in only 3 % of patients after 5 years of onset [91]. and Gary D. Klasser have no conflict of interest.
Burning symptoms are common upon awakening with inten-
sification as the day progresses and climaxing in the evening. Human and Animal Rights and Informed Consent This article does
Aggravating factors responsible for burning intensification are not contain any studies with human or animal subjects performed by any
personal stressors and fatigue and eating acidic/hot/spicy of the authors.
foods. Paradoxically, in about 50 % of patients, oral intake/
stimulation and distraction reduce or alleviate the symptoms
[92]. An association with anxiety, depression, and personality References
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ical disorder or vice versa [93]. highlighted as:
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