PART 8 Functional Pain
53 
Trigeminal Neuralgia
DAVID C. STRAUS, ANDREW L. KO, LALIGAM N. SEKHAR
CLINICAL PEARLS
• Careful clinical diagnosis is key to appropriately selecting
patients who will benefit from surgical treatments for
trigeminal neuralgia.
• During microvascular decompression, the entire cisternal
segment of cranial nerve V must be inspected from the
brainstem to the entrance into Meckel’s cave. It is not
Introduction and History
Trigeminal neuralgia, first described in detail by Dr. James
Fothergill in the 18th century, is an affliction of such severe
facial pain that it has previously been dubbed the “suicide
disease.” Early treatments primarily focused on peripheral neu-
roablative procedures. Carnochan documented the first suc-
cessful surgical treatment of the disease in 1856, which used a
transantral approach to follow the maxillary nerve back to the
gasserian ganglion, which was subsequently excised. In the
1890s Victor Horsley developed a subtemporal approach to
the gasserian ganglion where he sectioned the preganglionic
nerve fibers. Also in the 1890s Hartley and Krause indepen-
dently described the extradural approach for gasserian ganglio-
nectomy. In the late 1890s Cushing developed a modification
of this extradural ganglionectomy that utilized a more basal
trajectory to avoid bleeding from the middle meningeal artery.1
Dandy was the first to perform a lateral suboccipital approach
(“cerebellar route”2) to the trigeminal nerve for treatment of
trigeminal neuralgia in the 1920s. Similar to other techniques,
his involved sectioning of the preganglionic trigeminal nerve.
As a result of his intracranial approach through the posterior
fossa, he was the first to note the frequent incidence of vascular
compression on the trigeminal nerve in its cisternal segment
and postulate that sensory root compression may be an impor-
tant factor in the pathogenesis of trigeminal neuralgia.3
Gardner4,5 furthered this theory in the 1960s and published
successful results from vascular decompression of the nerve
root. With the advent of the surgical microscope, Jannetta6–8
solidified the theory of vascular compression as the underlying
FPO
Optional
Photo/Art Inset
(10p x 10p)
uncommon to identify multiple offending vessels, all of which
require decompression for optimal results.
• Treatment recommendations should be tailored to the specific
patient, weighing the distinct advantages and disadvantages
of each modality.
etiology for trigeminal neuralgia and demonstrated the excel-
lent response rate and surgical safety for microvascular decom-
pression (MVD) of the trigeminal nerve in a large series of
patients.
Percutaneous techniques also evolved in parallel to open
surgical treatments for trigeminal neuralgia. As early as 1910,
Harris documented the percutaneous injection of alcohol into
the gasserian ganglion in the treatment of a patient with tri-
geminal neuralgia. In 1914 Härtel described the landmarks
and trajectory for accessing the gasserian ganglion through an
anterior trajectory. Sweet further established the methods of
radiofrequency rhizotomy (RFR),9 and Mullan developed the
balloon compression technique.10 The application of the radia-
tion to achieve lesioning of the trigeminal nerve was the first
clinical application of stereotactic radiosurgery (SRS) by Leksell
in the 1950s.11 Taken together, these techniques—MVD,
RFR, balloon compression, glycerol rhizotomy, and SRS—
continue to represent the current interventional armamentar-
ium for treating trigeminal neuralgia.
Pathogenesis
One important hypothesis regarding the mechanism for tri-
geminal neuralgia attributes causation to demyelination of
the trigeminal sensory fibers (typically in the nerve root, but
occasionally in the brainstem). In most cases demyelination
involves the proximal part of the nerve root that is techni-
cally within the central nervous system (CNS) and myelin-
ated by oligodendroglial cells rather than Schwann cells (the
745
746 PART 8 Functional Pain
Obersteiner-Redlich zone).4 Demyelination is commonly
caused by arterial compression. Less common causes of demy-
elination are venous compression, demyelination from mul-
tiple sclerosis (MS), or compressive lesions in the posterior
fossa. These focal areas of demyelination enable direct apposi-
tion of the axons from larger Aα and Aβ sensory fibers with
neighboring axons of unmyelinated small Aδ and C fibers
transmitting pain signals. This anatomic configuration enables
both ephaptic conduction between these apposed fibers as
well as ectopic generation of spontaneous nerve impulses.
This spontaneous activity is further exacerbated by the defor-
mity associated with vascular indentation. Surgical decom-
pression of the nerve root provides rapid relief of pain by
releasing the focal pulsatile distortion of the nerve rootlets
and causing separation of the demyelinated rootlets, thus pre-
venting both ectopic nerve signals and the ephaptic spread
of these signals. The impact of remyelination over time may
play a role in preventing recurrence of the neuralgia over the
long term.12
An alternative hypothesis, first suggested by Devor in 1994,
states that a cluster of damaged neurons in the gasserian gan-
glion becomes hyperexcitable, forming an “ignition focus” and
subsequent autonomous firing within the ganglion that ceases
once the neural refractory period is reached.13 This may explain
the not infrequent (up to 17%14 of cases) instance of trigeminal
neuralgia that occurs in the absence of mass lesions, demyelin-
ating diseases, or neurovascular compression.
Clinical Features and Diagnosis
The annual incidence of trigeminal neuralgia is ~4.5 per
100,000. The overall prevalence is up to 27 cases per 100,000
people-years. It is about twice as common in females as in
males, and peak incidence occurs between 50 and 60 years of
age.15 The classic description of facial pain associated with
trigeminal neuralgia is a unilateral, sharp, lancinating, electric-
shock–like pain that is episodic in nature with interval pain-
free periods. Frequently, there are trigger areas or activities (eg,
eating, dental care) that provoke pain episodes. Though mild
hypesthesia may be present, trigeminal nerve function typically
does not show impairment on physical exam.
The majority of patients will have an initial response to
anticonvulsant medications such as carbamazepine, and about
50% of patients will achieve remission of pain for 6 months
or more. However, in nearly four of five patients, pain will
recur after the initial diagnosis.16 The frequency of pain may
vary substantially between patients, from occasional paroxysms
to incessant twinges of “status trigeminus.” Distribution of
pain is most frequently in the V2 and V3 branches of the
trigeminal nerve (one-third of patients); configuration of pain
in V2 or V3 alone, or in V1 and V2 alone, occurs in about
15% of patients; pain in V1 alone is rare (~4%).17 In evaluating
patients with pain in the trigeminal distribution, it is impor-
tant to assess for other potential causes of facial pain. These
include dental pathology, temporomandibular joint pain,
migraines, postherpetic neuralgia, and temporal arteritis.18 It
is also important to realize that trigeminal neuralgia may go
unrecognized by other providers less attuned to the diagnosis,
and patients with tic pain may undergo numerous dental pro-
cedures or other such treatments before the correct diagnosis
of trigeminal neuralgia is reached.
The International Headache Society distinguishes neuro-
genic facial pain in the distribution of the trigeminal nerve as
either symptomatic trigeminal neuralgia or “idiopathic” tri-
geminal neuralgia.19 Symptomatic trigeminal neuralgia refers
to trigeminal nerve pain related to an identifiable pathology,
such as CP angle tumors; idiopathic trigeminal neuralgia refers
to trigeminal nerve pain without an identifiable pathology. It
is important to differentiate between cases of symptomatic tic
pain and idiopathic cases, as treatment strategies will differ
between the two groups. Symptomatic cases, such as those due
to MS, schwannomas, meningiomas, metastatic tumors, epi-
dermoid cysts, arachnoid cysts, or other pathologies, are best
addressed by direct treatment of the underlying pathology. In
cases of new onset trigeminal neuralgia without additional
cranial neuropathies, magnetic resonance imaging (MRI)
reveals an underlying pathology (not including vascular com-
pression of the trigeminal nerve) in approximately 15% of
cases.20 Pooled data from MRI studies reveal vascular compres-
sion of the symptomatic nerve in 77% (sensitivity) of patients,
whereas there is no vascular compression in asymptomatic
nerves in 71% (specificity) of cases.
Trigeminal neuralgia in the setting of MS is particularly
important to consider. Patients with MS are 20 times more
likely to suffer from trigeminal neuralgia than those without
MS; about 5% of patients with trigeminal neuralgia also have
MS, whereas about 2% of patients with MS will develop
trigeminal neuralgia. These patients typically do not tolerate
the anticonvulsant medicines as well as non-MS patients and
thus more frequently experience medically intractable pain.
They also do not respond as well to MVD in comparison to
idiopathic cases of trigeminal neuralgia and are more prone to
surgical complications.21 Special consideration should be made
in these cases; in many cases the pain may be well controlled
with less invasive procedures such as RFR or SRS. Idiopathic
trigeminal neuralgia may be further characterized by its clini-
cal manifestations. Typical trigeminal neuralgia (type 1 TN)
is pain that is >50% sharp, lancinating, and shocklike with
pain-free intervals and atypical trigeminal neuralgia; “atypi-
cal” (type 2 TN) is pain for which >50% of symptoms are
constant with an aching, throbbing, or burning character.22
Patients with typical trigeminal neuralgia more frequently
are found to have arterial vascular compression at surgery
and have both more frequent and more durable responses
to microvascular decompression. Although they have a less
favorable outcome profile compared to “typical” trigeminal
neuralgia, patients with atypical trigeminal neuralgia still
demonstrate a meaningful response to treatment and remain
surgical candidates. Other forms of trigeminal nerve pain
exist—such as deafferentation pain (related to prior rhizoto-
mies), neuropathic pain (related to peripheral trigeminal nerve
trauma), and atypical facial pain.23 These categories and their
optimal management, however, are less well defined in the
literature.

Treatment Modalities and Results
Medical Treatment
Medical intervention is the first-line therapy for classic trigemi-
nal neuralgia. Patients often demonstrate excellent initial
response to medical treatments. Typical narcotic pain medi-
cines do not provide adequate relief for tic pain. Anticonvul-
sants are typically used as first-line therapy. Strong data exist
to support the use of carbamazepine (200–1200 mg/day).
Four placebo-controlled studies have demonstrated its efficacy
in treating classic trigeminal neuralgia. It is shown, reliably, to
reduce both the frequency and the intensity of painful parox-
ysms. The number needed to treat in these trials was only 1.7
to 1.8, demonstrating carbamazepine’s efficacy in ameliorating
pain in classic trigeminal neuralgia. Its utility, however, is
limited by its relatively narrow therapeutic index and with a
number needed to harm of only 3.4 for minor side effects and
24 for severe adverse events.
Oxcarbamazepine (600–1800 mg/day)—a sodium channel
blocker with a structure that is biochemically analogous to
carbamazepine—has also been well studied in clinical trials.
Three double-blind randomized-controlled trials (RCTs) com-
paring oxcarbamazepine to carbamazepine show that it is non-
inferior, producing a >50% reduction of attacks in 88% of
patients. Oxcarbamazepine has the advantage of more stable
pharmacodynamics and also minimized exposure to some
of the more severe side effects of carbamazepine, specifically
agranulocytosis and aplastic anemia. Given its equivalent effi-
cacy and its more favorable risk profile, oxcarbamazepine is
often used as a first-line medication in treating classic tic pain.
A number of other drugs have been investigated in the
treatment of trigeminal neuralgia, but none has as robust
an evidence base as carbamazepine and oxcarbamazepine.
Phenytoin was the first anticonvulsant to be applied to tic pain
with reported success; however, there have been no controlled
trials evaluating its efficacy. Baclofen has been shown in a single
trial to reduce the number of pain paroxysms. Lamotrigine has
been shown to be effective as an add-on therapy. Pimozide and
tocainide showed efficacy in comparison with carbamazepine
in single trials. Other antiepileptics, such as gabapentin, clon-
azepam and valproate, have demonstrated efficacy as well but
all are less efficacious than carbamazepine. Topical ophthalmic
anesthesia has been shown to be ineffective in a placebo-
controlled RCT. There is insufficient evidence to evaluate the
utility of intravenous medications in the acute treatment of tic
pain. There is also insufficient evidence to evaluate the use of
drugs commonly used in neuropathic pain, such as pregabalin
and serotonin-noradrenaline reuptake inhibitors. In summary,
carbamazepine and oxcarbamazepine are first-line treatments
for classic trigeminal neuralgia. If either one of these drugs is
not effective or has intolerable side effects, then the next step
should be surgical referral.20 Second-line medications are also
available. Frequently used are lamotrigine and gabapentin,
which are felt to have comparable efficacy and fewer adverse
reactions,24 though the quality of evidence supporting these
claims is poor.
CHAPTER 53  Trigeminal Neuralgia 747
Surgical Interventions
Despite the excellent initial response many patients have with
medical treatment, up to 50% of patients eventually become
refractory to medical therapy or suffer intolerable medication
side effects at the dosages required to control their pain. Surgi-
cal interventions are the next option for patients with medi-
cally refractory trigeminal neuralgia. There is some evidence
that patients should be referred early for surgical intervention.
In a study of 245 patients who were treated surgically, 78%
reported that they would have preferred to have had their
intervention performed at an earlier time point in the course
of their disease25 (this study, however, has the selection bias of
only addressing patients who proved to be medically refractory
and went on to have surgery). There are three primary surgical
treatment strategies for trigeminal neuralgia: stereotactic radio-
surgery, percutaneous rhizotomy, and microvascular decom-
pression. Use of one procedure does not preclude use of the
other treatment options or repeat treatment.
Percutaneous Rhizotomy
Percutaneous rhizotomies are achieved by one of three methods:
radiofrequency thermoablation, balloon compression, or glyc-
erol rhizolysis. All techniques involve accessing the gasserian
ganglion through a needle puncture in the cheek. The physi-
ologic goal is to selectively destroy the nociceptive Ad and C
fibers and preserve the Aa and Ab (touch) fibers.
The radiofrequency rhizotomy procedure is performed
under monitored anesthesia care with a quickly reversible agent
such as propofol. The neck is slightly extended and the head
rotated to the contralateral side. The cheek is prepped, and a
needle is used to puncture the skin in the cheek at a point
2.5 cm lateral to the oral commissure. The needle is then
advanced to a point aimed superiorly to a point 2.5 cm ante-
rior to the tragus and medially to a point at the medial margin
of the ipsilateral pupil. The trajectory transverses the buccal
muscles to pass medial to the coronoid process of the mandi-
ble, through the pterygomaxillary fossa to the skull base. At
this point, a modified submentovertex view fluoroscopy may
be used to identify the foramen ovale and to finalize the trajec-
tory of the needle (Fig. 53.1A). The needle is then advanced
through the foramen ovale. Entry into the Meckel cave is felt
as a “pop” through the outer layer of dura and may also be
evidenced by a jaw jerk or CSF egress from the needle. The
head is returned to a neutral position, and the fluoroscopy unit
is rotated to a true lateral image. The depth of needle insertion
should correlate to the distribution of the patient’s pain: the
clival line can be used to approximate the location of V2 fibers
in the Meckel cave; V1 lies 1 mm beyond the clival line, and
V3 lies 1 mm ventral to it (Fig. 53.1B). At this point the
patient may be awakened and low frequency stimulation is
used to confirm the placement in the proper location within
the trigeminal nerve rootlets to treat the appropriate nerve
distribution. Once confirmed, the patient is reanesthetized and
a radiofrequency-induced thermal lesion is sequentially created
using higher-frequency stimulation.
748 PART 8 Functional Pain
A B
• Figure 53.1  (A–B) Trajectory of needle entry to the Meckel cave.
• Figure 53.2  Shape of balloon filling the Meckel cave after inflation with
radiopaque dye.
Balloon compression rhizotomy is most often done under
general anesthesia. Access to the Meckel cave is obtained in an
analogous fashion with a 14-gauge needle. A 4-Fr Fogarty
balloon is then inserted and slowly inflated with radiopaque
dye and observed to assume the shape of the Meckel cave as it
expands (Fig. 53.2). The balloon is further inflated to a set
pressure of 1.25 atm for a period of 1 minute to cause the
rhizotomy.
Glycerol rhizolysis may also be performed by accessing the
Meckel cave in an analogous manner. After confirmation of
needle placement in the Meckel cave by fluoroscopy and a
radiopaque dye injection, the patient is placed in the seated
position (which he or she will maintain for 2 hours after the
injection), and anhydrous glycerol is injected to fill the cistern.
These percutaneous techniques offer a relatively noninvasive
approach to treating trigeminal neuralgia and immediately
improve symptoms. Up to 90% of patients have relief of their
pain immediately after treatment, and around 75% of patients
are pain free at 1 year. However, the durability of this relief is
suboptimal with around 50% of patients having recurrent pain
at 5 years. These procedures may be repeated after pain recur-
rence with comparable results. Side effects from percutaneous
rhizotomy procedures include a nearly 50% rate of sensory
loss, and 6% of patients report troubling dysesthesias. Around
4% of patients develop corneal numbness, and up to 4% may
develop anesthesia dolorosa. The risk of other complications—
such as other cranial neuropathies, meningitis, and mortality—
is minimal (<1%).20 Intraprocedurally, there is a risk of reflex
bradycardia or asystole during manipulations within the
Meckel cave; the anesthesia team should be aware of this risk
and prepared for intervention in the event of hemodynamic
instability (glycopyrrolate, atropine, transcutaneous pacing in
order of application). The choice of percutaneous procedure to
utilize is in part determined by the surgeon’s comfort level.
Glycerol rhizolysis may be less durable than either radiofre-
quency rhizotomy or balloon compression. It is also more
difficult to precisely target the injection as well, though there
is a slightly lower risk of numbness or anesthesia dolorosa.
Balloon compression may be preferable in patients who are
unable to tolerate an awake procedure or are unable to effec-
tively communicate with the surgical team during the proce-
dure. It is also preferable in the rare patients who have
predominantly V1 segment symptoms, as there may be a
slightly lower risk of corneal anesthesia. Balloon compression
has a significantly higher risk of masticatory weakness, however.
Radiofrequency rhizotomy is the most precise method, but it
is a slightly more technically difficult procedure, requires
patient cooperation, and may harbor a slightly higher risk
of complications such as corneal anesthesia and anesthesia
dolorosa.

CASE 53.1
A 69-year-old male suffered from a spontaneous onset of
lancinating right-sided V2 and V3 pain 5 years ago. It is
triggered by eating, drinking, and brushing his teeth. He has
developed a dull, aching component to the pain during the past
2 years. He had some response to escalating medical therapy,
but he presently requires carbamazepine, gabapentin, and
phenytoin to tolerate his pain. With this polypharmacy, he has
developed significant and intolerable side effects, including
imbalance and cognitive decline. He underwent stereotactic
radiosurgery in 2012 but did not have any response to this
treatment. His neurologic exam is notable only for mild right V2
hypesthesia. MRI with fast imaging employing steady-state
acquisition (FIESTA) sequencing did not show any evidence of
neurovascular compression on the right trigeminal nerve. He was
presented with the options for repeat radiosurgery, percutaneous
rhizotomy, or microvascular decompression. He opted to proceed
with balloon compression rhizotomy, which was subsequently
performed without complication (Fig. 53.3). He was discharged
home the same day, has nearly completely tapered off of his
medications, and has remained pain free since the procedure.
Radiosurgery
Similar to the percutaneous techniques, stereotactic radiosur-
gery offers a less invasive method to treat trigeminal neuralgia.
The most data exist for treatment with the frame-based Gamma
Knife radiosurgery system, though there are no data that other
radiosurgery platforms differ in their results. This technique
exerts its physiologic effect by injuring the nerve rootlets. The
radiosurgical target is defined as the cisternal segment of the
nerve as it courses toward the Meckel cave. After application
of the head frame, a stereotactic MRI is obtained to identify
the nerve for treatment planning. It is targeted between 3 and
8 mm ventral to the junction of the trigeminal nerve with the
pons using a 4-mm isocenter. Typically an 80-Gy median
maximum radiation dose is prescribed, taking care to have the
brainstem located beyond the 20% isodose line. Typically,
patients do not have any change in their symptoms immedi-
ately after treatment. Pain relief typically occurs in the first
month after treatment and is maintained in 69% of patients
at 1 year. The durability of radiosurgery is less than with the
percutaneous techniques, with around 52% of patients main-
taining pain relief at 3 years.26 It is important to note that
pain improvement following stereotactic radiosurgery groups
patients who remain on trigeminal neuralgia medications and
those who are pain-free without medication together. Facial
numbness may occur in between 9% and 37% of patients,
though troublesome paresthesias or sensory loss only occurs in
6% to 13% of patients. Anesthesia dolorosa is exceedingly
uncommon, as are complications outside of the trigeminal
nerve. For recurrent cases, repeat SRS is an option, although
a slightly different target is typically selected and a reduced
dosage of 70 Gy is used for the second treatment.
Microvascular Decompression
Open surgical techniques for treating trigeminal neuralgia
attempt to address neurovascular compression while maintain-
ing trigeminal nerve function. Neuromonitoring is typically
used with somatosensory evoked potentials (SSEPs)/motor
CHAPTER 53  Trigeminal Neuralgia 749
evoked potentials (MEPs) and cranial nerve monitoring for
cranial nerves V, VII, and brainstem auditory evoked responses
(BSAERs). A retrosigmoid craniotomy is used to expose the
posterior fossa dura. Further bone removal is performed to
expose the junction of the transverse and sigmoid sinuses. The
dura is opened, and cerebrospinal fluid (CSF) is drained from
the lateral cerebellomedullary or cerebellopontine (CP) angle
cistern to relax the posterior fossa. The cerebellum is gently
retracted, and the arachnoid overlaying the cranial nerves is
opened sharply. Care is taken not to avulse the petrosal vein
during this exposure. The trigeminal nerve is found in the
superior portion of the opening. After identifying the trigemi-
nal nerve, it is inspected circumferentially paying particular
attention to the root-entry zone region near its junction with
the pons and following it out to its entrance to the Meckel
cave. Vessels contacting the nerve are carefully dissected free,
and small pieces of shredded and rolled-up Teflon felt are used
to buttress the artery off of the nerve (Video 53.1). In some
cases, an internal neurolysis may be performed as well, separat-
ing the individual nerve fascicles.27 Neurovascular compression
is identified in up to 89% of cases, with the superior cerebellar
artery (SCA) being the most frequently involved vessel com-
pressing the nerve from above (~75% of cases). In ~10% of
cases the anterior inferior cerebellar artery (AICA) is involved;
venous compression is found in ~10% of cases. Outcome from
surgery is excellent and offers the most durable treatment for
trigeminal neuralgia available. About 90% of patients obtain
pain relief initially; over 80% will be pain free at 1 year. At 5
years, 73% of patients remain pain free.6 Complication rates
are low, with 4% of patients suffering a significant complica-
tion such as CSF leak, infarction, or hematoma. Aseptic men-
ingitis is relatively more common (11%). Permanent injury
to cranial nerves IV, VI, or VII is exceedingly rare. The most
common cranial nerve injury is ipsilateral hearing loss (up to
10% in some case series), though permanent hearing loss is
rare with the use of intraoperative BSAERs. Sensory loss occurs
in 7% of patients, though this is typically not dysesthetic.20
Overall, microvascular decompression is a very well tolerated
procedure that offers an excellent response rate and provides
the most durable treatment for patients with trigeminal neural-
gia. There are small, upfront risks that are necessarily associated
with general anesthesia and posterior fossa surgery.
CASE 53.2
A 55-year-old, otherwise healthy, female patient suffered from 5
years of severe and intractable paroxysms of sharp, stabbing pain
localized to her left jaw. Several factors triggered the left face pain
including eating, talking, cold objects, washing her face, and
brushing her teeth. Initially she was submitted to a dental
treatment, which included tooth extraction, prior to arriving at
the diagnosis of trigeminal neuralgia. She tried several different
pain medications, including carbamazepine and gabapentin, but
none provided durable relief from the pain. She was referred for
surgical evaluation and a preoperative MRI scan was performed,
showing a vessel in contact with the trigeminal nerve on the left
(Fig. 53.4A–B). She underwent a left retrosigmoid craniotomy and
microvascular decompression of the fifth cranial nerve (Fig. 53.4C–D,
Video 53.2). Postoperatively her pain completely resolved. She
has remained pain free and off of medication since surgery.
750 PART 8 Functional Pain

C-arm monitor
C-arm

OR staff

Patient

Anesthesia
Instruments
Surgeon
Anesthesia
machine

RF generator
RF cable IV on left

A B

F.Sp

C D

PCL

P.Sph.
Pet.

E F
• Figure 53.3  Case example of percutaneous rhizotomy. (A) Preoperative MRI. (B) Room setup. (C–F)
Targeting and needle positioning.
 CHAPTER 53  Trigeminal Neuralgia 751

A B

SCA

CN V
minor portion

Petrosal vein
preserved

CN V
decompressed

SCA

Teflon felt

• Figure 53.4  Case example of microvascular decompression. (A–B) Preoperative imaging. (C–D)
Diagram of surgical microvascular decompression.
752 PART 8 Functional Pain

AVERAGE REPORTED COMPLICATION RATE ACROSS DIFFERENT TREATMENT MODALITIES FOR

TRIGEMINAL NEURALGIA
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• Figure 53.5  Average reported complication rate across different treatment modalities for trigeminal
neuralgia.

Other Treatments dermatotopic distribution of the trigeminal nerve segments

The surgical treatments described here are the most commonly
used treatment strategies for trigeminal neuralgia. There are a
few alternative treatments that may be applied in unusual
cases. Peripheral nerve procedures—such as peripheral radio-
frequency neurotomy; injections of anesthetics or destructive
agents such as streptomycin, alcohol, or phenols; cryoablation;
or surgical neurectomy—have been applied but show signifi-
cantly lower response rates and rapid recurrence of symptoms
as soon as 1 year after the destructive peripheral procedure.
Given their relative inferiority compared to the techniques
described earlier, they are not commonly in use but may be
applied in rare situations. In cases of macrovascular compres-
sion from a dolichoectatic vertebrobasilar artery, microvascular
decompression with Teflon pledgets alone may be insufficient
to relieve the arterial impaction. In such selected cases, arterial
pexy may be of use in treating recurrent facial pain.28 Addition-
ally, a transpetrosal approach may be needed to open the
Meckel cave in cases where there is ongoing pathology or nerve
compression. Finally, in the most extreme refractory cases, a
trigeminal tractotomy may be performed. Here anatomic and
neurophysiologic localization is used to create a lesion in the
descending trigeminal tract in the medulla in order to produce
a loss of pain and temperature sensation in the face and pharynx
while sparing the sense of touch.
Fig. 53.5 shows composite complication rates across the
different surgical treatments discussed earlier.20
Summary and Treatment Algorithm
Classic trigeminal neuralgia consists of episodic, sharp, electric
shock–like, lancinating pains that occur clearly in the
(most commonly in V2 and V3). The diagnosis is made on
clinical history and exam, though it is critical in all cases to
radiographically exclude the possibility of an underlying lesion
as the causative factor. A trial of medical treatment, typically
with carbamazepine or oxcarbamazepine, is appropriate as the
first-line treatment. In patients who are refractory to medica-
tion or develop intolerable side effects, surgical treatment with
microvascular decompression, percutaneous rhizotomy, or ste-
reotactic radiosurgery is indicated.
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Please go to ExpertConsult.com to view the complete list of references.

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