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Review Article

Trigeminal Neuralgia
Address correspondence to
Giorgio Cruccu, Department
of Neurology and Psychiatry,
Viale Universitá 30, Rome,
Italy 00185, Giorgio Cruccu, MD
giorgio.cruccu@uniroma1.it.
Relationship Disclosure:
Dr Cruccu has received
personal compensation for ABSTRACT
serving on the advisory board Purpose of Review: Although trigeminal neuralgia is well known to neurologists,
of and as a consultant for
Angelini and Biogen, recent developments in classification and clinical diagnosis, new MRI methods, and a
Inc and has received personal debate about surgical options necessitate an update on the topic.
compensation for serving on Recent Findings: Currently, a worldwide controversy exists regarding the classification,
the advisory board of and as a
speaker for Sigma Tau diagnostic process, and surgical treatment of trigeminal neuralgia. This controversy has
Pharmaceuticals, Inc. been caused on one side by the recognition that some 50% of patients with trigeminal
Dr Cruccu has received neuralgia, apart from characteristic paroxysmal attacks, also have continuous pain in
research/grant support
from Sapienza University of the same territory, which results in greater diagnostic difficulties and is associated with
Rome and Sigma Tau a lower response to medical and surgical treatments. In contrast, recent developments
Pharmaceuticals, Inc. in MRI methods allow differentiation between a mere neurovascular contact and an
Unlabeled Use of
Products/Investigational
effective compression of the trigeminal root by an anomalous vessel, which implies
Use Disclosure: more difficulties in the choice of surgical treatment, with the indication for
Dr Cruccu discusses the microvascular decompression becoming more restricted.
unlabeled/investigational use
of BIIB074 for the treatment
Summary: This article proposes that the diagnosis of trigeminal neuralgia, with or
of elderly patients with without concomitant continuous pain, must rely on clinical grounds only. Diagnostic
trigeminal neuralgia. tests are necessary to distinguish three etiologic categories: idiopathic trigeminal neu-
ralgia (nothing is found), classic trigeminal neuralgia (an anomalous vessel produces
morphologic changes of the trigeminal root near its entry into the pons), and
secondary trigeminal neuralgia (due to major neurologic disease, such as multiple
sclerosis or tumors at the cerebellopontine angle). Carbamazepine and ox-
carbazepine (ie, voltage-gated, frequency-dependent sodium channel blockers)
are still the first-choice medical treatment, although many patients experience
significant side effects, and those with concomitant continuous pain respond less
well to treatment. The development of sodium channel blockers that are selective
for the sodium channel 1.7 (Nav1.7) receptor will hopefully help. Although all the
surgical interventions (percutaneous ganglion lesions, gamma knife radiosurgery,
and microvascular decompression) are very efficacious, precise MRI criteria for
differentiating a real neurovascular compression from an irrelevant contact will be
of benefit in better selecting patients for microvascular decompression.

Continuum (Minneap Minn) 2017;23(2):396–420.

INTRODUCTION known as tic douloureux) is frequently
Facial pain is easily misdiagnosed. mistaken for dental pain, leading to
When the pain is intense and recurrent redundant diagnostic procedures such
and the underlying etiology is elusive, as x-rays of the jaw and, in more than
the condition is often labeled trigem- a few cases, unnecessary extractions
inal neuralgia, although other condi- of teeth.3
tions are much more likely to be the Accurate diagnosis of trigeminal
cause. The prevalence of trigeminal neuralgia depends critically on the
Supplemental digital content: neuralgia in the population is 0.07%, patient’s description of its characteris-
Direct URL citations appear in
the printed text and are in- compared to approximately 2% in tic features. Clarification of the char-
cluded in the HTML, PDF, and patients with facial pain in general.1,2 acteristics of the pain is therefore
app versions of this article.
Conversely, trigeminal neuralgia (also necessary to guide clinical diagnosis

396 ContinuumJournal.com April 2017

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

KEY POINTS
and management. Successful diagnostic and trigeminal neuralgia secondary h Although trigeminal
criteria must account for established to neurovascular contact. To solve neuralgia is
variants of the phenotype (eg, typical this problem, the International Clas- still frequently
versus atypical trigeminal neuralgia), sification of Headache Disorders misdiagnosed, its
incorporate symptoms or signs that (ICHD) endorsed the term classic, peculiar clinical features
correlate with different etiologies (pri- specifying that classic trigeminal neu- are unmistakable.
mary trigeminal neuralgia versus trigem- ralgia should be diagnosed when no h A neurovascular
inal neuralgia secondary to a major cause other than neurovascular contact compression is
neurologic disease), and identify pain is apparent.8 acknowledged as
features that indicate underlying patho- The author agrees with this solu- the most frequent
physiologic mechanisms (peripheral ver- tion because it avoids confusion. cause of trigeminal
sus central), as they are relevant to direct However, the author favors additional neuralgia (classic
further investigations or treatment de- differentiation of idiopathic trigeminal trigeminal neuralgia).
cisions (pharmacologic therapy versus neuralgia from classic trigeminal neu- h Notwithstanding the
surgery). Physicians should be aware ralgia. Even after surgical exploration most accurate and
that the literature on trigeminal neural- of the posterior fossa at the base of advanced investigations,
gia has been hampered by a terminolog- the skull for microvascular decom- no cause can be found
ical dishomogeneity, which must be pression, approximately 11% of pa- in about 11% of
patients with trigeminal
solved to the benefit of researchers, tients with trigeminal neuralgia
neuralgia (ie, idiopathic
clinicians, and, ultimately, patients. remain without diagnosis of an appar-
trigeminal neuralgia).
Although tic douloureux is fre- ent cause.7,9 The frequency of cases
quently used as a synonym for trigem- without an etiology justifies their
inal neuralgia, the term was originally designation as idiopathic. For trigem-
introduced to describe the involuntary inal neuralgia caused by a neurologic
wincing associated with the occur- disease other than neurovascular com-
rence of pain. Other diagnostic labels pression, the author prefers the term
have been proposed to indicate differ- secondary rather than symptomatic
ences in the etiology or clinical pre- because it is less ambiguous. The term
sentation of trigeminal neuralgia. symptomatic may also indicate the
Variable use of seemingly inter- painful side of the face or the affected
changeable labels, such as classic and trigeminal root on MRI.
idiopathic or secondary and symp-
tomatic, has been a major source of CLINICAL DIAGNOSIS OF
confusion. To differentiate idiopathic TRIGEMINAL NEURALGIA
trigeminal neuralgia from manifesta- The International Association for the
tions of neuralgia that are secondary Study of Pain (IASP) defines trigeminal
to an identified disease, in 1973 neuralgia as ‘‘sudden, usually unila-
Strandjord4 established the term pri- teral, severe, brief, stabbing, recurrent
mary trigeminal neuralgia, which episodes of pain in the distribution of
contradicts the notion of trigeminal one or more branches of the trigem-
neuralgia as a condition of neuropathic inal nerve.’’10 The ICHD, Third Edi-
pain. MRI shows neurovascular contact tion, beta version (ICHD-3 beta)
in 70% to 83% of patients with typical describes trigeminal neuralgia in sim-
trigeminal neuralgia.5,6 In neurosurgical ilar terms, ‘‘as a disorder characterized
case series, this frequency increases by recurrent unilateral brief electric
to 89%.7 Hence, primary trigeminal shocklike pains, abrupt in onset and
neuralgia was loosely used by many termination, limited to the distribu-
authors to describe both trigeminal tion of one or more divisions of the
neuralgia without identifiable cause trigeminal nerve and triggered by
Continuum (Minneap Minn) 2017;23(2):396–420 ContinuumJournal.com 397
Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

Trigeminal The paroxysmal characteristic of neuralgia must be considered when trigeminal neuralgia. Typical Pain episodes in trigeminal neuralgia descriptions of temporal and sensory occur and end abruptly. is unmistak- characteristics laid out in the defini.com April 2017 Copyright © American Academy of Neurology. 252 MS patients with trigeminal neu- an electric shock. Refuting earlier assumptions. they are only a few seconds long. are short and qualities of trigeminal neuralgia in- severe. tric shockYlike. stabbing. ter of the pain. with its abrupt episodes of orofacial pain exhibit the onset and termination.15 except for secondary trigeminal neu.18 found only one case of bilateral pain Previous definitions of trigeminal neu- out of 74 patients with secondary ralgia emphasize a stereotypic charac- trigeminal neuralgia. and are felt on only one side of clude brief. and its distribu- of trigeminal neuralgia include unilat.15 These trigeminal neuralgia in 234 patients periods may last from weeks to years.’’11 Although these NEURALGIA descriptions are certainly correct. The of trigeminal neuralgia paroxysms may sensory characteristics of the pain are last up to 2 minutes.13 A recent geminal neuralgia may enter into meta-analysis of clinical studies did periods of complete pain remission not find any report of truly bilateral in up to 63% of patients. range from zero to more than 50. sudden.16 a re- ralgia in multiple sclerosis (MS).15.’’ According to the their recent meta-analysis.12 vary from patient to patient. pain that cannot be felt innervation territory of the trigeminal outside the trigeminal territory. POSSIBLE TRIGEMINAL cular compression. Stereotypic pain character 398 ContinuumJournal. however. Oc. they A patient’s history must fulfil two do not allow for evaluating the strength requirements for the identification of of the diagnostic criteria. The parable to an electric shock. additionally. There may or may not be. and nerve (Figure 3-1). tion must be consistent with the eral facial pain. tri- neously on both sides. a frequency of slightly less cial pain of moderate intensity. number of paroxysms per day may eral trigeminal neuralgia is very rare. cent study of 200 patients with classic casional reports of bilateral classic trigeminal neuralgia did not find evi- trigeminal neuralgia reflect successive dence that frequency or duration of episodes of unilateral pain that move trigeminal neuralgia paroxysms in- to the opposite side of the face rather crease with duration of the disease. in most patients usually described as stabbing or com. trigeminal neuralgia ‘‘may MS associated with trigeminal neural- short-lasting pain develop without apparent cause or gia and identified a total of 24 cases of usually described as be a result of another diagnosed dis. 6 This meta. is analysis included mixed causes of not a unique feature of trigeminal secondary trigeminal neuralgia.17 than pain episodes that occur simulta. bilateral trigeminal neuralgia out of stabbing or similar to order. persistent background fa. Unauthorized reproduction of this article is prohibited. with classic trigeminal neuralgia and but most often last a few months. Unlike other neuropathic pains. Although the duration tory of the trigeminal nerve. Stereotypy. . even if the verbal descriptors tions provided by IASP and IHS.11. Bilat. pain that is paroxysmal. In neuralgia. trigeminal neuralgia develops without apparent cause other than neurovas. Classic than 10%). or elec- the face within the innervation terri. Cruccu trigeminal neuralgia is International Headache Society (IHS) and colleagues14 reviewed studies of a very abrupt and definition. able. possible trigeminal neuralgia: the pain The starting points for a diagnosis must be paroxysmal. ralgia (ie. Trigeminal Neuralgia KEY POINT h Paroxysmal pain in innocuous stimuli.

f Advanced MRI techniques can demonstrate neurovascular compression with morphologic changes of the trigeminal nerve root. It does not extend to the posterior third of the scalp. et al. the posterior part of the external ear. . Unauthorized reproduction of this article is prohibited. but they almost never present with simultaneous bilateral pain. d Trigger maneuvers include innocuous mechanical stimuli. Few patients develop trigeminal neuralgia on both sides of the face over the course of a disease (eg. Reprinted with permission from Cruccu G. Neurology. e MRI readily identifies major neurologic diseases. or complex activities such as shaving or applying makeup.FIGURE 3-1 New classification and diagnostic grading system for trigeminal neuralgia (TN). neurology. Other investigations may include the neurophysiologic recording of trigeminal reflexes and trigeminal evoked potentials.23(2):396–420 ContinuumJournal. Continuum (Minneap Minn) 2017. but may be accompanied by continuous pain. b The pain strictly follows the distribution of the trigeminal nerve branches.14 B 2016 American Academy of Neurology.com 399 Copyright © American Academy of Neurology. c Paroxysmal pain is the most noted symptom. such as tumors of the cerebellopontine angle or multiple sclerosis. which become necessary in patients who cannot undergo MRI. or the angle of the mandible (Figure 3-2). Confined trigger zones and a common combination with brisk muscle contractions (tics) help distinguish triggered trigeminal neuralgia from allodynia in other conditions of neuropathic pain. a Trigeminal neuralgia is typically a unilateral condition. Trigger maneuvers may be tested by the examiner.org/content/87/2/220. in multiple sclerosis). facial or oral movements.short.

Light gray areas in the back of tongue and throat are innervated by the glossopharyngeal nerve.com April 2017 Copyright © American Academy of Neurology. or the skin overlying the angle of before or after surgery.14 B 2016 American Academy of Neurology. The TRIGGERED PAIN AS A territory of the mandibular division CRITERION OF CLINICALLY extends up to the temple: a patient ESTABLISHED TRIGEMINAL with trigeminal neuralgia in the man. neurology. White areas are innervated by cervical nerves. Trigeminal Neuralgia KEY POINT h Stimulus dependence is may be observed with other forms of trigeminal divisions. this no- (Figure 3-2).16.16. as these territories are innervated by cervical nerves. ear. maxillary (green). Unauthorized reproduction of this article is prohibited. The examining physician tion has not been adequately scruti- should ascertain that the pain does not nized in clinical studies.6 Of note. the extend to the posterior third of the affected division of the trigeminal nerve scalp. it is not uncommon nation of the maxillary and mandibular neuralgia.short. Neurology. and mandibular (orange). Reprinted with permission from Cruccu G.20 division or the tongue has long been Pain should be felt in one or more considered an indication of secondary divisions of the trigeminal nerve trigeminal neuralgia.14. .20 the mandible. Facial and intraoral territories of innervation of the three trigeminal branches: ophthalmic (yellow). NEURALGIA dibular branch of the trigeminal nerve Stimulus dependence is one of the most may therefore describe pain at the striking features of trigeminal neuralgia. pain of variable sensory characteristics Trigeminal neuralgia in the ophthalmic over the course of the disease. light mechanical stimuli FIGURE 3-2 Innervation territories of the trigeminal nerve.org/content/87/2/220. for trigeminal neuralgia to produce branches of the trigeminal nerve). 400 ContinuumJournal.19. they should be one of the most striking neuropathic and non-neuropathic contiguous (most frequently a combi- features of trigeminal pain.5. In addition. pain is evoked by If trigeminal neuralgia involves two non-noxious. et al. the posterior part of the external and the side of the face may change. In most patients. However. temple and the lower lip (Figure 3-2).19.14.

23(2):396–420 ContinuumJournal. The sciatica). Circles denote the typically small areas where light touch or other innocuous mechanical stimuli trigger the pain paroxysms. trigger. Move.21 movement is evoked by noxious or are unique to Subtlety of the trigger maneuvers is potentially noxious stimuli. The suffice to provoke a pain attack. after inadvertently bit.com 401 Copyright © American Academy of Neurology. in the few patients with no apparent washing or shaving of the skin. author proposes that the presence tion to the evoked pain). appli. and the or ‘‘without trigger’’ and did not pain can be felt as radiating (similar to find these terms in any article.21 B 1959 British Medical Journal. of trigeminal neuralgia and qualifies voked movement of the face is similar the patient as having clinically to other reactions to acute nocicep.bmj. Distribution of 31 trigger zones in 30 patients. established trigeminal neuralgia tive pain (eg. In other diseases.23 Hence. such as eye blinking or a ment alone (eg smiling. The author searched the literature for location of the evoked pain may differ reports of pain with ‘‘no trigger’’ from the site of the stimulation. Because triggered pain ing one’s tongue or a tooth with paroxysms are a unique somatosensory FIGURE 3-3 Mechanism of pain in trigeminal neuralgia. talking) may twitch of other facial muscles. The Although pain paroxysms may orig- stimulus may simply be a touch or a inate spontaneously. trigeminal neuralgia. patients with a whiff of air. In some patients. the pain attacks are evoked by cation or removal of makeup. However. Continuum (Minneap Minn) 2017.short. they may also be or maneuvers in classic trigeminal tested by the examiner. Lindblom U. pulpitis). . into the presence of trigger stimuli tient. eating movements that the patients are un- or drinking) are also common.22. (Figure 3-1). this brisk h Trigger maneuvers ing the oral cavity (Figure 3-3). the involuntary facial movement in reac. Reprinted with permission from Kugelberg E. Unauthorized reproduction of this article is prohibited. The term tic of triggered pain matching the above refers to the abruptness and short description confirms the diagnosis duration of the movement. jnnp. These triggers are usually few studies that looked specifically spontaneously reported by the pa. J Neurol Neurosurg Psychiatry. the 94% of patients. unique to trigeminal neuralgia. It is possible that stimuli and facial movement (eg. the trigger zones are larger (dashed areas) or intraoral (ovals). who should neuralgia reported triggered pain in pay attention to the typical tic (ie. aware of.com/content/22/1/36. although more complex history of exclusively spontaneous maneuvers involving both tactile attacks are very rare. includ. KEY POINT within the trigeminal territory.15. The pro.

No generally agreed-upon term are performed. neuralgia has well defined the charac- h Treatment of trigeminal TRIGEMINAL NEURALGIA teristics of this other phenotype and neuralgia can be WITH CONCOMITANT has brought far more attention to it. dull.19. After 3 weeks.25 A recent cross-sectional the etiology in cases of clinical trial for trigeminal neuralgia. Unauthorized reproduction of this article is prohibited. Brain MRI showed a neurovascular compression that distorted and flattened the affected trigeminal root near its entry into the pons. The distri- continuous pain ered probable neuropathic pain. study in 158 patients with trigeminal trigeminal neuralgia. She had already been treated with several pain killers and benzodiazepines by her primary physician with no improvement. The patient was diagnosed with trigeminal neuralgia with concomitant continuous pain.24 bution of this continuous pain co- adds to the typical Clinically established trigeminal neu. or tingling. The neurologic examination was normal.26 diagnostic investigations Some patients with trigeminal neural. MRI of her brain with contrast was ordered to rule out major neurologic diseases. reporting resolution of her symptoms. Comment. initiated before CONTINUOUS PAIN reporting a frequency of almost 50%. and constructive interference in steady state (CISS) sequences were also ordered. She also stated that when drying her face. she needed to slowly press the towel without brushing it up and down. This patient’s symptoms were typical of trigeminal neuralgia with concomitant continuous pain. been known by several designations. A baseline complete blood count and comprehensive metabolic profile completed the investigations. and fluctuations of its intensity h Diagnostic investigations diagnostic certainty to implement parallel in time those of the paroxys- are needed to establish treatment or enroll patients in a mal pain. Trigeminal Neuralgia KEY POINTS h In almost 50% of phenomenon.’’ where she could pat a towel slowly to her face but could not brush the towel up and down because of the pain that was triggered. apart from the patient grimacing when a cotton swab was touched to the right side of her face. The patient was prescribed oxcarbazepine and titrated up to 300 mg 4 times a day. a lightninglike pain would go from her nose to her lip. including the presence of a trigger mechanism (in this case the patient exhibited the ‘‘sign of the towel. Its sensory char. concomitant pain so that it should also be consid. otherwise. She described the pain as being on the right side only and consisting of ‘‘a burning and stabbing pain’’ in her cheek that sometimes lasted for hours. . but may vary in continuous pain is present.). Although diagnostic investigations to ascertain etiology must be performed in all patients. ralgia represents a sufficient degree of pain. Case 3-1 A 77-year-old woman presented to the neurology clinic for a 1-month history of facial pain. it also increases the acteristics differ from the paroxysmal patients with trigeminal diagnostic certainty of neuropathic pain and are commonly described as neuralgia. incides with that of the paroxysmal paroxysmal pain.com April 2017 Copyright © American Academy of Neurology. the patient returned. This pain is continuous or inal neuralgia in which concomitant nearly continuous. 402 ContinuumJournal. To look for a possible neurovascular compression. time-of-flight magnetic resonance angiography (MRA). medical treatment can be implemented early based on clinical information only. burning. It has intensity and quality. gia experience pain between attacks exists to describe the form of trigem- (Case 3-1). but she had not tried voltage-gated sodium channel blockers. three-dimensional reconstruction.

The author prefers central mechanisms. they are considered to have trigeminal neuralgia with concomitant continuous pain. . Except for trigeminal neuralgia caused by multiple sclerosis. is associated with poorer outcome assess for secondary tinuous refers strictly to the temporal after surgical intervention. KEY POINTS including atypical trigeminal neural. the pain affects one side of the face. Continuous pain may develop as may occur in idiopathic.28 Several authors h MRI is the most widely describing the pain as continuous have suggested that continuous pain used diagnostic tool to rather than persistent because con. Either phenotype (purely paroxysmal pain or with additional continuous pain) may occur with any of the three categories. Classic trigeminal neuralgia is caused by vascular compression of the trigeminal nerve root. Several authors have favored ently after microvascular decompres- describing the pain as constant.29Y32 It is trigeminal neuralgia. Classification Trigeminal neuralgia is classified in three etiologic categories. trigeminal neuralgia. However.33 intensity or sensory quality of the pain. Patients usually do not experience pain between paroxysms. because it is highly in idiopathic. continuous pain because it directly a result of progressive root damage after classic. It is abrupt in onset and typically lasts only a few seconds (2 minutes at maximum). or secondary conveys the difference from typical prolonged compression27 or reflect trigeminal neuralgia. Patients may report their pain as arising spontaneously. major neurologic with persistent idiopathic facial pain. which sion. Thus. MRI is the most widely used diagnos- The presence of continuous pain is tic tool to assess for secondary tri- not related to etiology and may occur geminal neuralgia. The mechanisms h The presence of gia and trigeminal neuralgia type 2. Idiopathic trigeminal neuralgia occurs without apparent cause. paroxysmal pain. If they do report additional continuous pain. Unauthorized reproduction of this article is prohibited.23(2):396–420 ContinuumJournal. convinc.19. which is an unrelated painful condi. continuous is the description ETIOLOGY least susceptible to confusion (Table 3-1). whereas unclear to what extent these reports because it is highly persistent may imply refractoriness to reflect patient selection or differences sensitive for detecting treatment (and can also be confused in nerve pathology. underlying continuous as opposed to continuous pain is not The author prefers the term trigemi. in the same distribution and in the same periods as the paroxysmal pain. a tumor of the cerebellopontine angle or multiple sclerosis). paroxysmal pain may improve differ- tion).com 403 Copyright © American Academy of Neurology. but these pain paroxysms can always be triggered by innocuous mechanical stimuli or movements. manifestation of the pain. Secondary trigeminal neuralgia is the consequence of a major neurologic disease (eg. or secondary sensitive for detecting major neurologic TABLE 3-1 Definition and Classification of Trigeminal Neuralgia Definition Trigeminal neuralgia is orofacial pain restricted to one or more divisions of the trigeminal nerve. related to etiology and nal neuralgia with concomitant stood.20. paroxysmal pain are not fully under. ing evidence exists that continuous and diseases such as a tumor or multiple sclerosis.32. indicating that the mechanisms is nearly synonymous with continuous responsible for the two pain compo- but may also refer to unchanging nents may be distinct. Continuum (Minneap Minn) 2017. classic.

34. indicating high and colleagues14 became convinced sensitivity but low specificity. Two schematic drawings show axial sections at the level of the trigeminal roots where gray indicates nervous tissue. MRI cation of morphologic changes of the neurovascular contact may reveal neurovascular contact of the compressed trigeminal root. recent studies have emphasized studies. distorted. Sup. but the frequency of mere contact between root and are highly suggestive of physical alter- of mere contact blood vessels in trigeminal nerves in ation and have a high predictive value between root and blood asymptomatic patients cautions against for pain relief after decompression. Compression of the trigemi- neurovascular contacts is poorer com. to the point that Cruccu asymptomatic nerves. ical diagnosis of trigeminal neuralgia FIGURE 3-4 Morphologic changes of the trigeminal root showing examples of classic right trigeminal neuralgia.14 The degree of morphologic results are corroborated by two pro- trigeminal root changes is therapeuti. nal nerve at its entry into the brain- pared to the decompression of dis. stem increased the specificity to 100%. These of the trigeminal nerve trigeminal nerve root. or flattened nerve It is important to acknowledge that roots (Figure 3-4). located.14 vessels in trigeminal its use as a diagnostic criterion.7 Nerve that the reintroduction of the term dislocation or signs of atrophy in- idiopathic trigeminal neuralgia was creased the specificity to 97%. high-quality blinded and controlled patients cautions tion. and black indicates bone. 404 ContinuumJournal. Trigeminal Neuralgia KEY POINT h MRI may reveal diseases such as a tumor or MS. red indicates arteries. The long-term outcome neurovascular contact appears to be after surgical correction of simple relevant.33 Advanced MRI all the studies cited here rely on a clin- techniques now allow radiologic verifi.com April 2017 Copyright © American Academy of Neurology. type of contact and its physical impact tomatic nerves and in 244 out of 681 on the nerve. Atrophy of the right trigeminal root caused by a crossing artery (A) and a downward loop of the superior cerebellar artery that provokes distortion of the right trigeminal root at its entry into the pons (B) can be seen. spective studies. .35 Location of the cally relevant. In a recent meta-analysis of nine nerves in asymptomatic ported by negative findings at opera. These needed.31. Unauthorized reproduction of this article is prohibited. but the frequency changes of symptomatic nerve roots root. mere neurovascular contact against its use as a the importance of differentiating the was found in 471 out of 531 symp- diagnostic criterion.

signs and morphologic changes caused ment of nerve function (Figure 3-539). masseter muscles.34. MRI techniques. trigeminal neuralgia. and mental nerves and for sion requires the use of specific imaging recording uses surface electrodes paradigms with three-dimensional re. dis. mean specificity of 64% is low. Allowing a between- creasing number of imaging options side quantitative assessment of the are available to depict the nerve and ophthalmic. but their several DTI abnormalities at the tri. for stimulation. KEY POINT prior to MRI. infra- Detection of neurovascular compres.com 405 Copyright © American Academy of Neurology. trigeminal re- dimensional time-of-flight magnetic flex testing achieved a sensitivity of resonance angiography (MRA) for 94% and a specificity of 87% in iden- visualization of arteries. or atrophy of the inal reflex testing is particularly helpful trigeminal root (ie. lination and edema. constructive interference in steady the evaluation of neuropathic pain state [CISS]) for a detailed exami. placed over the orbicularis oculi and construction MRI techniques. diagnostic accuracy of MRI. contrast to trigeminal reflex testing.5. evoked ment for trigeminal neuralgia reverses potentials may be altered. will reliably demonstrate microstruc. Trigeminal reflex testing is an reconstruction However.6 Trigem- tortion. the use of specific preceded by an evaluation of clinical tigation.37 The nec.40 In a nation of the cisternal and cavernous meta-analysis of 629 patients with segments of the nerve and three. Typical imaging reliable method to detect secondary paradigms include sequences for forms of trigeminal neuralgia and has three-dimensional T2-weighted MRI been recommended in guidelines for (eg. with three-dimensional presence of trigeminal neuralgia.12. In tractography to measure focal demye. so far the available evidence imaging paradigms symptoms and signs that indicate the is still insufficient.36. MRI find. orbital.5. emergence of the supraorbital. it uses etiology of classic trigeminal neuralgia surface electrodes placed over the (Figure 3-1). maxillary. and mandibular any blood vessels in proximity to divisions. 36. the morphologic if a patient cannot undergo MRI or if changes considered essential to distin. by a vascular compression involving the Trigeminal reflex testing requires only symptomatic trigeminal nerve provides standard nerve conduction study strong enough evidence to confirm the equipment. tifying patients with secondary trigem- essary but sufficient scope of the MRI inal neuralgia.23(2):396–420 ContinuumJournal. many believe that in the future DTI h Detection of ings alone cannot be used as bio. Unauthorized reproduction of this article is prohibited. involving the trigeminal nerve. . neurovascular markers to diagnose trigeminal tural damage in the trigeminal root compression requires neuralgia unless the investigation is and thus become the ultimate inves.28 geminal root entry zone. a combination of clinical established neurophysiologic assess. Consequently. An in. trigeminal neuralgia secondary to tri- guish between a mere contact and a geminal neuropathy is suspected in real compression)14 must still gain spite of a normal MRI result (refer to wide consensus. classic trigeminal neuralgia. trigeminal reflex testing is a the posterior fossa. compression-induced microstructural Various evoked potentials after changes may be estimated using electric or thermal stimuli have been diffusion-tensor imaging (DTI) and studied in trigeminal neuralgia.38 A recent which is normal in idiopathic or report suggests that effective treat. the following section on secondary Several studies suggest that trigeminal neuralgia). comparable to the evaluation to identify dislocation. flattening.38 Although Evoked potentials are adjuvant measures Continuum (Minneap Minn) 2017.

compression induces focal demyelin- root. Unauthorized reproduction of this article is prohibited. infraorbital (V2).12 In a clinical setting. et al. (Figure 3-642). Evidence of tumors as a cause of secondary trigeminal neural- SECONDARY TRIGEMINAL gia comes from four main studies that NEURALGIA reported a total of 20 (8%) out of Trigeminal neuralgia caused by a ma. Calibration is 10 ms/100 2V. tinuous pain rather than trigeminal neuralgia. acoustic neu- tials whose generation site has been romas. trigeminal tions within the trigeminal territory are neuralgia is caused by benign tumors bound to elicit reflex responses that un. stimulation sites at the supraorbital (V1). In 15% of patients emphasizing that all electric stimula. the cause is a major neurologic disease. at the cerebellopontine angle or MS avoidably contaminate the scalp signals. and mandibular (V3) divisions. Trigeminal Neuralgia KEY POINT h In some 15% of patients with trigeminal neuralgia. age by malignant tumors is commonly tification of the affected trigeminal associated with hypesthesia and con- division under general anesthesia. and cholesteatomas. and recording from the orbicularis oculi (A) and masseter (B) muscles. maxillary (V2). or pons.39 B 2006 American Academy of Neurology. Schematic drawing of the ophthalmic (V1). Right. to demonstrate functional abnormalities tified by MRI or other appropriate in trigeminal neuralgia.5. whereas infiltrative Leandri and Gottlieb41 is useful during tumors lead to axonal degeneration. omas. 243 patients with trigeminal neuralgia. Local located near the trigeminal ganglion. this ation and may trigger paroxysmal method of stimulation detailed by ectopic discharges. Reprinted with permission from Cruccu G.org/content/66/1/139. Early (R1) and late (R2) blink reflex (V1-A). Neurology. and early (SP1) and late (SP2) masseter inhibitory reflex (V2-B and V3-B). neurology. They include meningi- recording of subcortical far-field poten. . epidermoid cysts. FIGURE 3-5 Trigeminal reflex test to disclose secondary trigeminal neuralgia.long. It is worth investigations. Left.com April 2017 Copyright © American Academy of Neurology. and mental (V3) nerves. and compress the root near its entry fraorbital foramen provides a safe scalp into the pons. with typical pain attacks.6 jor neurologic disease is readily iden. most often multiple sclerosis or benign tumors in the cerebellopontine angle (ie.6 Tumors causing tri- Only electric stimulation via two fine geminal neuralgia are mostly benign needle electrodes inserted into the in. secondary trigeminal neuralgia). about 20% of 406 ContinuumJournal. On the other hand. radiofrequency thermocoagulation of The different pathology of nerve dam- the ganglion because it allows the iden.

51 be one of several other common MS Very recently. typically have multiple demyelinated Patients with MS have a 20-fold areas on MRI and strongly delayed increased risk of trigeminal neuralgia.47. Demyelinating plaques along the intraaxial course of the trigeminal afferents (arrows). B. Reprinted with permission from Cruccu G.43 All symptomatic manifestation for all their life. additive mechanism. however. thus tumors compress the trigeminal nerve being classified as having clinically root.com 407 Copyright © American Academy of Neurology. et al.30 These patients never produce trigeminal neuralgia.52 Continuum (Minneap Minn) 2017. some patients have tri. Unauthorized reproduction of this article is prohibited. cerebellopontine angle tumors produce geminal neuralgia as their sole clinical trigeminal neuralgia.48 It has been sion exert a dual. . It trigeminal neuralgia has conventionally has been hypothesized that the pontine been attributed to demyelinating plaque and a neurovascular compres- plaques in the pons. sound evidence. which are characteristic of MS.FIGURE 3-6 Common causes of symptomatic trigeminal neuralgia. crush syndrome on the same primary though trigeminal neuralgia in MS may afferents near the root entry zone. Handb Clin Neurol. vascular compression)50 create a double cantly higher than that of MS. Benign tumors along the extraaxial course of the trigeminal root (arrows). this theory has found disturbances.18. that the onset in which inflammatory demyelination age of the population with trigeminal (the intraaxial plaque)48 and mechani- neuralgia and MS is lower than that of cal demyelination (the extraaxial neuro- classic trigeminal neuralgia but signifi.42 B 2010 Elsevier. A.45.com/science/article/pii/ S0072975210970565. sciencedirect.18 responses on neurophysiologic tests The prevalence of trigeminal neuralgia (trigeminal reflexes and evoked poten- in MS is 2% to 5%.46 The cause of tials).44 Trigeminal neuromas almost isolated syndrome.49 Al. clearly shown.23(2):396–420 ContinuumJournal.

The author proposes that. Hence. but trigeminal reflexes are theory.57 Indeed a paroxysmal dence in animal models of focal demy- pain similar to that of trigeminal neu. and most patients also de. or because of a local bilateral but may begin asymmetrically direct mechanical stimulus such as and occasionally present with parox. pain. and histologic afferents near the entry come toxic for the liver. the primary insufficiently to pharmacologic treat. becomes necessary sooner or later. the primary of the trigeminal root procedure for trigeminal neuralgia mechanism is focal demyelination of into the pons. admittedly more debatable. disease or genetic disorder is usually Spontaneously. order of frequency: posttraumatic.29.56 dence at all at this time. axon. microvascular evidence. then the axons do not have scribe continuous pain. More supported by evi- ralgia. dental procedures.25. where Schwann cells are substituted These neuropathies may be divided by oligodendroglia in providing the into three subgroups in descending myelin sheath.56. with almost no sound evi- invariably delayed or absent. ectopic activity is ysmal pain similar to trigeminal neu. apparatus necessary to pump sodium sometimes these focal neuropathies off are physiologically concentrated present with episodes of paroxysmal at the level of the nodes of Ranvier. as. of focal demyelination become a facial or neurosurgical procedures may source of ectopic generation of im- damage branches of the trigeminal pulses. the artery pulsation. Facial damaged primary afferents in the area trauma.53. ity to damage) because it is the site ondary to a trigeminal neuropathy. neuroimaging. The pain attacks are usually longer when the demyelinating process allows than those associated with trigeminal the passage of ions in and out of the neuralgia. is that the eases. inal root into the pons.59Y61 pain. siologic. Trigeminal Neuralgia KEY POINT h Both in classic and Because patients with MS-related PATHOPHYSIOLOGY OF secondary trigeminal trigeminal neuralgia usually respond TRIGEMINAL NEURALGIA neuralgia. and idiopathic/genetic. is that the 408 ContinuumJournal. In primary afferents near the entry these patients. sociated with connective tissue dis. however. healthy nerve The patients will eventually develop bilat. A second pathophysiologic theory. which clarifies the diagnosis. Painful trigeminal neu. Although the primary symptom cause mitochondria and the energetic in trigeminal neuropathy is sensory loss. ropathy caused by a connective tissue which makes them hyperexcitable. elination of the trigeminal root is the ralgia may be the first symptom of an concept of ephaptic transmission underlying connective tissue disease. . fibers and the generation of high- eral sensory deficits and continuous frequency discharges. generated.com April 2017 Copyright © American Academy of Neurology.54 locus minoris resistentiae (a site of A smaller group of patients may lower resistance or higher susceptibil- present with trigeminal neuralgia sec. the benefit (extraaxial or intraaxial) of the trigem- yielded by any type of surgical treat.55 The trauma enough energy to promptly reestablish or the intervention should not escape the resting potential. the axons medical history. tend toward a depolarization level. Some investi- ment is shorter in duration than in gators believe this area represents a classic trigeminal neuralgia. Both in classic and second- (extraaxial or intraaxial) decompression or another surgical ary trigeminal neuralgia. MRI A third potential pathophysiologic is normal. or maxillo.58 (cross talk) from close. be- nerve. Unauthorized reproduction of this article is prohibited. One aspect of pathophysiology is mechanism is focal ment or must stay on high dosages supported by established neurophy- demyelination of primary that worsen their fatigue or may be.

unfortunately. of the .com/ responders nor nonresponders. Both sodium channel drugs. in. . Although pimozide was found ous side effects and allergic dermatitis. Unauthorized reproduction of this article is prohibited. confusion. 5. in this third these agents.6 Based on evidence. These h The adverse events management that were agreed upon central side effects. pa. in the case of carbamaze. Societies (EFNS) are very clear as to medical treatment (Supplemental group of patients. Indeed. Hence naturally. pine. the drugs can be tried. analysis of the evidence- choice is oxcarbazepine because of its based trials led to the following sug- better tolerability. it was reactive (ie. The guidelines on trigeminal neuralgia lence. no adequate trials in trigeminal neuralgia. was believed to be very prom- patient exists who requires some ising because it was well supported by consideration.67 Some reports about allergic reaction to one of the two the efficacy of gabapentinoids and anti- drugs cannot be switched to the depressants exist. or imbalance. the side effects restrict the (most frequently cardiac conduction oral dosage to a level lower than the problems or severe arrhythmias). a third type of receptor.17. should be add to those of carbamazepine or proposed. which would in trigeminal neuralgia.lww. baclofen.28. however. Some patients cannot animal experiments.6 oxcarbazepine. In this case. carbamazepine.63. other drug will be enough. no imposes a very slow titration. a small head-to-head clinical trial. the relief (ie. she or he is one of the rare comparatively high risk of dermatitis cases of a real nonresponder). are expectedly more Continuum (Minneap Minn) 2017. which are more caused by both and jointly published by the American frequent with carbamazepine than oxcarbazepine and Academy of Neurology (AAN) and the oxcarbazepine (Figure 3-7).64 Unfortunately. but there have been other) or.23(2):396–420 ContinuumJournal. who are neither Digital Content 3-1.66 Now it is known take either of the two choice drugs that unless baclofen is administered because of specific contraindications intrathecally.63 If the patient gestions: lamotrigine. being extremely efficacious side effects on the CNS.17 may carbamazepine may often prevent patients from maintaining require discontinuation of European Federation of Neurological adequate doses. 1800 mg/d. blockers.65 and. or platelets) rarely sants. namely MEDICAL TREATMENT OF duce central nervous system (CNS) oxcarbazepine and TRIGEMINAL NEURALGIA depression. one necessary to reach antinociceptive Some other patients encounter seri. a fall in blood elements (white Both gabapentinoids and antidepres- cells. this drug is not devoid of surgery. being antiepileptic drugs.6 Lamotrigine is supported patients (1200 mg/d to 1500 mg/d) by evidence if used as an add-on to without achieving the desired pain carbamazepine.com 409 Copyright © American Academy of Neurology. h Medical treatment ondarily induces central sensitization tients on carbamazepine must under. Baclofen. tend to be cross. KEY POINTS hyperactivity of primary afferents sec. effects. other CONT/A215). the patients who had the never tried again. Hence. red cells. reaching aplastic anemia. Both drugs may cause frequency-dependent more central changes.-aminobutyric acid B (GABA-B) responders. presenting as somno. the treatment should begin either with AAN/EFNS guidelines suggest trying carbamazepine 400 mg/d to 1200 mg/d other pharmacologic options as or with oxcarbazepine 900 mg/d to monotherapy or add-on medications. an agonist Aside from responders and non. more efficacious than carbamazepine in which. however. links.62 sodium depletion (Case 3-2). The author’s first-line In particular. of trigeminal neuralgia of wide dynamic range neurons in the go a complete blood count every 3 to is based on spinal trigeminal nucleus or even 4 months. and reaches the dosages adequate for most pimozide.

which she felt was tolerable. other major neurologic diseases (eg. and combing her hair. who quickly tapered and stopped oxcarbazepine. Regarding medication side effects. The possibility of an endovascular intervention was discussed. Trigeminal Neuralgia Case 3-2 A 67-year-old woman with a history of hypertension presented with a 6-month history of right-sided facial pain. The pain was paroxysmal (she described it as similar to an electric shock). sodium depletion occurs in 6% to 8% of patients. In this case. the patient suddenly developed severe weakness and confusion and was seen in a local emergency department. this patient’s cardiologist had recently introduced a diuretic to her antihypertensive regimen that probably added to oxcarbazepine in depleting sodium. and a dedicated three-dimensional MRI and magnetic resonance angiography (MRA) study were ordered to check for a neurovascular compression.com April 2017 Copyright © American Academy of Neurology. as well as an interventional neuroradiologist who. in retrospect. The patient returned for follow-up 3 weeks later. but its efficacy was considered uncertain. She was also seen by another neurologist. imbalance). Within 24 hours after the intervention. proceeded with endovascular intervention first with a coil in the aneurysm and then with a stent in the artery. she had complete disappearance of the neuralgic pain attacks and continued to have no further symptoms when seen in follow-up 6 months later. where she was diagnosed with severe hyponatremia (120 mEq/L) and was begun on saline infusions. eyelid movement when looking upward. the dedicated MRI study for possible neurovascular compression showed a very rare compression by a wide-collar berry aneurysm of the superior cerebellar artery. In addition. One week later. the carbamazepine induced central nervous system side effects (eg. With oxcarbazepine. and her pain had disappeared. Her problems were twofold: first. . Unauthorized reproduction of this article is prohibited. the only unusual clinical factor was the location of her pain. as soon as the electrolyte abnormality resolved. and it was evoked by typical trigger maneuvers for trigeminal neuralgia: light touch on the forehead and eyebrow. however. monitoring of serum sodium is necessary at least once. with increasing doses up to 1200 mg/d. a standard brain MRI. and the standard MRI showed some small ischemic lesions in the cerebral white matter. although secondary trigeminal neuralgia is usually attributed to tumors or multiple sclerosis. The artery looped downward. and she still had central nervous system depression. dizziness. which she found unbearable. although to a far lower degree. Regarding the etiologic classification of this patient. the rare trigeminal isolated sensory neuropathy or aneurysms) should be kept in mind when something in the history or symptoms suggests a secondary origin. She was switched to oxcarbazepine. which exclusively involved the ophthalmic division (this was long considered a Continued on page 411 410 ContinuumJournal. somnolence. She had previously been prescribed carbamazepine 600 mg/d. and the aneurysm distorted the trigeminal root. although oxcarbazepine by no means requires the three to four checks per year of blood elements that are mandatory for the duration of therapy for patients on carbamazepine. Neurologic examination was normal. The trigeminal reflex testing was normal. trigeminal reflex testing. In this case. and second. no investigation had yet occurred to ascertain the etiology. Comment.

This case suggests the need for a pulsating stimulus on the demyelinated nerve fibers to induce the ectopic generation of high-frequency discharges. Continuum (Minneap Minn) 2017. combinations been verified. Regarding pathophysiology.68Y71 The amount of published inal neuralgia with concomitant contin. Continued from page 410 sign of probable secondary trigeminal neuralgia. may not accept ysmal pain and are often tried as an add. nor has the safety of these the safety profile is very high. In microvascular decompression. although this association was not confirmed by the American Academy of Neurology [AAN] and the European Federation of Neurological Societies [EFNS] 2008 guidelines6). The author believes on to oxcarbazepine or carbamazepine that in those patients who do not want in patients with the atypical form of to undergo any kind of surgical in- trigeminal neuralgia with concomitant tervention. it is well known that microvascular decompression relieves neuralgic pain far before a remyelinating process might take place. the pain relief lasts several months. Often. Unauthorized reproduction of this article is prohibited. efficacious in continuous than parox. botulinum toxin injec- continuous pain. patients. the artery pulsation was eliminated by the stent. Reportedly.com 411 Copyright © American Academy of Neurology. this third group of patients and the main side effect is a transient is eventually referred for surgery. and uous pain. evidence is growing day by day. In this case. . MRI = magnetic resonance imaging. tried. surgery that easily. Many weakness of the facial muscles in the FIGURE 3-7 Trigeminal neuralgia (TN) treatment algorithm. A dedicated clinical tions of the trigger areas should be trial has never been reported in trigem. however.23(2):396–420 ContinuumJournal. the neurosurgeon leaves a tiny sponge to keep the artery and the nerve root separate.

All these procedures inclination.7 (Nav1. of the trigeminal terminal nerves at sion of CNS excitability. a new voltage. adding further mech. radio- human genetic linkage. BIIB074.6.73 Furthermore. Zakrzewska and col. alcohol injections. in the brain. but no Nav1. three types of lesions can be treatment. botulinum where surgery is most effective.77 experiencing the long-lasting benefit.com April 2017 Copyright © American Academy of Neurology. linum toxin injections for other estab. entially damage the small pain fibers. where the gasserian some patients. that the first treatment should be lished indications. groups: lesions distal to the ganglion. to reach the infratemporal fossa. each procedures for trigeminal toxin injections should be performed surgical method entails its own poten- neuralgia exist that are by neurologists experienced in botu. thus the author believes very efficacious.7 receptors promises to prevent includes all sorts of peripheral lesions any side effects associated with depres. . has standard dosages are not enough or the not yet achieved US Food and Drug side effects are too severe. When on choice between medical and surgical target. lesion of been discovered. after tion of high-concentration glycerol. has lesions at the ganglion level.70 In loss of function mutations lead to the fact.76 chemical lesion by injec- neuralgia found that many. or cryolesions. haps the neuropathic pain condition Balloon compression and glycerol 412 ContinuumJournal. a long cannula or geminal neurons. methods involve percutaneous gas- leagues74 have now demonstrated that serian (ie.7) subtype. difficult question is whether Meckel cave. so oxcarbazepine or carbamazepine. already been proved in patients in a The second group of surgical phase 2 trial. sions. Finally.71 Naturally.7 receptors exist microvascular decompression. If the efficacious in other conditions. None function mutations are linked to a of these methods has ever been severe chronic pain syndrome. sodium receptor in the nociceptive and posterior fossa intervention of system. dium channel 1. Unauthorized reproduction of this article is prohibited.7 has their emergence from the facial bones: been validated as a key pain target by neurectomy. In all cases.and Surgical methods for treating trigem- frequency-dependent sodium channel inal neuralgia can be divided in four blocker that has selectivity for the so. tial problems. then surgery Administration (FDA) indication for should at least be proposed and dis- trigeminal neuralgia. A study in patients who done: thermocoagulation by radio- had undergone surgery for trigeminal frequency. This absence of brain The first group of surgical methods Nav1.78 Radiofrequency thermo- the very beginning. or mechanical compression by balloon would have opted for surgery from inflation. Nav1. electrode is inserted first through the anistic support to the potential of this cheek. then between the mandibular new molecule. trigeminal) ganglion le- BIIB074 can inhibit the firing of tri.7 is a major the root by gamma knife radiosurgery. as gain of frequency lesions. arch and the maxillary bone. whereas supported by adequate trials. cussed with the patient. This treatment.75 coagulation was conceived to prefer- Although trigeminal neuralgia is per. through which it TRIGEMINAL NEURALGIA penetrates the skull base reaching the A first. should be offered the early need fluoroscopic guidance. these lesions were often the inability to feel pain. Trigeminal Neuralgia KEY POINT h Several surgical injected area. and aimed at SURGICAL TREATMENT OF the foramen ovale. its source of anesthesia dolorosa (pain efficacy and extreme tolerability has in area of sensory loss). according to their ganglion lies.72 Nav1.

including the intraoperative reliability and accuracy of the recording of trigeminal evoked poten. Continuum (Minneap Minn) 2017.23(2):396–420 ContinuumJournal. This study (one follow-up studies report a variable of the very rare randomized con- duration of pain relief. trigeminal division because the dam. where the radiation beams should age to small fibers entails corneal collimate). Whereas balloon mater covering the Meckel cave. the amount dent with the painful division. that the root entry zone is the key spot trast. . from can be performed under continuous burning of an oculomotor nerve to general anesthesia. Only the occur- neous ganglion lesion techniques. the pain- frequency. is not supported by evidence. Unlike the other patients submitted to pulsed radio. is not immediate and generally re- cutaneous ganglion lesion procedures quires 6 to 8 weeks to develop. one study reported that in all geminal neuralgia. Naturally. the irradiated area. the (which is close to the trajectory toward rationale is that of blocking the trig. types of intervention. however.injection preferentially damage the are piercing of the maxillary artery large myelinated fibers.20 The success ing because it conveys strong evidence of ‘‘pulsed’’ radiofrequency. radiosurgery interventions (ie. persisting in trolled trials of stereotactic radiosurgery about 70%. However. and the irradiated area. and more severe and longer lasting cause they must report in what areas after radiofrequency (Figure 3-8). the veloped. and in trigeminal neuralgia) is very interest- 5 years. thus. the foramen ovale). patients compression and glycerol injection must be awakened in between be. Unauthorized reproduction of this article is prohibited. is the same as for all stereotactic Sophisticated methods have been de. the original pain returned relieving effect of gamma knife therapy by 3 months. and then of favorable evidence is increasing the patient is anesthetized again before rapidly. the rence of facial numbness or pares- pain relief is immediate and complete thesia correlated with the length of in a high percentage of cases.79 The major risks of all per. The electrode is moved slightly fewest number of patients who have until the evoked paresthesia is coinci. radiofrequency infusion of glycerol into the CSF of the thermocoagulation requires anesthe. and that of the dura gering impulses. Almost unavoid- sia when the electrode is moved to able are trigeminal sensory deficits. Balloon trial studied whether expanding the compression and glycerol injection irradiated area more distally along are devoid of the risk of corneal the root would increase the rate of keratitis because they damage large responders80: the total success rate myelinated fibers only. and 50% at 1.com 413 Copyright © American Academy of Neurology. 60%.6. 3. middle cranial fossa. Hence. of the face they feel the paresthesia Stereotactic radiosurgery (gamma evoked by electric impulses delivered knife) is the most recent type of in- from the tip of the electrode to prevent tervention applied to trigeminal neu- damaging the wrong trigeminal divi. In in the origin and maintenance of tri- fact. been treated.41 In any event. respectively. A randomized controlled deafferentation and keratitis. the target and then again at the which are usually transient with balloon moment of the lesion. in con. the ordinates of the trigeminal root just electrode cannot be aimed at the first before its entrance into the pons. Regarding the was 68% regardless of the length of general pros and cons of the percuta. the main problem the actual thermocoagulation begins. ralgia and therefore the one with the sion. with compression and glycerol injection various possible consequences. methods of finding the exact co- tials.

and microscopy to ade- analysis of gamma knife interventions. or thrombocytes. pression is the only causal cure and is the only causal tion occurs in up to 69% of patients. The 34% of patients do not reach 1 year of neurosurgeon may then disentangle pain relief. Blood cells = white cells. With the sponge to keep the pulsating artery increasing number of interventions. Facial gone this procedure. cutting Cochrane Review81 does not add to the dura mater. Note that central nervous system (CNS) disturbances affected patients on carbamazepine far more frequently than patients on oxcarbazepine. toxicity also increases. hemisphere. nately. repeated administration of the looping artery and leave a small radiations were necessary. patients (although it tends to improve dence to be considered in a Cochrane with time). found that. . whereas hyponatremia only affected patients on oxcarbazepine. It requires general anesthe- been reported.6 at patients at 1-year follow-up. blinded operators are unthinkable. shifting the cerebellar the 2008 guidelines. separated from the trigeminal root. The most recent sia. intubation.com April 2017 Copyright © American Academy of Neurology. red cells. Trigeminal Neuralgia FIGURE 3-8 Dropouts due to adverse events in 100 patients on carbamazepine and 100 patients on oxcarbazepine.82 decompression requires 1 year after gamma knife therapy. and troublesome sensory Review. Unfortu. quately visualize the nerves emerging however. because about from the cerebellopontine angle. No complications done as an outpatient surgical pro- outside the trigeminal nerve have cedure. with Importantly. Although microvascular decom- major surgery but complete pain relief with no medica.81 Microvascular decompres- loss or paresthesia is reported in 6% sion is the only type of surgery for to 13%.6 A recent meta. in about 11% of patients 414 ContinuumJournal. KEY POINT According to the 2008 AAN/EFNS facial hypesthesia persisting in 50% of h Microvascular guidelines on trigeminal neuralgia. the rate of success and the pain-free Naturally. a placebo intervention or time increase significantly. whereas anesthesia dolorosa trigeminal neuralgia that cannot be is practically absent. no reported trial trigeminal neuralgia numbness is reported in 9% to 37% of meets the minimal criteria of evi- and offers longer-lasting pain relief. huge numbers of patients have under- intervention of This falls to 52% at 3 years. Unauthorized reproduction of this article is prohibited. craniotomy.

. Diplopia to distinguish three etiologic catego- is usually transient.7 receptor has such as how clear the neurovascular promise of efficacy without inducing compression is on MRI.2%. ous pain. with microvascular de. A leagues and the patient. but they report a neuralgia in patients with MS. still the meta-analyses of logic role exerted by neurovascular the largest studies make microvascular compression would seem to favor the decompression the most efficacious choice of microvascular decompres- of the surgical interventions for clas. and those with concomi- fashion with our neurosurgical col. The recent demon- Allowing for the lack of evidence. Most surgeons in port or refute the effectiveness of the trigeminal neuralgia these latter cases interpose the separat. cular decompression) are all very Continuum (Minneap Minn) 2017. KEY POINT referred for this type of intervention. whether the side effects related to CNS depres- patient also has involvement of the sion. knife are efficacious in mere contact that apparently is not Insufficient evidence exists to sup. and into the pons).com 415 Copyright © American Academy of Neurology.14 the surgical option. gamma knife. and facial palsy is ries: idiopathic trigeminal neuralgia rare. and whether the patient terventions (percutaneous ganglion is prepared to wait at least 1 month to lesions. Three categories of surgical in- first division. Aseptic meningitis is the most only. and carbamazepine are still the first- When considering the choice of sur. When the decision is difficult. must rely on clinical grounds tomas. sion in the posterior fossa. percutaneous gasserian of the trigeminal root near its entry ganglion lesions. the best h Percutaneous ganglion the surgeons do not find any neuro. cerebellopontine angle). although gical treatment. Unauthorized reproduction of this article is prohibited. or hema. classic tri- tients. surgical management of trigeminal and can be repeated in ing sponge anyway. and secondary trigem- microvascular decompression may all inal neuralgia (due to major neurologic be considered. new sodium channel blocker that is acteristics should also be considered. infarctions. believes that MS pa- to establish MRI criteria that ensure tients with evidence of drug-resistant that morphologic changes of the tri. trigeminal neuralgia should be offered geminal root are observed. 4% of patients incur major problems with or without concomitant continu- such as CSF leaks. Oxcarbazepine tion of pain relief.6 90% of main types of intervention. however. the treatment of damaging the nerve. option is referral to a large center that lesions and gamma vascular compression9.23(2):396–420 ContinuumJournal. choice medical treatment. gamma knife. Diagnostic tests are necessary common complication (11%). The major long-term complication geminal neuralgia (an anomalous is ipsilateral hearing loss (Figure 3-9). 75% at 3 years. including patients obtain pain relief. The cases of relapse.54 at 1 year. Sensory loss occurs in 7% of pa. Up to The diagnosis of trigeminal neuralgia. greater rate of failure. vessel produces morphologic changes In conclusion. stration of the concurring pathophysio- based data. disease such as MS or tumors at the compression offering the longest dura. (nothing can be found).52 However. More than percutaneous ganglion lesions and 80% of patients will still be pain free gamma knife. selective for the Nav1. Specific char.14 or they find a is led by experienced neurosurgeons. hence the need author. the treating neurologist many patients experience significant should be involved in a collaborative side effects. The average mortality associ. CONCLUSION ated with the operation is 0. and 73% at 5 years. sic trigeminal neuralgia: according to positive reports occur with all the the AAN/EFNS guidelines. and microvas- get the pain relief from gamma knife. tant continuous pain respond less.

fashion with the patient and the doi:10.com April 2017 Copyright © American Academy of Neurology. Reprinted with permission from Gronseth G. ogist should work in a collaborative J Oral Maxillofac Res 2014. Macfarlane GJ. 416 ContinuumJournal. PGL = percutaneous ganglion lesions.5037/jomr.full. Beasley M. neurology. et al.org/content/71/15/1183. Trigeminal Neuralgia FIGURE 3-9 Complications of surgery for trigeminal neuralgia.6 B 2008 American Academy of Neurology. Macfarlane TV. Precise MRI criteria for neurosurgeon to determine when and differentiating a real neurovascular what type of surgical procedure to try. compression from an irrelevant con- tact will be of benefit in better REFERENCES selecting patients for microvascular 1. a Many Class IV studies on gamma knife surgery report trigeminal sensory disturbances in 9% to 37% of patients. efficacious.5(3):e2. Neurology.2014. CSF = cerebrospinal fluid.5302. Self-reported facial pain in UK Biobank decompression. MVD = microvascular decompression. The treating neurol- Study: prevalence and associated factors. Unauthorized reproduction of this article is prohibited. . GKS = gamma knife radiosurgery.

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