They theorized that this type was a progression of untreated classic trigeminal neuralgia, and represented worsening neural injury. There were seven proposed sub-types of trigeminal neuralgia (TN) in this classification (see table), and the final category was reserved for facial pain caused by somatoform disorder. This last category (TN7) was termed atypical facial pain, although many cases that would otherwise be traditionally labelled as AFP would fall into other groups in this classification, especially into the second group. In a publication of the Trigeminal Neuralgia Association (TNA), the following was said about this new classification and AFP:

"The term atypical facial neuralgia or pain was a wastebasket term applied by a serious contributor of a former era to a group of patients he did not understand. Many of these patients were our trigeminal neuralgia type 2 patients. It is unfortunate that many of these people were told they had psychological problems. Many developed psychological problems after the fact when told by everyone that such was their problem. Over the years, our areas of ignorance have progressively narrowed. ... A non-pejorative and, hopefully, reasonable term for the ever-narrowing group of undiagnosed face pain problems: Facepain of Obscure Etiology (FOE or POE) to replace atypical facial pain in the Burchiel classification." As a result, some sources list terms such as "atypical trigeminal neuralgia", "trigeminal neuropathic pain" and "atypical facial neuralgia" as synonyms of AFP. ICHD-2 Diagnostic criteria
The ICHD-2 lists diagnostic criteria for "persistent idiopathic facial pain" (the term that replaces AFP in this classification):

A.
Although it is a centrally acting sympathomimetic, it does not block reuptake or transporters. It may reduce the dopaminergic and serotonergic transmission in the peripheral nervous system and it indirectly affects norepinephrine (noradrenaline) synthesis. Methyldopa acts on alpha-2 adrenergic receptors, which are found on the pre synaptic nerve terminal. This inhibits the synthesis of norepinephrine by inhibiting tyrosine hydroxylase. The S-enantiomer of methyldopa is a competitive inhibitor of the enzyme aromatic L-amino acid decarboxylase (LAAD), which converts L-DOPA into dopamine. L-DOPA can cross the blood brain barrier and thus methyldopa may have similar effects. LAAD converts it into alpha-methyldopamine, a false prescursor to norepinephrine, which in turn reduces synthesis of norepinephrine in the vesicles. Dopamine beta hydroxylase (DBH) converts alpha-methyldopamine into alpha-methylnorepinephrine, which is an agonist of the presynaptic α2-adrenergic receptor causing inhibition of neurotransmitter release. Pharmacokinetics
Maximum decrease in blood pressure occurs 4-6 hours after oral dosage. The half-life of methyldopa is 105 minutes. Methyldopa exhibits variable absorption from the gastrointestinal tract. It is metabolized in the liver and intestines and is excreted in urine. History
When methyldopa was first introduced, it was the mainstay of antihypertensive treatment, but its use has declined on account of relatively severe adverse side effects, with increased use of other safer and more tolerable agents such as alpha blockers, beta blockers, and calcium channel blockers. Additionally, it has yet to be associated with reducing adverse cardiovascular events including myocardial infarction and stroke, or overall all-cause mortality reduction in clinical trials.