Mechanism underlying cranial nerve rhizopathy.

The cranial nerve rhizophathy, commonly presented with trigeminal neuralgia (TN) or hemifacial spasm (HFS), is a sort of hyperexcitability disorders with higher incidence in senior Asian. In this paper, a novel hypothesis on the pathogenesis is proposed and with which some clinical phenomena are explained. In those with crowded cerebellopontine angle in anatomy, the cranial nerve root and surrounding vessel are getting closer and closer to each other with aging and finally the neurovascular conflict happens. As the interfacial friction associated with pulse, the nerve incurs demyelination. Since this pathological change develops to a certain degree, some transmembrane proteins emerge from the nerve due to a series of signaling pathway mediated by inflammatory cytokines. Among them, voltage-gated (Na1.3) and mechanosensitive (Piezo2) ion channels may play the important role. With pulsatile compressions, the Piezo2 drives the resting potential toward depolarization forming a state of subthreshold membrane potential oscillation. Under this condition, just an appropriate pressure can make the membrane potential easy to reach threshold and activate the sodium channel, eventually generating conductible action potentials from the axon. When these ectopic action potentials propagate to the central nerve system, an illusion of sharp pain is perceived; while to the nerve-muscle junctions, an attack of irregular muscle constriction occurs. This hypothesis can well explain the symptomatic manifestation of paroxysmal attacks aroused by emotions. When we get nervous or excited, our heart rate and blood pressure alter correspondingly, which may give rise to "a just right pressure" - with specific frequency, amplitude and angle - impacting the suffered nerve to reach the threshold of impulse ignition. After a successful microvascular decompression surgery, the trigger is gone (there is no compression anymore) and the symptom is alleviated. While the postoperative recurrence could be attributable to Teflon granuloma development if had been placed improperly - for this nerve root has been susceptible no matter to arteries or to neoplasms. Besides, it may illustrate the clinical phenomenon that secondary TN or HFS cases are seldom caused by schwannoma: with a proliferative sheath, the nerve root is actually insulated. By contrast, not all neurovascular contacts can lead to the onset: it demands an exclusive extent of demyelination firstly.