fbpx

Trigeminal Neuralgia

Updated : February 16, 2024





Background

Trigeminal neuralgia (TN) is a painful condition caused by brief, sudden, and severe pain attacks, also described as an electric shock-like pain affecting the fifth cranial nerve (trigeminal), which supplies the cheek, jaw, and forehead.

It is also known as tic douloureux, as the facial spasms accompany the pain. It is one of the most common causes of craniofacial pain. This condition is unilateral and rarely stimulates on both sides of the face, affecting other trigeminal nerve divisions.

Epidemiology

Annually 4-13 per 100,000 individuals are affected. Compared to males, females are affected more often. Trigeminal neuralgia is rare in children and often observed in adults above 50; few cases are seen in the second and third decades.

In population-based studies, lifetime prevalence was estimated at approximately 0.3% to 0.16%. The development of this condition in younger adults is associated with multiple sclerosis. Patients with comorbidities such as hypertension and diabetes mellitus have a higher risk of developing trigeminal neuralgia.

Anatomy

Pathophysiology

Trigeminal neuralgia is caused mainly by the compression of the trigeminal nerve, and demyelination occurs at the site of nerve compression. Ectopic impulses are generated from the demyelinated lesion, which results in the ephaptic transmission. The ephaptic relation between the fibers responsible for the generation of pain and regulating light touch describes the precipitation of shock-like pain.

The presence of the central pain mechanisms in TN is indicated by triggered episodes observed by refractory periods and stimuli, which leads to pain sensations. Alterations in the grey matter and motor cortex have also been reported. Whenever the vibrational frequency of the trigeminal nerve comes close to its surrounding structure, the nerve fibers damage, resulting in abnormal impulse transmission and facial pain.

Trigeminal neuralgia is classified as:

Classic: Caused by vascular compression

Secondary: Caused due to tumor or an underlying disease

Idiopathic: Has unknown cause

Etiology

The most common cause of TN is compression of the trigeminal nerve. It starts at the pons and is divided into three branches, namely, V1 (Ophthalmic) responsible for supply to the eye and forehead, V2 (Maxillary) supplies to the upper jaw, and V3(Mandibular) supplies to the lower jaw.

An adjacent vein or artery compression causes about 80-90% of cases. The superior cerebellar artery, in most cases, is implicated. Other blood vessels such as the vertebral artery, inferior cerebellar artery, and petrosal vein are identified to trigger TN.

Nerve compression is also caused by an epidermoid cyst, meningioma, and acoustic neuroma and is rarely due to saccular aneurysm or arteriovenous malformation. Patients with multiple sclerosis (MS) have a higher risk of developing TN if the demyelination of the nerve is caused by multiple sclerosis itself.

Genetics

Prognostic Factors

Trigeminal neuralgia is not a severe condition. It can, however, cause lifelong pain and be debilitating. The progression of TN is uncertain. Some individuals experience episodes that last weeks or months, followed by pain-free spells. Some individuals experience persistent background facial pain.

Some patients’ pain attacks deteriorate over time, with fewer and shorter pain-free intervals between attacks. Furthermore, the drugs‘ effectiveness diminishes with time. Accurate diagnosis and management benefit patients and lead to a good prognosis

Clinical History

Physical Examination

Age group

Associated comorbidity

Associated activity

Acuity of presentation

Differential Diagnoses

Laboratory Studies

Imaging Studies

Procedures

Histologic Findings

Staging

Treatment Paradigm

by Stage

by Modality

Chemotherapy

Radiation Therapy

Surgical Interventions

Hormone Therapy

Immunotherapy

Hyperthermia

Photodynamic Therapy

Stem Cell Transplant

Targeted Therapy

Palliative Care

Medication

 

carbamazepine 

Immediate release::

Initial dose:
Tablets: 100mg orally twice a day
Oral suspension: 50mg orally every 6 hours
Increase every week by 200mg/dose divided every 6-8 hours
Maintenance dose: 400 to 800mg /day
Maximum dose: 1200mg /day

Extended-release:
Initial dose:
Tablets: 200mg orally once a day/100mg orally twice a day
Increase every week by 200mg/dose divided every 6-8 hours
Maintenance dose: 400 to 800mg /day
Maximum dose: 1200mg /day



 
 

Media Gallary

References

https://www.ncbi.nlm.nih.gov/books/NBK554486/

Trigeminal Neuralgia

Updated : February 16, 2024




Trigeminal neuralgia (TN) is a painful condition caused by brief, sudden, and severe pain attacks, also described as an electric shock-like pain affecting the fifth cranial nerve (trigeminal), which supplies the cheek, jaw, and forehead.

It is also known as tic douloureux, as the facial spasms accompany the pain. It is one of the most common causes of craniofacial pain. This condition is unilateral and rarely stimulates on both sides of the face, affecting other trigeminal nerve divisions.

Annually 4-13 per 100,000 individuals are affected. Compared to males, females are affected more often. Trigeminal neuralgia is rare in children and often observed in adults above 50; few cases are seen in the second and third decades.

In population-based studies, lifetime prevalence was estimated at approximately 0.3% to 0.16%. The development of this condition in younger adults is associated with multiple sclerosis. Patients with comorbidities such as hypertension and diabetes mellitus have a higher risk of developing trigeminal neuralgia.

Trigeminal neuralgia is caused mainly by the compression of the trigeminal nerve, and demyelination occurs at the site of nerve compression. Ectopic impulses are generated from the demyelinated lesion, which results in the ephaptic transmission. The ephaptic relation between the fibers responsible for the generation of pain and regulating light touch describes the precipitation of shock-like pain.

The presence of the central pain mechanisms in TN is indicated by triggered episodes observed by refractory periods and stimuli, which leads to pain sensations. Alterations in the grey matter and motor cortex have also been reported. Whenever the vibrational frequency of the trigeminal nerve comes close to its surrounding structure, the nerve fibers damage, resulting in abnormal impulse transmission and facial pain.

Trigeminal neuralgia is classified as:

Classic: Caused by vascular compression

Secondary: Caused due to tumor or an underlying disease

Idiopathic: Has unknown cause

The most common cause of TN is compression of the trigeminal nerve. It starts at the pons and is divided into three branches, namely, V1 (Ophthalmic) responsible for supply to the eye and forehead, V2 (Maxillary) supplies to the upper jaw, and V3(Mandibular) supplies to the lower jaw.

An adjacent vein or artery compression causes about 80-90% of cases. The superior cerebellar artery, in most cases, is implicated. Other blood vessels such as the vertebral artery, inferior cerebellar artery, and petrosal vein are identified to trigger TN.

Nerve compression is also caused by an epidermoid cyst, meningioma, and acoustic neuroma and is rarely due to saccular aneurysm or arteriovenous malformation. Patients with multiple sclerosis (MS) have a higher risk of developing TN if the demyelination of the nerve is caused by multiple sclerosis itself.

Trigeminal neuralgia is not a severe condition. It can, however, cause lifelong pain and be debilitating. The progression of TN is uncertain. Some individuals experience episodes that last weeks or months, followed by pain-free spells. Some individuals experience persistent background facial pain.

Some patients’ pain attacks deteriorate over time, with fewer and shorter pain-free intervals between attacks. Furthermore, the drugs‘ effectiveness diminishes with time. Accurate diagnosis and management benefit patients and lead to a good prognosis

carbamazepine 

Immediate release::

Initial dose:
Tablets: 100mg orally twice a day
Oral suspension: 50mg orally every 6 hours
Increase every week by 200mg/dose divided every 6-8 hours
Maintenance dose: 400 to 800mg /day
Maximum dose: 1200mg /day

Extended-release:
Initial dose:
Tablets: 200mg orally once a day/100mg orally twice a day
Increase every week by 200mg/dose divided every 6-8 hours
Maintenance dose: 400 to 800mg /day
Maximum dose: 1200mg /day



https://www.ncbi.nlm.nih.gov/books/NBK554486/

Free CME credits

Both our subscription plans include Free CME/CPD AMA PRA Category 1 credits.

Digital Certificate PDF

On course completion, you will receive a full-sized presentation quality digital certificate.

medtigo Simulation

A dynamic medical simulation platform designed to train healthcare professionals and students to effectively run code situations through an immersive hands-on experience in a live, interactive 3D environment.

medtigo Points

medtigo points is our unique point redemption system created to award users for interacting on our site. These points can be redeemed for special discounts on the medtigo marketplace as well as towards the membership cost itself.
 
  • Registration with medtigo = 10 points
  • 1 visit to medtigo’s website = 1 point
  • Interacting with medtigo posts (through comments/clinical cases etc.) = 5 points
  • Attempting a game = 1 point
  • Community Forum post/reply = 5 points

    *Redemption of points can occur only through the medtigo marketplace, courses, or simulation system. Money will not be credited to your bank account. 10 points = $1.

All Your Certificates in One Place

When you have your licenses, certificates and CMEs in one place, it's easier to track your career growth. You can easily share these with hospitals as well, using your medtigo app.

Our Certificate Courses

Up arrow