Trigeminal Neuralgia
Historically called tic douloureux – occurs in the distribution of one or more of the three branches of the trigeminal or 5th cranial nerve. This disorder may be characterized as:
Type 1 (“Typical” or “Classic” TN) which presents as volleys of sharp, stabbing, electric-shock pain, with individual spasms lasting up to two minutes and volleys lasting up to two hours.
Type 2 (“Atypical” TN) is characterized by constant, searing, burning, crushing, throbbing, grinding pain, in the eye, ear, sinus, palate and/or upper and lower teeth and jaw area. ATN attacks may last for days, weeks, months or years.
Both types sometimes display spontaneous remissions of weeks or months duration, particularly early in development of the disorder. Both types of TN occur most often as unilateral pain (one side). Pain is experienced between the top of the head and the jaw line, forward of the mid-line of the skull and passing just behind the ear. Although less common, TN may also be bilateral (both sides) on the face, most often with different symptoms or timing (switching sides) of symptoms on the two sides.
Some patients can have both Type 1 and Type 2 symptoms, while others can begin with Type 1 and graduate to Type 2.
Both types of TN pain may be initiated by light stimulus on trigger zones that can move dynamically from hour to hour, across the distribution of the trigeminal nerve. Stimulus may comprise heat, cold, or even moving air. Some patients cannot wash their hair or brush their teeth -- or walk in a light breeze -- without fear of initiating an attack.
The mechanism which causes Type 1 (Typical or "Classic") TN is thought to be primarily one of nerve compression by small veins or arteries in the region close to emergence of the cranial nerves from the brain stem. Compression and mechanical stimulation of the nerve are believed to compromise the outer Myelin layer around the nerve, allowing abnormal cross-talk between nerve fibers and initiation of uncontrolled pain cascades.
With Type 2 (Atypical) TN, the cause(s) are not as well understood and may possibly involve Central Nervous System sensitization, generalized arachnoiditis, or generalized trigeminal neuropathy of unknown origin. A recent trend in pain research among organizations such as the International Association for the Study of Pain has been to recognize differences between trigeminal neuropathy and neuralgia as potentially artificial.
Neuralgia is by definition an inflammation process, while Neuropathy is pain due to mechanical damage. Professionals have questioned whether "Typical" TN is an inflammatory process at all. Patient pain-free response of Type 1 TN to microvascular decompression surgery is often immediate after nerves and blood vessels are physically separated - a result not expected if the primary mechanism of pain is due to physical damage to the nerve.
Medical treatments for these two variant disorders tend to be highly similar. However, Type 1 TN is more frequently responsive to anti-seizure medications such as Tegretol (Carbamazepine) or Trileptal (Oxcarbamazepine). Type 2 TN might not respond to anti-seizure meds, but frequently responds to tri-cyclic anti-depressant meds such as Amitriptylene, even at dose levels below those normally associated with management of depression. It is theorized by some investigators that there may be a chemical cross-over effect between pain relief response and anti-depressant response, in a common or shared chemical process of the nerves.
In significant numbers of cases, emergence of either type of TN and some other forms of chronic face pain can be attributed to either whiplash automobile injury or blunt force trauma to the head and neck.
For additional information, please check out our Resources Tab and Google "trigeminal neuralgia".
Attribution: The material on this page is drawn from an article by Richard A "Red" Lawhern, Ph.D, on "Classification and Treatment of Chronic Face Pain"
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