Trigeminal neuralgia (tic doloreaux)


Shocklike pain in one or more divisions of the trigeminal nerve, usually in older individuals.

A chronic neuropathic pain disorder characterized by spontaneous and elicited paroxysms of electric shock-like or stabbing pain in the region of the face.
Paroxysmal facial pain is the hallmark of TN, yet 24-49% of patients have continuous or long lasting pain between paroxysmal attacks.
Background fluctuating pain is described as burning, throbbing or aching.
The mechanism of trigeminal neuralgia with continuous pain is different then underlying paroxysmal pain, by lesser degree of alleviation of continuous pain as compared with proximal pain after treatment was sodium channel blockers or microvascular decompression.
Burning, throbbing, aching pain probably mediated by impaired C fibers, which are unmyelinated sensory neurons t that transmit impulses slowly.
Loss of C fibers in the trigeminal sensory route may cause abnormal spontaneous activity in the second order neurons in the brain stem as a result of denervatiin super sensitivity of exposed postsynaptic membranes to neurotransmitters.

Trigeminal neuralgia occurs later in life, from middle age onwards, most often after age 60, and is a condition typically associated with very strong pain distributed over the area innervated by the maxillary or mandibular nerve divisions of the trigeminal nerve (V2 and V3).

In 15% of patients with typical pain attacks TN is caused by multiple sclerosis or benign tumors in the cerebellopontine angle.
The risk of trigeminal  neuralgia increased 20 fold  among patients with multiple sclerosis, with the prevalence of 2-5% among patients with multiple sclerosis.

Pain may occur in the eyes, lips, nose, scalp and forehead and jaw.

Prevalence of 155 per million people with a 3:3 female-:male ratio.

When present in persons younger than 40 years multiple sclerosis and disorders that can cause vascular compression such associated tumors must be considered.

Microvascular compression of the nerve root is often present in older patients.

Initial evaluation must rule out structural neoplastic or demyelinative processes with an MRI examination.

Neurovascular compression can be seen with the use of MRI and three dimensional reconstruction.
Three types of TN are noted: classical, secondary, and idiopathic.
The forms of trigeminal neuralgia are usually clinically indistinguishable.
The classical type is most common and is caused by intracranial vascular compression of the trigeminal nerve root.
Pathophysiology is considered to be compression of the sensory portion of the trigeminal nerve, close to its root entry in the pons, by an adjacent small branch of the basilar artery, most often the superior cerebellar artery.
With the classical type, the responsible blood vessel is usually the superior cerebellar artery which causes changes in the adjacent trigeminal nerve root.
Secondary TN accounts for approximately 15% of cases and is attributed to multiple sclerosis or tumor in the  cerebropontine angle which alters the entry of the trigeminal nerve or compresses the nerve in its extracranial course.
Secondary trigeminal neuralgia patients are usually younger, more likely to have sensory loss on a portion of the face, and are more likely to have bilateral pain.
Idiopathic trigeminal neuralgia has no apparent cause and accounts for approximately 10% of cases.
Diagnosis is clinical and based on three main criteria: 1-pain restricted to one with more divisions of the trigeminal nerve, 2-paroxysms of pain that is sudden, intense, and of very short duration from less than 1 second  to two minutes, but usually a few seconds and are described as a shock or electric sensation, and 3-pain triggered by innocuous stimuli on the face or intraoral trigeminal territory.
Triggered paroxysmal pain is reported in 91-99% of patients, and may be considered pathognomonic of trigeminal neuralgia.
The trigeminal nerve loses Schwann cell myelin  sheath  at its entrance into the pons and is replaced by central myelin generated by oligodendroglia.
The zone of transition is vulnerable to damage and demyelinization so that vascular compression at this area can occur.
Vascular compression is the usual cause of the myelinization at the site before the nerve enters the pons, and multiple sclerosis is the typical cause at the site just after the entry into the pons.
When the myelin sheath becomes thin enough, it allows transmembrane passage of ions into the underlying axon, and the axon is not equipped to pump out sodium.
The sodium deposition makes the axon hyperexcitable, causing ectopic impulses and high frequency afterdischarges.
Nerve fibers most involved are a-beta fibers susceptible to demyelination from mechanical damage or multiple sclerosis: High frequency discharges from the A-beta primary afferents are redirected by the brainstem to be perceived as paroxysmal pain.
It can be triggered by light touch, toothbrushing, eating, or talking.
Patients will at times present with half-shaved face or partially employed make up because of trade trigeminal pain being triggered.
The pain of TN most frequently involves the second (maxillary) or third (mandibular) division of the trigeminal nerve.
The pain involves the right side of the face more than the left side.
Bilateral TN suggests another neurologic disease or a disease affecting the cranium.
The incidence of TN is higher for women than men and increases with age.
Pain involving the posterior third of the scalp, the outer ear, the skin of the angle of the mandible are not related to trigeminal nerve innervation and are not size of pain due to TN.
The pain can be triggered by common gestures of daily life, and are in small receptive sensory zones.
The location of the pain in TN is not always concordant with the site of the trigger sensation.
Observation of the face during an attack a blink or a small mouth movement may be appreciated, even if the patient is unaware.
Rarely patients experience a forceful contraction of facial muscles called tic convulsif.

Treatment antiseizure medications.

Carbamazine, among antileptics, can alleviate such pain in 40-80% of patients.

Carbamazepine and oxcarbazepine are the drugs of choice for trigeminal neuralgia.

Sumatriptan can provide safe and effective treatment.

For trigeminal neuralgia dilantin is a second choice drug to carbamazepine.


Other drugs include oxcarbazepine, baclofen, and lamotrigine.


Some benefit has been demonstrated from gabapentin, pre-gabalin, and topical lidocaine.


For intractable cases, microvascular decompression, gamma knife therapy, or radio frequency ablation can be performed.


Microvascular decompression involves surgery where the trigeminal nerve and offending blood vessel or mobilized.



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