Pain

Pain is, an unpleasant sensory and emotional

experience associated with actual or potential tissue
damage. Acute pain resulting from injury will generally
initiate a reflex withdrawal thus ensuring minimal or
no tissue damage (nociceptive pain).
The physiologic aspect of pain involves pain receptors
stimulation, pain transmission, transduction,
modulation and central integration in higher thought
and emotional centers.
Terms
Allodynia: the injured region becomes sensitive to even light
touch it refers to central pain sensitization (increased
response of neurons) following normally non-painful, often
repetitive, stimulation. Allodynia can lead to the triggering of a
pain response from stimuli which do not normally provoke
pain.
Hyperalgesia: over reactive to painful stimuli An increased
response to a stimulus that is normally painful, at the site of
injury or inflammation. ... Primary hyperalgesia results from
the direct effects of injury to skin and nerve tissue, whereas
secondary hyperalgesia involves the increased pain sensitivity
of the surrounding tissue
 Nociceptive pain occurs in 5 phases
1) Transduction, 2) Conduction, 3)
Transmission, 4) Modulation, 5)
Perception. Transduction begins when
peripheral terminals of nociceptive C
fibers and A-delta (Aδ) fibers are
depolarized by noxious mechanical,
thermal, or chemical energy. The
spinal cord carries the pain message
from its receptors all the way up to
the brain, where it is received by the
thalamus and sent to the cerebral
cortex, the part of the brain that
processes the message.
Nociceptive pain occurs in 5 phases
Cellular damage and inflammation increase concentrations
of other chemical mediators such as histamine, bradykinin,
and prostaglandins in the area surrounding functional pain
units Endorphin and enkephalin are the body's natural
painkillers. ... Enkephalins block pain signals in the spinal
cord. Endorphins are thought to block pain principally at
the brain stem. Both are morphine-like substances whose
functions are similar to those of opium-based drugs
CLINICAL EVALUATION OF PAIN
Clinical evaluation of pain requires an understanding of
the patient's subjective perception of the discomfort. To
reach such an understanding the following aspects must
be studied
A- Onset of pain
B- Localization of the pain
C- Characters of pain
D- Course of pain
E- Factors that alter pain
F- Associated findings
Orofacial Pain
As a symptom, it may be due to disease of the orofacial
structures, generalized musculoskeletal, peripheral or central
nervous system disease, or psychological abnormality; or the
pain may be referred from other sources (e.g. cervical
muscles or intracranial pathology ) 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.
Anatomic consideration
• Cranial nerve V (CN V), the trigeminal nerve, is the
dominant nerve that relays sensory impulses from the
orofacial area to the central nervous system
• The facial (CN VII), glossopharyngeal (CNIX), and
vagus (CN X) nerves and the upper cervical nerves
(C2 and C3) also relay sensory information from the
face and surrounding area.
• By intense or noxious stimuli. Some are unimodal and
respond only to thermal or mechanical stimuli; others
are polymodal and respond to mechanical, thermal, and
chemical stimuli. Nociceptors encode the intensity,
duration, and quality of a noxious stimulus
Clinically COFP may be subdivided into
three main symptomatic classes
1- Musculoskeletal
2- neuropathic
3- Neurovascular
Musculoskeletal entities are dealt with Temporomandibular Disorders.
Possible causes of Facial Pain:
• Dental pain
• TMJ
• Neuropathic pain (neuralgias)
• Pathology in related str. (salivary gland , sinus ,eyes , cervical
spine,nasopharyns)
• Vascular disorder (headaches)
• Intracranial lesions (neoplasm, MS)
• Referred pain (angina pect.)
• Psychogenic facial pain.
Differential Diagnosis of Orofacial Pain
1- Intracranial pain disorders Neoplasm, aneurysm, abscess, hemorrhage, hematoma,
edema
2- Primary headache disorders (neurovascular disorders ) Migraine,
cluster headache, paroxysmal hemicrania, cranial arteritis.
3- Neurogenic pain disorders Paroxysmal neuralgias (trigeminal,glossopharyngeal,
nervus intermedius)Continuous pain disorders (neuritis, post herpetic neuralgia,
post-traumatic and postsurgical neuralgia)
4- Intraoral pain disorders Dental pulp, periodontium, mucogingival
tissues, tongue.
5- Temporomandibular disorders Masticatory muscle, temporomandibular joint,
associated structures
6- Associated structures Ears, eyes, nose, paranasal sinuses, throat, lymph nodes,
salivary.
If the cause is intra-cranial; more than one division may be involved. And
in advanced lesion there may be signs of elevation in the intra-cranial
pressure (I.C.P). If the cause is intra-cerebral; then there may be
neurological deficits to be demonstrated.
Classic signs of intracranial pressure include a headache and/or the
feeling of increased pressure when lying down and relieved pressure
when standing., vision changes, changes in behavior, and seizures can also
occur.
Clinical features of raised I.C.P
• Headache.
• Impairment of conscious level.
• Papilloedema
• Nausea, vomiting
• Raised arterial pressure
• Bradycardia
Brain swelling can be caused by a number of injuries
and conditions, including:
• traumatic injury to the head
• not having enough red blood cells or hemoglobin
(anemia)
• CSF buildup in the brain (hydrocephalus)
• brain bleeding (hemorrhage)
• brain inflammation (encephalitis)
• brain tissue inflammation (meningitis)
• high blood pressure (hypertension)
• collection of infected pus in the brain
(abscess)
• brain tumor
CHRONIC OROFACIAL PAIN
1- Musculoskeletal
2- Neuropathic Orofacial Pain.
3-Neurovascular Pain includes
Neuralgias
The classic neuralgias that affect the craniofacial region
are a unique group of neurological disorders involving
the cranial nerves and are characterized by
(a) Brief episodes of shooting
(b) Trigger zones on the skin or mucosa that precipitate
painful attacks when
touched
(c) Pain-free periods between attacks and refractory
periods immediately after an attack, during which a new
episode cannot be triggered
 Trigeminal Neuralgia
It is sever recurrent shooting pain, sharp,
stabbing or electrical lasting within seconds
or minutes and provoked by talking, eating
or touching specific areas called the
"trigger zone", is an excruciating, short-
lasting, unilateral facial pain. It is
characterized by sever paroxysmal pain in
one or more branches of trigeminal nerve.
Usually affecting the middle aged and
elderly and often women are more affected
than men. The most common sites involved
are the mandibular mental area and the
maxillary canine area. The ophthalmic
distribution of the trigeminal nerve is
rarely affected.
The most common forms:
1- Classical unrelated to pathology and most
probably caused by neurovascular compression of
the trigeminal nerve root.
2- 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
Types of attack
There are two attack-related phenomena that are particular
to TN.
Latency refers to the short period of time between
stimulation of a trigger area and pain onset.
A refractory period occurs following an attack and during
this time pain may not be initiated.
Attacks begin and end abruptly, lasting from a fraction of a
second up to 2 minutes. Longer attacks, increasing with
disease duration, have been reported.
Most paroxysms occur during waking hours, but may awaken
Pain paroxysms are usually accompanied by spasm of the
ipsilateral facial muscles (hence the name tic douloureux)the
patient.
Etiology:
The etiology of neuralgia is unclear and 10% of
cases have detectable
underlying pathology such as:
1- Tumors of the cerebellar pontine angle,
2- demyelinating plaque of multiple sclerosis
3- Vascular malformation.
The remainder of cases of TN is classified as
idiopathic.
 Pre trigeminal Neuralgia (PTN).
An early form of TN termed “pretrigeminal neuralgia”
(PTN) has been reported in 18% of TN patients
characterized by a dull continuous pain (days to years) in
one of the jaws. As PTN progresses it becomes more
typical with characteristic flashes of pain. Thermal stimuli
may cause triggering at a relatively higher rate, and a
throbbing quality to PTN pain is sometimes present
mimicking dental pathology. These qualities combined with
the success of regional anesthesia have led to misdiagnosis
of PTN as pain of dental origin PTN is however highly
responsive to carbamazepine, and careful dental
assessment should help differentiate it.
Diagnosis
The diagnosis of TN is usually based on the history
of shooting pain along a branch of the trigeminal
nerve, precipitated by touching a trigger zone, and
possibly examination that demonstrates the
shooting pain MRI of the brain is indicated to rule
out tumors, multiple sclerosis, and vascular
malformations.
 Treatment
1- Anticonvulsant; Carbamazepine (Tegretol) remains
the drug of choice for TN. Initial low-dose therapy (100
mg with food) and a slow increase (byl00-200 mg) on
alternate days will minimize side effects. In responsive
cases,
therapeutic effects are observed rapidly or within
three days. Titration to final dose (800-1200 mg/d)
should continue slowly based on response and side
effects
Main side effects:
a- Transient elevation in liver enzymes may occur b- Transient
leucopenia
c- Aplastic anemia is a serious effect that may occur.
d- Hyponatremia is observed in carbamazepine-treated cases and
requires drug withdrawal.
e- Skin rashes occur in patients and may signal the onset of
antiepileptic drug hypersensitivity syndrome. Patients receiving
carbamazepine must have periodic hematologic laboratory
evaluations because serious life threatening blood dyscrasias occur.
Monitoring of hepatic and renal function is also recommended.

Baclofen has a strong synergistic effect with carbamazepine ,

making it suitable for combined therapy.
2-Surgical
Peripheral Procedures
Peripheral neurectomy carries the danger of
inducing traumatic neuropathic pain and is not
recommended. Cryotherapy of peripheral branches
may give pain relief for six months. Pain recurrence
is at the original site, repeated cryotherapy often
produces better results.
Central Procedures:
Percutaneous Trigeminal Rhizotomy
Microvascular decompression of the nerve root at the brainstem
Gamma Knife
Historically, alcohol injections have been used but are painful and
cause fibrosis. Alcohol may induce herpes zoster (HZ)
reactivation and bony necrosis.
Pain control after alcohol block lasts just over one year, and
there have been reports of post injection neuropathic pain.
Peripheral glycerol injection has been employed, but success
seems short term.
Complications were as follows; dysesthesia ,hypertension, and
hypesthesia ,headache ,ocular dysesthesia, masseter weakness
hyperalgesia ,attack of paroxysmal pain.
 Glossopharyngeal neuralgia (GN)
The location of the trigger zone and pain sensation
follows the distribution of the glossopharyngeal nerve,
namely, the pharynx, posterior tongue, ear, and
retromandibular area.
Pain is triggered by stimulating the pharyngeal mucosa
during chewing, talking, and swallowing The application
of topical anesthetic to the pharyngeal mucosa
eliminates glossopharyngeal nerve pain and can aid in
distinguishing it from the pain of other neuralgias
Features:
The glossopharyngeal (IX) nerve has two main sensory branches:
the auricular (tympanic) and the pharyngeal.
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. GN is a
paroxysmal, unilateral, severe pain that is sharp, stabbing, shooting,
or lancinating . Patients often feel a scratching or foreign body
sensation in the throat.
 Pathologies Mimicking GN
1- A significant association between symptomatic GN and multiple
sclerosis has been reported
2- Regional diseases such as infectious or inflammatory processes
3- tonsillar carcinoma
4- Other regional tumors (tongue, oropharyngeal)
5- Cerebellopontine angle or pontine lesion

Treatment
Carbamazepine is usually successful and is the favored medication.
Alternatives include baclofen (muscle relaxant), gabapentin and
phenytoin. Permanent neurological deficits are rare and may include
mild hoarseness and/or dysphagia, or facial nerve paresis
Facial Pain Associated With Herpes Zoster
Post herpetic neuralgia: Acute Herpes Zoster
(shingles) is a reactivation of latent varicella virus
infection that may occur decades after the primary
infection. HZ is a disease of the dorsal root ganglion
and therefore induces a dermatomal vesicular eruption.
Definitive diagnosis may be obtained by identification of
viral DNA from vesicular fluid employing the
polymerase chain reaction. he ophthalmic branch is
affected in more than 80% of the trigeminal cases,
particularly in elderly males, and may cause sight-
threatening keratitis.
Clinical Features
Usually begins with a prodrome of regional pain,
itching and malaise.
Pain precedes typical vesicular eruption by <7
days, usually 2-3 days. The dermatomal vesicular
or herpetic eruption will rupture and “dry out”
over 7-10 days, but complete healing may last
up to one month. Accompanying pain is
moderate to severe and may persist for three
to six months.Very rarely dermatomal pain
occurs with no rash.
Treatment of shingles

Therapy is directed at controlling pain, accelerating healing,

and reducing the risk of complications such as meningitis,
post herpetic neuropathy (PHN), and local secondary
infection. Antiviral should be initiated within 72 hours from
onset of rash, and will significantly decrease rash duration,
pain severity, and the incidence of PHN. This is particularly
effective in patients >50 years old. Use of glucocorticoids is
controversial, but may help reduce acute pain; they should
always be used together with antivirals.Vaccinating at risk
individuals markedly reduces the incidence of PHN among
older adults.
PHN
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 year), severe prodromal
pain, 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.
Treatment
Early treatment of established PHN improves prognosis.
Prevention Use of antiviral famciclovir 500 mg 3 times daily
for 7-10 days. Short course of systemic corticosteroid during
the active phase of the disease. Topical therapy includes the
use of topical anesthetic agents, such as lidocaine, or
analgesics.

Ophthalmic PHN seems to have the worst prognosis.

Evidence-based treatment options for PHN include tricyclic
antidepressant (TCA) drugs and gabapentin
Invasive therapies include epidural and intrathecal steroids
and a variety of neurosurgical techniques.
Burning Mouth Syndrome (BMS)
Is a poorly understood pain condition that is most probably
neuropathic. The condition is also known as stomatodynia
and is characterized by a burning mucosal pain with no
significant physical signs and is common in postmenopausal
women. BMS may be sub classified 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. BMS is characterized by resistance to
a wide range of treatments and is one of the most challenging
management problems in the field of OFP.
Clinical Features
The primary location of the burning complaint is the
tongue, usually the anterior 2/3. However, usually more
than one site is involved and in addition to the tongue,
hard palate, lips, and gingiva are frequently involved. Pain
is most commonly described as burning or hot and
intensity varies from mild to severe. BMS is typically of
spontaneous onset and lasts from months to several
years. Pain pattern may be irregular, but some patients
may complain that pain increases toward the end of the
day.
Common aggravating factors include personal
stressors, fatigue, and specific foods (acidic, hot, or
spicy). More than two-thirds of the patients
complain of altered taste sensation (dysgeusia)
accompanying the burning sensation, in many cases
described as a spontaneous metallic taste. Abnormal
sensations, such as feeling of dry mouth, are
common but true hyposalivation is less common
and should be considered under secondary or
symptomatic BMS.
Oral and perioral burning sensation as a result of
local or systemic factors or diseases is classified as
SBMS.
1- Local factors and diseases known to induce SBMS
include oral candidiasis , lichen planus, and allergies.
2- Systemic disorders that induce SBMS include
hormonal changes, deficiencies of vitamin B12, folic
acid or iron, diabetes mellitus, side effects of
medications, and autoimmune diseases. Successful
treatment of the primary disease will usually alleviate
the burning sensation in SBMS patients.
Treatment

Topical therapies may be effective and are useful in elderly,

medically compromised patients. The most established is
clonazepam(1 mg) which should be sucked and subsequently spat
out three times daily. Topical anesthetics may decrease or
increase pain and are therefore unpredictable.
Systemic therapies include paroxetine (antidepressant) (20 mg/d)
These may reduce pain and improve anxiety and depression.
A two-month course of 600 mg daily of alpha-lipoic acid may be
beneficial. A combination of alpha-lipoic acid (600 mg/d) and
gabapentin (300 mg/d) results in greater improvement of the
burning symptoms compared to these medications taken alone.
Painful Posttraumatic Trigeminal
Neuropathy (PTTN)
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. Following dental implant surgery l%- 8% and
following orthognathic jaw surgery 5%-30% of patients may
remain with permanent sensory dysfunction but the
incidence of chronic pain is unclear.Third molar extractions
may lead to disturbed sensation in the lingual or inferior
alveolar nerve for varying periods. Patient complaints of
tongue dysesthesia after injury may remain in a small group of
patients (0.5%). Persistent pain after successful root canal
therapy may occur; also surgical root therapy may resulted in
chronic neuropathic pain.
Treatment
Topical anesthetics may be successfully employed in the management
of painful neuropathies.
Systemic Pharmacotherapy Available data confirm that ant epilepsy.
Drugs AEDs and tricyclic antidep.TCAs are most effective. For many
of the drugs used in the therapy of traumatic neuropathies, response
is dose dependent and subsequently accompanied by significant side
effects Therapy of neuropathic pain with any one of the established
drug groups ,like Antidepressant, anticonvulsants medications leads to
improved quality of life, sleep, and mood.
Neurovascular Pain
Cluster Headache is a distinct pain syndrome characterized
by episodes of severe unilateral head pain occurring chiefly
around the eye and accompanied by a number of autonomic
signs (AS), with severe pain and major autonomic activation.
The precise genetics of CH are unclear but is likely to involve
an autosomal dominant gene with low penetrance. CH
typically appears between the ages of 20-29 years, is more
common than previously thought, and seems to affect men
more than women.
Episodic CH: commonly occurs at least once daily for a
period of weeks, at the same time of day or night. Active
periods (or “clusters” of 6-12 weeks) are followed by a
temporary remission that may last from weeks to years.
Features

Pain in CH is usually periorbital or ocular but varies. In

“upper CH” the forehead, temporal, and parietal regions
are involved, whereas in “lower CH” the temporal and
suboccipital regions are affected with radiation to the
teeth, jaws, neck, and cheeks. Pain is unilateral and in 20%
of cases may change sides. Severity is excruciating and
rated as 8-10 on a visual analog scale. Quality is
nonspecific and is variably described as throbbing or
boring, burning, stabbing
CH attacks last 15-180 minutes reaching peak intensity
very rapidly—within 3 minutes (up to 9-10 minutes).
Longer attacks lasting from 3 to 48 hours are rare and
frequency is one every other day to 8/d. Pain is most
usually accompanied by at least one ipsilateral autonomic
sign (AS); conjunctival injection/lacrimation, nasal
congestion/rhinorrhea, eyelid edema, forehead/facial
sweating, miosis, and ptosis. The vast majority (>80%) of
patients are markedly restless during an attack. Patients
appear agitated; continually move around, particularly
during more severe attacks; in sharp contrast to the quiet-
seeking behavior observed in migraine
The cause of cluster headache is unknown Cluster
headaches were historically prsent as dilation of
blood vessels which in turn, was thought to create
pressure on the trigeminal nerve. 1. Genetics Cluster
headache may, but rarely, run in some families in an
autosomal dominant inheritance pattern.
2.Tobacco smoking
3.Hypothalamus A review suggests that the
suprachiasmatic nucleus of the hypothalamus, which is
the major biological clock in the human body
Differential Diagnosis and Secondary CH
CH is often misdiagnosed as dental or maxillary sinus pathology
CH Treatment
patients should avoid daytime naps, alcoholic
beverages, and other triggers.
Pharmacologic Treatment may be abortive, transitional, or preventative
or prophylaxis.
1- Abortive symptomatic relief may be rapidly attained with oxygen
inhalation.
2-Subcutaneous sumatriptan (neuro active alkaloids) Rapid transitional
therapy.
3- Prophylactic or preventive (In both episodic and chronic CH.)is
usually with verapamil ( calcium channel blockers )
 Migraine
Migraine is the most common headaches, which may occasionally also
cause pain of the face and jaws. It may be triggered by foods such as
nuts, chocolate, and red wine; stress; sleep deprivation; or hunger.
Migraine is more common in women. The migraine headache is
frequently accompanied by nausea, vomiting, photophobia, phonophobia
and osmophobia. It may be preceded by an aura of neurological
dysfunction, such as visual disturbances, vertigo, numbness, or weakness.
In many patients, migraine is triggered by specific factors, such as
menses, weather changes, irregular sleep, alcohol, or certain foods.
Migraine is also often relieved by sleep. The life time prevalence of
migraine is estimated to be near 35%, and it affects greater than 17% of
women and 6% of men.
Etiology and Pathogenesis
1 - There appears to be a genetic and familial risk as more than half
of all migraineurs report having other family members who suffer
from migraine. The concordance for migraine in monozygotic twins
is greater than that for dizygotic twins.

2- Vascular Theory
The aura of migraine was once thought to be caused by cerebral
vasoconstriction and the headache by reactive vasodilation, which
explained the throbbing quality of migraine and the relief of pain
by ergots.
3- Neuronal Theory
Migraine aura is believed to result from a slow-moving, spreading
depression of cortical activity that liberates potassium and is
preceded by a wave front of increased metabolic activity, suggesting
that dysregulation of normal neuronal function is a cause of
migrainous attacks. Migraine probably results from pathologic
activation of meningeal vessel nociceptors combined with a change
in central pain modulation.
4- Role of Serotonin and Dopamine
Pharmacologic data point to a strong role of the neurotransmitter
serotonin in migraine, the “triptan” class of drugs has renewed interest
in the role of 5- hydroxytryptamine (5-HT) in migraine .
Biologic, genetic, and pharmacologic evidence includes the following: (1)
most migraine symptoms can be induced by dopamine, (2) there is
dopamine receptor hypersensitivity in migraineurs, and (3) dopamine
receptor antagonists are effective agents in treating migraine.
The clinical features of migraine are separated into two types of
headache:
1- Migraine without aura (common migraine)
2- Migraine with aura (classic migraine).
Classic migraine starts with a prodromal aura that is usually visual but
that may also be sensory or motor.
The aura is followed by an increasingly severe unilateral throbbing
headache that is frequently accompanied by nausea and vomiting. The
patient characteristically lies down in a dark room and tries to fall
asleep. Headaches characteristically last for hours up to 2 or 3 days.
Common migraine Is not preceded by an aura,
but patients may experience irritability or other
mood changes. The pain of common migraine
resembles the pain of classic migraine and is
usually unilateral, pounding, and associated with
sensitivity to light and noise. Nausea and
vomiting are also common.
Treatment
Generally, migraine management is divided into three specific components:
(1) Prophylactic or preventative therapy
(2) Abortive therapy
(3) Palliative or rescue therapy.
Patients experiencing more than three migraines per month are candidates for
prophylactic therapy. Patients with migraine should be carefully assessed to determine
common food triggers. Attempts to minimize reactions to the stress of everyday living
by using relaxation techniques may also be helpful to some patients. Drugs that are
useful in aborting migraine include ergotamine and sumatriptan, which can be given
orally, nasally, rectally or parenterally. Ergotamine Initial dose: Oral, Sublingual: 2 mg
ergotamine in fixed combination with caffeine given as quickly as possible after the
first symptom of headache. Additional 1 mg doses can be given every 30 minutes until
the headache has been aborted or until a total dose of 6 mg has been reached or 10
mg/week.
Atypical Facial Pain (AFP)
Is a persistent facial pain that does not follow any anatomical
pattern, and not responding to any treatment, The major
manifestation of AFP is a constant dull aching pain without an
apparent cause that can be detected by examination or
laboratory studies. It occurs most frequently in women in the
fourth and fifth decades of life, and most studies report that
women make up more than 80% of the patients. Symptoms
may remain unilateral, cross the midline in some cases, or
involve both the maxilla and mandible.The pain is described
as a constant dull ache, instead of the brief and severe attacks
of pain that are characteristic of TN. There are no trigger
zones, and lancinating pains are rare.
MANAGEMENT
Patients should be reassured that they do not have an undetected
life threatening disease and that they can be helped without
invasive procedures. When indicated, consultation with other
specialists such as otolaryngologists, neurologists, or psychiatrists
may be helpful. TCAs such as amitriptyline given in low to
moderate doses, are often effective in reducing or (in some cases)
eliminating the pain. Other recommended drugs include
gabapentin and clonazepam. Some clinicians report benefit from
topical desensitization with capsaicin, topical anesthetics, or
topical doxepin.
Vascular Pain

CRANIAL ARTERITIS
(temporal arteritis, giant cell arteritis) is an
inflammatory Orofacial Pain disorder involving the
medium-sized branches of the carotid arteries. The
temporal artery is the most commonly involved
branch.
Etiology and Pathogenesis caused by immune
abnormalities that affect cytokines and T -lymphocytes,
resulting in inflammatory infiltrates in the walls of
arteries. This infiltrate is characterized by the formation
of multinucleated giant cells. The underlying trigger of
the inflammatory response is unknown.
Clinical Manifestations

Cranial arteritis most frequently affects adults above the age of 50

years. Patients have a throbbing headache accompanied by
generalized symptoms including fever, malaise, and loss of appetite.
Dull temporal pain, fatigue of the masticatory muscles, joint pain,
and headache of recent onset that is chronic and possibly
progressive. Moderate-to-severe headache, polymyalgia, and
claudication of the masticatory muscles may be present. There may
be a swollen and tender scalp artery, usually the superficial
temporal artery, pain radiate to face, neck, maxilla and mandible.
Blindness may develop in 50% of patients. Examination of the
involved temporal artery reveals a thickened vessel with burning
sensation over the artery
Treatment Individuals with cranial arteritis should be
treated with systemic corticosteroids as soon as the
diagnosis is made. The initial dose ranges between 40 to
60 mg of prednisone per day, and the steroid is tapered
once the signs of the disease are controlled. The ESR
may be used to help monitor disease status. Patients are
maintained.
Treatment
Individuals with cranial arteritis should be treated with
systemic corticosteroids as soon as the diagnosis is made.
The initial dose ranges between 40 to 60 mg of
prednisone per day, and the steroid is tapered once the
signs of the disease are controlled.
Patients are maintained on systemic steroids for 1 to 2
years after symptoms resolve. Steroids may be
supplemented by adjuvant therapy with
immunosuppressive drugs, such as cyclophosphamide, to
reduce the complications of long-term corticosteroid
therapy.
Cardiac Toothache (referred pain)
Angina pectoris or acute myocardial infarction, refer
pain to the shoulder, arm, the jaw and to the teeth.
Associated with chest pain (substernal),Tooth ache
increases with exercises and decreased with medication
specific for the heart (nitroglycerin).Treatment is
directed to the underlying heart problem, after dental
evaluation.When pain occurs after exertion, cardiogenic
etiology should be suspected. If patients are
experiencing a cardiogenic toothache give them an
aspirin, and make sure they get to a hospital emergency
room immediately.
Sinusitis and orofacial pain
Acute sinusitis, is a short-term infection or inflammation of the
membranes that line sinuses. It prevents mucus from draining from
nose. Symptoms of acute sinusitis include:
• nasal congestion
• thick, yellow, or green mucus discharge from the nose
• sore throat
• a cough (usually worse at night)
• drainage of mucus in the back throat (post nasal drip)
• headache
• pain, pressure, or tenderness behind eyes, nose, cheeks, or
forehead
• earache
• toothache
• bad breath reduced sense of smell reduced sense of taste and
fever