Introduction
Facial pain, often referred to as orofacial pain, refers to any type of discomfort localized to the face, from the hairline to the lower mandibles, including the oral and nasal cavities. When all causes are considered, the prevalence has been estimated to be as high as 26% of the general population with 7% experiencing chronic pain. The differential diagnosis is extensive and includes structural pathology, both malignant and nonmalignant, inflammatory disorders, dental disease, infection, primary headache disorders, and neuropathic/neuralgic syndromes. Females are affected more frequently than males, and patients often are suffering from a concomitant chronic pain condition involving another area of the body. Underlying psychological disorders and a smoking history may be contributing factors. Because of the broad range of etiologic possibilities, the treatment of facial pain may fall into the purview of multiple disciplines including, dentistry, primary care, ophthalmology, otolaryngology, oncology, neurology, and neurosurgery. The International Classification of Headache Disorders, Third Edition (ICHD-3) focuses predominantly on the neurologic causes of facial pain, and while the International Classification of Orofacial Pain also addresses the dental disorders, neither classification includes the myriad of potential etiologic possibilities.
Paroxysmal painful disorders involving the face and head are referred to as the cranial neuralgias. The pain is usually unilateral, lancinating, and electric shock–like in character with each episode lasting a short period of time. While the cranial neuralgias are rare, a diagnosis must be made with alacrity, as the pain is disabling, often the result of underlying compression or inflammation. It is important to distinguish neuralgic pain from neuropathic pain. With a neuropathy the pain is more often constant and burning in character, and there may be specific deficits in the distribution of the involved nerve. In addition to the persistent discomfort of neuropathic pain, there may be brief intermittent paroxysmal neuralgic discomfort. In evaluating a patient with neuralgic pain, it is important to determine whether the pain is idiopathic or the cause is structural, inflammatory, or infectious. In this chapter we will review facial pain and then the cranial neuralgias.
Disorders of Cranial Bone
While cranial bones are relatively insensate, blood vessels, muscles, skin, and the periosteum are highly pain sensitive. The typical pain is dull and aching in character and is always secondary to underlying pathology. The differential diagnosis may include multiple myeloma, Paget disease, fibrous dysplasia, metastatic disease, and scalp infection/osteomyelitis. Osteomas, consisting primarily of mature cancellous bone, are benign slow-growing tumors commonly affecting the craniofacial region. They may involve the skull, jaw, or sinuses and present with facial deformity and, at times, orofacial pain. Osteomas are usually solitary tumors, but multiple osteomas may develop in patients with Gardner syndrome, which is a type of autosomal dominant familial adenomatous polyposis. The diagnosis of cranial bone disorders requires palpation of the affected area and observing for tenderness, erythema, increased warmth, and evidence of a mass. Workup should include skull x-rays, computed tomography (CT) of the skull, and potentially a bone scan. Treatment is specific to the underlying cause. The pain of osteomas usually responds to aspirin or other nonsteroidal antiinflammatory medication. Indications for surgical treatment of osteomas include cosmetic disfigurement, progressive increase in volume, impingement on underlying structures, and limitation of function, which may occur with a tumor in the mandible.
Disorders of the Eye
Eye pain is a common cause of primary care and emergency room visits. When eye pain is accompanied by visual difficulty, the patient requires an emergent ophthalmology evaluation. Decreased visual acuity with accompanying eye pain occurs in acute angle closure glaucoma, scleritis, optic neuritis, orbital cellulitis, pituitary apoplexy, anterior uveitis, and keratitis.
Acute closed-angle glaucoma will cause retro-orbital and periorbital pain with severe central visual field defects accompanied by corneal clouding, fixed mydriasis, and conjunctival injection. Patients must receive immediate ophthalmologic treatment.
The sclera is the protective fibrous coating of the eye. The episclera is continuous with the cornea and covers the sclera. Scleritis causes severe boring eye pain that intensifies with movement of the eye and may precipitate a more generalized headache. The eye appears red with a bluish discoloration of the sclera, and vision is impaired. Episcleritis causes engorgement of superficial blood vessels but is not painful, and there is no accompanying visual loss or bluish discoloration. Scleritis is usually the result of an underlying rheumatologic disease, but infection must be ruled out. For noninfectious scleritis, initial treatment is with nonsteroidal antiinflammatory medication.
Optic neuritis causes orbital pain that increases with eye movement. Visual loss occurs over days, and on examination an afferent pupillary defect will be detected. Optic neuritis may be the result of multiple sclerosis or an underlying systemic inflammatory disorder. Patients should receive high-dose intravenous corticosteroids under the care of neurology and ophthalmology.
Pituitary apoplexy is a sudden infarction or hemorrhage of the pituitary gland within a pituitary adenoma and presents with the apoplectic onset of headache, eye pain, visual loss, and an oculomotor nerve deficit with ptosis, dilated pupil, and lateral eye deviation. Adrenal crisis occurs, and the patient requires immediate corticosteroid replacement. Patients with visual loss will require emergency neurosurgical intervention.
Orbital cellulitis presents with eye pain and swelling, diplopia with diminished eye movement, proptosis, visual loss, and ptosis. Associated paranasal sinusitis may be present, and treatment with intravenous antibiotics is indicated.
The uvea is the pigmented layer of the eye lying beneath the sclera comprising the iris, ciliary body, and choroid. Anterior uveitis, which is inflammation of the iris and ciliary body, presents with pain, photophobia, meiosis, and ciliary flush. This is often associated with underlying systemic inflammatory disorders such as sarcoidosis, rheumatoid arthritis, syphilis, reactive arthritis, or seronegative spondyloarthropathies. Treatment will depend on the cause. For noninfectious disorders, topical steroids and an immunosuppressant are indicated.
Infectious keratitis (inflammation of the cornea) due to herpes simplex virus, herpes zoster ophthalmicus, bacteria, or acanthamoeba causes eye pain, eye redness, photophobia, and visual loss due to corneal damage. Management by ophthalmology is indicated.
There are multiple disorders of the eye that cause pain without visual loss. The most common are corneal abrasions, hordeolum, and conjunctivitis. Dry eye syndrome may present with a burning discomfort.
Eye pain with ophthalmoplegia involving the oculomotor, abducens, and trochlear cranial nerves may occur as the result of an ischemic neuropathy usually due to diabetes mellitus, giant cell arteritis, or a systemic inflammatory disorder. The oculomotor nerve is most commonly involved, followed by the abducens nerve. The trochlear is rarely affected. The ophthalmoplegia lasts from weeks to months and then usually spontaneously resolves. Contrast-enhanced brain magnetic resonance imaging (MRI) and a magnetic resonance angiogram (MRA) should be performed, and the patient should also undergo testing to rule out giant cell arteritis.
Cavernous sinus thrombosis is a rare life-threatening disorder that presents with unilateral eye pain with proptosis, chemosis, and ophthalmoplegia. It may be the result of a facial infection, orbital cellulitis, sinusitis, pharyngitis, otitis media, surgery, or trauma. Fever will be present if there is an underlying infection. The oculomotor, abducens, and trochlear nerves and the first two divisions of the trigeminal nerve reside in the cavernous sinus, and involvement of several or all the cranial nerves located in the cavernous sinus may occur secondary to compression and inflammation. Contrast-enhanced brain MRI, MRA, and magnetic resonance venogram should be performed emergently. A lumbar puncture is required to exclude meningitis. Treatment is with parenteral antibiotics and anticoagulation.
Tolosa Hunt syndrome is a relatively benign idiopathic granulomatous inflammatory disorder of the cavernous sinus, superior orbital fissure, and occasionally the orbital apex. Symptoms include severe periorbital pain extending into the frontal and temporal regions. The pain increases with eye movement, and the oculomotor, abducens, and trochlear cranial nerves are involved, resulting in ophthalmoparesis and diplopia. Dramatic improvement usually occurs within 2–3 days after treatment with corticosteroids has begun. Untreated, symptoms will usually resolve within 8 weeks. Brain MRI with contrast and an MRA are indicated.
Trochlear headache presents with unilateral periorbital and frontal pain due to trochlear inflammation. The pain increases with eye movement and responds to nonsteroidal antiinflammatory drugs or a direct injection of a local anesthetic or steroid.
Heterophoria, heterotropia, and refractive errors may cause mild dull eye pain or frontal aching discomfort but not a severe headache.
Paroxysmal sharp stabbing pain into the eye lasting seconds is referred to as ophthalmodynia periodica and is an uncommon presentation of primary stabbing headache. While confined to the eye, the pain is not secondary to ocular pathology.
Rhinosinusitis
Although rhinosinusitis is often implicated as a cause of headaches, studies have shown that approximately 90% of patients who believe that they are suffering from “sinus” headaches fulfill the ICHD-3 criteria for migraine without aura. Chronic sinusitis persisting for more than 12 weeks rarely causes facial pain or headache. The location of pain is similar for both types of headaches, and migraine is often pressure-like in character and not uncommonly accompanied by nasal congestion and discharge. Both types of headaches can be precipitated by changes in barometric pressure, but whereas migraines last from hours to 1–2 days, a true sinus-related headache can persist for days to weeks. The pain from rhinosinusitis is secondary to inflammation of the sinus and nasal cavity, but pain is not the hallmark of the disorder, and only approximately one-third of patients experience facial pain or headache. Most infections are viral, and symptoms include nasal congestion, postnasal drip, runny nose with discolored mucus, facial tenderness, and typical symptoms of an upper respiratory infection. With bacterial sinusitis, patients will be febrile and experience fatigue and pressure in the ears. Halitosis may be present. Sphenoid sinusitis is rare but more likely to cause a headache than infection in the other sinuses and is usually not accompanied by nasal congestion or discharge. The pain may be frontal, periorbital, temporal, or occipital in location. Thunderclap headache has been described with sphenoid sinusitis, and the pain may be accompanied by nausea and vomiting and photophobia. Complications include bacterial meningitis, subdural abscess, and cavernous sinus thrombosis.
Rhinosinusitis should be managed by ENT with antibiotics if a bacterial infection is suspected. A CT of the sinuses and a brain MRI may be required.
Dental Disease
Dental pathology, specifically caries and apical root infections, is the most common cause of lower orofacial pain. The character is usually constant and aching, but intermittent jabbing pain may occur. Diagnosis is facilitated by evidence of inflammation in the oral cavity and pain when palpating the affected tooth. Odontogenic pain is usually precipitated by intake of cold or hot liquids. Diseases of the oral mucosa may cause facial pain and disorders of the salivary glands due to sialolithiasis, sialadenitis, infection, Sjögren syndrome, or benign or cancerous tumors.
Burning Mouth Syndrome
Burning mouth syndrome (BMS) is a rare chronic disorder characterized by a burning sensation in the oral cavity without evidence of oral mucosal pathology. The tip of the tongue is usually involved, and there is often accompanying dysgeusia and a sense of dryness. It occurs more commonly in perimenopausal or postmenopausal females, and onset is spontaneous. With primary or idiopathic BMS a cause cannot be identified. Secondary BMS may be due to candidiasis, vitamin or nutritional deficiencies, diabetes mellitus, Sjögren syndrome, or psychosocial stressors. A small fiber neuropathy has been proposed as the potential etiology. If an underlying cause is not detected, then treatment may include topical lidocaine, capsaicin, alpha-lipoic acid, tricyclic antidepressant, gabapentin, pregabalin, venlafaxine, or duloxetine. Cognitive behavioral therapy may also be helpful.
Eagle Syndrome
Eagle syndrome, often referred to as stylohyoid syndrome, is a rare disorder that is the result of an elongated or disfigured styloid process. Neck movement can provoke orofacial and cervical pain by compressing adjacent structures, most commonly the glossopharyngeal nerve, but multiple cranial nerves can be stretched or compressed, accounting for the facial pain. The pain is usually unilateral, but bilateral discomfort may occur. It was initially described following tonsillectomy but usually there is no history of surgery. Impingement of the internal carotid artery will result in ipsilateral supraorbital pain and rarely transient neurologic symptoms. Surgical intervention may be indicated, but pain can often be managed with nonsteroidal antiinflammatory drugs, antidepressant medication, anticonvulsant medication, or transpharyngeal injections of a steroid and local anesthetic.
Gradenigo Syndrome
The classic triad of Gradenigo syndrome, also referred to as petrous apicitis, includes suppurative otitis media, abducens nerve palsy, and pain in the distribution of the trigeminal nerve. Patients present with retro-orbital and periorbital pain due to involvement of the trigeminal ganglion and diplopia due to a sixth nerve palsy. Ipsilateral peripheral facial weakness occurs if the seventh cranial nerve is affected, and rarely deficits of cranial nerves VIII, IX, and X are seen. Possible complications include meningitis and intracranial abscess. Both high-resolution temporal bone CT and brain MRI are required to evaluate the underlying pathology. Patients usually respond to high-dose antibiotic therapy, obviating the need for surgical intervention. In the postantibiotic era, the syndrome with the classic triad has become extremely rare.
Neck-Tongue Syndrome
Neck-tongue syndrome is characterized by episodes of severe sharp and stabbing pain lasting seconds to minutes in the neck extending into the occipital region. Unilateral auricular pain extending into the face may occur, and the discomfort is accompanied by numbness and dysesthesias of the ipsilateral tongue. Symptoms are precipitated by sudden rotation of the head and neck and typically occur in the pediatric and adolescent age group. The most likely cause is transient subluxation of the lateral atlantoaxial joint due to ligamentous laxity. Cases have been observed to occur in families, suggesting a genetic predisposition. An MRI scan of the cervical spine and base of the brain should be performed. Most patients do not require treatment, but for persistent symptoms, cervical spine immobilization, spinal manipulation, and surgery to stabilize the spine have been used with reported success. Spinal manipulation is contraindicated if there is evidence of atlantoaxial instability, and there is the risk of vertebral artery dissection.
Carotid Artery Dissection
Carotid artery dissection is the result of a tear of the intimal layer of the carotid artery either occurring spontaneously or as the result of trauma. Blood flow to areas of the brain may be compromised, potentially resulting in an ischemic stroke, and dissection is the leading cause of stroke in younger patients. The tear results in an intramural hematoma causing stenosis of the vessel and thrombus formation. Traumatic dissections can occur as the result of a forcible whiplash injury, blunt trauma, or violent coughing or sneezing. Fibromuscular dysplasia, Marfan syndrome, and Ehlers-Danlos syndrome may increase the risk of spontaneous dissection, and it has been reported with Eagle syndrome due to direct contact on the carotid artery by the elongated styloid process. The presentation can be widely varied from a devastating stroke to simply a headache and facial pain on the side of the dissection. An ipsilateral Horner syndrome is often observed. CT angiogram or MRA of the neck including axial fat-suppressed T1-weighted images should be performed emergently if dissection is suspected. A head CT will detect a hemorrhage, but a brain MRI with diffusion-weighted images is required to determine whether there is evidence of an acute stroke. While the optimal treatment remains somewhat controversial, a direct oral anticoagulant for 3 months followed by 81 mg of aspirin daily for at least 3 additional months is the most pragmatic approach. Follow-up imaging of the vessels should be performed at 6 months. Endovascular carotid artery stenting has been performed on patients with symptoms of ischemic stroke and evidence of significant hypoperfusion on imaging, but controlled studies comparing it to the best medical therapy have not been performed.
Cervicogenic Headache
Headache and facial pain may occur as a result of disorders of the cervical spine. The pain is most commonly unilateral, nonthrobbing, and nonlancinating in character, beginning posteriorly then extending into the frontal region and face. Neck pain always accompanies the headache and may involve the shoulder and arm on the same side. Cervical range of motion is reduced, and provocative maneuvers will exacerbate the pain The pain affects males and females equally beginning in the fourth and fifth decades of life. While cervical structural disease, such as a herniated nucleus pulposus or degenerative disease, may be the cause, many patients have no detectable cervical spine pathology. In the elderly, cervical spondylosis is often the source of the pain. Physiotherapy is usually beneficial, and medication options include acetaminophen, nonsteroidal antiinflammatory medication, muscle relaxants, and tricyclic antidepressants. Acupuncture can be considered. If the pain does not respond to treatment, then MRI scans of the brain and cervical spine should be performed.
Giant Cell Arteritis
Giant cell arteritis (GCA) is the most common systemic vasculitis in adults, and it occurs almost exclusively in patients over the age of 50, affecting females more than males. The granulomatous inflammation involves medium and large vessels, predominantly the temporal, ophthalmic, occipital, and vertebral arteries. The aorta and its proximal branches may also be involved and, rarely, intracranial vessels. Blood vessel inflammation can lead to stenosis, occlusion, or aneurysm formation. Headache is the presenting symptom in 80%–90% of patients, and the pain is usually unilateral, involving the temporal region with tenderness of the area, although any part of the head may be involved, and the pain may be bilateral. Other symptoms may include cramping pain in the jaw while chewing referred to as jaw claudication, malaise, fever, night sweats, and in 40%–60% of patients an accompanying rheumatologic condition, polymyalgia rheumatica, with pain and stiffness in proximal joints, typically the shoulders and hips. Patients who have a history of polymyalgia rheumatica alone have a 16%–21% chance of developing GCA especially if untreated. With GCA the sedimentation rate (ESR) and C-reactive protein (CRP) are usually significantly elevated, with CRP being the more sensitive test. However, 22.5% of patients who have GCA confirmed by temporal artery biopsy have a normal sedimentation, and 2%–14% of patients have a normal CRP. Four percent of patients with biopsy-confirmed GCA have both normal CRP and ESR. Blood work will often reveal anemia and thrombocytosis, and leukocytosis may also be present. Doppler ultrasonography is a first-line diagnostic tool with a sensitivity of 69% and specificity of 82%, but techniques are constantly improving. The classic finding is the halo sign, which is a hyperechoic ring around the arterial lumen indicating thickening of the arterial wall due to inflammation. MRA is an alternative with a sensitivity of 73% and a specificity of 88%, and positron emission tomography has also been used with a sensitivity of 73%–92% and a specificity of 83%–85%. Temporal artery biopsy remains the gold standard for diagnosis with a specificity of 98% but a sensitivity of only 61% as the biopsy may miss skipped lesions in the artery. GCA is a medical emergency, as visual loss, stroke, and death may occur if treatment is delayed. Patients should be placed on prednisone 60 mg daily, and treatment should optimally be initiated prior to the biopsy to prevent visual loss due to ophthalmic artery occlusion. There is no advantage to using intravenous corticosteroids compared to high-dose oral corticosteroids. The IL-6 receptor alpha inhibitor tocilizumab is now used for maintenance of remission and reduction in the dose of glucocorticoids, but it is not effective in the acute phase, as it does not prevent optic neuropathy.
Raeder’s Paratrigeminal Neuralgia
Raeder’s paratrigeminal neuralgia is a unilateral deep, boring, nonpulsatile periorbital and retro-orbital pain accompanied by ptosis, meiosis, eyelid edema, and nasal congestion or rhinorrhea. Facial sweating is preserved. The syndrome is more common in males between the ages of 40 and 50 years, although onset has been reported in the second through eighth decades. The disorder may be idiopathic or secondary due to a parasellar mass, internal carotid artery aneurysm, head trauma, vasculitis, or sinusitis. Johan Raeder first described the syndrome in 1918, and it appears, based on our current knowledge of headache disorders, that the idiopathic form may actually be a trigeminal autonomic cephalgia, hemicrania continua, and not a distinct entity. Evaluation would include gadolinium-enhanced MRI of the brain and MRA. If the workup is negative, then a trial of treatment with indomethacin should be initiated beginning at 25 mg three times per day and increasing up to 225 mg/daily. Topiramate is also an option.
Temporomandibular disorder
Patients with temporomandibular disorder (TMD) present with unilateral facial pain that is usually dull or aching in character and accentuated by palpation or movement of the temporomandibular joint or muscles of mastication. Intermittently, the patient may experience sharp stabbing pain in the temporomandibular region. Accompanying symptoms may include diminished excursion of the mandible on opening the jaw, deviation of the mandible suggesting subluxation and temporomandibular joint crepitations. Crepitations are significant only if there is accompanying pain, and restricted jaw movement is not required to make the diagnosis. The lower facial pain may extend into the temporal region, but the resultant headache does not have migraine-like features. TMD is more common in females, with a prevalence of 5%–15% in the general population and an incidence of 4% in adults. Risk factors for developing TMD include mood disorders, bruxism, migraine, tension-type headache, trauma, and other chronic pain conditions. Patients usually respond to a dental appliance and jaw exercises. Muscle relaxant medication such as orphenadrine or cyclobenzaprine or a tricyclic antidepressant medication, amitriptyline, or nortriptyline, may be beneficial. Surgical intervention should be considered as a last resort and only if MRI imaging of the temporomandibular joint is significantly abnormal. Botulinum toxin A injections into the masseter muscle may provide relief for up to 3–4 months.
Intracranial Lesions
Referred pain to the face may be the result of a mass lesion such as meningioma, schwannoma, neurofibroma, cholesteatoma, pituitary tumor, or nasopharyngeal cancer. The pain is caused by traction on or inflammation of meninges, cranial nerves, or blood vessels. The pain is most often dull, nonpulsatile, constant, and unremitting, aggravated by exertion and change in position, but intermittent neuralgic pain may occur. Headache and facial pain, however, are rarely the presenting symptom of tumor. Thalamic lesions such as stroke may cause unilateral burning facial pain accompanied by a dysesthetic sensation. Constant severe unilateral lower facial pain extending into the ear may be the presenting symptom of nonmetastatic lung cancer. If an underlying structural lesion is suspected, then an MRI of the brain with gadolinium should be performed. For unremitting lower facial pain without an obvious cause, a chest CT scan should be considered.
Primary Headache Disorders
The primary headache disorders are discussed in detail in another chapter, but clinicians must be mindful of the fact that the trigeminal autonomic cephalgias and migraine may present with middle and lower orofacial pain. It often takes years for a patient with cluster headache to be accurately diagnosed, and patients who report severe unilateral maxillary pain during an attack often undergo unnecessary dental procedures. Also due to the prominent autonomic symptoms, specifically nasal congestion and discharge, in association with the severe pain, many patients are subjected to sinus surgery. The interventions are not performed with any malice, as the treating clinicians are desperately trying to provide relief for their patients who are suffering from disabling head pain that is often referred to as the “suicide headache.” Severe retro-orbital and periorbital pain occurs with cluster headache, paroxysmal hemicrania, and short-lasting unilateral neuralgiform headache (SUNA). Migraine headache may also be confined to the face on occasion, and “facial migraine” and “lower half headache” are well described in the literature but not listed as a distinct diagnostic entities in the ICHD-3 classification. With “facial migraine” the pain is confined to the lower face and accompanied by typical migrainous features, including nausea, photophobia, and phonophobia.
CRANIAL NEURALGIA
Trigeminal Neuralgia
In 1677, John Locke provided the first detailed description of trigeminal neuralgia, and a French physician, Nicholas Andre, in 1756 coined the term “tic douloureux,” as the episodes of facial pain were associated with transient twitching of the facial muscles. The classification of trigeminal neuralgia has evolved over the years, and the most current criteria are listed in the ICHD-3 ( Box 12.1 ). The classification includes subdivisions, and a diagnosis of classical trigeminal neuralgia is made when there is evidence of neurovascular compression, usually by the superior cerebellar artery, on MRI/MRA sequences with nerve root atrophy or displacement. If the trigeminal neuralgia is due to compression from a mass or a demyelinating plaque, it is then referred to as secondary trigeminal neuralgia. If the etiology is unknown and imaging and electrophysiologic testing are normal, then the diagnosis is idiopathic trigeminal neuralgia. While most patients are pain free between the paroxysms of pain, some will experience continuous dull discomfort, which is officially referred to as tri-geminal neuralgia with concomitant continuous pain. Figure 12.1 depicts the nerves of the face.
Diagnostic criteria
Recurrent paroxysms of unilateral facial pain in the distribution(s) of one or more divisions of the trigeminal nerve, with no radiation beyond, and fulfilling criteria B and C
- A.
Pain has all of the following characteristics:
- 1.
lasting from a fraction of a second to 2 minutes
- 2.
severe intensity
- 3.
electric shock–like, shooting, stabbing or sharp in quality
- 1.
- B.
Precipitated by innocuous stimuli within the affected trigeminal distribution
- C.
Not better accounted for by another ICHD-3 diagnosis
Trigeminal neuralgia is rare, with a lifetime prevalence of 0.3%. The disorder is slightly more common in females, and while most patients are over 50 years of age, patients with idiopathic or secondary trigeminal neuralgia may present at a younger age. Trigeminal neuralgia is sporadic, but up to 11% of patients have a family history. While cluster headache has been referred to as the “suicide headache” trigeminal neuralgia has been described as the “suicide disease” because of the excruciating pain. Episodes are paroxysmal, brief, lancinating and shock-like with repetitive attacks occurring over a period of usually less than 1 hour. The pain is almost always unilateral, more often right sided, and predominantly confined to the second and third divisions of the trigeminal nerve ( Table 12.1 ). Bilateral trigeminal neuralgia should raise the possibility of a demyelinating lesion secondary to multiple sclerosis. Trigeminal neuralgia occurring in the distribution of the ophthalmic division of the trigeminal nerve occurs in fewer than 5% of affected patients and is often accompanied by mild autonomic symptoms, making the distinction between trigeminal neuralgia and short-lasting unilateral neuralgiform headache with cranial autonomic symptoms (SUNA) somewhat murky. Ninety-nine percent of patients with trigeminal neuralgia report triggers such as brushing teeth, chewing food, talking, shaving, applying makeup, touching the face, or exposure to a cold wind. After a series of severe paroxysmal attacks, patients often describe a refractory period during which the triggers no longer precipitate pain. It is interesting that SUNA patients also describe triggers but without a refractory period, and the age of onset is much later than with other trigeminal autonomic cephalgias. Patients with trigeminal neuralgia may experience random remissions from pain lasting from weeks to years.
| Ophthalmic (V1) | Frontal |
|
| Nasociliary |
| |
| Lacrimal | ||
| Maxillary (V2) | In middle cranial fossa |
|
| In pterygopalatine fossa |
| |
| Mandibular (V3) | In middle cranial fossa |
|
| Anterior division |
| |
| Posterior division |
|
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