Craniofacial Pain

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Transcript Craniofacial Pain

Chronic Craniofacial Pain
D
• An unpleasant sensory and
emotional experience associated
with actual or potential tissue
damage , or described in terms
of such damage
Pain is always subjective
What do we associate to?
Dental and Periodontal Pathology
Burning mouth syndrome
Atypical facial pain (phantom tooth pain)
Temporomandibular joint disorders
What may we visit?
Headache Syndromes
Otologic Problems
Ocular and Periocular Disorders
Facial nueralgias
What’s The Point?
Successful treatment
depends on making the
correct diagnosis
Despite all the
advancements in
medicine, it is not
possible to cure all
pain problems
History
 Hx of present illness
 Past medical hx
 Family hx
 Social hx
Physical examination
Careful detailed pain history
Location
Duration
Temporal characteristics
Quality
Severity
Circumstances of onset
Influencing factors
Neurological symptoms
Response to medications
Orofacial pain (OFP) is prevalent in the general population;
around 23%, of which 7%–11% is chronic.
Acute OR chronic
Acute OFP is primarily associated with the teeth and their
supporting structures. Most frequently, dental pain is due to dental
caries, although a broken filling or tooth-abrasion may also cause
dental sensitivity. Other oral pains are usually periodontal or
gingival in origin.
Chronic orofacial pain (COFP) is a term used to describe
painful regional syndromes with a chronic, unremitting
pattern.
Clinically COFP may be subdivided into three main
symptomatic classes:
1. Neuropathic
2. Neurovascular
3. Musculoskeletal
Neuropathic OFP includes a number of clinical Entities
the most common are:
1.
TN
2. Painful Posttraumatic Neuropathies
3. Burning Mouth Syndrome (BMS)
More rarely
1. Facial Postherpetic Neuropathy
2. Central Poststroke Pain
3. Glossopharyngeal Neuralgia (GN)
TN is an excruciating, short-lasting, unilateral facial pain.
The most common is the classical unrelated to pathology and
most probably caused by neurovascular compression of the
trigeminal nerve root.
In the new classification, secondary forms have been classified
separately, and these are related to a variety of clear pathologies
including tumors, cysts, viral infection, trauma, and systemic diseases
such as multiple sclerosis.
CLINICAL FEATURES
Location
Quality and intensity: paroxysmal, shooting, sharp, piercing, stabbing,
or electrical.
Pain paroxysms are usually accompanied by spasm of the
ipsilateral facial muscles (hence the name tic douloureux).
 Typically pain is precipitated by light, innocuous touch at
sites called “trigger areas.”
 Trigger factors such as: noise, lights, and stress may also
induce pain.
 There are two attack-related phenomena that are particular
to TN:
Latency
Refractory Period
The glossopharyngeal (IX) nerve has two main sensory branches:
1.
The Pharyngeal
2.
The Auricular (Tympanic)
In pharyngeal-GN, the pharynx or posterior tongue-base are
involved. Pain radiates to the inner ear or the angle of the
mandible, and may include the eye, nose, maxilla, or shoulder
and even the tip of the tongue.
In tympanic-GN, pain predominates in the ear but may radiate to the pharynx.
Bilateral pain occurs in up to a quarter of patients.
 Rare; occurs about 1 in 170,000; average age 50.
 Abrupt onset, painful attacks last 30-60 seconds.
 Talking, chewing, swallowing, yawning, touching the tonsil may
precipitate pain (trigger)
 May mimic TMD.
 Subject to remission and recurrences.
 Topical anesthetic tonsil/pharynx of affected side gives relief up to 90 min.
• Up to one-fifth of acute HZ patients will suffer persistent
pain three to six months after acute HZ. By one year however
only 5%–10% suffer pain.
• Advanced age (>50), severe prodromal pain (VAS>5), severe acute
pain, and severe rash are risk factors for persistent pain.
• In patients older than 60 years, 50% or more will continue to suffer
pain for more than one year.
 F > M, 4-7:1; rare before age 30; 14% of post-menopausal
women, 3-12 years after menopause.
BMS may be subclassified into:
1. “primary” or idiopathic BMS for which a
neuropathological cause is likely and cannot be attributed
to any systemic or local cause
2. “secondary BMS” (SBMS) resulting from local or systemic
pathological conditions.
 Spontaneous onset; burning of anterior third of dorsum
of tongue; mild on awakening increasing during the day;
altered or diminished taste; intensified by hot foods or
liquids.
 Pain is most commonly described as burning or hot and
intensity varies from mild to severe.
 Common aggravating factors include personal stressors,
fatigue, and specific foods (acidic, hot, or spicy).
 Anxiety, depression or irritability are common.
Oral and perioral burning sensation as a result of local or
systemic factors or diseases is classified as SBMS.
•
Local factors and diseases known to induce SBMS include:
oral candidiasis, lichen planus, and allergies.
• Systemic disorders that induce SBMS include
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hormonal changes,
deficiencies of vitamin B12, folic acid or iron,
diabetes mellitus,
Side effects of medications,
autoimmune diseases.
Some patients develop chronic pain following negligible nerve
trauma such as root canal therapy or following considerable
injury to nerve bundles, such as in fractures of the facial
skeleton.
 Also known as sphenopalatine neuralgia or Horton’s
syndrome.
 Pain in mid and upper face around eye.
 Attacks occur in clusters with extended periods of
remission.
 Associated with sleep apnea; 80% are smokers; alcohol,
cocaine or nitroglycerine may initiate attack.
 Prevalence is 1 in 10,0000; 6:1 male; most age 20-30; B > W;
familial (50-fold increase).
•
Pain unilateral follows
distribution of ophthalmic
division of trigeminal nerve;
may cause jaw or tooth pain.
•
Paroxysmal burning or
lancinating pain lasting 15min
to 3 hrs occurring up to 8
times/day for weeks; onset
often in middle of night @
same time (alarm clock
headache).
•
Nasal stuffiness, tearing, facial
flushing and conjuctival
redness.
CONDITIONS ASSOCIATED WITH CLUSTER
HEADACHE (HORNER’S SYNDROME)
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PICA syndrome (posterior inferior cerebellar artery occlusion)
Trauma - base of neck, usually blunt trauma.
Stroke
Middle ear infection
Aortic aneurysm, thoracic
Neurofibromatosis type 1
Goiter
Dissecting aortic aneurysm
Thyroid carcinoma
Bronchogenic carcinoma
Multiple sclerosis
Carotid artery dissection
Cavernous sinus thrombosis
Sympathectomy
Syringomyelia
Nerve blocks
 Common disabling paroxysmal
unilateral headache.
 Thought to be caused by
vasoconstriction or vasospasm
of cerebral artery, possible due
to reduced serotonin, leads to
nitric oxide mediated
vasodilation, with pain and
edema.
 First onset in teenagers and
young adults estimated at 21%
life-time risk.
 Females 3:1; ages 20-40.
 With aura or without; throbbing pain in temporal frontal or
orbital region starts mild becoming severe 30+ minutes.
 Can include nausea, vomiting, diarrhea photophobia,
phonophobia; can mimic toothache, sinusitis and allergic rhinitis.
 Wide variety of drugs are useful including ergotamine, caffeine,
aspirin, phenobarbital, belladonna, methergine, propranolol,
nefedipine, methysergide.
 Most common headache syndrome
 Episodic < 15 days per month
 Chronic > 15 days per month
 30 minutes to 7 days
 Pressing or tightening
 Mild to moderate pain
 Variable location, often bilateral
 Nausea and vomiting rare
TTH - TREATMENT
Stress management
 Biofeedback
CTTH
 Abortive
 Stress reduction
 NSAIDs
 Posture correction
 ASA-caffeine-butalbital
Medication rarely needed in
ETTH
 Phenacetin
 Preventative
 Benzodiazepines
 Antidepressants
 amitriptyline
 Muscle relaxants
 NSAIDs
 Multifocal vasculitis of cranial arteries, especially the temporal arteries.
 Possible autoimmunity to elastic lamina.
 Prevalence estimated at 6 in 100,000.
 W > B; older than 50, average age 70.
 Unilateral throbbing headache gradually replaced by burning temporal &
facial pain. Throbbing coincides with heartbeat.
 Pain during chewing or pressure on temple; can mimic toothache, jaw or
tongue pain.
 Vision loss; transient or permanent (50%).
 Treatment with systemic or local steroids.
 Atypical facial neuralgia is a persistent pain in the
maxillofacial region that does not fit the diagnostic
criteria of other causes of orofacial pain (diagnosis
by exclusion).
 “Traveling patient”; sometimes labeled as neurotic,
obsessive-compulsive, anxiety-depressive or a
hypochondriac.
 F > M; age 30-60.
 Present most often with continuous or deep gnawing ache,
intense burning, pressure or sharp pain on small area of
face, single alveolus or quadrant, temple, neck or occipital
area.
 Drug management includes tricyclic anti-depressants,
serotonin reuptake inhibitors & anticonvulsants (such as
gabapentin).
 Other treatments include psychotherapy, behavior
modification, transcutaneous electrical nerve stimulation
(TENS), nerve block and nerve obliteration.
TRATMENTS
 Rule out surgical lesions (tumor, etc.)
 Neuropathic vs. nociceptive?
 Develop a strategy
o Lay out a plan
 Conservative initial dosing to avoid side effects
 Monotherapy is preferable if possible
o Escalate dose to effect or toxicity
 If second drug needed, choose agent in different class
o Na+ channel blcoker, GABA agonist, etc.
PHARMACOLOGICAL THERAPY
 Non-opioid analgesic
 Opiates
 Anti-epileptics drugs (AEDs)
 Antidepressant medications
 Neuroleptics
 Antispasmodics
 Miscellaneous drugs
 Botox