Facial Pain & Atypical Sensory Symptoms

📋 Key Information Summary

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Facial pain encompasses a broad differential — always distinguish dental/orofacial causes from neurologic, vascular, and sinister aetiologies before initiating treatment.
Red flags requiring urgent referral include new-onset temporal headache in patients >50 years (giant cell arteritis), unilateral facial numbness with proptosis (malignancy/cavernous sinus lesion), progressive cranial nerve palsies, and jaw claudication.
Trigeminal neuralgia (TN) is the most common neurologic cause of facial pain — characterised by brief, electric-shock-like paroxysms in V2/V3 distribution, often triggered by light touch, eating, or wind.
Carbamazepine (200–1200 mg/day PO) remains first-line for classical TN; oxcarbazepine (300–1200 mg/day) is an effective alternative with a better side-effect profile. Both require HLA-B*1502 screening where feasible.
Temporomandibular disorders (TMD) are the most common cause of non-dental orofacial pain — managed with conservative measures (patient education, jaw exercises, occlusal splints), short-course NSAIDs, and physiotherapy.
Giant cell arteritis (GCA) is a medical emergency — initiate high-dose prednisolone (50–100 mg/day PO) immediately on clinical suspicion; do not wait for temporal artery biopsy to confirm.
Atypical facial pain (persistent idiopathic facial pain / burning mouth syndrome) is a diagnosis of exclusion — requires systematic elimination of dental, neurologic, vascular, and sinister causes before labelling.
MRI brain with trigeminal protocol is the investigation of choice for suspected TN, to exclude secondary causes (MS plaque, posterior fossa tumour, vascular loop compression).
Amitriptyline (10–75 mg nocte PO) is first-line prophylactic therapy for atypical facial pain and persistent idiopathic facial pain; duloxetine (30–60 mg/day PO) is a second-line option.
Aboriginal and Torres Strait Islander peoples experience disproportionately high rates of untreated dental disease contributing to orofacial pain — culturally safe oral health programmes and timely specialist access are essential.
Neurosurgical options (microvascular decompression, percutaneous rhizotomy, gamma knife radiosurgery) are reserved for medically refractory TN and require specialist referral.
Multidisciplinary pain services are integral for refractory atypical facial pain — combining pharmacotherapy, cognitive-behavioural therapy, and interventional procedures.

Introduction & Australian Epidemiology

Facial pain is a heterogeneous symptom complex that draws from dental, neurologic, musculoskeletal, vascular, and psychogenic domains. The face is among the most densely innervated regions of the body, supplied by the three divisions of the trigeminal nerve (V1 ophthalmic, V2 maxillary, V3 mandibular), the facial nerve (CN VII), and contributions from cervical nerve roots. This neuroanatomic complexity creates a wide differential diagnosis and significant potential for referred pain.

In Australia, orofacial pain affects an estimated 5–7% of the adult population at any given time, with temporomandibular disorders (TMD) accounting for the majority of non-dental cases. Trigeminal neuralgia has an incidence of approximately 12.6 per 100,000 person-years, with higher prevalence in women and those aged over 50 years. Aboriginal and Torres Strait Islander Australians experience orofacial pain at approximately twice the rate of the non-Indigenous population, driven largely by higher rates of untreated dental caries and periodontal disease (AIHW 2023).

Atypical facial pain — now classified under the International Classification of Headache Disorders, 3rd edition (ICHD-3) as persistent idiopathic facial pain (PIFP) — accounts for up to 10% of all facial pain presentations to neurology clinics. The condition is characterised by daily or near-daily facial pain that does not fulfil criteria for another cranial neuralgia and for which no structural cause has been identified. Burning mouth syndrome, another atypical sensory condition, predominantly affects post-menopausal women and has an estimated prevalence of 1–5% in the general population.

The diagnostic challenge lies in distinguishing benign, self-limiting causes from life-threatening conditions such as giant cell arteritis, nasopharyngeal carcinoma, or intracranial neoplasms. A structured, systematic approach to evaluation — incorporating history, examination, and targeted investigation — is essential to avoid both under-diagnosis of sinister pathology and over-investigation of benign conditions.

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Clinical pearl: Facial pain can be the presenting feature of serious systemic disease. New-onset unilateral facial pain in an older patient with jaw claudication, visual disturbance, and elevated ESR/CRP should be treated as giant cell arteritis until proven otherwise — steroid therapy must not be delayed for investigations.

Orofacial Pain Evaluation

The evaluation of orofacial pain requires a structured history and examination to categorise the pain as dental, neurologic, musculoskeletal, vascular, or secondary to systemic disease. The approach must be systematic to avoid premature closure of diagnosis.

History — Key Domains

Onset and duration: Acute (<3 months) vs chronic (>3 months); sudden vs gradual.
Character: Sharp, electric-shock-like (suggests neuralgia), dull aching (dental/TMD), throbbing (vascular), burning (neuropathic/small fibre).
Location and radiation: Unilateral vs bilateral; specific nerve distribution (V1, V2, V3); radiation to ear, temple, or neck.
Triggers and relieving factors: Light touch, wind, chewing (TN); jaw movement (TMD); hot/cold foods (dental); position (sinusitis).
Associated symptoms: Jaw claudication, visual disturbance (GCA); hearing change, facial weakness (acoustic neuroma); nasal obstruction, epistaxis (nasopharyngeal carcinoma); skin vesicles (herpes zoster).
Dental history: Recent procedures, multiple dental consultations without resolution, missing teeth, ill-fitting dentures.
Psychosocial factors: Depression, anxiety, sleep disturbance, medicolegal claims, illness behaviour — these are common in chronic facial pain and do not exclude organic disease but should be documented.

Examination — Structured Approach

Inspection: Facial symmetry, skin lesions (vesicles in zoster, erythema in cellulitis), temporal artery (tenderness, thickening, reduced pulse), nasal cavity (if accessible), oral mucosa.
Palpation: Temporal arteries bilaterally, parotid glands, TMJ (click, crepitus, tenderness), masticatory muscles (masseter, temporalis, medial/lateral pterygoids), trigger points in cervical and cranial musculature.
Neurologic examination: Testing of all three trigeminal divisions — light touch (cotton), pinprick, corneal reflex (V1), jaw jerk reflex, motor function of CN V (jaw opening/closing against resistance) and CN VII (forehead sparing vs complete facial palsy).
TMD assessment: Maximum inter-incisal opening (normal >40 mm), lateral excursion, joint sounds (clicking, crepitus), deviation on opening.
Dental examination: Percussion of individual teeth, vitality testing (if available), assessment for caries, abscess, cracked tooth syndrome.
Cranial nerve examination: Full screen of CN II–XII, with particular attention to V, VII, and VIII.

Distinguishing Dental vs Neurologic Causes

Feature	Dental / Odontogenic	Neurologic	Musculoskeletal (TMD)
Pain character	Dull, aching, throbbing	Electric, shooting, lancinating; or burning	Dull, aching, worse with jaw use
Location	Localised to a specific tooth or quadrant	Follows dermatomal distribution (V1–V3)	Pre-auricular, masseter, temporal region
Triggers	Hot/cold, sweet, biting pressure	Light touch, wind, talking, eating (TN)	Chewing, yawning, jaw clenching
Duration	Minutes to hours, may be constant	Seconds (TN); constant (PIFP, neuropathic)	Hours, worsens throughout the day
Associated signs	Swelling, caries, abscess, failed dental treatment	Sensory loss, trigger zones, corneal hyporeflexia	TMJ click/crepitus, limited opening, bruxism
Response to local anaesthetic	Pain resolves with dental block	Pain may persist or follow deeper nerve	Partial relief with trigger point injection

Temporomandibular Disorders (TMD)

TMD encompasses a group of musculoskeletal conditions affecting the masticatory muscles, temporomandibular joint, and associated structures. It is the most common non-dental cause of orofacial pain in Australian adults, with a peak incidence between ages 20 and 45, and a female-to-male ratio of approximately 3:1.

Classification (DC/TMD criteria):

Group I — Myofascial pain: Pain in the masticatory muscles with trigger points; most common subtype (approximately 45% of TMD cases).
Group II — Disc displacement: With or without reduction; presents with clicking, locking, or restricted opening.
Group III — Arthralgia, osteoarthritis, osteoarthrosis: Inflammatory or degenerative joint disease; crepitus, pain on jaw movement.

Management of TMD:

Patient education and self-management: Soft diet, avoidance of excessive jaw opening (yawning widely, chewing gum), warm compresses, jaw relaxation exercises, sleep hygiene, and stress management. This is the foundation of all TMD management.
Occlusal splint therapy: Hard acrylic stabilisation splint worn at night; reduces bruxism-related muscle fatigue. Fitted by dentist or prosthodontist.
Physiotherapy: Jaw exercises, manual therapy, postural correction, dry needling of trigger points. Referral to a physiotherapist experienced in orofacial pain.
Pharmacotherapy: Short-course NSAIDs (ibuprofen 400 mg PO TDS with food, 7–14 days), or naproxen 250–500 mg PO BD. Muscle relaxants (cyclobenzaprine 5–10 mg PO nocte) may be considered for myofascial pain but evidence is limited. Avoid chronic benzodiazepine use.
Invasive treatments: Arthrocentesis, botulinum toxin injection (off-label), and arthroscopy are reserved for refractory cases and require specialist (oral and maxillofacial surgery) referral.

Red Flags — When to Investigate Urgently

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Giant cell arteritis: Age >50, new temporal headache, jaw claudication, visual symptoms, ESR >50 mm/hr, weight loss, scalp tenderness. Treat empirically with high-dose prednisolone — do NOT await biopsy.
Malignancy: Unilateral facial numbness (especially V2 or V3), proptosis, unexplained cranial nerve palsy, nasal obstruction with epistaxis, unexplained weight loss, lymphadenopathy, non-healing oral ulcer >3 weeks.
Acute herpes zoster (shingles): Prodromal pain followed by vesicular eruption in a dermatomal distribution (V1 most common with risk to eye); requires urgent ophthalmology referral if V1 involved.
Cavernous sinus pathology: Multiple cranial nerve palsies (III, IV, V1, V2, VI), proptosis, chemosis — urgent MRI.
Cerebral aneurysm / SAH: Thunderclap facial or head pain, neck stiffness, loss of consciousness — emergency CT head ± LP.
Posterior fossa lesion: Facial pain with ipsilateral hearing loss, ataxia, or other cranial nerve signs — urgent MRI.

Atypical Facial Pain

Atypical facial pain is a term that encompasses several conditions in which facial pain does not conform to the diagnostic criteria of established cranial neuralgias, dental pathology, or identifiable structural disease. Under the ICHD-3 classification, the primary entities are persistent idiopathic facial pain (PIFP, previously "atypical facial pain") and burning mouth syndrome.

Persistent Idiopathic Facial Pain (PIFP)

PIFP is characterised by facial pain that is deep, poorly localised, constant or near-constant, and does not follow a peripheral nerve distribution. It is by definition a diagnosis of exclusion — all other facial pain aetiologies must be systematically ruled out.

ICHD-3 Diagnostic Criteria for PIFP:

A: Facial pain fulfilling criteria B and C
B: Recurring daily for >2 hours/day for >3 months
C: Pain is poorly localised, not following the distribution of a peripheral nerve, and is typically deep, dull, aching, or burning
D: Not better accounted for by another ICHD-3 diagnosis

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Diagnostic uncertainty: Atypical facial pain is one of the most challenging diagnoses in neurology. The critical principle is: the diagnosis of PIFP is a diagnosis of exclusion that must never be made on first presentation. Patients require thorough evaluation — including dental assessment, neuroimaging, and laboratory investigations — before this diagnosis is applied. Re-evaluation at 3–6 monthly intervals is recommended, as structural pathology may declare itself over time.

Burning Mouth Syndrome (BMS)

BMS presents as a burning, scalding, or tingling sensation of the oral mucosa — typically affecting the tongue, palate, and lips — in the absence of identifiable oral or systemic pathology. It predominantly affects post-menopausal women (female:male ratio approximately 7:1) and is thought to involve small-fibre neuropathy of intraoral sensory afferents.

Key features:

Burning pain that typically worsens throughout the day, often absent on waking and maximal by evening
Xerostomia (subjective dry mouth) in up to 70% of patients, though salivary flow is often objectively normal
Dysgeusia (altered taste — commonly metallic or bitter) in 50–65%
Oral mucosa appears clinically normal on examination
Significant psychological comorbidity — depression and anxiety are present in up to 50–70%

Secondary causes to exclude before diagnosing BMS:

Oral candidiasis (especially in denture wearers, inhaled corticosteroid users, immunocompromised patients)
Nutritional deficiencies: iron, folate, vitamin B12, zinc — request serum levels
Medication-related: ACE inhibitors, angiotensin receptor blockers, antiretrovirals, chemotherapeutic agents
Sjögren syndrome — consider anti-Ro (SSA) and anti-La (SSB) antibodies, Schirmer test
Contact allergy (dental materials, toothpaste ingredients — sodium lauryl sulphate)
Endocrine: diabetes mellitus, thyroid dysfunction — request HbA1c, TSH

Trial Treatments for Atypical Facial Pain

Management of PIFP and BMS requires a structured, stepped approach combining pharmacotherapy with non-pharmacological strategies.

Step 1 — Non-Pharmacological Interventions

Reassurance and education: Validation of the patient's pain experience, explanation that PIFP/BMS is a recognised neurobiological condition (not "imaginary"), and that effective treatments exist.
Cognitive-behavioural therapy (CBT): Addresses pain catastrophising, maladaptive coping, and mood disturbance. Best delivered by a psychologist with experience in chronic pain. Available through some publicly funded chronic pain programmes.
Physiotherapy: Orofacial relaxation techniques, jaw and neck exercises, posture correction — particularly when there is comorbid TMD or bruxism.
Topical capsaicin (0.025–0.075% cream): Applied to the affected area of the face 3–4 times daily. Evidence is modest but may provide relief via desensitisation of TRPV1 receptors. Requires several weeks of consistent use before benefit is apparent.

Step 2 — First-Line Pharmacotherapy

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Amitriptyline

Endep® · Trypizol® · Tricyclic antidepressant

Mechanism Inhibits serotonin and noradrenaline reuptake; central analgesic effect via descending pain modulation

Adult dose Start 10 mg PO nocte; titrate by 10 mg every 1–2 weeks; target 25–75 mg nocte

Paediatric dose Not routinely recommended for facial pain in children; specialist guidance required

Duration Minimum 8-week trial at adequate dose before declaring inefficacy; continue for 6–12 months if effective, then attempt slow taper

Renal adjustment No specific adjustment; use with caution

Hepatic adjustment Avoid in severe hepatic impairment; reduce dose in mild-moderate impairment

Key side effects Dry mouth, constipation, sedation, weight gain, urinary retention, QT prolongation

PBS status ✔ PBS General Benefit

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Nortriptyline

Allegron® · Tricyclic antidepressant

Mechanism Noradrenaline-predominant TCA; better tolerated than amitriptyline (less anticholinergic burden)

Adult dose Start 10–25 mg PO nocte; titrate to 50–100 mg nocte

Duration Minimum 8-week trial; continue 6–12 months if effective

PBS status ✔ PBS General Benefit

Step 3 — Second-Line Pharmacotherapy

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Duloxetine

Cymbalta® · SNRI

Adult dose 30 mg PO daily for 1 week, then 60 mg PO daily

Advantages Less sedating, less anticholinergic burden, useful when comorbid depression or generalised pain

Side effects Nausea, headache, dizziness, dry mouth, constipation

Renal adjustment Avoid if eGFR <30 mL/min

PBS status ⚠ PBS Authority Required

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Pregabalin

Lyrica® · Gabapentinoid

Adult dose 75 mg PO BD; titrate to 150–300 mg PO BD over 1–2 weeks

Advantages Effective for neuropathic pain component; anxiolytic properties when comorbid anxiety

Side effects Sedation, dizziness, weight gain, peripheral oedema

Renal adjustment Dose reduction required: eGFR 30–60 → max 150 mg BD; eGFR 15–30 → max 75 mg BD; eGFR <15 → 25 mg daily

PBS status ⚠ PBS Authority Required

Step 4 — Referral to Neurology or Pain Medicine

Referral is indicated when:

Diagnosis remains uncertain after comprehensive primary care evaluation
Two or more adequate pharmacotherapy trials (minimum 8 weeks at target dose) have failed
Significant diagnostic red flags require further investigation (MRI, nerve conduction studies)
There is diagnostic concern for secondary TN (MS, posterior fossa tumour)
Severe functional impairment with inability to work or maintain social participation
Significant psychological comorbidity requiring integrated management

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Medicare referral pathway: Neurology referrals can be made through public hospital outpatient departments (long wait times — 3–12 months depending on jurisdiction) or private practice with Medicare rebate (Item 110). For public pain service referral, most tertiary hospitals require a referral from a GP or specialist — include a comprehensive summary of prior investigations, medications trialled, and current functional status to expedite triage. Chronic pain management plans (Item 721) and Team Care Arrangements (Item 723) enable MBS-rebated allied health involvement.

Interventional Pain Procedures (Specialist Setting)

Procedure	Indication	Setting	Notes
Sphenopalatine ganglion block	PIFP, cluster headache, facial neuropathic pain	Pain medicine specialist / ENT	Trans-nasal approach; can be performed in clinic; repeated blocks may be needed
Trigger point injections	Myofascial TMD, referred facial pain	GP, dentist, pain specialist	Local anaesthetic ± corticosteroid; MBS Item 18356
Botulinum toxin type A	Refractory TMD, chronic migraine with facial pain	Neurologist, pain specialist	Off-label for TMD; TGA-approved for chronic migraine (≥15 days/month); PBS authority for chronic migraine
Peripheral nerve stimulation	Refractory neuropathic facial pain	Pain medicine specialist	Implanted; requires trial stimulation period; limited availability in Australia

Pathophysiology

Trigeminal Neuralgia — Classical

Classical TN is most commonly caused by neurovascular compression of the trigeminal nerve root entry zone (REZ) by the superior cerebellar artery (SCA) or, less commonly, the anterior inferior cerebellar artery (AICA). Pulsatile arterial contact demyelinates the nerve at the REZ, generating ephaptic transmission — ectopic impulse spread between adjacent demyelinated axons. This produces the characteristic paroxysmal, electric-shock-like pain triggered by innocuous stimuli (light touch, chewing, wind).

The pain-free refractory period following an attack is thought to result from post-excitatory hyperpolarisation of damaged neurons. Over time, repeated paroxysms can lead to central sensitisation in the trigeminal nucleus caudalis, resulting in background aching between paroxysms — a feature of long-standing, untreated TN.

Secondary TN

Secondary TN may result from demyelination (multiple sclerosis — TN occurs in 2–5% of MS patients, often bilateral), posterior fossa tumours (schwannoma, meningioma), arteriovenous malformations, or pontine infarction. These structural causes disrupt normal nerve conduction through direct compression or demyelination.

Persistent Idiopathic Facial Pain

The pathophysiology of PIFP is incompletely understood but is thought to involve a combination of peripheral and central mechanisms:

Peripheral sensitisation: Local tissue injury or inflammation (dental procedures, sinusitis, trauma) may initiate nociceptive input that persists after the inciting event has resolved.
Central sensitisation: Prolonged nociceptive input to the trigeminal nucleus caudalis produces neuroplastic changes (wind-up, expanded receptive fields, lowered activation thresholds) that maintain pain independently of peripheral input.
Descending modulation dysfunction: Impaired function of the periaqueductal grey–rostral ventromedial medulla–dorsal horn pathway reduces endogenous pain inhibition.
Psychological factors: Catastrophising, hypervigilance, and mood disturbance amplify pain perception through limbic system engagement — these are not causative but are powerful modulators.

Burning Mouth Syndrome

BMS is thought to involve small-fibre neuropathy of intraoral trigeminal afferents (C-fibres and Aδ-fibres) with subsequent central disinhibition. Neuroimaging studies demonstrate altered activity in the trigeminal sensory nuclei and insular cortex. The circadian pattern (worsening through the day) may relate to progressive depletion of inhibitory neurotransmitters (GABA, endogenous opioids) with sustained sensory input.

Giant Cell Arteritis

GCA is a granulomatous vasculitis affecting medium and large arteries, particularly the extracranial branches of the aortic arch. The temporal, vertebral, and ophthalmic arteries are commonly involved. Intimal hyperplasia leads to luminal stenosis and tissue ischaemia. Facial pain in GCA results from ischaemia of the masticatory muscles (jaw claudication) or ischaemic neuropathy of cranial nerves. Untreated, GCA can cause sudden irreversible blindness via posterior ciliary artery occlusion.

Clinical Presentation & Diagnostic Criteria

Trigeminal Neuralgia — ICHD-3 Criteria

A: Recurrent paroxysms of unilateral facial pain in the distribution of one or more divisions of the trigeminal nerve, with no radiation beyond the trigeminal distribution
B: Pain has at least 3 of the following: (1) paroxysms lasting from a fraction of a second to 2 minutes; (2) severe intensity; (3) electric-shock-like, shooting, stabbing, or sharp character; (4) precipitated by innocuous stimuli to the affected side of the face
C: Not better accounted for by another ICHD-3 diagnosis

Classical TN: Caused by vascular compression (MRI evidence of neurovascular contact); may have sensory deficit on examination.

Secondary TN: Caused by an identifiable underlying disease (MS, tumour, structural lesion).

Idiopathic TN: No demonstrable cause on imaging or investigation.

TN vs Symptomatic TN — Clinical Differentiation

Feature	Classical TN	Secondary / Symptomatic TN
Age of onset	Typically >50 years	Any age (younger in MS)
Side	Almost always unilateral; bilateral in <5%	Bilateral more common (especially MS)
Triggers	Well-defined trigger zones on face	May be spontaneous; triggers less consistent
Neurologic signs	Examination normal (though up to 30% may have subtle sensory loss)	Sensory loss, corneal hyporeflexia, motor weakness, other cranial nerve signs
Response to carbamazepine	Excellent (diagnostic aid)	Partial or poor response
MRI findings	Neurovascular contact at REZ	Structural lesion, MS plaque, tumour

Other Cranial Neuralgias

Neuralgia	Nerve	Pain Distribution	Distinguishing Features
Glossopharyngeal	CN IX	Posterior tongue, tonsillar fossa, ear	Triggered by swallowing, talking; may cause syncope (cardioinhibitory reflex)
Geniculate (Nervus intermedius)	CN VII sensory component	Deep ear, periauricular	Paroxysmal ear pain; may have herpetic vesicles in ear canal (Ramsay Hunt)
Occipital	Greater/lesser occipital nerves (C2–C3)	Posterior scalp, behind ear, periorbital referral	Tenderness over occipital nerve; may mimic frontal facial pain
Post-herpetic neuralgia	Any trigeminal division (V1 most common)	Dermatomal, within prior zoster distribution	Pain persisting >90 days after zoster rash; allodynia and burning

Giant Cell Arteritis — Diagnostic Criteria

ACR 1990 criteria (≥3 of 5 required for diagnosis):

Age at onset ≥50 years
New-onset or new-type headache
Temporal artery tenderness or reduced pulse
ESR ≥50 mm/hr (Westergren)
Abnormal temporal artery biopsy (showing necrotising arteritis with mononuclear cell infiltrate or granulomatous inflammation, usually with giant cells)

Note: Jaw claudication (pain in the jaw muscles with chewing, resolving with rest) is the most specific symptom for GCA but is not included in ACR criteria. Its presence markedly increases the likelihood of GCA.

Investigations

Investigation should be guided by clinical suspicion. Not all patients with facial pain require neuroimaging — those with a classic TN presentation in the correct age group and no red flags may be trialled on carbamazepine with imaging arranged electively. However, any atypical features mandate neuroimaging before treatment.

Essential

FBE, ESR, CRP, CMP

Screen for inflammatory markers (GCA), anaemia of chronic disease, renal function for medication dosing. Available at all Australian pathology services. MBS Item 65071/65080 (single pathology episode).

Essential

Serum B12, folate, ferritin, fasting glucose / HbA1c, TSH

Exclude nutritional deficiencies (burning mouth syndrome), diabetes mellitus (neuropathy), and thyroid disease. MBS Item 66839 (B12), 66555 (ferritin), 66500 (glucose).

Available

MRI Brain with Trigeminal Protocol

The investigation of choice for TN. High-resolution T2-weighted sequences (CISS/FIESTA) and MRA to assess neurovascular contact. Identifies posterior fossa tumours, MS plaques (FLAIR/T2), and vascular loop compression. Available at all major metropolitan radiology centres; MBS Item 63056 (MRI brain, Medicare rebatable with GP referral). Regional access may require transfer to metropolitan centre.

Available

Orthopantomogram (OPG) / Dental Radiograph

To exclude dental pathology (periapical abscess, impacted teeth, caries). Available at most dental practices; MBS Item 013 (if performed in hospital setting). Dental x-rays may also be covered under state-funded public dental services for eligible patients.

Referral

Temporal Artery Biopsy

Confirmatory for GCA; should be performed within 2 weeks of commencing corticosteroids. Sensitivity 70–90%; a negative biopsy does not exclude GCA if clinical suspicion is high. Arrange through vascular surgery or general surgery. Steroid treatment must not be delayed while awaiting biopsy.

Available

FDG-PET/CT

Increasingly used for large-vessel vasculitis assessment (GCA); sensitivity 70–90% for extracranial vessel involvement. Available at major PET centres; MBS Item 61370 (Medicare-rebatable when performed for suspected vasculitis). Useful when temporal artery biopsy is negative but clinical suspicion remains high.

Specialist

Quantitative Sensory Testing (QST)

Objective assessment of small-fibre function (thermal thresholds, mechanical detection). Available at select specialist pain medicine and neurology centres. Not routinely Medicare-rebatable.

Specialist

Trigeminal Reflex Testing (Electrophysiology)

Records the R1 and R2 components of the blink reflex and masseter inhibitory reflex. Abnormalities suggest structural trigeminal pathology. Available at select tertiary neurophysiology departments. Useful for differentiating classical TN from secondary TN when MRI is equivocal.

Available

Anti-Ro (SSA) / Anti-La (SSB) Antibodies

Screen for Sjögren syndrome when burning mouth syndrome is suspected and sicca symptoms are present. MBS Item 66800. Refer to rheumatology if positive.

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MBS notes: MRI brain (MBS Item 63056) is now Medicare-rebatable without prior specialist authorisation since November 2013, subject to clinical indication. GP referral is sufficient. However, MRI of the face/sinuses (MBS Item 63500 series) may require specialist referral depending on the item. Discuss with your radiologist if uncertain.

Risk Stratification & Severity

Low Risk

Benign / Self-Limiting

Dental caries, uncomplicated TMD, acute sinusitis, post-dental procedure pain. Clear precipitant, no red flags, examination normal aside from localised findings. Responsive to simple analgesia and conservative measures.

Setting: Primary care / Dental clinic

Moderate Risk

Neurologic — Requires Investigation

Suspected TN (classic presentation, V2/V3 distribution, triggerable paroxysms), persistent facial pain >3 months without clear cause, burning mouth syndrome, post-herpetic neuralgia. Requires neuroimaging, laboratory investigation, and likely pharmacotherapy initiation. Consider neurology referral.

Setting: Primary care with specialist input; neurology outpatient

High Risk

Urgent — Potential Serious Pathology

Giant cell arteritis (new headache + jaw claudication + visual symptoms in patient >50), suspected intracranial malignancy, cavernous sinus pathology, acute herpes zoster ophthalmicus with ocular involvement, progressive cranial nerve palsies, thunderclap facial/headache. Requires immediate investigation and treatment.

Setting: Emergency department / Urgent specialist referral

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Giant cell arteritis — do not delay: If GCA is clinically suspected (age >50, new headache, jaw claudication, visual symptoms, ESR >50), initiate prednisolone 50–100 mg PO immediately. Arrange urgent ESR/CRP and temporal artery biopsy within 2 weeks. Steroid treatment must not be delayed while awaiting investigations. Referral to rheumatology is mandatory. If visual symptoms are present (amaurosis fugax, diplopia, visual loss), treat as a medical emergency — consider IV methylprednisolone 500 mg–1 g daily for 3 days in consultation with rheumatology/ophthalmology.

Empirical Therapy

Trigeminal Neuralgia — First-Line

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Carbamazepine

Tegretol® · Tegral® · Anticonvulsant (sodium channel blocker)

Mechanism Blocks voltage-gated sodium channels on demyelinated nerve fibres, reducing ectopic impulse generation

Adult dose Start 100 mg PO BD with food; titrate by 100–200 mg every 3–7 days; effective range 200–1200 mg/day in divided doses

Paediatric dose 10–20 mg/kg/day in divided doses (specialist guidance required for TN in paediatrics)

Route Oral; liquid formulation available for those unable to swallow tablets

Duration Continue for as long as pain controlled; attempt dose reduction after 6–12 months of remission

Key monitoring FBE (risk of agranulocytosis — 1:10,000), LFTs, UEC at baseline, 2 weeks, 1 month, then 3-monthly for 12 months. Educate patient to report sore throat, fever, rash, mouth ulcers.

Renal adjustment No specific dose adjustment; use with caution

Hepatic adjustment Avoid in severe hepatic impairment; significant CYP450 inducer (many drug interactions)

PBS status ✔ PBS General Benefit

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Oxcarbazepine

Trileptal® · Anticonvulsant (sodium channel blocker)

Mechanism Keto-analogue of carbamazepine; similar sodium channel blockade with fewer drug interactions and lower risk of blood dyscrasias

Adult dose Start 150 mg PO BD; titrate by 150 mg every week; effective range 300–1200 mg/day in divided doses

Key advantages Better side-effect profile than carbamazepine; fewer drug interactions (weaker CYP inducer); no auto-induction; lower risk of agranulocytosis

Key side effects Hyponatraemia (check sodium at baseline, 2 weeks, and 3 months); dizziness, ataxia, diplopia, rash (cross-reactivity with CBZ ~25%)

Renal adjustment Start at half dose if eGFR <30 mL/min

PBS status ⚠ PBS Authority Required (trigeminal neuralgia)

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HLA-B*1502 screening: The TGA recommends HLA-B*1502 testing before initiating carbamazepine or oxcarbazepine in patients of Southeast Asian, Han Chinese, or Indian ancestry (including Aboriginal Australians in some regions), due to an increased risk of Stevens-Johnson syndrome / toxic epidermal necrolysis. Testing is available through most Australian pathology services (MBS Item 71147). If positive, avoid carbamazepine; oxcarbazepine risk is lower but use with extreme caution.

Acute Dental / Odontogenic Pain

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Ibuprofen + Paracetamol

Nurofen® + Panadol® · NSAID + Analgesic

Adult dose Ibuprofen 400 mg PO TDS with food + Paracetamol 1 g PO QDS (max 4 g/day). Combination provides superior analgesia to either alone.

Duration Short course (3–7 days); definitive dental treatment required

Caution Avoid NSAIDs in renal impairment, GI bleeding history, anticoagulant use. Consider paracetamol alone if NSAIDs contraindicated.

PBS status ✘ Not PBS listed (OTC)

Acute / Temporising Analgesia for All Facial Pain

Paracetamol: 1 g PO QDS (max 4 g/day) — foundation analgesic; safe in most populations. PBS General Benefit.
NSAIDs: Ibuprofen 400 mg PO TDS or naproxen 250–500 mg PO BD with food. Short course only. Avoid in renal impairment, GI bleeding risk, and anticoagulant use.
Topical agents: Lignocaine 5% medicated plasters (Versatis®) — cut to size and applied to the affected area of the face for up to 12 hours/day. Useful for localised neuropathic pain. PBS Authority Required.

Directed / Pathogen-Specific Therapy

TN — Second-Line (Carbamazepine Inadequate Response or Intolerance)

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Lamotrigine

Lamictal® · Anticonvulsant

Adult dose Start 25 mg PO daily for 2 weeks → 50 mg daily for 2 weeks → 100 mg daily → titrate to 200–400 mg/day in divided doses. SLOW titration essential (risk of SJS).

Advantages Good evidence for TN when used as add-on to carbamazepine or as monotherapy; less sedating than CBZ

Caution Risk of serious rash (SJS/TEN) increased with rapid titration, concomitant valproate (double lamotrigine levels), and age <16

PBS status ⚠ PBS Authority Required

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Baclofen

Lioresal® · Baclopar® · GABA-B agonist / muscle relaxant

Adult dose Start 5 mg PO TDS with food; titrate by 5 mg every 3 days; max 80 mg/day. Effective range for TN: 40–80 mg/day.

Advantages Useful as adjunct to carbamazepine; may be used alone; rapid onset of action

Side effects Drowsiness, dizziness, nausea; avoid abrupt withdrawal (risk of seizures, hallucinations)

Renal adjustment Significant dose reduction in renal impairment (eGFR <30 → start 5 mg daily)

PBS status ✔ PBS General Benefit

Neurosurgical Options for Refractory TN

Procedure	Mechanism	Success Rate	Recurrence	Setting
Microvascular decompression (MVD)	Surgical separation of compressing vessel from nerve REZ via posterior fossa craniotomy	70–90% pain-free at 1 year	15–25% at 10 years	Neurosurgery (major centres); MBS Item 39214
Percutaneous balloon compression	Meckel's cave catheter balloon compression of Gasserian ganglion	80–90% initial relief	20–30% at 3 years	Neurosurgery / interventional radiology
Stereotactic radiosurgery (Gamma Knife)	Focused radiation to trigeminal REZ	60–80% significant pain relief	30–50% at 3–5 years	Specialist radiosurgery centres (limited availability in Australia)
Percutaneous radiofrequency thermocoagulation	Controlled thermal lesion of Gasserian ganglion	85–95% initial relief	25–50% at 5 years	Neurosurgery

Referral for surgery: Indicated when two or more adequate medical therapies have failed or are intolerable, and quality of life is significantly impacted. Microvascular decompression offers the best long-term outcomes for classical TN with confirmed neurovascular contact on MRI. Percutaneous procedures (balloon compression, RF thermocoagulation) are preferred in elderly or medically unfit patients. Referral to a neurosurgeon with TN expertise is essential.

Giant Cell Arteritis — Directed Therapy

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Prednisolone

Panafcort® · Solone® · Corticosteroid

Adult dose — non-visual Prednisolone 50 mg PO daily for 3 weeks → taper by 10 mg every 2 weeks to 20 mg → then taper by 2.5 mg every 2–4 weeks → maintenance 5–10 mg/day. Total treatment duration 1–2 years (minimum).

Adult dose — visual symptoms Methylprednisolone 500 mg–1 g IV daily for 3 days → switch to oral prednisolone 1 mg/kg/day (max 80 mg). Arrange urgently with rheumatology/ophthalmology.

Bone protection Calcium + vitamin D supplementation (Caltrate® 600 mg + Vit D PO daily) from initiation; consider bisphosphonate (alendronate 70 mg PO weekly) if ≥3 months prednisolone expected. DEXA scan at baseline.

GI protection PPI (pantoprazole 40 mg PO daily) if risk factors for GI bleeding

Monitoring ESR/CRP at 2, 4, 8 weeks then monthly during taper; glucose monitoring; blood pressure; DEXA at 12 months

Steroid-sparing Tocilizumab (Actemra®) 162 mg SC weekly — increasingly used as steroid-sparing agent; PBS Authority Required. Refer to rheumatology for initiation.

PBS status ✔ PBS General Benefit (prednisolone)

Post-Herpetic Neuralgia (Facial)

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Pregabalin

Lyrica® · Gabapentinoid

Adult dose 75 mg PO BD; titrate to 150–300 mg PO BD over 1–2 weeks based on response and tolerability

Renal adjustment eGFR 30–60: max 150 mg BD; eGFR 15–30: max 75 mg BD; eGFR <15: 25 mg daily

PBS status ⚠ PBS Authority Required (neuralgia)

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Gabapentin

Neurontin® · Gabapentinoid

Adult dose Start 300 mg PO daily (day 1) → 300 mg BD (day 2) → 300 mg TDS (day 3); titrate to 600 mg TDS as tolerated (max 3600 mg/day)

PBS status ⚠ PBS Authority Required (neuralgia)

ℹ️

Acyclovir for acute herpes zoster: If facial pain presents with a vesicular eruption in a dermatomal distribution, initiate acyclovir 800 mg PO 5 times daily for 7 days (within 72 hours of rash onset). Valaciclovir 1 g PO TDS for 7 days is an alternative with simpler dosing. If V1 (ophthalmic division) is involved, urgent ophthalmology referral is mandatory (risk of keratitis). Both are PBS General Benefit.

Monitoring

Trigeminal Neuralgia — Carbamazepine / Oxcarbazepine Monitoring

Timepoint	Investigations	Clinical Assessment
Baseline (pre-treatment)	FBE, LFTs, UEC, serum sodium (if oxcarbazepine), HLA-B*1502 (if applicable)	Pain characterisation, dental examination, neurologic examination, MRI brain (trigeminal protocol)
2 weeks	FBE, LFTs	Side-effect screen, dose titration progress, pain response
1 month	FBE, LFTs, UEC, sodium	Pain diary review, functional assessment
3-monthly (first 12 months)	FBE, LFTs, UEC	Ongoing response, side effects, need for dose adjustment or second-line agent
Annually (ongoing)	FBE, LFTs, UEC	Review need for ongoing therapy; consider trial reduction if pain-free >6–12 months

Atypical Facial Pain — Monitoring Framework

4–6 weekly reviews during medication titration phase — assess pain intensity (NRS 0–10), functional status (work, sleep, social), side effects, and mood.
Validate treatment response at 8–12 weeks: If no clinically meaningful improvement (≥30% reduction in pain intensity or meaningful functional improvement) at adequate dose, consider dose escalation or switch to second-line agent.
Reassess diagnosis at 6 months: If pain persists and is unresponsive to treatment, reconsider the diagnosis — request neuroimaging (if not already performed), consider specialist referral. New neurologic signs may have emerged.
Long-term follow-up: 3-monthly during the first year; 6-monthly thereafter. Monitor for depression (PHQ-9), anxiety (GAD-7), sleep disturbance, and substance use.
Pain diary: Encourage patients to keep a simple daily pain diary recording intensity, triggers, medication use, and functional impact — invaluable for identifying patterns and assessing treatment response.

Giant Cell Arteritis — Monitoring

ESR and CRP at weeks 2, 4, 8, and then monthly during the steroid taper.
Rising ESR/CRP during taper suggests relapse — increase steroid dose and seek rheumatology guidance.
Blood glucose monitoring (steroid-induced hyperglycaemia); BP monitoring; DEXA at 12 months.
Relapse rate is approximately 50% during the first 2 years — prolonged treatment and close monitoring are essential.

Special Populations

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Pregnancy

Carbamazepine

Category D — teratogenic (neural tube defects, facial clefts, cardiac malformations). Use only if no alternative and benefits outweigh risks. Supplement with high-dose folic acid (5 mg/day). Discuss with obstetric medicine.

Oxcarbazepine

Category D — similar risk profile to carbamazepine but less human data. Avoid in pregnancy if possible.

Pregabalin

Category B3 — limited human data; animal studies show developmental toxicity. Use only if clearly needed.

Preferred approach

Conservative management where possible. Lamotrigine (Category B3) is generally considered the safest anticonvulsant in pregnancy. Neuropathic pain: consider lamotrigine or gabapentin with specialist input. TMD: physiotherapy and occlusal splints are safe.

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Paediatrics

TN in children

Extremely rare in children. When it occurs, a higher index of suspicion for secondary causes (MS, posterior fossa tumour) is required. MRI brain is mandatory. Neurology referral is essential. Carbamazepine is used with weight-based dosing (10–20 mg/kg/day) under specialist guidance.

Paediatric orofacial pain

Most common cause is dental. TMD can occur in adolescents, especially with bruxism or orthodontic appliances. Conservative management is first-line. Avoid TCAs in children without specialist oversight.

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Elderly

GCA consideration

Any new facial or temporal headache in a patient >50 years must prompt consideration of GCA. ESR and CRP are essential first-line investigations. Low threshold for empirical steroid initiation.

Carbamazepine

Start at lower doses (50–100 mg/day) in the elderly; increased risk of hyponatraemia, dizziness, falls, confusion, and drug interactions (polypharmacy). Oxcarbazepine is preferred by many clinicians for its better tolerability profile.

TCAs (amitriptyline, nortriptyline)

Use with extreme caution — Beers Criteria list TCAs as potentially inappropriate in older adults due to anticholinergic effects (sedation, confusion, urinary retention, constipation, falls, cardiac conduction abnormalities). Start at 5–10 mg. Nortriptyline is better tolerated than amitriptyline.

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Renal Impairment

Carbamazepine

No significant renal adjustment required; hepatic metabolism. Use with caution — albumin may be low, increasing free drug fraction.

Pregabalin

Significant renal adjustment required — see dosing table under directed therapy. Excreted renally unchanged.

Baclofen

Accumulates in renal impairment — start at 5 mg daily and titrate cautiously; risk of encephalopathy in CKD.

Gabapentin

Requires dose reduction: eGFR 30–59 → 200–700 mg BD; eGFR 15–29 → 200–300 mg daily; eGFR <15 → 100–300 mg daily.

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Hepatic Impairment

Carbamazepine

Hepatically metabolised (CYP3A4). Avoid in severe hepatic impairment (Child-Pugh C). Reduce dose and monitor closely in mild-moderate impairment. Risk of hepatotoxicity — monitor LFTs.

TCAs

Hepatically metabolised — avoid amitriptyline in severe liver disease. Nortriptyline may be used cautiously at reduced dose.

Prednisolone

Can be used in hepatic impairment — does not require hepatic activation (unlike prednisone). Standard dosing applies.

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Immunocompromised

Herpes zoster

Higher risk of zoster reactivation and more severe disease (disseminated zoster, multi-dermatomal). Treat aggressively with IV acyclovir (10 mg/kg TDS) if severe. Lower threshold for admission. Oral valaciclovir for mild cases. Consider long-term suppressive acyclovir post-recovery.

Atypical infections

Consider opportunistic causes of facial pain (mucormycosis, CMV, fungal sinusitis) in severely immunosuppressed patients (e.g. transplant recipients, uncontrolled HIV). ENT and infectious diseases referral required.

MS-related TN

TN in a young patient should prompt investigation for multiple sclerosis. MRI brain with contrast is essential. Neurology referral for disease-modifying therapy.

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Australians experience significantly higher rates of orofacial pain compared to the non-Indigenous population. According to the AIHW (2023), Indigenous Australians are approximately 2.5 times more likely to report toothache and 1.6 times more likely to have untreated dental decay. Access to timely dental care remains a major barrier, particularly in regional and remote communities.

Dental disease burden

Aboriginal and Torres Strait Islander adults have higher rates of dental caries, periodontal disease, and tooth loss. Many present to primary care or emergency departments with advanced dental disease that is the underlying cause of their facial pain. Ensure appropriate dental referral alongside symptom management.

Access barriers

State and territory public dental services have significant wait times (often 12–24 months). Access is particularly limited in remote communities where visiting dental services may operate on rotational schedules. Aboriginal Community Controlled Health Organisations (ACCHOs) provide integrated dental care in some jurisdictions — contact the local ACCHO to identify available services.

Cultural safety in pain assessment

Pain expression varies across cultures. Some Aboriginal and Torres Strait Islander patients may use different descriptors for pain or may underreport pain severity. Avoid assumptions — use validated pain assessment tools (e.g. the culturally adapted Faces Pain Scale) and take time to build rapport. Acknowledge the social and emotional wellbeing determinants of health that may influence pain perception and management.

CA-MRSA and facial infections

Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) prevalence is higher in remote Aboriginal and Torres Strait Islander communities. Facial soft tissue infections may require CA-MRSA-active agents — trimethoprim-sulfamethoxazole (2/160 mg PO BD) or clindamycin (450 mg PO TDS) as per local susceptibility patterns. Consult the local antibiogram and eTG Antibiotic guidelines.

Medication considerations

Polypharmacy is common in Aboriginal and Torres Strait Islander patients with multiple chronic conditions. Drug interactions with carbamazepine (CYP3A4 inducer) are a significant concern. Ensure a thorough medication review. Consider oxcarbazepine (weaker inducer) as a preferred alternative when clinically appropriate. Medication adherence may be affected by availability in remote communities — ensure continuity of supply through Remote Area Aboriginal Health Services.

Giant cell arteritis

GCA is reported less frequently in Aboriginal and Torres Strait Islander populations compared to Caucasians, but this may reflect underdiagnosis rather than lower incidence. Maintain clinical vigilance, particularly in older patients with new-onset headache and systemic symptoms.

Specialist access

Neurology, oral and maxillofacial surgery, and pain medicine specialists are concentrated in metropolitan areas. Telehealth (MBS Items 99200–99215 for GP and specialist video consultations) enables remote specialist input and is available through the Australian Telehealth framework. The Patient Assistance Travel Scheme (PATS) in each state/territory supports transport and accommodation for patients requiring specialist care away from home. Ring the local Aboriginal Health Worker or liaison officer to facilitate culturally safe referrals.

Social and emotional wellbeing

Chronic facial pain intersects with social and emotional wellbeing, grief, loss, and intergenerational trauma. A holistic approach — recognising the social, emotional, cultural, and spiritual determinants of health — is essential. Refer to culturally appropriate counselling services and social and emotional wellbeing teams within ACCHOs where available. Close the Gap PBS Co-payment Measure may assist with medication costs for eligible patients.

📚 References

1. Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition. Cephalalgia. 2018;38(1):1–211. doi:10.1177/0333102417738202.
2. Cruccu G, Di Stefano G, Truini A. Trigeminal neuralgia. N Engl J Med. 2020;383(8):754–762. doi:10.1056/NEJMra1914484.
3. Bendtsen L, Zakrzewska JM, Abbott J, et al. European Academy of Neurology guideline on trigeminal neuralgia. Eur J Neurol. 2019;26(6):831–849. doi:10.1111/ene.13950.
4. Hronis T, Roberts H, Engel J. Orofacial pain: an update for general dental practice. Aust Dent J. 2020;65(S1):S56–S65. doi:10.1111/adj.12757.
5. Benoliel R, Gaul C. Persistent idiopathic facial pain. Cephalalgia. 2017;37(7):680–691. doi:10.1177/0333102417706311.
6. Hutton A, Smith L, Wray A. Burning mouth syndrome: an update. Aust Dent J. 2021;66(3):248–256. doi:10.1111/adj.12846.
7. Hunder GG, Bloch DA, Michel BA, et al. The American College of Rheumatology 1990 criteria for the classification of giant cell arteritis. Arthritis Rheum. 1990;33(8):1122–1128. doi:10.1002/art.1780330810.
8. Stone JH, Tuckwell K, Dimonaco S, et al. Trial of tocilizumab in giant-cell arteritis. N Engl J Med. 2017;377(4):317–328. doi:10.1056/NEJMoa1613849.
9. Australian Institute of Health and Welfare (AIHW). Oral health and dental care in Australia. Canberra: AIHW; 2023. Available at: www.aihw.gov.au.
10. Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in general practice (Red Book). 9th edition. Melbourne: RACGP; 2016 (updated 2023). Chapter 10: Oral health.
11. Schiffman E, Ohrbach R, Truelove E, et al. Diagnostic Criteria for Temporomandibular Disorders (DC/TMD) for Clinical and Research Applications. J Oral Facial Pain Headache. 2014;28(1):6–27. doi:10.11607/ofp.1500.
12. Therapeutic Goods Administration (TGA). Medicines Safety Update: Carbamazepine and HLA-B*1502 in patients of Asian ancestry. Canberra: Department of Health and Aged Care; 2020. Available at: www.tga.gov.au.
13. Australian Pain Society. Pain in the community: a national strategy for pain management in Australia. Sydney: Australian Pain Society; 2019.
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