Microvascular Decompression For Neurogenic Sinus Bradycardia And Mechanism Exploring

We found a special phenomenon in our clinical practice of MVD (microvascular decompression) for HFS (hemifacial spasm) patients. Some HFS patients had NSB (neurogenic sinus bradycardia). In their MVD operations, we found that, besides the offending vessels at REZ (root exit zone) of facial nerve, there were also offending vessels at VN (vagal nreve) and (or) VMO (ventrolateral medulla oblongata). Decompression at VN and (or) VMO could result in HR (heart rate) increasing after MVD. We prospectively selected some HFS patients companied by NSB. We explored the VN and VMO in MVD for HFS patients. If there were offending vessels at VN and (or) VMO we would enforce MVD at VN and (or) VMO. We found that most patients are right HFS and there were offending vessels at ipsilateral VN and (or) VMO in all these patients. Postoperative HR at the time one week and one year were both statistically higher than that of preoperation. We proposed the following hypotheses. NSB in HFS might be caused by artery compression at VN and (or) VMO. Dorsal nucleus of VN and ambiguous nucleus in VMO or intracranial segement of VN were stimulated by artery compression at VN and (or) VMO. Excitability of VN increased due to the compression stimulation. Cardiac vagus has negative chronotropic and dromotropic action on heart which decreased the HR. The right preponderance could be explained by the fact that sinus node was mainly innervated by right cardiac vagus.To explore the mechanism of NSB and prove the hypotheses, we had carried out five stages animal tests. Stage-1: A segement of femoral artery was designed to be modelling offending vessel. VN were unilaterally compressed by modelling offending vessel. HR was proved to have no statistical variation after compression at both sides of VN, which meant that compression at VN was not the cause of NSB. Stage-2: Bilateral VMO was compressed by self-made sacculus in different diameter. HR statistically decreased in right VMO compression group. However, there was no statistical variation in HR in left VMO compression group. Results showed that compression at right VMO might be the cause of NSB. Stage-3: Compression and decompression at right VMO were executed. We found that the process of HR decreasing after compression at right VMO was relatively rapid and that the process of HR rebounding after decompression at right VMO was relatively slow. Stage-4: Right VMO was compressed by different diameter sacculus after cutting right VN. There were no statistical variations among HR of different diameter sacculus compression, which meant that VN is important in the mechanism of NSB due to artery compression at right VMO. Pathological imformation of brain stem was transmitted to sinus node through VN. Then HR decreased. Stage-5: Frequency of tonic impulse of right VN was measured before and after compression at right VMO. Frequencies of tonic impulse of right VN were all statistically increased after different diameter sacculus compression at right VMO. Frequencies of right VN decreased after decompression. This meant that compression and decompression at right VMO could lead to the increasing and decreasing in the frequency of tonic impulse of right VN. The five-stage animal test indirectly proved our hypothese and the mechanism of NSB was partially clear.Discovering the phenomena of NSB in HFS and exploring its mechanism was potential clinically important. Those NSB patients with insufficient heart output might need heart pacemaker. If MVD could increase their HR and then increase their hear output, those patients might avoid pacemaker implantation. There are still many problems to be resolved before MVD clinically applied for NSB patients. MVD might be a new method for symptomatic NSB in the future.