Trigeminal Neuralgia - Causes

Causes

The trigeminal nerve is a mixed cranial nerve responsible for sensory data such as tactition (pressure), thermoception (temperature), and nociception (pain) originating from the face above the jawline; it is also responsible for the motor function of the muscles of mastication, the muscles involved in chewing but not facial expression.

Several theories exist to explain the possible causes of this pain syndrome. It was once believed that the nerve was compressed in the opening from the inside to the outside of the skull; but newer leading research indicates that it is an enlarged blood vessel - possibly the superior cerebellar artery - compressing or throbbing against the microvasculature of the trigeminal nerve near its connection with the pons. Such a compression can injure the nerve's protective myelin sheath and cause erratic and hyperactive functioning of the nerve. This can lead to pain attacks at the slightest stimulation of any area served by the nerve as well as hinder the nerve's ability to shut off the pain signals after the stimulation ends. This type of injury may rarely be caused by an aneurysm (an outpouching of a blood vessel); by a tumor; by an arachnoid cyst in the cerebellopontine angle; or by a traumatic event such as a car accident.

Short-term peripheral compression is often painless, with pain attacks lasting no more than a few seconds. Persistent compression results in local demyelination with no loss of axon potential continuity. Chronic nerve entrapment results in demyelination primarily, with progressive axonal degeneration subsequently. It is, "therefore widely accepted that trigeminal neuralgia is associated with demyelination of axons in the Gasserian ganglion, the dorsal root, or both." It has been suggested that this compression may be related to an aberrant branch of the superior cerebellar artery that lies on the trigeminal nerve. Further causes, besides an aneurysm, multiple sclerosis or cerebellopontine angle tumor, include: a posterior fossa tumor, any other expanding lesion or even brainstem diseases from strokes.

A large portion of multiple sclerosis patients have TN, but is not a symptom of MS. Only two to four percent of patients with TN, usually younger, have evidence of multiple sclerosis, which may damage either the trigeminal nerve or other related parts of the brain. It has been theorized that this is due to damage to the spinal trigeminal complex. Trigeminal pain has a similar presentation in patients with and without MS.

Postherpetic neuralgia, which occurs after shingles, may cause similar symptoms if the trigeminal nerve is damaged.

When there is no structural cause, the syndrome is called idiopathic.