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Trigeminal Neuralgia

Diagnosis, symptoms, and treatment methods.

General Information About Trigeminal Neuralgia

Trigeminal neuralgia is one of the most agonizing neuropathic pain syndromes documented in medical history, arising from injury to the fifth cranial nerve (Trigeminal Nerve) typically caused by neurovascular compression. It is characterized by paroxysmal lancinating pain resembling an electric shock or a lightning bolt in the face. It is treated in our Neurology and Neurosurgery clinics with antiepileptic drugs or microvascular decompression (MVD) surgery.

Disease Details and Frequently Asked Questions

You can access detailed information about the disease under the headings below.
What is Trigeminal Neuralgia?

It represents paroxysmal episodes of excruciating electric shock-like and lancinating pain in the face, resulting from demyelination and short-circuiting of the trigeminal nerve sheath which provides sensation to three facial zones (ophthalmic, maxillary, and mandibular branches).

What is the Pain Like? How is it Differentiated from a Toothache?

It is NOT continuous, dull, or aching like typical headaches or dental pain. The paroxysm lasts for seconds (or a maximum of 1-2 minutes), but at that exact moment, the individual jumps in agony as if they stuck their finger into an electrical socket, clutches their face, and screams. Patients commonly attribute the pain to dental caries and erroneously undergo extraction of 3-4 perfectly healthy teeth, yet the pain never relents.

Trigger Points (What Initiates the Pain)?

The most devastating aspect of the disorder is that even the most innocent stimuli can trigger a paroxysm. Washing the face, shaving, brushing teeth, eating, speaking, smiling, applying makeup, or even a light breeze (air conditioning) blowing across the face is sufficient to flip that electrical switch and trigger a catastrophic pain attack.

What Causes It? What is Vascular Compression?

In the vast majority of cases, the etiology is Microvascular Compression (Neurovascular Conflict). A normal intracranial artery elongates and ectasias with age, encroaching directly onto the root entry zone of the trigeminal nerve. The pulsatile mechanical force of the artery with every heartbeat erodes the protective myelin sheath like sandpaper. The demyelinated nerve transmits innocent tactile facial sensations to the brain as catastrophic pain signals (short-circuiting).

How is it Diagnosed? Is a Brain MRI Mandatory?

Diagnosis relies entirely on the pathognomonic clinical history of paroxysmal 'lightning-like' pain related by the patient. A neurologist establishes the diagnosis 100% clinically. However, a High-Resolution, Contrast-Enhanced Cranial MRI (FIESTA/CISS sequences) must be performed to evaluate for neurovascular conflict or to rule out secondary etiologies such as an intracranial tumor or Multiple Sclerosis demyelinating plaques compressing the nerve root.

How is it Treated? What is MVD Surgery?

This neuropathic pain NEVER responds to conventional Analgesics (such as paracetamol, NSAIDs, or morphine). The cornerstone of first-line pharmacotherapy (and diagnostic confirmation) is Carbamazepine, an antiepileptic agent. If pharmacological tolerance develops, the Gold Standard intervention is Surgery (Microvascular Decompression - MVD). A neurosurgeon creates a small suboccipital craniotomy behind the ear, identifies the offending vessel compressing the nerve, and dissects it away. A Teflon felt pad (sponge) is interposed between them. Upon emergence from anesthesia, the patient experiences immediate, permanent liberation from the electric shocks.

Our health library contents are prepared for informational purposes only and with scientific data available at the time of recording. For all your questions, concerns, diagnosis, or treatment regarding your health, please consult your doctor or a healthcare institution.


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