Trigeminal neuralgia is a chronic pain condition that affects the trigeminal or 5th cranial nerve, causing extreme, sporadic, sudden facial pain. It most often affects people over 50 but can occur at any age. Treatment options include medications like anticonvulsants, surgery, and complementary approaches. The National Institute of Neurological Disorders and Stroke funds research into better understanding the mechanisms of chronic pain like trigeminal neuralgia as well as developing new diagnostic methods and treatments.

1. Prepared By Shekh Md. Sami
Product Executive, PMD

2.  What is trigeminal neuralgia?
Trigeminal neuralgia (TN), also called tic douloureux,
is a chronic pain condition that affects the trigeminal
or 5th cranial nerve, one of the most widely
distributed nerves in the head. TN is a form of
neuropathic pain (pain associated with nerve injury or
nerve lesion.) The typical or "classic" form of the
disorder (called "Type 1" or TN1) causes extreme,
sporadic, sudden burning or shock-like facial pain that
lasts anywhere from a few seconds to as long as two
minutes per episode.

3.  Who is affected?
Trigeminal neuralgia occurs most often in people over
age 50, although it can occur at any age, including
infancy. The possibility of TN being caused by
multiple sclerosis increases when it occurs in young
adults.

4.  How is trigeminal neuralgia treated?
Treatment options include medicines, surgery, and
complementary approaches.
 Medications
 Anticonvulsant medicines—used to block nerve
firing—are generally effective in treating TN1 but often
less effective in TN2. These drugs include
carbamazepine, oxcarbazepine, topiramate,
gabapentin, pregabalin, clonazepam, phenytoin,
lamotrigine, and valproic acid.

5.  Surgery
 Several neurosurgical procedures are available to treat
TN, depending on the nature of the pain; the
individual’s preference, physical health, blood
pressure, and previous surgeries; presence of multiple
sclerosis, and the distribution of trigeminal nerve
involvement (particularly when the upper/ophthalmic
branch is involved). Some procedures are done on an
outpatient basis, while others may involve a more
complex operation that is performed under general
anesthesia.

6.  What research is being done?
The National Institute of Neurological Disorders and
Stroke (NINDS), a part of the National Institutes of
Health, is the federal government’s leading supporter
of biomedical research on disorders of the brain and
nervous system. NINDS-funded projects are exploring
the mechanisms involved with chronic pain and
trigeminal neuralgia, as well as novel diagnostic
methods and treatments. Other research addresses TN
through studies associated with pain research.

8.  What Are the Symptoms of Trigeminal Neuralgia
 Trigeminal neuralgia causes a sudden, severe, electric
shock-like, or stabbing pain that lasts several seconds. The
pain can be felt on the face and around the lips, eyes, nose,
scalp, and forehead. Symptoms can be brought on when a
person is brushing the teeth, putting on makeup, touching
the face, swallowing, or even feeling a slight breeze.

9.  How Is Trigeminal Neuralgia Diagnosed?
 Magnetic resonance imaging (MRI) can be used to
determine whether a tumor or multiple sclerosis is
irritating the trigeminal nerve. Otherwise, no test can
determine with certainty the presence of trigeminal
neuralgia. Tests can, however, help rule out other
causes of facial disorders. Trigeminal neuralgia usually
is diagnosed based on the patient's description of the
symptoms.

10.  How Is Trigeminal Neuralgia Treated?
 Trigeminal neuralgia can be treated with antiseizure
drugs such as Tegretol (carbamazepine) or Neurontin
(gabapentin). The medicationsKlonopin (clonazepam)
and Depakote (divalproex sodium) may also be
effective and may be used in combination with other
drugs to achieve pain relief. Some antidepressant
drugs also have significant pain relieving effects.
 If medications are ineffective or if they produce
undesirable side effects, neurosurgical procedures are
available to relieve pressure on the nerve or to reduce
nerve sensitivity.

11.  Medical Treatment for Trigeminal Neuralgia:
The goal of initial medical treatment is to achieve pain relief.
Anticonvulsants drugs like carbamazepine (Tegretol, Mazetol- trade
names) or gabapentin are the first line drug. However, there is a need
for further randomized clinical trials to establish the effectiveness of
these medications. Once patients have been in remission for 1 month
the dosage should be gradually reduced and withdrawn.
Carbamazepine may not be as effective for Atypical Trigeminal
Neuralgia.
 Some Tricyclic antidepressants drugs also have significant pain relieving
effects.
 If medications are ineffective or if they produce undesirable side effects
such as lethargy, loss of memory, nausea, weakness of bones
(osteoporosis), giddiness, low energy, etc., neurosurgical procedures are
available to relieve pressure on the nerve or to reduce nerve sensitivity.

13.  Ophthalmic division (V1) provides sensation to the forehead and eye.
 Maxillary division (V2) provides sensation to the cheek, upper lip, and
roof of the mouth.
 Mandibular division (V3) provides sensation to the jaw and lower lip; it
also provides movement of the muscles involved in biting, chewing,
and swallowing.
 Figure 1. The trigeminal nerve supplies feeling and movement to the
face. It has three divisions that branch from the trigeminal ganglion:
ophthalmic division (V1) provides sensation to the forehead and eye,
maxillary division (V2) provides sensation to the cheek, and
mandibular division (V3) provides sensation to the jaw.

14.  What are the symptoms?
 Patients describe an attack as a "pins and needles" sensation that turns
into a burning or jabbing pain, or as an electrical shock that may last a
few seconds or minutes. In some cases of extreme pain, patients have
even considered suicide. Everyday activities can trigger an episode.
Some patients are sensitive in certain areas of the face, called trigger
zones, which when touched cause an attack (Fig. 2). These zones are
usually near the nose, lips, eyes, ear, or inside the mouth. Therefore,
some patients avoid talking, eating, kissing, or drinking. Other
activities, such as shaving or brushing teeth, can also trigger pain.
 Figure 2. Facial areas of trigger zones. Trigger points (circles) have the
greatest sensitivity.

15.  Pharmacology
 Appears to provide anticonvulsant effects by reducing polysynaptic responses and blocking posttetanic potentiation.
Mechanism of action for other effects is unknown.
 Slideshow: View Frightful (But Dead Serious) Drug Side Effects
 Pharmacokinetics
 Absorption
 Therapeutic levels are 4 to 12 mcg/mL.
 Suspension T max is approximately 1.5 h.
 Tablets T max is 4 to 5 h.
 Extended-release T max is 3 to 12 h ( Tegretol XR ).
 Distribution
 76% protein bound. Rapidly crosses the placenta.
 Metabolism
 Induces its own metabolism; metabolized in the liver by CYP3A4 to the active metabolite carbamazepine-10,11-epoxide
(shown to be equipotent to carbamazepine).
 Elimination
 Initial t ½ is 25 to 65 h, decreasing to 12 to 17 h on repeated doses. 72% is excreted in the urine (3% as unchanged drug)
and 28% in the feces.
 Special Populations
 Children
More rapidly metabolized to 10,11-epoxide.
 Indications and Usage
 Treatment of epilepsy (eg, partial seizures with complex symptoms, generalized tonic-clonic seizures, mixed seizure
patterns, other partial or generalized seizures); treatment of pain associated with trigeminal neuralgia.
 Equetro only Treatment of acute manic and mixed episodes associated with bipolar 1 disorder.
 Unlabeled Uses
 Treatment of restless leg syndrome; alternative/adjunctive treatment for certain symptoms associated with borderline
personality disorder; alternative to benzodiazepines for managing alcohol withdrawal; adjunctive therapy for
schizophrenia; treatment of postherpetic neuralgia.

16.  Contraindications
 Hypersensitivity to tricyclic antidepressants or carbamazepine; history of bone marrow depression; concomitant use of
MAOIs. Discontinue MAOIs at least 14 days before administration of carbamazepine.
 Dosage and Administration
 Epilepsy
Adults and Children older than 12 yr of age Initial dosage PO 200 mg twice daily (tablets) or 100 mg (1 tsp) 4 times
daily (suspension). Increase weekly by up to 200 mg/day in 2 divided doses for extended-release or 3 to 4 divided doses
for other formulations to reach minimum effective dose (max, 1,000 mg/day in children 12 to 15 yr of age; 1,200 mg/day
in children older than 15 yr of age; 1,600 mg/day in adults).
 Maintenance 800 to 1,200 mg/day.
 Adults and Children older than 12 yr of age (extended-release) Initial dosage PO 200 mg twice daily.
 Children 6 to 12 yr of age Initial dosage PO 100 mg twice daily (tablets) or 50 mg 4 times daily (suspension).
Increase weekly by 100 mg/day in 3 to 4 divided doses (extended-release formulations use a twice-daily regimen) to
reach minimum effective dose (max, 1,000 mg/day).
 Maintenance 400 to 800 mg/day in 3 to 4 divided doses.
 Children younger than 6 yr of age Initial dosage PO 10 to 20 mg/kg/day in 2 or 3 divided doses (tablet) or 10 to 20
mg/kg/day in 4 divided doses (suspension). Increase weekly to achieve optimal clinical response when administered in
3 or 4 divided daily doses (max, 35 mg/kg/day).
 Maintenance Less than 35 mg/kg/day.
 Trigeminal Neuralgia
Adults Initial dosage PO 100 mg twice daily (tablets) or 50 mg 4 times daily (suspension). May increase by up to 200
mg/day (tablets, 100 mg increments every 12 h; suspension, 50 mg 4 times daily) as needed (max, 1,200 mg/day).
 Maintenance Usually 400 to 800 mg/day. Attempt to reduce the dosage or discontinue the drug once every 3 mo.
 Adults (extended-release) Initial dosage PO 100 mg twice daily (tablets) or 200 mg once daily (capsules) (max,
1,200 mg/day).
 Bipolar Disorder ( Equetro only)
Adults Initial dosage PO 200 mg twice daily. Increase in 200 mg/day increments to optimal clinical response (max,
1,600 mg/day).

17.  General Advice
 May be used alone or in combination with other antiepileptic drugs (AEDs) for treatment of seizures or with analgesics
for treatment of trigeminal neuralgia.
 Extended-release capsules
 Administer without regard to meals. Administer with food if GI upset occurs.
 Advise patient to swallow whole and to not crush or chew the capsule.
 Inform patient that capsules may be opened and beads sprinkled over food (eg, tsp of applesauce or similar food
product) and immediately swallowed without chewing. Caution patient not to chew the beads.
 Extended-release tablets
 When converting from tablets to extended-release tablets, administer same number of mg per day divided into 2 daily
doses.
 Inspect tablet for chips or cracks. Do not administer damaged tablets.
 Administer prescribed dose with food. Advise patient to swallow tablet whole and to not crush or chew the tablet.
 Suspension
 When converting from tablets to suspension, start the suspension at a lower dose and increase the dose slowly to
minimize adverse reactions.
 Shake suspension well before measuring dose. Measure dose using dosing cup, spoon, or syringe.
 Do not administer carbamazepine suspension simultaneously with other liquid medications or diluents.
 Ensure that lower initial doses and slower dose escalation are used when treating with suspension because a given dose
of suspension will produce higher blood levels than the same dose given as a tablet.
 Administer prescribed dose with food.
 Tablets
 Administer prescribed dose with food.
 Storage/Stability
 Store all doseforms at controlled room temperature (59° to 86°F). Protect from light and moisture. Protect suspension
from freezing.

18.  Trigeminal neuralgia associated with sinusitis
 Author information
 Abstract
 When a patient presents with trigeminal neuralgia, one usually thinks
of a vascular loop at the root entry zone of the nerve and consequently
of vascular decompression. An image of sinusitis on the MRI may be
considered an incidental finding. We present a case of an elderly
woman who experienced severe neuralgic pain in the distribution of
the trigeminal nerve on the left side following a mild upper respiratory
tract infection. Routine MRI revealed severe sinusitis with no
pathology in the brain. Following antibiotic treatment for the sinusitis,
the symptoms of the neuralgia resolved completely and no other
therapy was necessary. A review of the literature reveals a wide variety
of etiologies for trigeminal neuralgia. A vascular loop compressing the
nerve may be the most frequent cause of trigeminal neuralgia.
Nevertheless, other etiologies must be considered prior to
decompressive surgery since some can be treated medically.