Trigeminal neuralgia

1. TRIGEMINAL NEURALGIA
Aditya Johan Romadhon, SST.FT, M.Fis

2. Introduction
The incidence in woman is higher, with a female–male ratio of approximately 2–3:1
90% trigeminal neuralgia present in elderly 50 years old, while peak incidence 60-70 years old
The prevalence of trigeminal neuralgia is 4,3 / 100.000 case worldwide
Neuralgia trigeminal is unilateral, chronic and recurring facial pain syndromes, in which pain is distributed following
trigeminal nerve branches
The International Association for the Study of Pain describes trigeminal neuralgia as “a sudden usually unilateral severe brief
stabbing recurrent episodes of pain in the distribution of one or more branches of the trigeminal nerve
The trigeminal nerve (V) is the fifth and largest of all cranial nerves, and it is responsible for detecting sensory stimuli that
arise from the craniofacial area

3. Trigeminothalamic tract
The primary function
of the trigeminal
nucleus is to carry
temperature, touch,
and pain inputs from
the ipsilateral side of
the face to the
contralateral thalamus
via the ventral
trigeminothalamic tract

4. Trigeminal branches
The superior region of the head, that is, meninges and cornea
are innervated mainly by the ophthalmic branch (V1)
The upper lip, maxillary teeth, and mucosa are innervated by
the maxillary branch (V2)
While the mandibular branch (V3) innervates mainly the
mandibula, lower lip, mucosa, and mandibular teeth
The V1 and V2 branches are purely sensory, whereas V3 has
motor fibers which are responsible for innervation of the jaw
muscles
The fibers that form the trigeminal nerve are classified into
nociceptive fibers (Ad and C fibers) and low-threshold
mechanoreceptors (LTMs; Aa and Ab fibers)

5. Trigeminal sensory system is
composed of peripheral structures,
such as the trigeminal nerve (V)
and trigeminal ganglia (TG)
Central structures,
such as the
trigeminal brainstem
sensory nuclear
complex (VBSNC)

6. Classification of Trigeminal Neuralgia
Secondary/symptomatic TN may be caused by an underlying disease such as tumors or artery malformations
(aneurysm) and has been associated with multiple sclerosis (multiple sclerosis patients show a 20-fold high
prevalence of TN)
Classic TN is associated with neurovascular compression (NVC) in the trigeminal root entry zone, which causes
nerve root atrophy or displacement
Idiopathic TN (unknown causes)approximately 10% of patients, even after surgical procedures or magnetic
resonance imaging, the disease remains without a diagnosed cause
The etiology of trigeminal neuralgia (TN) and the underlying mechanisms of this condition are still poorly
understood and based on the etiology, TN is classified into idiopathic TN, classic TN, and
secondary/symptomatic TN

7. Classic Trigeminal Neuralgia
According to the International Classification
of Headache Disorder- Classical TN is
caused by NVC, most frequently by the
superior cerebellar artery of the trigeminal
nerve roots into the pons
This compression usually results in the
demyelination of nerve fibers, which then
start firing ectopically (no sensory loss)
The NVC hypothesis is
supported by evidence that
after surgical procedures
that lead to microvascular
decompression, the
majority of patients
achieve sustained pain
relief

8. Clinical Manifestation (SOCRATES)
SITE : In approximately 60% of
the cases, there is an
involvement of only one branch,
the maxillary or mandibular
branch, whereas in
approximately 35% of the cases
both are involved
ONSET : Pain attacks usually
occur by stimulating trigger
points, usually located in the
territory innervated by the
trigeminal nerve
CHARACTERISTIC : Pain is
usually described as stabbing,
paroxysmal, reminiscent of
electric shock
RADIATED : radiated to ear
(mandibular branches), radiated
to nostril (maxillary branch)
radiated to eye (ophthalmic
branch)
ASSOCIATED : winses or tic
doulourues (muscle spasm)
TIME : Each episode of pain is
followed by a refractory period
that can last from a few seconds
to several minutes (1-2 minutes)
EXACERBATION : Examples of
stimuli that trigger attacks of
pain include a slight touch of the
face, tooth brushing, and
activation of the masticatory
and facial muscles during
speech and feeding
SEVERITY : When attacks of
pain become very frequent,
patients become unable to
perform their daily activities,
and even avoid eating and
communicating for fear of
triggering a new crisis

9. Early Treatment
The first-line treatment
for patients with classic
TN and idiopathic TN is
pharmacologic therapy.
The most commonly
used medication is the
anticonvulsant drug,
carbamazepine
It is usually started at a
low dose, and the dose
is gradually increased
until it controls the pain
It controls pain for most
people in the early
stages of the disease,
however, in some
patients, the
effectiveness of
carbamazepine
decreases over time
Possible side effects of
carbamazepine include
drowsiness, dizziness,
double vision, and
nausea
Patients with secondary
TN also can respond
well to
pharmacotherapy,
however, it is
recommended to treat
the underlying lesion or
disease (MRI or specific
assessment mandatory)

10. Prognosis
Trigeminal neuralgia is not a life-threatening
condition, however, it can lead to life long pain
and can be disabling
Some patients may have episodes lasting weeks
or months, followed by pain-free intervals
Some patients have persistent background facial
pain concomitantly with TN, in some patients,
the pain attacks worsen over time, with fewer
and shorter pain-free intervals before they recur
Also, the medications might lose effectiveness
over time, so correct diagnosis and proper
management can be beneficial to the patients
and leads to a good prognosis

11. THANKS