Facial Pain

Presented to the Pan-Pacific Surgical

Conference , January 2006

Jeff Burgess DDS MSD

Boarded in Oral Medicine

Director – Oral Care Research Associates

Facial Pain

Comments made herein are

solely those of the author and

provided for educational

purposes only. If any condition

described is thought to be

present the reader should

consult their physician or

dentist

Facial Pain, like all pain, is a complex phenomena involving multiple

peripheral and central processes. Interpretation and augmentation occurs in

many regions within the spinal cord and brain. Multiple brain systems

influence the perception of pain via central and other body functions.

This Lecture covers the different

conditions and diseases in various

locations that can cause oral, facial, and

head pain.

Differential Diagnosis

Pain referred from the chest or neck

Pain caused by systemic disease

Pain caused by regional disease

Intracranial disease

Neurogenic pain conditions

Neurovascular disorders

Temporomandibular disorders (TMD)

Intraoral disease/pain problems

Disease of the ear, eye, nose, sinuses, lymph nodes, and salivary glands

Atypical facial pain

What will be covered in this power point presentation

Differential Diagnosis

Let us begin by taking a look at an

unusual case involving facial and

tooth pain.

Pain Referred From the Chest

33 y/o female with painful mandibular left premolar.

Intermittent, spontaneous pain x one month: toothache

Medical history apparently non-contributory but with recent loss of

appetite, 7% weight loss, dry cough not attributed to URI or smoking

Examination without evidence of dental disease or pulpal

involvement. Block without effect. Subsequent referral to

pulmonary specialist – large mediastinal mass surrounding the

trachea

Ultimate diagnosis:

Large cell lymphomaKant: JADA, 1989

Pain Referred from the Chest

Mediastinal lymphoma

Cardiac disease

Lung cancer

Liver Cancer

A Number of conditions in the region of the chest

can cause Face Pain including:

Pain Referred from the Chest

Case report – Australian Radiology, 1996

(Shakespeare TP)

Face pain from lung cancer did not

involve metastatic lesions. Pain

preceded the final diagnosis by 9

months

Liver Cancer

Case files from my Oral Medicine

practice: Mandibular pain arising

from metastatic lesion in the lower

jaw of a 69 y/o man from primary

liver tumor – Pain not recognized by

prior provider as potentially from the

metastatic cancer

- Delayed diagnosis resulted

ultimately in patient‟s premature

death

Lung Cancer

Suboccipital and Cervical Problems

Facial Pain is also referred from the

neck and inferior region of the

skull. The following conditions are

known to cause facial pain:

Suboccipital and Cervical Problems

Lymphatic disease / infection

Neoplasm (in spine or elsewhere)

Developmental abnormality (lymphoepithelial cyst)

Lymphangitis, pharyngitis, tracheitis, thyroiditis

Tonsillitis, peritonsillar infection/neoplasm

Myofascial abnormality

Cervical trigger point syndrome

Cervicogenic headache

Vascular developmental abnormality

Primitive trigeminal artery or carotid-basilar anastomosis

Carotidynia (classic, migrainous, arteriosclerotic)

Stylohyoid process syndrome (eagles)

Fracture

Fracture of lamina

Anterior or posterior arch of atlas

Burst fracture

Suboccipital and Cervical Problems

Neoplasm

Carcinoma of the thyroid

Recurrent neck cancer

Occipital neuralgia

Acceleration-deceleration injury of the neck

(cervical sprain)

Cervical muscle sprain

Suboccipital and Cervical Problems

Suboccipital and Cervical Problems

CarotidyniaThree types: Classic,

Migrainous,

Arteriosclerotic)

Now lets take a closer look at one neck

condition that refers pain to the face and teeth.

It is called:

CarotidyniaSymptoms include the following:

Moderate, constant, dull

ache/throb

Neck radiates to

face/temple/mastoid

region of the head

Unilateral Pain

Increased by

swallowing, laughing,

head movement

And There may be nausea

and vomiting

Facial Pain Can Also Be Caused

by Systemic Disease

Pain Caused by Systemic Disease

Diabetes

Connective tissue diseases

Allergy

Sickle cell Disease: Sickle cell disease causes diffuse abdominal pain secondary to blood flow abnormality and lowered oxygen tension. Facial pain may be an initial symptom.

Cherry, et al, in Clinical Preventive Dentistry, 1992, report a case involving severe mandibular neuropathy.

Thyroiditis Thyroiditis typically occurs 2-3 weeks after a URI

Pain occurs in the thyroid and may radiate into the face. There is also pressure and fullness in the throat. Swallowing increases symptoms. There may be fever and malaise. The condition may occur over months.

Immunologic disease periarteritis nodosa

giant cell arteritis ( with temporal arteritis)

Medications vincristine

Pain Caused by Systemic Disease

Pain Caused by

Intracranial Disease

Subarachnoid and intracerebral hemorrhage Vernon et al; J of Craniomandib Pract, 1987: 33y/o male post fall with cc face pain, HA.

Edema right max, man region, swallowing caused pain. Pain lancinating. MRI with arachnoid cyste anterior temporal fossa.

Intracranial infection

Other conditions arachnoid cysts

cholesterol granulomas

ventral pontine infarction

acute ischemic cerebrovascular disease

intracranial hematoma

low cerebrospinal fluid pressure

Intracranial Disease

Pain Caused by

Neurogenic Pain

Conditions: Paroxysmal (Shock-Like,

Brief Duration, Repeated)

Trigeminal Neuralgia

Primary (essential)

Secondary

Glossopharyngeal Neuralgia

Trigeminal

NeuralgiaLocation of Facial Pain: Typically

in the region of the second (nose,

upper lip, upper teeth) or third

division (lower jaw, lower teeth) of

the Fifth Cranial Nerve

Pain is described as an intense shock that lasts for seconds and repeats multiple

times. It is „triggered‟ by manipulation of the lip or jaw such as occurs with

eating, brushing ones teeth, kissing, shaving, applying makeup.

Other Types of

Trigeminal Neuralgia

“Idiopathic” (essential)

trigeminal neuralgia

Atypical trigeminal neuralgia

Symptomatic trigeminal neuralgia

“Pre” trigeminal neuralgia

Pain characteristics

Sudden, severe, agonizing, episodic, recurrent

Shock-like, electric – typically unilateral

Brief (seconds) with pain free intervals

Pain perceived superficially in the skin but also in

teeth, intraoral mucosa

Triggered by light touch to external skin, teeth,

gingiva or buccal mucosa

Episodic (will go away on its own without

apparent reason but then return without reason

Trigeminal Neuralgia

Trigeminal Neuralgia

Prevalence rare 2.7/100,000 men,

5/100,000 women

Occurs after fourth decade – peak during

the fifth and sixth decade

Prior to 40 should be investigated for

other causes: MS or intracranial tumor

Trigeminal Neuralgia

Be aware of neurologic symptoms

In essential “idiopathic” TIC

neurologic examination should be

normal; MRI and CT should be

normal

Trigeminal Neuralgia

Tumors

meningioma

epidermoid tumor

acoustic neurinoma

metastatic tumors

brainstem glioma

Arnold Chiari malformation

Demyelinating disease

(Multiple Sclerosis)

Vascular lesions

basilar artery or cavernous sinus aneurysm

arteriovenous malformation

tortuous basilar artery

Bone disease

Paget‟s disease

acromegaly

Secondary Trigeminal Neuralgia

Trigeminal NeuralgiaSecondary Trigeminal Neuralgia

•Prevalence data suggests that anywhere from 2% to 45% of TIC

patients can have brain tumors

•Pain from traction on intracranial structures (the venous sinuses, dural

and cerebral arteries, pia and dural mater and cranial nerves

(e.g. tumor) or specific disease (meningitis).

•Site of pain depends on location of tumor (I.e. compression of III and

periorbital pain). Pain quality varies considerably. May be

throbbing, dull aching, sharp or paroxysmal like a neuralgia.

•Typically worsens over time and non-responsive to appropriate

medication.

•Associated with focal neurological signs or deficits such as weakness,

dizziness, difficulty with speech or swallowing, ptosis,

tingling or numbness, memory loss or confusion.

Secondary Trigeminal Neuralgia

43 y/o female with shock-like pain

beginning in the maxillary left cuspid,

corner of the mouth with superior-lateral

radiation to the ear. Began after fall.

Present 6 months without change

Pain free intervals, triggered by

mouth movement and chewing;

also subtle „numbness‟ above

cuspid tooth

Medical, family social history

unremarkable; examination

unremarkable – no apparent

dental pathology

Final diagnosis: brain tumor

- Meningioma

The Case of a Patient seen in

my Oral Medicine Practice:

CT of brain was negative. Patient

elected to have surgery to place a

plastic placed between the carotid

artery and the trigeminal nerve and at

surgery the tumor was found.

Treatment/Management

PharmacotherapyAnticonvulsants

SurgeryGangliolysis (RF or Glycerol

Neurectomy

Microvascular decompression

Gamma Knife

Gamma knife radiosurgery for trigeminal

neuralgia: the

Washington University initial experience

•Stereotact Funct Neurosurg. 2005;83(4):148-52.

Epub 2005 Oct 3

Drzymala RE, Malyapa RS, Dowling JL et al

Lets take a look at one of many studies and see

what it suggests: Gamma knife radiosurgery

Gamma knife radiosurgery for trigeminal

neuralgia: the

Washington University initial experience

Seventy-three patients

changes in pain relief, numbness and

paresthesias

dose of 76-87 Gy

Results

59% attained complete pain relief without

prior surgery (33% with prior surgery)

25% achieved > or = 50% pain reduction (28%

with prior surgery)

11% of surgery patients obtained minor pain

relief

16% of patients without surgery had no relief

(28% with prior surgery)

Results and conclusions

Numbness/paresthesias developed slowly over the first 12-15 months

Bothersome levels were experienced by 15% of the patients without prior surgery (22% with prior surgery)

2% of all patients had persistently bothersome side effects

radiosurgery is an effective treatment of trigeminal neuralgia

An open study of botulinum-A toxin

treatment of trigeminal neuralgia.

Neurology. 2005 Oct 25;65(8):1306-8.

Piovesan EJ, Teive HG, Kowacs PA et al

Thirteen subjects

Botulinum-A neurotoxin (BoNT/A)

Visual analog scale score, surface area of pain,

and therapeutic coefficient were reduced

No RCTs to date

Glossopharyngeal

NeuralgiaLocation: Tonsillar fossa, tongue, and

adjacent areas with radiation to the

external auditory canal (otic variety) or

the neck (cervical variety)

Glossopharyngeal Neuralgia

Pain: shocking, electrical, or stabbing

Severe, debilitating

Precipitated by tongue movement,

swallowing, yawning

Shooting to the ear, tonsillar region, or

neck

Pain free intervals

Other Neurogenic Pain

Conditions Conditions causing continuous facial

Pain Neuralgias have been reported to follow 3rd molar extraction, orthognathic

surgery, and dental anesthetic injection.

Pretrigeminal neuralgia

Postherpetic neuralgia

Trauma induced neuralgia

Anesthesia dolorosa

Neuritis / Neuroma

RSD (Complex regional pain syndrome)

Pre-Trigeminal

NeuralgiaLocation: In the face, typically in

region of the second or third

division of V

Pre-trigeminal neuralgia has been described as pain that is localized to the

alveolus. Can last up to 2 years as a dull aching or burning or sharp/burning

pain. Can be incorrectly diagnosed as odontogenic pulpal pain, or in cases of

ear/preauricular radiation - TMD.

Response to tegretol, dilantin, or blacofen with Pre-trigeminal neuralgia

suggestive of the diagnosis.

Post Herpetic

NeuralgiaLocation: Face, typically

in the 1st (ophthalmic)

division of V

Post Herpetic Neuralgia

• Location: Face, typically in the 1st

(ophthalmic) division of V (forehead,

scalp)

• Pain Duration: Constant

• Pain Quality: Burning, dull

• Pain Severity: Severe (8-10 level)

• Other Symptoms: Tingling, Numbness

Now Lets Look at Some Research

Conclusions: chronic pain studies of

lidocaine patch 5% using the

Neuropathic Pain Scale.

Curr Med Res Opin. 2004 Nov;20 suppl.

2(1):29-31

Argoff CE

Lidocaine patch 5% was effective in treating

chronic pain of both neuropathic and non-

neuropathic origins

Research assessing treatment of Post-herpetic Neuralgia:

Psychosocial risk factors for

postherpetic neuralgia: a prospective

study of patients with herpes zoster.

J Pain. 2005 Dec;6(12):782-90

Katz J, McDermott MP, Cooper EM, et al

Prospective study - 110 patients with herpes zoster

Assessed within the first month after rash onset with

measures of acute pain and five broad domains of

psychosocial functioning-physical, role, social, and

emotional functioning, and stress and social support.

And what about the psychological and social implications:

Psychosocial risk factors for

postherpetic neuralgia: a prospective

study of patients with herpes zoster.

Twenty of the 102 patients with follow-up data were diagnosed with PHN

Measures of role functioning, personality disorder symptoms, and disease conviction during herpes zoster each made independent contributions to predicting either presence or intensity of PHN in logistic and linear regression analyses that controlled for relevant demographic and clinical variables, including age and acute pain intensity

Pregabalin: a new agent for the

treatment of neuropathic pain

Drugs Today (Barc). 2005 Aug;41(8):509-16

Zareba G

Antiepileptic, analgesic and anxiolytic activity

Peak plasma levels occur approximately 1 hour after oral doses and oral bioavailability is about 90

Not protein-bound; plasma half-life about 6 hours

Hepatic metabolism negligible; most of the oral dose (95%) appears unchanged in the urine

RCTs?

Innovative management of neuropathic pain, drug study:

Facial Pain Caused by Neurovascular Disorders

Immune system mediated: Temporal arteritis

(giant cell arteritis)

Other:

Cluster-tic syndrome

Hemicranias

Migraine variants Syndrome of “jabs and jolts”

SUNCT syndrome

Mixed headache

Chronic tension type headache (mixed headache)

Neurovascular Disorders

Temporal Arteritis

> age of 70 but in 50-70 y/o can be delayed

diagnosis

Headache (temple), jaw claudication,

polymyalgia rheumatica, and visual symptoms

40% of patients present with atypical

manifestations, including fever of unknown

origin, respiratory tract symptoms (especially

dry cough), and large artery involvement, chin

hypoesthesia

Temporal Arteritis

Temporal artery biopsy remains the only

confirmatory procedure, newer laboratory

investigations and blood flow studies with fundus

fluorescein angiography may be useful

Abnormal temporal artery on physical examination

and anemia are factors that may predict the risk of

severe ischemic complications related to GCA.

Sanchez-Andrade A, Llorca J. J Rheumatol. 2005

Sep;32(9):1737-41.

Temporal Arteritis

Only 7 (22.6%) of the 31 patients who suffered

permanent visual loss had an ESR at the time

of disease diagnosis greater than 100 mm/h. Gonzalez-Gay MA, Lopez-Diaz MJ, Barros S, Garcia-Porrua C, Sanchez-

Andrade A, Paz-Carreira J, Martin J, Llorca J Giant cell arteritis: laboratory

tests at the time of diagnosic Medicine (Baltimore). 2005 Sep;84(5):269-76

Vertebrobasilar ischemia is an uncommon

complication of TA (but can occur) Pfadenhauer K, Esser M, Berger K. J Rheumatol. 2005 Dec;32(12):2356-60.

Trigeminal autonomic cephalalgias.

Pathophysiology and classification.

Rev Neurol (Paris). 2005 Jul;161(6-7):692-5

Goadsby PJ

Trigeminal Autonomic Cephalalgias (TACs) is a grouping of headache syndromes that includes cluster headache, paroxysmal hemicrania and short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT)

Trigeminal Autonomic Cephalalgias

Clinical presentation: episodic, stereotypic attack profile and very often prominent cranial autonomic symptoms, such as lacrimation, conjunctival injection or rhinorrhea

afferent activation of the trigeminal innervation of intracranial pain-producing structures, or the perception of that activation, and reflex activation of the seventh cranial nerve

Dysfunction in the brain, specifically in the posterior hypothalamic gray matter

Neurovascular Disorders

ClusterLocation: ocular, frontal, temporal,

infraorbital, ipsilateral upper teeth,

back of head, entire hemicranium,

neck, or shoulder

Cluster Periorbital or temple region, but may also be

perceived initially in the maxillary posterior teeth or palate.

Severe and typically unilateral although some bilateral

Facial sweating and nasal congestion, lid edema and ptosis, conjunctival injection, miosis, general restlessness

Pain will usually awaken the patient

Lets Look at the Research

Assessing the Cause of

Cluster

Genetics of cluster headache: an

update

J Headache Pain. 2005 Sep;6(4):234-6

Pinessi L, Rainero I, Rivoiro C et al

Genetic epidemiological surveys have shown that

first-degree relatives of CH patients are more likely to

have CH than the general population. CH has been

reported in some concordant monozygotic twin pairs

association between the HCRTR2 gene and the

disease

The Research related to the cause of Cluster:

Familial cluster headache. Is

atypical cluster headache in family

members part of the clinical

spectrum?

Cephalalgia. 2005 Nov;25(11):1068-77

Sjostrand C, Russell MB, Ekbom K

21 Swedish families

affected, of whom 42 had episodic or chronic CH, one had probable CH and 12 had atypical symptoms

mean age at onset was significantly lower in the second/third generation than in the first generation

CH in CH families may represent an expanded spectrum of the disease with a common aetiology, i.e. a common genetic background.

Cluster - Treatment Treatment: 100% oxygen delivered via non-

rebreather mask at 10 liters per minute for 15 minutes.

Subcutaneous sumatriptan (3-6mg) or IV/SQ/IM dihydroergotamine at .5-1mg].

Indomethicin 25-50mg tid

Prednisone as a preventive (high dose with taper)

Lithium carbonate 300mg bid to qid (adverse effects)

Calcium antagonists (verapamil) (120-160 mg in three or four divided doses

Suboccipital injection with a mixture

of rapid- and long-acting steroids in

cluster headache: a double-blind

placebo-controlled study.

Pain. 2005 Nov;118(1-2):92-6. Epub 2005 Oct 3

Ambrosini A, Vandenheede M, Rossi P et al

mixture of long- and rapid-acting betamethasone (n=13; Verum-group) or physiological saline (n=10; Plac-group

A single suboccipital steroid injection completely suppresses attacks in more than 80% of CH patients. This effect is maintained for at least 4 weeks for the majority

New Treatment Strategy – The Research:

Neurovascular Disorders

Paroxysmal Hemicrania

Remitting or Unremitting (chronic) form (CPH)

Location: Ocular, frontal, temple,

occasionally infraorbital maxillary

region

Paroxysmal Hemicrania

Remitting

Multiple episodes of throbbing pain persisting

for 5 to 20 minutes (relatively pain free

intervals)

More frequent in young women

Localized to midface, orbit, or temple

Ipsilateral conjunctival injection and tearing

with nasal congestion and rhinorrhea

Response to indomethacin

Neurovascular Disorders That Can Cause

Chronic Paroxysmal

HemicraniaC7 disc herniation

Occipital infarction

Gangliocytoma within the sella

Ophthalmic herpes-zoster infections

Cerebrovascular disease (e.g. arteriovenousmalformation)

Orbitocavernous

sinus syndrome

Parasellar pituitary

microadenoma

Maxillary cyst

Meningioma in the

roof of the

cavernous sinus

Lower-half facial migraine: a report

of 11 cases

J Oral Maxillofac Surg. 2004 Dec;62(12):1453-6

Penarrocha M, Bandres A, Penarrocha M, Bagan JV

11 cases of lower-half facial migraine

Location of the pain often mimics dental pain

About half had had root canal treatment; 1/3 Ext

Ergotamine 9 cases; 2 patients indomethacin

RESULTS: Nine patients (82%) improved as a result of treatment

Temporomandibular Disorders (TMD)

AAOP Taxonomy

cranial bones including themandible

temporomandibular jointarticular disorders

masticatory muscle disorders *****

temporomandibular joint dislocation

congenital or developmentaldisorders

aplasia

hypoplasia

neoplasia

inflammatory conditions

sprain/strain - trauma

related

perforation of the

posterior ligament/disk

collagen vascular diseases

ankylosis

fracture

American Association of Orofacial Pain

Muscle Problems – and Referral

Jaw muscles may refer pain directly

to the teeth P Svensson et al, PAIN 92, 2001, 399-409

Study assessing stimulus evoked pain in patients with TMD

Saline infused into the deep masseter in patients and controls age

and sex matched

Saline injection induced pain in teeth in 62% of both groups

Studies: Stohler and Lund – 1995 and Svensson and

Arendt-Neilson –2000 as well as others

TMD (Temporomandibular Disorders)

18-45; prevalence 12% - 5% needing Tx; 10% chronic

Etiology: bruxism (nocturnal and daytime parafunction, other oral habits); trauma (overt/blunt); systemic diseases (immunologic, infectious, neoplastic); psychophysiologic factors (somatic focus, depression), hormonal factors (estrogen)

Self-limiting for the most part (not involving disease or profound psychological/dysfunctional factors)

Non-invasive treatment is appropriate

Pain of Intraoral Origin

Glossodynia and sore mouth

Pain associated with mucosal disease

Pain associated with bone pathology Chronic diffuse osteomyelitis

Neoplasm

Cracked teeth (cracked tooth syndrome)

Location: tip and lateral borders of

tongue, entire tongue, lips, cheeks,

anterior hard palate; typically bilateral

Glossodyniaor Burning Mouth

Syndrome

Glossodynia Etiology: For idiopathic glossodynia – unknown

Differential diagnosis for tongue burning:

Candidiasis (erythematous or atrophic)

B-complex deficiency

Systemic disease (diabetes, anemia)

Local factors (trauma, nerve injury, tumor)

Local mucosal disease (lichen planus, areata migrans)

Allergy (contact type)

Psychological factors (depression, anxiety)

Glossodynia Clinical features:

Women over 50

Postmenopausal

Pain quality: constant burning/tender but also nagging, discomforting, tiring

Increases towards afternoon/evening

Associated symptoms: taste dysfunction, oral dryness

Pain increases with hot food, fatigue, tension, speaking

Glossodynia Remission within 6-7 years common

Responds to TCAs, anti-anxiety

medications (Topical clonazepam (.5 to 2mg tid))

Has been found to reduce lancinating phantom

pain (Bartusch et al; Clin J Pain 1996:59) Mechanisms unclear – probable effect on GABA and supression of

polysynaptic activity in the cord, neuronal activity in the

mesencephalic reticular system. Serotonin also potentially altered.

Possible peripheral effect as well.

Glossodynia

Pathophysiology – unclear

Theories:

Glossodyniaor Burning Mouth SyndromeFDOPA PET scans done on 10 BMS and 14 healthy

control subjects

Results: presynaptic

dopaminergic function with

significant decrease right

putamen (20%) with right

change non-significant

(17%)

Non-

significant

change in

the caudate

nucleus

Jaaskelainen, S et al: Role of the dopaminergic system in chronic pain – a

fluorodopa-PET study; Pain 2001:257

Glossodyniaor Burning Mouth SyndromeFDOPA PET scans done on 10 BMS and 14 healthy

control subjects

Jaaskelainen, S et al: Role of the dopaminergic system in chronic pain – a

fluorodopa-PET study; Pain 2001:257

Authors feels that this study is the first to elucidate in vivo

evidence of dopaminergic dysfunction in clinical pain

Suggest that there is existence of purely nociceptive projection

neurons from the substantia nigra to the striatum

This and previous studies suggest that the nigrostriatal pathway

is involved in the processing sensory gating of nociceptive

information

Glossodynia Effects of near-infrared irradiation to

stellate ganglion in glossodynia.

Oral Dis. 2004 Jul;10(4):217-20

Nakase M, Okumura K, Tamura T

Purpose: Assess the effect of stellate ganglion

near-infrared irradiation (SGR)

Glossodynia Thirty-seven patients

SGR once weekly for 4 weeks

Temperature and blood flow of the

tongue measured before and after first

SGR

Mean pain intensity decreased

significantly over 4 weeks of therapy

Glossodynia Tongue blood flow at rest in the patients with

glossodynia [7.2 +/- 1.6 ml min(-1) (100 g)(-1)] was significantly lower than that in the healthy subjects [7.8 +/- 0.23 ml min(-1) (100 g)(-1)]. Five minutes after SGR, the temperature of the tongue rose 1.5 +/- 0.21 degrees C, and blood flow increased to 8.5 +/-1.2 ml min(-1) (100 g)(-1). Tongue blood flow (at rest) after 4 weeks of SGR had increased to 7.7 +/- 1.1 ml min(-1) (100 g)(-1).

Glossodynia Implications: mechanism by which SGR

improves symptoms associated with

glossodynia: SGR inhibits abnormally

increased sympathetic activity associated with

glossodynia. This is followed by normalization

of decreased tongue blood flow, thereby

alleviating pain

Pain Genetics Some evidence that genetic variation may

account for migraine, menstrual pain, back pain, and fibromyalgia

Menopausal or post-menopausal women appear more prone to AFP, AO, and TMD

TMD is more prevalent during period of fertility, between puberty and menopause (LeResche, Pain 1997)

Pain Genetics In animal studies there is a reoccurring theme

of sex-specific genetic effects

Sensitivity to the supraspinal effects of

morphine

The direction of sex differences in thermal

nociception and morphine antinociception

are strain dependent in the animal model

Pain Genetics Estrogen appears to alter the receptive field properties

of primary afferents in the peripheral nervous system (Sato, 1990; Smith, et al 1998)

Estrogen appears to enlarge the peripheral receptive fields (Berieter, 1980)

In the CNS gonadal hormones influence endogenous opioid systems (Berglund et al 1988, Smith et al 1998)

Gonadal hormones influence the activity of neuromodulators including substance P (Duval et al 1996)

Incidence and treatment of dysgeusia

in patients with glossodynia

Acta Otolaryngol Suppl. 2002;(546):

142-5

Tanaka M, Kitago H, Ogawa S, et al

Research directed towards the

management of Glossodynia:

Glossodynia 96 patients

Gustatory tests, measured serum zinc and

copper levels, examined lingual papillae using

biomicroscopy, used psychological tests

Results:

Gustatory test results showed that 43 (44.8%) of

the patients had dysgeusia, which was mild in

62.8%, moderate in 30.2% and severe in 7.0%.

Glossodynia Priority was to treating the gustatory

abnormality

Gustatory sensation improved in 27 (62.8%) of

these 43 patients. Overall, pain disappeared or

was improved in 65 (67.7%) cases

Meaning (recent study suggests development

of glossodynia higher in „super-tasters‟ – 7th

nerve inhibition?

Remember that teeth

cause pain

Dental Pathology

Incompletely

fractured teeth

•32 patients with 46 teeth found to have

incomplete fractures

•Most fractures in heavily restored teeth

•Poorly localized facial pain: jaw, neck, ear,

muscles of mastication, TMJ

•Often projected to opposite arch

•Pain often anterior to affected tooth

•The longer the pain, the more diffuse the

presentation

Brynjulfsen A, et al:

Incompletely fractured teeth

associated with diffuse

longstanding orofacial pain:

diagnosis and treatment

outcome; Internat Endod J

35:461,2002

Atypical Odontalgia

Definition/Terminology –

Atypical Odontalgia

Historical terminology:

Atypical facial pain, Phantom tooth pain, Idiopathic

odontalgia, Vascular toothache, Migrainous neuralgia,

Neurovascular odontalgia, Neuropathic orofacial pain

IASP Taxonomy: Atypical odontalgia

Severe throbbing pain in the tooth without pathology

IHS Taxonomy: no definition (suggested by

Graff-Radford – Idiopathic toothache)

Epidemiology-AO

No specific epidemiologic research for this condition

In general, facial pain is widely reported Locker/Grushka; Toronto,1986; random sample

1014; 39.7%

Generally female over-representation for all types of idiopathic orofacial pain problems

Epidemiology-AO Predictive factors largely unstudied (e.g.

prehistory of pain, type of trauma, co-morbid pain problems, presence of infection, age, co-morbid depression, behavioral issues)

Imura, et al: Int Endod J 1995 looked at factors associated with post-treatment flare-ups: 1.58% of 1012 cases; two factors of potential implication – periradicular pain and patients taking analgesic or anti-inflammatory drugs

Studies - AO Epidemiology

Vickers, R et al (in Australia) report 25% of presenting patients referred to their pain center with AO (Vickers et al;

Analysis of 50 patients with atypical odontalgia; Oral Surg Oral Med Oral Pathol, Oral Radiol Endod, 1998:24)

Campbell et al (1990) and Marbach et al (1982)

Retrospective studies assessing patients with AFP post endodontic treatment (2.5-3.%)

Campbell: 118 non-surgical endo then surgery

79 with pain presurgery; 39 pain free

Post surgery 6 with continued pain (5%); 3 with ‟post-traumatic‟ dysesthesia; 3 with „phantom tooth pain

Most likely to occur between 40-51 years

Etiology - AO Typically attributed to dental treatment

Endodontic therapy

Tooth restoration (e.g. caries removal, crown preparation)

Periodontal scaling

Tooth extraction

Occlusal adjustment

Trauma Blunt/overt facial impact

Bruxism (?)

Underlying sinus hyper-reactivity(Emshoff et al: Idiopathic maxillary pain; OOO 87,1999: 685)

Mechanisms - AO Peripheral

Peripheral sensitization arising as a consequence of treatment

Deafferentation

Other: thrombophilia and hypofibrinolysis in focal areas of bone

Localized osteonecrosis / hole in bone

Thrombophilia (inacreased tendency to intravascular thrombosis)

Hypofibrinolysis (reduced ability to lyse thrombi)

Coupling of sympathetic and somatosensory pathways during healing

Mechanisms - AO Central

sensitization arising from persistent peripheral nociceptor barrage

Altered segmental inhibitory descending controls

Coupling of sympathetic and somatosensory pathways in the DRG

Dopaminergic Function (?)

Cortical area (S1, S2, Insula, ACC) activation

Jaaskelainen, S et al: Role of the

dopaminerigc system in chronic

pain – a fluorodopa-PET study;

Pain 2001:257

Symptoms Classical description is of dull, aching, persistent pain

like „toothache‟

Frequency of sensory words chosen on the McGill in the Vickers‟ study(of 40 subjects): throbbing (18), aching (15), tender (15), sharp (11), pulsing (10), shooting (10), stabbing (9), burning (9), gnawing (8)

Frequency of affective words: nagging (16), tiring (12), annoying (12), intense (10), sickening (9), exhausting (8), miserable (8)

Vickers et al; Analysis of 50 patients with atypical odontalgia; Oral Surg Oral Med Oral Pathol, Oral Radiol

Endod, 1998:24

Symptoms Pain may cross the midline

Pain may radiate superiorly (e.g. to maxillary region, eye, forehead, head vertex)

Pain of moderate to severe intensity

Occurs in single or multiple teeth

Premolars / molars; maxillary teeth > mandibular teeth

Migrates post intervention (RCT, tooth extraction, sinus surgery)

Other facial/head and non-head pain problems are likely to be present

Painful areas identified by „phantom‟ tooth

pain patients by Marbach (JADA, 127:221,

1996

1 - nasolaabial fold

2 – mental nerve

3 – maxillary sinus

4 – infraorbital nerve

5 – palpebral nerve

6 – supraorbital nerve

7 – temporalis muscle

8 – occipital nerve

9 – pterygoid muscle

Signs

Dental examination is typically negative or

findings are conflicting

Other diagnostic tests

Standard dental imaging

Functional brain imaging

SPECT bone scans

Thermography

Studies assessing possible confounding biobehavioral or psychological factors limited

Disability issues unknown

Coping factors unstudied Lennon et al: J Pers Soc Psychol 1990 report that

cases with facial pain secondary to TMD cope very differently than controls with pain and other stressful life events and have more changes in usual activities following negative events

Co-morbid depression

Psychosocial Issues

Therapy Typical intervention

If Dentist is first contact: Periodontal or Root canal treatment

Multiple antibiotic trials

Retreatment of root canal/additional RCTs

Surgical endodontics

Tooth extraction

Narcotics

Psychology

Therapy Typical intervention

If Physician is first contact: Multiple antibiotic trials

ENT evaluation (sinus CT) and sinus surgery

Neurosurgical evaluation (head CT or MRI)

Mutiple medication trials (anticonvulsants/other)

Ablative neurosurgical procedures

Psychology or psychiatry

Depression/disability Association with depression

1992 Graff-Radford reports 42% of AO with depression

Non-association with psychological

dysfunction Graff-Radford and Solberg, report that MMPI scores

for AO and HA within normal ranges and not

supportive of psychological dysfunction (1993, OOO,

75:579)

Activity limitation/disability Vickers, et al, report excess treatment seeking and 66% of

AO patients with concurrent stress (OOO 1998, 85:24)

Therapy - Pharmacy

Topical anesthetics (assuming a neuropathic etiology)

EMLA (eutectic mixture lidocaine and prilocaine) (1-4 applications x 5 minutes)

Lidocaine patch (minutes to hours)

Topical clonidine (.2% mg in cream base qid)

Topical capsaicin (0.025%) (pre-application of benzocaine 15% x 3 min, then Cap bid x 3 min)

Other: NSAID gels, anticonvulsants, tetracycline, TCA (no IO studies)

Therapy - Pharmacy

Anesthetic blocks Stellate ganglion block

Potentially useful for differentiating SMP from sympathetically

independent pain

Repeated injections can lead to prolonged pain relief

Sphenopalatine ganglion block

Lidocaine

30-40% aqueous cocaine

Sensory Abnormalities in

Patients With Chronic Pain

Moriwaki et al / Pain 81(1999): 1-6

Secondary trigeminal neuralgia after injury to the infraorbital nerve during sinus

surgery. VAS pain ratings are shown for first visit, 15 minutes after stellate

ganglion block with 1% mepivacaine (a-2); end of first course of tx with repeated

SGB and local infiltration of triamcinolone with local anesthetics for 3 weeks (a-3);

worsening of pain at 2 months (A-4) and end of a second series of tx (A-5)

Therapy - Pharmacy

Compounding pharmacy: (In pluronic lecithin organogel)

Lidocaine 4%

Carbamazapine 4%

Ketoprofen 5-10%

Doxipin 10%

Clonidine (if response to stellate block) .2-.4%

Katamine .5%

Capsaicin .025% (added later)

Therapy - Pharmacy

PO Medication

Few available studies

Drugs reported to be useful include:

Tricyclic antidepressants (25-100mg)

Feinman et al: Psychogenic pain, presentation and treatment;

Br Med J, 1984. Dothiepin (doxepin) 150mg with placebo– at

9 weeks 71% pain free; best result with drug for one year

Therapy - Pharmacy

Benzodiazepines such as clonazepam

(0.5-2.0mg). Concern regarding

depression (Reviewed by Dellemijin, Fields (Do

benzodiazepines have a role in chronic pain?) Pain 1994, 57:137)Dellemijin, Fields conclude:

• Little evidence to support action via reduced anxiety

• Only uncontrolled studies/case reports suggesting clonazepam helpful for TIC or

neuropathic pain. Studies mixed for various problems (no studies for

AO)

• No convincing evidence that demonstrate a significant deepening of

depression with benzodiazepams. Some controlled studies suggest no

such effect

• Risks associated with sleep problems, abuse, psychomotor and cognitive

disturbance, ½ life in elderly

Therapy - Pharmacy

Anticonvulsants

Carbamazepine

Tegretol, Lamotrigine

Gabapentine

Neurontin

Sodium valproate

Other: Baclofen, Klonopin, Pimozide, Phenytoin

Therapy - Pharmacy

Dosage

Therapeutic window for each individual

Carbamazepine:100 mg bid x 3 days with

increases at 100-200mg every three or four days

to 1200mg

Gabapentine (Neurontin): 100 mg or ½ tab x 3

days with slow increase to 2400mg

Baclofen: 5 mg (1/2 tab) tid for 3 days to 20mg

tid (40-80mg/day)

Therapy - Pharmacy

Other Medications

NMDA receptor antagonists (dextromethorphan)

Preemptive use of NMDA receptor antagonist may reduce postoperative analgesic requirements

May be limited use with respect to reducing neuropathic facial pain conditions (Gilron, et al: A

randomized, controlled trial of high-dose dextromethorphan in facial neuralgias; Neurology, 2000:964)

Randomized, double-blind, crtossover trial 6 weeks of oral dextromethorphan with active placebo (lorazepam)

N=19 in three groups: possible TIC, 5 anesthesia dolorosa, 3 idiopathic TIC

Dosage titrated to highest level without disruption of normal activities

Only 2-4% reduction in pain

Conclusion: drug shows little or no analgesic efficacy in pain with above conditions.

Therapy - PharmacyOther: polypharmacy

TCA and Clonazepam (divided doses)

TCA and gabapentine

TCA with phenothiazines (fluphenazine - 1-

2.5mg PO BID)

Topical and systemic approaches

Tramadol hydrochloride (Ultram) or opioid with

TCA

Combination of peripheral and central acting

medication

Neurovascular relationship at the

trigeminal root entry zone in persistent

idiopathic facial pain: findings from

MRI 3D visualisation.

J Neurol Neurosurg Psychiatry. 2005 Nov;76(11):1470-1

Lang E, Naraghi R, Tanrikulu L et al

TREZ was visualised by 3D CISS MRI in 12 patients with unilateral PIFP

TREZ contacts on the symptomatic and asymptomatic sides did not differ significantly

Symptomatic side, vessel-TREZ contact was found in 58% of patients (sensitivity)

ConclusionThe next slide summarizes all of the factors

that confound the presence of facial pain

and the differential diagnosis. The

knowledgeable clinician considers all of

these when evaluating facial pain and

establishing its diagnosis and management

Differential

Diagnosis of Non-

Dental Pain

Neurophysiology / Pain

mechanisms

Pathology:

local,

regional,

systemic

Psychological Confounders

Behavioral Issues

PeripheralCentral Sympathetic

Age and Gender Effects

Management

Atypical Presentation

The History

Stress

Depression

For more information about this subject see

the following Medical Texts:

• Burgess, J: Craniofacial Pain. In: Pain Surgery, Eds Kim

Burchiel, Thieme, New York, Chapter 20.

• Burchiel K, Burgess J. Facial and Cranial Pain. In:

Neurosurgical Management of Pain, Editors:

Richard B North and Robert M Levy, New York,

Chapter 7

• Orbach R, Burgess J: Temporomandibular Disorders

and Craniofacial Pain. In: Conn‟s Current

Therapy, 1st Edition R.E. Rankel, Section 14.