In this paper the authors present neuroanatomical and neurophysiological arguments against the microvascular compression in the root entry zone of trigeminal nerve nerve as an ethiopathogenetic factor of ITN. Clinical experience has proven that compression of mixed sensorymotor nerve (peripheral or central one), cannot provoke paroxysmal neuralgic pain. The authors conclude that the well known fact that dental pulp has only pain sensory modality brings up the question what might be consequence of tooth extraction where neural fibers are broken in the innervation areas of maxillar and mandibular nerve. The answer could be only one. If exclusive algophoric deafferentation hypersensitivity after tooth extraction exceeds a certain threshold, patients will experience paroxysmal neuralgic pain. Broken neural fibers develop pathological ephaptic communication with other trigeminal sensory modalities through supraspinal central structures responsible for the transmision of dental pulp pain. This can explain trigger phenomena and latency between the touching of circumoral areas and onset of neuralgic paroxysm, which is a central epileptic phenomenon. In conclusion, the so-called idiopathic trigeminal neuralgia (ITN) is the expression of algophoric deafferentation hypersensitivity after tooth extraction.
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