|Clinicians need to recognize and understand that not all “toothaches” are of odontogenic origin.|
|Neuropathic pains, episodic or continuous, may present with symptoms that mimic odontogenic pain but require medical or surgical intervention instead of routine dental intervention.|
|Clinicians should have an understanding of neuropathic processes to avoid misdirected or incomplete treatment.|
|Referral to other health care providers should be a consideration when patients present with complex and confusing symptoms.|
|Management of neuropathic pain often requires a multidimensional and multidisciplinary approach.|
Neuropathic pain is defined as pain that arises from injury, disease, or dysfunction of the peripheral or central nervous system,1 as compared with somatic pain, which occurs in response to noxious stimulation of normal neural receptors. Neuropathic pain is generally classified according to the agent of insult and anatomical distribution of the pain. Neuropathic pain, based on temporal features, can be episodic or continuous and can be peripherally generated or centrally mediated. Often both central and peripheral sensitization play a role in the continuation of the condition. Patients experiencing neuropathic pain may complain of a combination of spontaneous (stimulus-independent) or touch-evoked (stimulus-dependent) pain.2 Characteristically, sensory signs and/or symptoms accompany neuropathic pain. These signs may be either positive (eg, hyperalgesia) or negative (eg, numbness).3 Thermal or mechanical allodynia are also signs significantly associated with neuropathic pains.4
Throughout this chapter, the codes from the International Headache Society (IHS) and The International Classification of Diseases, Tenth (ICD-10) and Ninth (ICD-9) Editions are presented for each disorder.
Head and neck pain are mediated by afferent fibers in the trigeminal nerve, nervus intermedius, glossopharyngeal and vagus nerves, and the upper cervical roots via the occipital nerves. Neuralgia results when these nerves are stimulated by compression, distortion, exposure to cold, or other forms of irritation or by a lesion in the central pathways. A common characteristic of this pain is a paroxysmal, sharp, stabbing, or electric shock–like quality felt in the area innervated by the involved nerve. The pain is often triggered by mild and innocuous stimuli. Neuralgia is named according to the nerve involved, with the most common type of neuralgia being trigeminal neuralgia.
Trigeminal neuralgia (IHS 13.1; ICD-10 G50.0; ICD-9 350.1)
Trigeminal neuralgia (also known as tic doulou-reux) is a painful condition that affects the face unilaterally in the distribution of one or more divisions of the trigeminal nerve. The condition is characterized by brief (paroxysmal) electric shock–like or lancinating pains that are typically precipitated by nonpainful stimuli, such as washing or lightly touching the face, shaving, talking, and brushing the teeth. The pain may also be spontaneous in nature. The paroxysmal pains are usually severe, with a duration of seconds to a few minutes. Frequently, there is a refractory period in which an outburst cannot be provoked. Sometimes several paroxysms will occur in succession and “fuse,” with the patient describing a longer duration of pain. In addition, some patients who have frequent attacks of pain will describe a longer-lasting burning sensation in the same distribution.
The condition is marked by remission periods lasting days to years during which little or no pain is noted. The pain-free intervals usually become shorter and the exacerbations intensify as the neuralgia progresses.5–7 Attacks usually occur during waking hours but may also awaken the patient from sleep.8,9 Clinically, there do not appear to be any neurologic deficits.10 The second and third divisions of the trigeminal nerve are most commonly affected; the first division is affected in only 1% to 2% of patients. The right side of the face is more often involved than the left. The pain does not cross the midline of the face, although the condition may affect the face bilaterally in as many as 3% to 5% of patients. The neurologic examination is normal.10 The average age of onset is approximately 50 years, and the prevalence has been estimated to be 107.5 males/million and 200.2 females/million.11
The pathogenesis of trigeminal neuralgia is not completely understood, but there are many hypotheses. Trigeminal neuralgia has been investigated as a result of demyelination, or the loss of the insulating myelin sheath that separates individual nerve fibers. The cause of the demyelination is most frequently a result of compression of the trigeminal nerve root close to its entry into the pons by overlying blood vessel(s).12 This compression and resultant deformation of the trigeminal nerve root and some of its insulating myelin is thought to allow for spontaneous nerve firing and ephaptic cross-talk among adjacent fibers (cross stimulation of C fibers).13 This hypothesis may account for the presentation of innocuous stimuli resulting in spontaneous perception of pain.
Other possible causes for demyelinating compression of the trigeminal nerve include a variety of compressive or invasive tumors.14 This compression can be caused by invasion of the tumor itself or by the trigeminal nerve being trapped between the tumor and an adjacent structure. Rarely is trigeminal nerve compression caused by a bony malformation or a disease process. Tumors, usually carcinoma, can cause infiltration of the trigeminal nerve root or ganglion, as well as any other part of the trigeminal nerve, and rarely are a cause for typical trigeminal neuralgia. Occasionally, saccular aneurysm, arteriovenous malformation, or other vascular anomalies can be the cause for the compression and resultant demyelination.13 Clinically, suspicious signs of intracranial tumor include reduced corneal reflex and hypoesthesia. Diagnosis is confirmed by magnetic resonance imaging (MRI).
Primary demyelinating disorders, such as multiple sclerosis (MS), may also be associated with the symptoms of trigeminal neuralgia. MS increases the risk of developing trigeminal neuralgia by a factor of 20.15 Bilateral trigeminal neuralgia (14% to 31% in MS) or trigeminal neuralgia in a young patient may be indicative of underlying MS.16,17 Trigeminal neuralgia will precede MS in only 0.3% of patients.18 Interestingly, only a minority of patients with MS show vascular compression of the trigeminal nerve root. Decompression procedures on these few specific patients often relieve the neuralgia-like symptoms.19
Nondemyelinating lesions, such as those associated with an infarction of the brainstem or angioma, can also be the cause of trigeminal neuralgia.20 Some researchers have reported familial trigeminal neuralgia, suggesting that there are genetic traits that are autosomal dominant. Charcot-Marie-Tooth disease is an autosomal-dominant sensory motor type I neuropathy associated with peripheral demyelination and hence could produce trigeminal neuralgia–like symptoms.21
Although there appears to be a strong association between demyelination and trigeminal neuralgia, demyelination theories alone do not account for many of the characteristics of this particular neuropathy. Devor et al22 proposed the ignition hypothesis, which takes the demyelination theories one or more steps further. The ignition hypothesis attempts to explain the phenomena of:
• Triggering, or how a trigger stimulus such as light touch can cause severe pain that long outlasts the stimulus.
• Amplification, or how the innocuous stimulus results in a spreading response far beyond the area innervated by the originally stimulated nerve fibers.
• Stop mechanism, or how the pain response is sustained for a period of time and then actually stops itself.22
Earlier, Rappaport and Devor23 explained 13 out of 14 key features of trigeminal neuralgia based on neuronal abnormalities related to nerve injury. In most cases, this injury is related to nerve root compression, but other forms of injury may apply. Nerves that are injured become hyperexcitable and therefore may fire with little or no stimulus. These so-called ectopic pacemaker sites may actually be at points of demyelination or at the ends of severed nerves.22 Some sites may fire continuously at a low level and produce a dull, background, burning pain, and yet others may require only the slightest stimulation to produce a long-lasting burst of impulses that result in severe pain lasting long beyond the initial stimulus.24
Nerve fibers may recruit other adjacent fibers and so on, causing short-lasting shooting pain from one point to another.23 Once ignited, there can be further amplification of the pain by ephaptic transmission or electrical cross-talk between nerve fibers at a site of injury or compression, whereby the adjacent nerve fibers have lost their insulating neural sheaths, allowing direct “short circuit” stimulation.25
The stop mechanism can be explained by hyperpolarization of the neuron. This stops the burst, and until the ionic imbalance returns to its prestimulation levels, the nerve fiber can no longer be stimulated.22 Not only is the burst of pain stopped, but for a period of time it cannot be triggered again. This period is called the refractory period.
In the majority of patients who have undergone surgical treatment for trigeminal neuralgia, microvascular compression of the trigeminal nerve root was identified. These patients mostly responded well to microvascular decompression surgery. Compressive damage of trigeminal ganglion has been found in patients as well.26
If no pathologic factor other than vascular compression is identifiable, the neuralgia is classified as “Classical (idiopathic or primary) trigeminal neuralgia” (IHS 13.1.1). The vast majority (> 85%) of trigeminal neuralgia patients are diagnosed with classical trigeminal neuralgia. If the neuralgia is caused by a verifiable lesion such as a tumor, epidermoid cyst, (eg, acoustic neurilemoma or meningioma), cholesteatoma, osteoma, aneurysms, or vascular malformations,27 it is classified as “Symptomatic or secondary trigeminal neuralgia” (IHS 13.1.2). Trigeminal neuralgia must be differentiated from other causes of facial pain, including local dental disorders, sinus disease, head and neck neoplasms and infections, atypical postherpetic neuralgia, persistent idiopathic facial pain, and headache or facial pain associated with a temporomandibular disorder (TMD) (IHS 11.7). Additionally, two other pain conditions that have to be considered in the differential diagnosis are short-lasting, unilateral, neuralgiform headache with conjunctival injection and tearing (SUNCT) (IHS 3.3) and primary stabbing headache, previously called the jabs and jolts syndrome (IHS 4.1). As part of identifying other causes of the pain, imaging studies of the head and brain may be indicated.
The treatment for classical trigeminal neuralgia can be divided into two modalities, medical and surgical.
Medical management. Carbamazepine is the most effective medication for trigeminal neuralgia. The initial response to carbamazepine is good (70%) but drops dramatically (20%) after 5 to 16 years of use.28 The starting dosage is 100 mg/day, and then the dosage is increased by 100 mg every 2 days to a maximum of 1,200 mg/day in a divided-dose regimen. A beneficial effect is often apparent within hours to a couple of days after starting this medication. The most common side effects include drowsiness, dizziness, unsteadiness, nausea, and anorexia. These are often transient and can be reduced by starting with a low dose and increasing the dose slowly. Aplastic anemia is a rare side effect, while a transient elevation in liver enzymes may occur in 5% to 10% of paitients and transient leukopenia may manifest in 5% of patients (persistent in 2%). Therefore, patients taking this drug need to have their blood levels carefully monitored for these potential complications. Sustained preparations have improved compliance and reduce the medication’s sedating side effects. A recent Cochrane Database systematic review concerning the efficacy of carbamazepine for the treatment of trigeminal neuralgia revealed only five placebo and three active randomized controlled trials (RCTs). The numbers in the studies that could be evaluated were small but showed that there is evidence that carbamazepine is effective in the treatment of trigeminal neuralgia.29
Phenytoin has been prescribed for the treatment of trigeminal neuralgia. However, long-term success was achieved in only 25% of cases when used alone. The combination of phenytoin and baclofen appears to be more effective.30,31 Common side effects are drowsiness, dizziness, asthenia, and gastrointestinal discomfort.
Gabapentin may be a useful alternative first-line treatment. Compared to carbamazepine and phenytoin, gabapentin has minimal side effects and is better tolerated by older patients.32,33 However, there are no RCTs specifically investigating the efficacy of phenytoin or gabapentin for trigeminal neuralgia.34,35 Pregabalin, an antiepileptic drug structurally related to gabapentin, has shown to be efficacious in the treatment of trigeminal neuralgia in an open-label study36 and according to patient-reported outcomes.37
Oxcarbazepine, a keto-analog of carbamazepine that has no known potential for bone marrow or hepatic toxicity, has also shown efficacy in the treatment of trigeminal neuralgia.38,39 Oxcarbazepine is started at 150 mg twice daily, and the daily dose is increased as tolerated to 300 to 600 mg twice daily with a maximum dose of 2,400 mg/day. Side effects are similar to those from carbamazepine except that hyponatremia occurs more frequently. There are no controlled clinical trials studying the efficacy of oxcarbazepine compared with a placebo for the treatment of trigeminal neuralgia.
One small, double-blind, placebo-controlled study showed that lamotrigine was superior to placebo in trigeminal neuralgia.40 It has recently been validated for refractory cases, especially in trigeminal neuralgia due to MS, with doses between 100 and 400 mg daily.41 Side effects may include diplopia, ataxia, dizziness, headache, and gastrointestinal discomfort. Lamotrigine should be promptly discontinued at the first sign of any rash, as serious rashes, including Stevens-Johnson syndrome, have occurred in approximately 0.1% of patients and usually appear within 2 to 9 weeks of starting treatment.40
Topiramate has shown initial promise in one very small, randomized, placebo-controlled pilot study.42,43 In a meta-analysis comparing topiramate with carbamazepine, it was reported that there seemed to be no differences in the overall effectiveness and tolerability between these two medications in the treatment of classical trigeminal neuralgia; however, a favorable effect of topiramate was present after a 2-month duration.44 Topiramate is started at 25 mg twice daily and increased slowly by 100 mg/day every 1 to 2 weeks, aiming for a daily dosage of 100 to 400 mg divided twice daily. Side effects can include anorexia, weight loss, somnolence, anxiety, fatigue, psychomotor slowing, urolithiasis, and glaucoma. For all of the newer anticonvulsants, including gabapentin and oxcarbazepine, larger RCTs are needed to more precisely estimate their treatment effectiveness.
Cochrane Database systematic reviews concluded that there is insufficient evidence from RCTs to advocate the use of nonseizure medications, including baclofen, tizanidine, tocainide, proparacaine hydrochloride, pimozide, clomipramine, and amitriptyline, for the treatment of trigeminal neuralgia. Overall, the methodologic quality of the studies was considered poor, and side effects associated with the medications were common.45,46
Surgical management. Several peripheral and central surgical procedures have been recommended to treat trigeminal neuralgia. Peripheral procedures include neurectomy, cryotherapy, and alcohol injection. Procedures aimed at traumatizing or destroying nerve tissue in or near the gasserian ganglion include radiofrequency thermocoagulation, percutaneous glycerol rhizotomy, and percutaneous balloon microcompression. The central surgical procedures include microvascular decompression and stereotactic radiosurgery (gamma knife) surgery.
Neurectomy is a peripheral ablative procedure in which the offending trigeminal nerve branch is avulsed under local or general anesthesia. Success rates for neurectomy are conflicting (50% to 64%) and involve relatively small series with short-term follow-up.47 Common side effects are hypoesthesias and paresthesias, 48,49 and pain recurrence is frequent.
Cryotherapy is a peripheral ablative procedure in which the offending trigeminal branch is frozen under general or local anesthesia. A recently designed probe allows the procedure to be performed without surgical exposure of the nerve.50 Generally, the effects of cryotherapy are short lasting (6 to 12 months),50,51 although longer pain relief has been reported.52 Side effects may include atypical facial pain and sensory deficits.
Alcohol injections are performed under local anesthesia. After the affected branch of the trigeminal nerve is anesthetized, a small amount of absolute alcohol is deposited. Compared to neurectomy and radiofrequency thermocoagulation, alcohol blocks result in a higher percentage of recurrence but fewer side effects.48 Side effects typically include hypoesthesia, paresthesia, and dysesthesia as well as the potential for tissue fibrosis, reactivation of herpes zoster, and bony necrosis.47 Duration of pain relief is generally less than 1 year.53 However, the procedure can be repeated without impact on the extent or duration of pain relief.53 Because of the risk of developing neuropathic pain, peripheral procedures should be reserved for patients with significant medical problems that make other procedures unsafe.47
Three types of gasserian ganglion procedures are available for treatment of trigeminal neuralgia. Percutaneous radiofrequency ther-mocoagulation and percutaneous glycerol rhizotomy are neurosurgical procedures in which a needle, guided by radiographic fluoroscopy, is placed into the foramen ovale of the sedated patient. After careful manipulation and feedback from the patient, the selected nerve fibers are destroyed by thermal lesioning54 or by injection of anhydrous glycerol.55,56 Corneal numbness and masseter weakness are the most common complications of radiofrequency thermocoagulation (10% to 12%).57 Corneal numbness and dysesthesia are the most common complications of percutaneous glycerol rhizotomy (8% each).57
Percutaneous balloon microcompression is a neurosurgical procedure in which the trigeminal nerve is compressed by inflating a tiny balloon in the area of the involved nerve fibers.58,59 The needle placement is similar to that of the other two procedures. Reports show high rates of immediate pain relief with balloon compression (91% to 100%),60–62 and the recurrence rates at 12 to 18 months were low (2.5% to 5%).60,62 A retrospective study with an average follow-up time of almost 11 years reported 19% recurrence within a 5-year period and 32% recurrence over a 20-year period.63 Side effects of this procedure include numbness and dysesthesia, the severity of which may be related to the amount of compression applied.60 Transient masseter weakness is reported with high frequency.64 Other complications include arterial and cranial nerve injuries.
An alternative to rhizotomy is microvascular decompression of the gasserian ganglion and dorsal root, first described in 1952 by Taarnhoj65 in Denmark and by Love66 in the United States. Jannetta67 refined and popularized this procedure, which involves a craniotomy in which the posterior fossa is opened and explored. The cortex is carefully lifted, exposing the root entry zone of the trigeminal nerve while the offending vessel or lesion responsible for compressing the nerve root is located. The superior cerebellar artery is the most common offending vessel. The vessel is carefully dissected from the trigeminal nerve, and a sponge is placed between the structures, often resulting in immediate success. Although microvascular decompression appears to have great long-term success, a major surgical procedure is required, along with its accompanying morbidity (0.3 to 3%) and mortality.68 Patient selection is therefore extremely important. Relatively young, healthy patients are the best candidates.
A minimally invasive method to treat trigeminal neuralgia is stereotactic neurosurgery (gamma knife surgery). Precisely focused radiation of 40 to 90 Gy emitted from 201 photo beams is applied to the trigeminal root entry zone in the posterior fossa. Compared to other procedures, onset of pain relief is delayed.69 Reports of pain relief vary from 61% to 92%,69–72 while recurrence rates vary from 10% to 27%.70–72 Dysesthesia is the most prominent side effect related to stereotactic radiosurgery (9%),57 and this appears inversely related with pain control.73–75 Repeat surgeries seem to be as efficacious as initial surgeries.73–76 Safety and efficacy of the procedure after more than one repeat surgery have not been established, and repeat surgery should be used selectively because no data are available on the effects of cumulative radiation dose.
There are no RCTs comparing different types of surgeries or comparing surgeries with medications for trigeminal neuralgia. A recent thorough systematic review including only high-quality studies with actuarial data evaluated the treatment efficacy of radiofrequency thermocoagulation, percutaneous glycerol rhizotomy, percutaneous balloon compression, and stereotactic radiosurgery.57 This review revealed that, whereas radiofrequency thermocoagulation showed the longest pain relief, the complications, though transient, were also the most frequent. Radiofrequency thermocoagulation and percutaneous glycerol rhizotomy yielded higher percentages of complete pain relief at 6, 12, and 24 months than stereotactic radiosurgery. However, after 2 years, the pain-relieving effects of glycerol rhizotomy rapidly declined. From a recent study, it appears that microvascular decompression and balloon compression have the best prospects to improve the quality of the patient’s life. Percutaneous glycerol rhizotomy and radiofrequency thermocoagulation also yielded favorable results, whereas medications were the least likely to improve the patient’s quality of life.77
A recent Cochrane Database systematic review concluded that there is a very low quality of evidence for the efficacy of most neurosurgical procedures (no studies of microvascular decompression met inclusion criteria) because of the poor quality of the trials. All procedures produced variable pain relief, but many resulted in sensory side effects.78
The American Academy of Neurology and the European Federation of Neurological Societies have published guidelines regarding trigeminal neuralgia management (medical and surgical).79
Pretrigeminal neuralgia (no IHS category; ICD-10 G50.9; ICD-9 350.9)
Pretrigeminal neuralgia was first described in the literature by Sir Charles Symonds.80 Fromm at al81 reported on 16 patients who initially complained of a dull, continuous toothache in the maxilla or the mandible and whose pain changed to classic trigeminal neuralgia. Tri-geminal neuralgia can be accompanied by a dull, continuous pain in between attacks. A retrospective chart review revealed that 35 of 83 patients with trigeminal neuralgia also reported continuous dull, achy pain in the same area. Of these patients, 14% reported that the dull, achy pain preceded the development of trigeminal neuralgia, which may have been cases of pretrigeminal neuralgia.82 No reports on the prevalence of pretrigeminal neuralgia are available. The diagnosis is based on the description of a dull toothache-like pain, normal neurologic and dental examinations, and a normal computerized tomography (CT) or MRI scan of the head. Pretrigeminal neuralgia has been treated successfully with medications traditionally used for trigeminal neuralgia.83
Glossopharyngeal neuralgia (IHS 13.2.x; ICD-10 G52.1; ICD-9 352.1)
“Classical glossopharyngeal neuralgia” (IHS 13.2.1) is similar in character to trigeminal neuralgia but is present in the distribution of the glossopharyngeal nerve and may be present in the distribution of the auricular and pharyngeal branches of the vagus nerve. The pain is typically severe; transient; stabbing or burning; and located in the ear, base of the tongue, tonsillar fossa, or beneath the angle of the jaw. The pain is unilateral, although 1% to 2% of patients may experience nonsimultaneous bilateral pain. The paroxysms of pain usually last seconds to 2 minutes and are provoked by swallowing, chewing, talking, or yawning. It may relapse and remit like trigeminal neuralgias. The incidence of glossopharyngeal neuralgia is estimated to be 50 to 100 times less than trigeminal neuralgia.84 The co-occurrence of trigeminal neuralgia and glossopharyngeal neuralgia is common and expected to occur in 10% to 12% of glossopharyngeal neuralgia patients.84 The neurologic examination is normal. The pathophysiology is thought to be similar to that of idiopathic trigeminal neuralgia.
The evaluation of a patient with glossopharyngeal neuralgia should include an MRI scan with contrast to exclude “Symptomatic glossopharyngeal neuralgia” (IHS 13.2.2), which may arise due to posterior fossa tumor, fusiform (dolichoectatic) vertebral or basilar arterial pathology, and vascular anomalies. Additionally, local causes for the pain, such as infection and nasopharyngeal tumor, must be excluded.
Effective treatment can often be accomplished with the same anticonvulsant medications used for the treatment of trigeminal neuralgia, such as carbamazepine, oxcarbazepine, baclofen, phenytoin, and lamotrigine either alone or in combination.38,85 Surgical procedures include intracranial sectioning of the glossopharyngeal nerve and the upper rootlets of the vagus nerve and microvascular decompression of the glossopharyngeal nerve or gamma knife surgery.86,87
Nervus intermedius neuralgia (IHS 13.3; ICD-10 G51.9; ICD-9 351.9)
Nervus intermedius neuralgia is a rare condition that is characterized by unilateral paroxysms of pain felt in the depth of the ear and lasting seconds or minutes. An alternative term used for this condition is geniculate neuralgia, because the cell bodies of the sensory afferents are located in the geniculate ganglion. There is often a trigger zone in the posterior wall of the auditory canal. Disorders of lacrimation, salivation, and taste are sometimes present. This type of neuralgia is frequently associated with herpes zoster.3,88–90 Medications used for trigeminal neuralgia may be tried. Surgical section of the nervus intermedius or chorda tympani may relieve the pain. Local ear disorders must be ruled out.
Superior laryngeal neuralgia (IHS 13.4; ICD-10 G52.2; ICD-9 352.3)
Superior laryngeal neuralgia is a rare condition with severe paroxysmal pain felt in the throat, submandibular region, or under the ear, with a duration of minutes to hours. Episodes of pain are precipitated by swallowing, straining of the voice, or head turning, and a trigger point is located on the lateral aspect of the throat overlying the hypothyroid membrane, through which the internal branch of the superior laryngeal nerve enters the laryngeal structures.91 Disorders that must be considered in the differential diagnosis include neoplasms, bursitis lateralis, neuritis, and neuritis laryngei cranialis (seen during influenza epidemics). Medications traditionally used for trigeminal neuralgia may be effective. Repeated nerve blocks with high doses of lidocaine (5% to 10%) have shown lasting effects.92
Painful ophthalmoplegia (IHS 13.16; ICD-10 H51.9; ICD-9 378.9)
Painful ophthalmoplegia is characterized by episodes of orbital pain accompanied by paralysis of one or more of cranial nerves III, IV, or VI. Lesions of one or more of these nerves, caused by vascular, neurologic, inflammatory, infiltrative, or space-occupying processes, may underlie the symptoms. Such lesions may be demonstrated on CT or MRI carotid angiography. Episodes are said to have a duration of 8 weeks in untreated patients; patients experience relief of pain within 72 hours of initiation of corticosteroid therapy. The differential diagnosis includes pseudotumor of the orbit and temporal arteritis, vascular lesions, and ophthalmoplegic migraine.93
Idiopathic (trigeminal) neuropathic pain (ICD-10 G50.9; ICD-9 350.9)
This category has historically been referred to as atypical facial pain or more recently by the IHS classification as “Persistent idiopathic facial pain” (IHS 13.18.4). Because both of these terms may be regarded as catch-all terms, it is preferred to refer to this category as idiopathic continuous neuropathic pain. More recently, it has been proposed that this entity be termed peripheral painful trigeminal traumatic neuropathy. 94 This term has recently been field-tested and was reported to be clinically applicable in the detection and characterization of relevant cases.94