Management of Trigeminal Neuropathies and Other Facial Pains

Introduction to trigeminal neuropathic pain

This review serves as a guide in the evaluation and management of facial neuropathic pain. Many facial pains mimic a neuropathy and the patient and clinician need a systematic and careful approach to diagnosis.  Common conditions such as myofascial pain, temporomandibular disorder (TMD), dental pathology (caries or gum disease), cracked teeth, infectious causes, sinusitis, or neurovascular causes, like migraine headache must be considered in the differential diagnosis. Myofascial Pain and TMD are very common and will also be reviewed.

It is not uncommon for a dentist to mistake the pain as dental-related and proceed with unnecessary dental treatments, which can worsen a neuropathy. Similarly the diagnosis of sinus pathology or atypical facial pain (a wastebasket term) by a physician may lead to unnecessary therapies and additional frustration and suffering for the patient. Through better medical understanding by the patient, such unnecessary treatments and misdiagnoses can hopefully be avoided and prompt referral to the proper orofacial pain specialist can be made. Likewise, patients should be made aware of the various new treatment options available to them. One reason for poor response to treatment may be inaccurate diagnosis. Differentiating between the various types of facial pains and mechanisms associated with neuropathies can sometimes be confusing, especially if the symptoms are complex and don’t fall into any one specific category. 

Neuropathies Defined 

Neuralgia is defined as pain in the distribution of a nerve or nerves. Simply put, pain involved in the nervous system is considered a neuralgia. Stimulation of these nerves, by mechanical, thermal or chemical energy may create pain, which is generically neuralgia. Clinically neuralgia can present as a continuous or intermittent pain characterized as stabbing, shooting, electric or sometimes constant burning-like sensation. The pain is felt along the nerve distribution.  

The term neuropathic actually requires there to be the presence of a lesion or disease within the neural system. By definition, the “pathic” part of the word tells us that there’s some sort of “pathological” abnormality as a causal factor. Pathologies refer to any sort of abnormality, including injury, tumor, or disease affecting the neural structure. Neuropathic pains can then also be sub-classified even further based on their location as being either central or peripheral; meaning is the pathology (abnormality) located in the brain/spinal cord (centrally) or outside the brain (peripherally). So a neuropathy is basically thought of as a disturbance in function or pathological change in a nerve or nerves.

If only one nerve is involved, it’s called mononeuropathy. If several nerves are involved, it’s referred to as mononeuropathy multiplex. And if it’s diffused throughout the body, it’s called polyneuropathy. Although “trigeminal neuralgia” is caused by a blood vessel compressing and injuring the nerve it is actually a neuropathy, but received its name prior to our current understanding. The term neurogenic is a temporary pain in the nervous system, a nerve disturbance caused by a transient process. This can be thought of as a short-term issue, like a “bruising of the nerve” from something like a blow or stretch that will cause pain for a while, but will then fully recover later.

Clinically neuropathic pain presents with allodynia (increased response to a non-painful stimulus), hyperalgesia (increased response to painful stimulus), hyperpathia (abnormally painful response to a repetitive stimulus), pseudo motor abnormalities (temperature changes), and a block effect, where blocking the sensory or autonomic nerves provides information as to the mechanisms.   

Neuropathic pain can also be further classified based on whether the pain is characterized as being episodic (i.e. cranial neuralgia) or continuous (ie traumatic trigeminal neuropathy, post-herpetic neuralgia, etc.). In the trigeminal nerve neuropathic pain commonly occurs in females in their forties. The relationship to estrogen is clear, with 90-100% of patients with neuropathy in the trigeminal nerve distribution being female. The injury causing neuropathy may range from a minor procedure such as an injection, filling or crown preparation to endodontic intervention, extraction, or complete reconstructive jaw surgery.  

Trigeminal Neuralgia

Classical trigeminal neuralgia (TN) is characterized by sharp, stabbing, paroxysms of severe pain, typically lasting a fraction of a second to two minutes. The paroxysms are very severe in intensity, usually having a trigger zone or an action that will trigger that will activate the shock-like jolt. The pain is almost always unilateral and located in the second (midface or maxilla) or third (mandible or jaw) trigeminal nerve branches. Pain rarely is seen in the first division (forehead or ophthalmic). Short lasting pain in the forehead should be considered as something other than trigeminal neuralgia. 

The most common alternative diagnosis is SUNCT (Short lasting, unilateral neuralgiform pain with conjunctival injection and tearing). It’s duration is usually 5-250 seconds and is accompanied by the eye tearing and redness. SUNCT is classified as a Trigeminal Autonomic Cephalalgia. Epidemiological studies report an incidence of 4-6 per 100,000 patients and that it occurred in the 50-70 age group and was more common in women than men.  However, more recent studies carried out in research primary care practices, suggest the incidence is actually closer to 28 per 100,000 patients. The cause is typically nerve compression by a vessel, usually the superior cerebellar artery on the trigeminal nerve root as it leaves the brain stem or pons. 

Multiple sclerosis, which causes demyelination of the nerve may also cause trigeminal neuralgia. Tumors in the posterior cranial fossa may also cause trigeminal neuralgia. It is essential that patients with pain in the trigeminal nerve distribution obtain appropriate imaging to help define the diagnosis and etiology. This is usually an MRI of the brain with and without contrast with specific attention to the trigeminal nerve.  

Classical trigeminal neuralgia with purely paroxysmal pain is also marked by periods of complete pain-free remissions. However, there is another subtype of classical trigeminal neuralgia which has the same paroxysmal sharp pains, but with a concomitant continuous, persistent dull, aching background pain that is mild to moderate in intensity. This subtype used to be called TN Type 2 or Atypical TN due to the “atypical” nature of its presentation.  

The diagnostic classification of classical trigeminal neuralgia from the 3rd edition of The International Classification of Headache Disorders, devised by the International Headache Society, is as follows: 

 Classical Trigeminal Neuralgia

  1. At least 3 attacks of unilateral facial pain fulfilling criteria B and C
  2. In more than or equal to 1 divisions of trigeminal nerve, with no radiation beyond trigeminal distribution
  3. Pain has more than or equal to 3 of the 4 characteristics:
  1. Recurring in paroxysmal attacks lasting from a fraction of a second to 2 min.
  2. Severe intensity
  3. Electric shock-like, shooting, stabbing, or sharp in quality
  4. Precipitated by innocuous stimuli to affected side of face

     D. No clinically evident neurological deficit

     E. Not better accounted for by another ICHD-3 diagnosis



There remains little doubt as to the efficacy of carbamazepine in the management of trigeminal neuralgia. The drug is highly effective and provides excellent pain relief within a few days.  The dose is between 100 mg and 1200 mg daily. Because there are potential side effects, baseline blood tests should be obtained and repeated every few months to ensure there is no anemia or drop in sodium (hyponatremia). 

Oxcarbazepine is a very useful alternative as it has similar efficacy but greatly improved tolerability and relative lack of interaction with other drugs.  The dosing is between 150 mg and 1500 mg daily in two or three doses. As with carbamazepine blood tests to evaluate anemia and hyponatremia must be considered. 

Lamotrigine is a useful drug in patients who develop allergies to carbamazepine and oxcarbazepine but the need for slow escalation in order to reduce skin reactions means it is not useful for rapid relief. It is used in doses of 12.5 -300 mg daily. It may also be useful in those patients who have been mistakenly diagnosed as trigeminal neuralgia but in fact have SUNCT or SUNA. 

The second generation anticonvulsant drugs like gabapentin may be used as a third line drug.  Although the side-effects of gabapentin are quoted as being low, sleepiness, weight gain and edema seem to be frequently reported.  

Pregabalin appears to be a promising drug in that it can be escalated more rapidly and can be used on a twice daily dosage scheme and does appear to have some effect on reducing anxiety often present in these patients. In the type II trigeminal neuralgia where there is a continuous or longer lasting dull, burning, aching background pain, the addition of a tricyclic antidepressant such as nortriptyline, in doses around 50-100mg, at bedtime, may be helpful.  

Other anticonvulsants such as levetiracetam and zonisamide  may be useful, but have not been studied in placebo controlled trials.   Baclofen is a muscle relaxant that is very effective in trigeminal neuralgia in doses between 5 and 80 mg daily. Sedation is the most significant side effect.  Phenytoin may be used as an alternative in doses of 100 – 300 mg per day. 

Surgical management for trigeminal neuralgia is very effective. The most effective surgery being microvascular decompression. Other options include stereotactic radiosurgery, balloon gangliolysis and radiofrequency rhizotomy.  

Glossopharyngeal neuralgia 

Description: The International Association for the Study of Pain defines glossopharyngeal neuralgia as a sudden severe brief recurrent pain in the distribution of the glossopharyngeal nerve.  This disorder may be due to symptomatic causes again due to compression of the nerve by tumors, malformations or vascular compression. Glossopharyngeal neuralgia is a severe, transient, stabbing, unilateral pain experienced in the ear, base of the tongue, tonsillar fossa and/or beneath the angle of the jaw.

It is commonly provoked by swallowing, talking and/or coughing, and may remit and relapse in the fashion of classical trigeminal neuralgia.  The pain can also be felt in the auricular and pharyngeal branches of the vagus nerve.  The pain can be present for years and may have spontaneous remissions. The pain attacks last for no more than 2 minutes.  Glossopharyngeal neuralgia is even rarer than trigeminal neuralgia, with an incidence rate of 0.7 per 100,000 patients.  It occurs in the older age group and seems to predominate more in women.  The drugs used in trigeminal neuralgia are also effective for glossopharyngeal neuralgia  

Surgical management includes nerve sectioning of glossopharyngeal and pharyngeal branches of the vagus. Microvascular decompression is also a possible treatment.  

Burning mouth syndrome (BMS):  

BMS is a sensation of intraoral burning or dysesthetic sensation, recurring daily for more than two hours per day over more than three months, without clinically evident causative lesions. It is important to exclude other causes both local and systemic which can cause burning especially drugs such as the ACE inhibitors or infections such as candida or herpes simplex. It is particularly common in perimenopausal or post-menopausal women. This is not a psychological disorder, rather there is evidence it is a neuropathic pain due to loss of the small pain fibers called c fibers.   

Management of BMS is best treated with topically applied clonazepam. The patient is asked to suck a 0.5 mg tablet three times per day for three minutes and the tablet and saliva are spat out. This gives immediate relief.  Continuing to do this for up to a month may be necessary to quiet the burning. Alternative topical agents with peppermint, spice such as chili flakes, or capsaicin may also be useful. The addition of tricyclic antidepressants or antiepileptic agents may also be beneficial.  

Post traumatic trigeminal neuropathy 

The most common cause of facial neuralgia is painful trigeminal neuropathy. This may be triggered by injury to any branch of the trigeminal nerve. Commonly this is secondary to a surgical or dental procedure, but can also occur with viral injury (post herpetic neuralgia). The injury may be a perfectly performed procedure that inadvertently sensitizes the nerve. An example would be following a root canal therapy. The purpose of this treatment is to remove an abscess or dead pulp in a tooth. This requires the removal of the nerve in the tooth. The nerve is a branch of the trigeminal nerve and when it is removed it can result in nerve sensitization and persistent pain.

This form of neuropathy occurs predominantly in females in their forties and is likely linked to a genetic predisposition and hormonally affected.  The neuropathic pain following tissue or nerve injury in the trigeminal nerve distribution may be called a painful post traumatic trigeminal neuralgia or trigeminal dysesthesia (TD). PPTN is defined as a continuous pain following complete or partial damage to a peripheral nerve or central nervous system structure. The pain is described as a continuous, burning numbness and often pulling pain.  

There are a number of mechanisms described as causing traumatic induced neuropathy. They can be described as a) peripheral sensitization, b) ectopic activity due to sodium channel expression, c) central sensitization, d) A beta fiber reorganization, e) alteration in central inhibition systems, and f) sympathetically maintained pain due to alpha receptor sprouting. 

More than one mechanism may be active to create individual clinical presentations.  

a) Peripheral sensitization: Once stimulated or traumatized the peripheral nociceptors will release a variety of peptides including substance p, calcitonin gene related peptide (CGRP), and neurokinins. This results in a peripheral sensitivity that is characterized by an increased response to non-noxious (allodynia) and noxious stimuli (hyperalgesia).   

b) Ectopic firing results after trauma, likely due to the sprouting of sodium channels. The nerve is easily depolarized and spontaneous shooting pains result. 

c) Central sensitization develops once the peripheral stimuli trigger second or third order neurons. Once again there is the release of peptides, though now in the dorsal horn (trigeminal nucleus) or thalamus, resulting in pain being generated without the presence of an ongoing peripheral stimulus. The role of glial cells and release of proinflammatory cytokines also plays a role in the central nervous system causing pain. 

d) A beta fiber reorganization is another mechanism causing centrally mediated pain. It is described as occurring when the c fibers are destroyed, which usually have their second order neurons in lamina II,  allowing for spontaneous growth of A beta fibers from lamina III into lamina II, making proprioceptive and temperature stimuli activate c fiber second order neurons. Hence non nociceptive activity causes pain.  

e)  Alterations in central inhibition, or disruption of normal pain inhibiting systems may also cause chronic pain. The brain has powerful opioid and non-opioid inhibitory systems. Neurochemicals such as serotonin, norepinephrine, and GABA all help the brain modulate nociception. If these inhibitory pathways are not efficient chronic pain may exist. 

f) Sympathetically maintained pain (SMP) may be a result of alpha receptors sprouting on peripheral nociceptors resulting in norepinephrine release peripherally causing pain. There is evidence that following neural injury, the sympathetic innervation in the dorsal root ganglia increases with age. It is not surprising that there is a higher incidence of neuropathic pain as we age. SMP is aggravated by non-noxious stimuli and interrupted temporarily by sympathetic block or alpha-adrenergic block with phentolamine. 

Therapy for trigeminal dysesthesia

The therapy for trigeminal dysesthesia is aimed at reducing peripheral nociceptive inputs and simultaneously enhancing central nervous system pain inhibitory systems. Management of neuropathy is achieved with integrating four treatment strategies: topicals, pharmacologic agents, nerve blocks/ nerve procedures, and behavioral strategies. 

Topical therapy allows a medication to be delivered to the source of pain via the skin or the mucosa in the mouth. An impression can be taken of the site of pain and the dentist can construct a plastic stent that fits over the pain site, called a “neurosensory shield”. The patient can take this in an out of their mouth and apply topical medications. The common medications include benzocaine, capsaicin, and compounded agents including tricyclic antidepressants, anti-inflammatories and antiepileptic agents. The use of clonazepam suck and spit as discussed in BMS may also be useful. 

Pharmacology often requires a combination of agents. Tricyclic antidepressants, such as nortriptyline in doses of 10 mg-100 mg is the first line therapy, followed by the use of antiepileptic agents such as pregabalin 50 mg-300 mg, or gabapentin 100mg-3000 mg. Nerve blocks help define if there is involvement of the sympathetic nervous system. Seeing the result of doing a sympathetic nerve block, either stellate ganglion block or sphenopalatine ganglion block will help the clinician choose a course of care. If there is a positive response to the procedure (greater than 60% reduction in pain) the patient may be a candidate for repeated blocks (up to 6 weeks apart), or a radiofrequency (burning) procedure to the ganglion. 

Stimulation of the nerves may also be useful although experimental. Onabotulinum toxin injected to the injured peripheral sensory nerve may desensitize it. Care should be taken not to create a weakness of the face, as this agent also paralyzes the muscles. Behavioral therapy is very useful on its own or in combination with any pain management technique. This comes in many options. Use of cognitive behavioral techniques, stress management, biofeedback, hypnosis, and mindfulness are all very powerful tools that enhance the brain’s natural inhibitory systems. This can help the effectiveness of medications, procedures and natural healing.  

Temporomandibular disorders (TMD)

TMD is a collective term which may include a number of different clinical entities including muscle and joint components. Pain in the temporomandibular joint may occur in 10% of the population and TMD has been reported in 46.1% of the US population. In non-patient population studies, 75% have at least one joint dysfunction sign and about 33% have at least one symptom. Out of the 75% with a sign or symptom, fewer than 5% require treatment. 

Inflammation within the joint accounts for TMD pain and the dysfunction is due to a disk/condyle incoordination. Common suggested etiological factors for TMD include bruxism

trauma, bite abnormalities, and emotional stressors. Occlusal interferences (bite abnormalities) are by far the most controversial aspect of etiology and treatment in TMD. A literature meta-analysis does not support the theory that occlusion is a factor in TMD etiology.  

Trauma to the TMJ may result in acute capsulitis but this inflammatory process tends to resolve quickly without complication.  Chronic joint disorders are more frequently associated with painful derangement of the TMJ.  Articular disc displacement frequently underlies the mechanism of joint derangement but the etiology is unclear. The remarkable adaptive capacity of TMJ is well documented.  Failure of this mechanism may lead to tissue destruction and disc displacement.  This may be affected by age, stress, gender, systemic illness and previous trauma.  However, acute and chronic disc displacement is not always painful.  

The TMJ is unique in its bilateral location with an upper and lower compartment separated by a fibrocartilaginous disc. This diarthrodial structure allows for both rotatory and translational movement of the mandible.  Although the TMJ is subject to the same pathological disorders that affect other synovial joints, it is unique in certain anatomical aspects.  Both joints move as a functional unit and are lined by a fibrous connective tissue, which is more resistant to degenerative change and has a greater capacity for repair. 

The masticatory system includes the articulation of the upper and lower dentition that may limit or support joint function and stability. A major component in TMD is joint noise and incoordination of the disc condyle relationship. This presents as noise in the joint with or without locking, or the inability to open with a normal range of motion. This is often referred to as an “internal derangement.” Articular disk displacement is the most common temporomandibular arthropathy and is characterized by an abnormal relationship or misalignment of the articular disk relative to the condyle. This is known as a disk derangement disorder and is classified as disk displacement with reduction and disk displacement without reduction.

In disk displacement with reduction during mouth opening, the disk that begins in a misplaced position reduces or improves its structural relationship with the condyle. As it reduces, a sound often described as a clicking or popping is heard. When the mouth closes, a second sound called a “reciprocal click” may be audible as the disk moves off the condyle just before the teeth come together upon closing. Usually the closing noise is of less magnitude.

Clicking sounds are not necessarily a sign of degeneration or an indication for treatment. Over one third of an asymptomatic sample can have moderate to severe derangement as seen on imaging and as many as 25% of clicking joints show normal or slightly displaced disks. Asymptomatic clicking does not require treatment.  A disc displacement without reduction is described as an altered or misaligned disc-condyle structural relationship that is maintained during mandibular translation. This is also referred to as a “closed lock.”  

Management of TMD is usually achieved with reducing stress on the joint through exercises and splint therapy, coupled with medications such as anti-inflammatories and muscle relaxants. If locking occurs, an injection or flushing the joint may be necessary.  

Myofascial pain 

Pain associated with temporomandibular disorders (TMD) may often be muscular in origin.  The most frequent diagnosis is myofascial pain. Myofascial pain is characterized by regional muscle pain, described as dull or achy and associated with the presence of trigger points in muscles, tendons or fascia. Myofascial pain is a common cause of persistent regional pain involving the neck, shoulder head, and orofacial regions. The precise etiology of myofascial pain is unclear, but there are some developmental (e.g. stress or oral habits) and perpetuating (e.g. poor sleep, postural abnormalities, depression) factors that have been identified. The major characteristics of myofascial pain include trigger points in muscles and local and referred pain.  

Management of myofascial pain is best achieved with a series of posture, stretching and strengthening exercises, coupled with physical medicine techniques such as spray and stretch and trigger point injections. Medications helpful in myofascial pain are muscle relaxants, tricyclic antidepressants and selective serotonin / norepinephrine reuptake blockers.  


Facial pain is a complex disorder with many causes and diagnoses. When suffering with facial pain the most important component in management is diagnosis. Too often the wastebasket term “atypical facial pain” is used and if so the patient should challenge the clinician for a clearer diagnosis. It is clear that psychological factors may aggravate facial pain of any cause, but they are not to be blamed as the primary etiology. Once a diagnosis is established, persistence and perseverance in therapy will help the majority of those who suffer.

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