Chapter 42 Orofacial Pain Flashcards
KEY POINTS 1. Diagnosis guides management; an algorithmic approach is necessary to treat patients with headache and facial pain. Accurate diagnosis requires knowledge of the ICHD-2 criteria, and stepwise elimination of primary and secondary headaches. 2. Red flags in the history and physical examination require further investigation. 3. Treatment centers on preventive and abortive strategies. The appropriate timing for interventional treatment needs to be measured against the severity of th
The ICHD-2 criteria provide a systematic classification for headache and orofacial pain and are divided into three
parts:
the primary headaches, the secondary headaches,
and cranial neuralgias central and primary facial pain
before considering the
diagnoses that are commonly attributed to orofacial pain
it is relevant to provide a brief comment on eliciting the
key components of the history and physical examination in
the evaluation of headache and orofacial pain. It is important to take a stepwise, systematic approach to the patients pain.
An appropriate physical examination includes
a thorough neurologic assessment (including gait, pronator drift, Romberg’s sign, and reflex testing, that is, Hoffman and Babinski signs), heart and carotid auscultation, fundoscopic examination, cervical range of motion (ROM including atlantoaxial and atlantoocciptial joint), a musculoskeletal evaluation with careful detail to myofascial tenderness and trigger points, maneuvers that provoke radicular signs (Spurling’s test), cervical facet examination, and Waddell’s signs of nonorganic pain (tenderness to palpation, stimulation, distraction, regional disturbance in function, and overreaction).
The Primary Headaches
- Migraine
- Tension-type headache
- Cluster headache and other trigeminal autonomic cephalalgias
- Other primary headaches
The Secondary Headaches
- Headache attributed to head and/or neck trauma
- Headache attributed to cranial or cervical vascular disorder
- Headache attributed to nonvascular intracranial disorder
- Headache attributed to a substance or its withdrawal
- Headache attributed to infection
- Headache attributed to disorder of homoeostasis
- Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth, or other facial or cranial structures
- Headache attributed to psychiatric disorder
Cranial Neuralgias Central and Primary Facial Pain and Other Headaches
- Cranial neuralgias and central causes of facial pain
14. Other headache, cranial neuralgia, central or primary facial pain
Headache with “Red Flag” Symptoms and Signs That Require Further Work-up
Sudden onset of headache (thunderclap headache)
Fever, rash, and/or stiff neck (meningismus) associated with the headache
Papilledema (optic nerve head swelling)
Dizziness, unsteadiness, dysarthria, weakness, or changes in sensation (numbness or tingling) especially if profound, static, and occurring
for the first time
Headache with “Red Flag” Symptoms and Signs That Require Further Work-up
Migraine auras or other previously experienced neurologic migraine accompaniments lasting longer than 1 hr
Presence of confusion, drowsiness, or loss of consciousness
Headache is triggered by exertion, coughing, bending, or sexual activity
Headache is progressively worsening and/or resistant to treatment
Previously experienced headache characteristics or accompaniments have substantially changed
Persistent or severe vomiting accompanies the headache
Headache with “Red Flag” Symptoms and Signs That Require Further Work-up
Headaches beginning after age of 50 are associated with a higher risk of arteritis or intracranial tumors. Inquire about unexplained weight loss,
sweats, fevers, myalgia, arthralgia, and jaw claudication, which are typical accompaniments of giant cell (temporal) arteritis
Headache occurring in a patient with human immunodeficiency virus or cancer
Frequent emergency department or acute care use
Daily or near-daily use of pain relievers or the need to take more than the recommended dosage of pain relievers to control headache symptoms
Indications for Neuroimaging in Headaches- Urgent
Thunderclap headache with neurologic deficit Headache with altered mental status or seizure Prior intervention (if reduced intracranial compliance focal defects suspected, meningismus)
Indications for Neuroimaging in Headaches- Routine
Thunderclap headache without focal neurologic deficit
Change in headache characteristics (severity, side shift, worsening)
Headache accompanied by neurologic deficit or abnormality (disequilibrium, pronator drift, weakness, papilledema)
Headache in immunocompromised patients, cancer patients
The trigeminal system provides
the relay system for pain
and touch sensation to the face, as well as motor function
to the muscles of mastication. The trigeminal system is a
bilateral structure that spans from the midbrain to the
medulla and is composed of four nuclei: the mesencephalic
nucleus, the main sensory nucleus, a spinal nucleus of V,
and the motor nucleus.
The caudal portion of the trigeminal system nucleus is referred to as the spinal nucleus of V and is composed of three regions
in cephalad to caudal
order, the subnucleus oralis, the subnucleus interplaris,
and the subnucleus caudalis.
The subnucleus caudalis
very similar in structure and function to the dorsal horn and extends down to the second or third cervical level.
In the trigeminal system the primary afferent synapses
ipsilaterally in the nucleus caudalis and then the second-order neuron crosses
to join the contralateral spinothalamic tract.
The trigeminal pathway is termed the
ventral trigeminothalamic
tract and terminates in the ventral posteromedial (VPM)
nucleus of the thalamus.
Activation of nuclei in close proximity to the trigeminocervical complex may explain
the associated aura and symptoms attributed to different headache disorders by either activation of wide dynamic neurons, ephaptic transmission, or by sheer close proximity to the complex (solitary nucleus, nucleus ambiguous, or dorsal nucleus of vagus nerve).
HEADACHE ATTRIBUTED TO
DISORDER OF CRANIAL BONE
The diagnostic criteria include
pain in one or more
regions in the head and face with clinical, laboratory, or imaging evidence of a lesion within the cranial bone
known to be valid evidence of generating headache
HEADACHE ATTRIBUTED TO
DISORDER OF CRANIAL BONE
The source of the pain must be
in close temporal association to and is maximal over the bone lesion, and
with resolution of the pain after successful treatment of the bone lesion.
HEADACHE ATTRIBUTED TO
DISORDER OF NECK
These constellations of disorders involve
pain referral from neck structures to the head/and or face.
Cervicogenic headache
pain attributed to a disorder or
lesion within the cervical spine or soft tissues that is generally accepted to cause headache or facial pain.
Retropharyngeal tendonitis (also called longus colli tendonitis
described as either unilateral or bilateral nonpulsatile
pain in the posterior neck radiating to the occiput
or entire head accompanied by swollen prevertebral soft
tissue measuring more than 7 mm in adults anterior to
the upper cervical vertebral bodies.
Retropharyngeal tendonitispain is exacerbated by
neck extension, and less commonly with neck
rotation and swallowing. The transverse process of the
upper three vertebral bodies is tender to palpation.
Retropharyngeal tendonitis treatment
pain is alleviated within 2 weeks of treatment with antiinflammatory medications.
In Retropharyngeal tendonitis Imaging studies are needed to
rule out carotid dissection and in some cases CT aspiration
of amorphous calcific material from the swollen periverterbal tissues
Acute retropharyngeal presents as a triad of tendinitis
neck pain, odynophagia, and fever.
Acute retropharyngeal tendinitis treatment is
usually conservative and includes NSAIDS or a short
course of corticosteroids and it is self-limited in most
cases.
Craniocervical dystonia (CCD) is characterized by
crampy or “tension-type pain” in the posterior neck radiating to the occiput or entire head accompanied by defective posture of the head or neck due to muscular hyperactivity.
Craniocervical dystonia (CCD) pain is exacerbated by
muscle contraction, movement, external pressure, or sustained posture.
Craniocervical dystonia (CCD) treatment
The pain resolves within 3 months of successful treatment of the underlying
muscle hyperactivity. Treatment involves physical therapy, muscle relaxants,
and botulinum toxin injections.
Craniocervical dystonia (CCD) dystonias include
pharyngeal dystonia, spasmodic torticollis, mandibular dystonia, or
lingual dystonia
pathophysiology of Craniocervical dystonia suggest
functional defects in dopamine signaling.
HEADACHE ATTRIBUTED TO
RHINOSINUSITIS
This is a secondary cause of frontal headache and pain in
one or more region of the face, ears, or teeth that is
accompanied by clinical, radiographic, endoscopic, or laboratory evidence of acute rhinosinusitis
RHINOSINUSITIS Clinical causes include
purulence within the nasal cavity, nasal obstruction, new onset hyposmia/anosmia, and/or fever. The headache/facial pain onset must be congruent
with the acute rhinosinusitis and must resolve within
7 days after remission or successful treatment.
Conditions that are not considered as causing RHINOSINUSITIS headache include
deviated septum, nasal turbinate hypertrophy, and sinus membrane atrophy.
Disorders of the teeth, jaws, or related structures typically
cause
toothache and facial pain, and less commonly headache.
Acute periodontal nociceptive pain is treated with
rest
(reduced mechanical stimulation), NSAIDs, topical
local anesthetics, and analgesics
Chronic periodontal
disease is
an immune mediated inflammatory process that
results in destruction of the teeth and the surrounding
anchoring bone
Common Intraoral Causes of Oral Pain- Infections
Herpetic stomatitis
Varicella zoster
Candidiasis
Acute necrotizing gingivostomatitis
Common Intraoral Causes of Oral Pain- Immune/autoimmune
Allergic reactions (toothpaste, mouthwashes, topical medications) Erosive lichen planus Benign mucous membrane pemphigoid Aphthous stomatitis and aphthous lesions Erythema multiforme Graft-versus-host disease
Common Intraoral Causes of Oral Pain- Traumatic and
iatrogenic injuries
Factitial, accidental (burns: chemical, solar, thermal) Self-destructive behaviors (rituals, obsessive behaviors) Iatrogenic (chemotherapy, radiation)
Common Intraoral Causes of Oral Pain- Neoplasia
Squamous cell carcinoma
Mucoepidermoid carcinoma
Adenocystic carcinoma
Intracranial tumors
Common Intraoral Causes of Oral Pain- Neurologic
Burning mouth syndrome and glossodynia Neuralgias Postviral neuralgias Post-traumatic neuropathies Dyskinesias and dystonias
Common Intraoral Causes of Oral Pain- Nutritional and Metabolic
Vitamin deficiencies (B12, folate)
Mineral deficiencies (iron)
Diabetic neuropathy
Malabsorption syndromes
Common Intraoral Causes of Oral Pain- Miscellaneou
Xerostomia, secondary to intrinsic or extrinsic conditions Referred pain from esophageal or oropharyngeal malignancy Mucositis secondary to esophageal reflux Angioedema
HEADACHE OR FACIAL PAIN ATTRIBUTED TO TEMPOROMANDIBULAR JOINT DISORDER This is characterized by
recurrent pain in one or more
regions of the head/face from the temporomandibular
joint (TMJ). It is precipitated by jaw movements, chewing,
decreased or irregular range of motion, and TMJ
tenderness that resolves within 3 months after successful
treatment of TMJ disorder.
TEMPOROMANDIBULAR JOINT
DISORDER include
disc displacements, osteoarthritis, or joint hypermobility, rheumatoid arthritis, and can be associated with myofascial pain and headache.
The temporomandibular joint is a
bicondylar joint that
contributes to the important functions of mastication and
speech. The joint is unique in that the articular surface is
covered by fibrocartilage instead of hyaline cartilage.
In the temporomandibular joint a fibrocartilaginous disc is located between the
condyle and and the articular fossa and separates the joint cavity into the superior ad inferior compartment
temporomandibular joint: Intracapsular disorders and
extracapsular disorders
Intracapsular disorders include rheumatoid arthritis,
osteoarthritis, and articular disc displacement, while extracapsular disorders include myofascial masticatory
pain
temporomandibular joint Treatment includes
treatment of any secondary causes such as infection, treatment of somatization component (stress, anxiety), elimination of nocturnal clenching, jaw exercises, and pharmacologic therapy (muscle relaxants, neuropathic pain medications), anti-inflammatory medications).
Local anesthetic/steroid and/or botolinum toxin injections may be indicated in selected cases. Surgery should be considered in patients who do not respond to conservative treatment if anatomic disruption is noted.
temporomandibular joint surgical treatment
The procedures include total and partial meniscectomy,
disk repair, lysis of adhesions, lavage, and in rare instances
total joint arthroplasty. Total TMJ replacement has a poor outcome.
TRIGEMINAL NEURALGIA (TIC DOULOUREUX)
a unilateral pain disorder characterized by brief painful episodes described as is typically classified as intense, sharp, and stabbing within the innervation of the one or more divisions of the trigeminal
nerve.
Trigeminal neuralgia disorder usually starts in the
second or third divisions with the first division affected in less
than 5% of the patients
in Trigeminal neuralgia Involvement of the first division hints towards a
postinfectious HSV.
in Trigeminal neuralgia the duration of the paroxysmal attack
can vary from seconds to 2 min and may be precipitated by trivial stimuli from the trigeminal nerve (such as small trigger areas in the nasolabial folds) or by stimuli remote to the trigeminal area, such as other sensory stimulation
(i.e., lights, sounds, or tastes).
If there is a causative
lesion identified, outside of vascular compression, then
trigeminal neuralgia is
secondary, or “symptomatic trigeminal neuralgia.”
The pathogenesis of trigeminal neuralgia
caused by compression of the trigeminal root by tortuous or aberrant vessels, as identified by MRI.
The trigeminal nerve
the fifth cranial nerve and resides in the Meckel’s cavity posterolateral to the cavernous
sinus adjacent to the sphenoid bone. Medial to the ganglion
in Meckel’s cavity is the internal carotid artery,
which is located in the posterior portion of the cavernous sinus
The ophthalmic division (V1) of the trigeminal nerve
The ophthalmic division (V1) courses in the lateral wall of the cavernous sinus and exits via the superior orbital fissure.
The maxillary division (V2) of the trigeminal nerve
The maxillary division (V2) exits the skull base through the foramen rotundum inferolateral to the cavernous sinus. It then enters the pteyrogopalatine
fossa.
The manibular (V3) component of the trigeminal nerve
The manibular (V3) component courses along the base of the skull and exits the cranium via the foramen ovale.
Treatment of trigeminal neuralgia
Treatment centers on prevention and abortive therapy. Trigeminal neuralgia usually responds to pharmacotherapy and should be employed before
interventions are attempted. Generally, after patients
fail conservative treatment, young patients with MRI evidence of vascular compression should be considered for microvascular decompression. Elderly patients or those with no evidence of vascular compression may be a candidate for gamma knife or radiofrequency thermoablation.
Conservative treatment strategies of trigeminal neuralgia
antidepressants and antiepileptics. First-line therapy is carbamazepine
or oxycarbamazepine, while second-line treatment is
baclofen.
Interventional modes of treatment of trigeminal neuralgia
decompressive, ablative, and neuromudulatory strategies using surgical and percutaneous routes
Interventional Approaches to Trigeminal Neuralgia- Surgical Approaches
Microvascular decompression (MVD): The vessels in contact with the trigeminal root entry zone are coagulated or separated from the nerve using an inert sponge.
Interventional Approaches to Trigeminal Neuralgia- Percutaneous Approaches
Gamma knife
Stereotactic radiation therapy: high dose of irradiation to a small section of the trigeminal nerve leading to nonselective damage.
Interventional Approaches to Trigeminal Neuralgia- Percutaneous Approaches
Percutaneous balloon microcompression:
Pressure-induced ischemia. The technique may be more suitable for treatment of V1 trigeminal neuralgia of the first branch as the corneal reflex tends to remain intact
Interventional Approaches to Trigeminal Neuralgia- Percutaneous Approaches
Percutaneous glycerol rhizolysis
Under fluoroscopy, predetermined volume of glycerol is injected for neurolysis
Interventional Approaches to Trigeminal Neuralgia- Percutaneous Approaches
Percutaneous radiofrequency
thermocoagulation
This is usually considered for the elderly patient who is high risk for surgical MVD. The outcome may be less favorable than MVD, but it is less invasive with lower morbidity and mortality rates
Interventional Approaches to Trigeminal Neuralgia- Percutaneous Approaches
Pulsed radiofrequency ablation (RFA):
Although it would seem a safer alternative than the commonly used thermal RFA, its efficacy is questioned in a randomized controlled study.
Interventional Approaches to Trigeminal Neuralgia- Neuromodulation
Gasserian ganglion Neuromodulation stimulation was reported either via a subtemporal craniotomy, or a
percutaneous approach
Glossopharyngeal neuralgia
an uncommon facial pain
syndrome characterized by transient severe, sharp, stabbing pain experienced in the ear, base of tongue, tonsillar fossa, or beneath the angle of the jaw. It is unilateral in presentation, lasts for seconds to 2 min, and may be precipitated by swallowing, talking, coughing, chewing, or
yawning
Glossopharyngeal neuralgia
The pain is transmitted via the
auricular and pharyngeal branches of the glossopharyngeal nerve, along
with the auricular and pharyngeal branches of the vagus nerve.
If a causative lesion is identified,
then the neuralgia is
secondary, and becomes “symptomatic
glossopharyngeal neuralgia.”
The glossopharyngeal nerve location
exits the brain stem and
descends through the base of the skull through the jugular
foramen.
The glossopharyngeal nerve receives contributions
from the solitary nucleus,
the nucleus ambiguous, and the inferior salivatory nucleus
The glossopharyngeal nerve branches include
.the tympanic, stylopharyngeal, tonsillar,
carotid sinus, linguinal branches, and communicating
branches to the vagus nerve.
pathophysiology of glossopharyegnal neuralgia
Vascular impingement of the nerve roots has been implicated in the pathophysiology of glossopharyegnal neuralgia, commonly microvascular compression by the posterior cerebellar artery
glossopharyegnal neuralgia treatment
Treatment is primarily conservative medical management with anticonvulsants and analgesics. Refractory cases to conservative management are candidates for surgical or
percutaneous treatments, including lesioning and nerve blocks.
NERVUS INTERMEDIUS NEURALGIA
(GENICULATE NEURALGIA, RAMSAY-HUNT
SYNDROME)
This is a rare disorder characterized by transient bouts of pain in the internal auditory canal, not attributed to any structural lesion, and is intermittent in onset and may last for seconds to minutes.
NERVUS INTERMEDIUS NEURALGIA symptoms
Disorders of salivation, lacrimation, or taste can accompany the pain and are commonly associated with herpes zoster.
Typical cases of Ramsay-Hunt
Syndrome (RHS) demonstrate the triad of
auricular vesicles, ipsilateral facial palsy, and vestibular/cochlear symptoms.
nervus intermedius
part of the facial nerve
(cranial nerve VII) and is located between the motor
component of the facial nerve and the vestibulocochlear
nerve (cranial nerve VIII).
nervus intermedius contains
sensory branches
(external auditory meatus, floor of mouth, and palate, and mucosa of nose, and provides taste to the anterior two
thirds of tongue,) and parasympathetic fibers (superior
salivatory nucleus) of the facial nerve
nervus intermedius joins the
motor root of the facial nerve in the facial canal, at the geniculate
ganglion.
NERVUS INTERMEDIUS NEURALGIA treatment
Conservative treatment involves the use of neuropathic
pain medications. The treatment of herpes zoster, if RHS is suspected, or surgical decompression.
SUPERIOR LARYNGEAL NEURALGIA
This is characterized by severe pain paroxysms, lasting
seconds to minutes, in the lateral aspect of the throat and
submandibular region and underneath the ear, precipitated
by swallowing, shouting, or turning of the head.
SUPERIOR LARYNGEAL NEURALGIA trigger
point
identified along the lateral aspect of the ipsilateral
hyoid bone or hyothyroid membrane that is relieved by
superior laryngeal nerve block, ablation, and/or resection of the superior laryngeal nerve.
superior laryngeal nerve
a terminal branch of the
vagus nerve (cranial nerve X) and receives sympathetic
input from the superior cervical ganglion. It divides into
the internal and external superior laryngeal nerve (which
innervates the cricothyroid muscle)
recurrent laryngeal
nerve
innervates all other laryngeal muscles, particularly
the abductors, and when damaged can cause vocal
cord paralysis (injury results in unilateral adduction of
vocal cord) and bilaterally can cause airway obstruction
NASOCILIARY NEURALGIA (CHARLIN’S NEURALGIA)
This is a transient, lancinating pain in the nostril that
radiates to the medial/frontal region. It lasts seconds to
hours. It is precipitated by touching the ipsilateral nostril
and abolished by blockade of the nasociliary nerve
The nasociliary nerve
a branch of the ophthalmic
nerve (V1) and enters the orbit between the lateral rectus
muscles and continues obliquely beneath the superior rectus and superior oblique muscle to the medial wall of the orbital cavity.
nasociliary nerve terminal branches include
the posterior
ethmoidal nerve, the long cilliary nerves, the infratrochlear
nerve, the communicating branch of the ciliary ganglion,
and the anterior ethmoidal nerve
SUPRAORBITAL NEURALGIA
This pain disorder is characterized by transient or constant pain in the forehead and supraorbital area supplied by the supraorbital nerve (terminal branch of the ophthalmic nerve V1). The pain can be precipitated or reproduced by pressure over the nerve in the supraorbital notch and diagnosis is confirmed by pain relief with local anesthetic
blockade.
The terminal branches of the trigeminal nerve include the
infraorbital,
lingual, alveolar, and mental nerves
Occipital neuralgia
described as paroxysmal stabbing and sharp pain in the distribution of the greater or lesser occipital nerves or third occipital nerve, sometimes accompanied by paresthesia or dysesthesia or tenderness
overlying the nerve that is involved.
Occipital neuralgia constant pain is caused by
compression, irritation or distortion of cranial nerves or upper cervical roots by structural lesions
Optic neuritis
described as pain behind one or both eyes
accompanied by central vision impairment due to a central
or paracentral scotoma
Optic neuritis caused by
It is not caused by compressive
lesion but is thought to be due to optic nerve (CNII)
inflammation. The onset of pain and visual impairment are
separated by less than 1 month and the pain is self-limited
with resolution within 4 weeks.
In Optic neuritisIf pain precedes the visual impairment by more than 4 weeks then it is classified as
“probable optic neuritis.” Optic neuritis is often a presenting manifestation of multiple sclerosis.
OCULAR DIABETIC NEUROPATHY
This condition is described as pain around the eye and forehead with paresis of one or more ocular cranial nerves in a patient with diabetes mellitus. Usually the pain is
centered on one eye with pain developing over approximately 2 hr.
OCULAR DIABETIC NEUROPATHY cranial nerve paresis is
most commonly the third cranial nerve (oculomotor) and less commonly, the fourth (trochlear) and sixth (abducens) cranial nerves.
In OCULAR DIABETIC NEUROPATHY It is important
to rule out other causes of cranial nerve palsies, including
infection, infarction, hemorrhage, or neoplasm.
HEAD OR FACIAL PAIN ATTRIBUTED
TO HERPES ZOSTER
Head or facial pain can be caused by herpes zoster.
The pain usually precedes the herpetic eruption by less
than 7 days, and the pain is congruent with herpetic
nerve eruption. Typically, pain resolves within 3 months.
The herpetic zoster affects what branch of the trigeminal nerve
The herpetic zoster affects the trigeminal nerve in
approximately 10% of patients, with the V1 or ophthalmic
division most commonly affected (80% of the time). In contrast, idiopathic trigeminal neuralgia usually affects the V2/3 distribution.
ophthalmic herpes can be associated with what nerve palsies
third, fourth, and six cranial nerve palsies
Postherpetic neuralgia (PHN)
facial pain in the distribution
of the affected nerve that persists 3 months after
the skin eruptions
The pathophysiology of acute herpes zoster correlates
with the
replication of varicella zoster virus and spread within the dorsal root or ganglion and along the peripheral sensory nerve. It may disseminate locally to adjacent structures, including the spinal cord.
The characteristic
dermatomal distribution of acute herpes zoster
is related to the anatomical
or functional disruption of the nervous system. Necrosis
of the dorsal root ganglion, the presence of the virus
within the nerve elements, and atrophy of the dorsal
horn characterize PHN.
Management of herpetic pain includes
antiviral medications.
The more bioavailable medications valaciclovir and famciclovir are more effective than acyclovir in treating
acute herpes zoster. The efficacy of steroid use is equivocal.
Neuropathic pain medications for herpetic pain
anticonvulsants
(gabapentin, pregabalin) and antidepressants (amitriptyline,
nortriptyline). Other medications commonly employed include topical agents (lidocaine patch), capsacin, opioids, and NMDA antagonists.
In extreme cases, Management of herpetic pain includes
Sympathetic blockade (e.g., stellate ganglion blockade) may be helpful specially if performed within the first year. some patients may resort to surgery, including cordotomy, rhizotomy, sympathetcomy, trigeminal tractomy, mesencepalotomy, retrogasserian rhizotomy, or superfical greater petrosal neurotomy
TOLOSA-HUNT SYNDROME
This syndrome is characterized by episodic orbital pain with paralysis of one or more of the third, fourth, and sixth cranial nerves that resolves spontaneously. Usually, it has a waxing and waning course.It is a painful ophthalmoplegia; the pain and paresis occur within 2 weeks of onset and resolve within 72 hr of treatment with corticosteroids.
TOLOSA-HUNT SYNDROME
can also involve divisions of the
trigeminal nerve, along with the facial, optic, and acoustic
nerves.
TOLOSA-HUNT SYNDROME
It is important to carefully exclude other causes
of the painful ophthalmoplegia including
inflammatory (vasculitis, sarcoid), infectious (meningitis), and endocrinologic (diabetes mellitus) causes. It may also be due to cancer (pain is due to a mass effect) or to a primary headache (migraine).
Central causes of facial pain include
anesthesia dolorosa,
central poststroke pain, facial pain secondary to multiple
sclerosis, persistent idiopathic facial pain, and burning mouth syndrome.
Central causes of facial pain pathophysiology
two processes have been implicated: neuritis with reduction in nerve threshold for a given painful stimulus or a reduction in inhibition from “loss of inhibition.
Central causes of facial pain
Characteristically, the pain complaint
The pain may be cramping, constricting, crushing,
or shooting/lancinating in character. There may be a pins
and needles sensation or dysethesia. Physical examination may show allodynia. Triggering stimuli include extreme temperatures and emotional distress
Anesthesia dolorosa
a painful anesthesia or hypesthesia in the distribution of the trigeminal, or one of its divisions, or occipital nerve. It is caused by a lesion of the relevant nerve or its central connections and is characterized as persistent
pain with diminished sensory loss in the distribution
of the nerve
Anesthesia dolorosa etiology
It is often related to surgical trauma via rhizotomy or thermocoagulation of the occipital nerve or the trigeminal ganglion
Anesthesia dolorosa was reported in cases after
glycerol rhizotomy and
radiofrequency rhizotomy, respectively, in the treatment of trigeminal neuralgia
Central poststroke pain
a unilateral pain and dysesthesia
associated with loss of sensation to pinprick, touch,
and temperature of the ipsilateral face. There is usually a
history of symptoms suggestive of stroke, with a lesion
demonstrated radiographically
Central poststroke pain characteristics
The pain and dysesthesia
develop within 6 months after the stroke, is usually persistent,
and is usually attributed to a lesion of the trigeminothalamic
pathway, thalamus, or thalamocortical projection. It may affect the trunk and limbs on the ipsilateral or contralateral side.
FACIAL PAIN ATTRIBUTED TO MULTIPLE SCLEROSIS
characterized by unilateral or bilateral facial pain
with or without an associated dysesthesia attributed to a
demyelinating lesion in the pons or trigeminothalamic
pathway in patients who have multiple sclerosis.
PERSISTENT IDIOPATHIC FACIAL PAIN
ATYPICAL FACE PAIN
facial pain that is present daily and persists for the majority of the day, but does not have features attributed to any of the other cranial neuralgias. It is confined to a poorly defined area of the face and is “deep” in location, not associated with sensory loss or other physical signs. It
is not attributed to any other disorder.
ATYPICAL FACE PAIN location
pain is commonly in the nasolabial fold or side of the chin and may spread to the upper or lower jaw with a more generalized distribution. It may be triggered by surgery or injury to the face, cheek, and gums.
BURNING MOUTH SYNDROME
This pain is characterized by an intraoral burning sensation
wherein no medical or dental etiology is demonstrated.
The mouth pain is daily and persistent for most of
the day. Associated symptoms include subjective dryness of
the mouth, paresthesia, and altered taste
