School of Medicine, University of Zagreb, Zagreb, Croatia.
Psychiatr Danub. 2019 Dec;31(Suppl 5):724-731.
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.
本文从神经解剖学和神经生理学的角度出发，对三叉神经根入区微血管压迫作为 ITN 的病因学因素提出了质疑。临床经验已经证明，混合感觉运动神经（周围或中枢）的压迫不能引发阵发性神经痛。作者得出结论，众所周知牙髓只有痛觉模式这一事实引发了这样一个问题，即牙齿拔除后，在支配上颌和下颌神经的区域内神经纤维被切断会产生什么后果。答案只有一个。如果拔牙后独有的痛觉传入过敏超过一定的阈值，患者将会经历阵发性神经痛。断裂的神经纤维通过负责牙髓痛觉传递的脊髓中枢结构，与其他三叉神经感觉模式发生病理性的轴突间电传递，从而产生病理联系。这可以解释触发现象和触及其口腔周围区域与神经痛发作之间的潜伏期，这是一种中枢癫痫现象。总之，所谓的特发性三叉神经痛（ITN）是牙齿拔除后痛觉传入过敏的表现。
