br Introduction Trigeminal neuralgia TN is categorized into

Introduction Trigeminal neuralgia (TN) is categorized into typical and atypical forms. The symptoms of typical TN are severe, sporadic, and abrupt shock-like pain in facial areas where the trigeminal nerve is distributed, with the pain attacks occurring in swift succession and lasting a few seconds to minutes. Established pain-inducing triggers include chewing, talking, drinking cold fluids, touching on the face, tooth brushing, and encountering cold air. The predominant cause of typical TN is the compression of the trigeminal nerve by an artery at the root entry zone, resulting in a short circuit of neural impulse transmission. Microvascular decompression (MVD) is an effective method for treating TN (success rate, 80–90%) when conservative treatment and less invasive therapies such as antiepileptic medication and radiofrequency thermocoagulation fail to alleviate the neuralgia. Arachnoid adhesions with the trigeminal nerve or venous contact with the trigeminal nerve has been occasionally observed during MVD. Whether venous compression causes TN remains debatable. Similarly, the mechanism underlying the role of arachnoid thickening in causing TN remains unclear. In addition, Peker et al reported frequent vascular compression of the trigeminal nerve in asymptomatic, and not necessarily pathological, people.
Materials and methods All surgical procedures were performed by a senior physician (H.T.H.) at the Taipei Tzu Chi Neurosurgical Training Center, Taipei, Taiwan. Patients were placed in the lateral decubitus position, with the head held by a MAYFIELD® Modified Skull Clamp. Small retrosigmoid posterior fossa craniectomy was performed. The superior petrosal veins were routinely coagulated and cut for visualizing the trigeminal nerves. Any ceramidase contacting (Figure 1A) or distorting (Figure 2A) the trigeminal nerve at or near the point of entry into the brain stem were repositioned using shredded Teflon (Figures 1B and 2B). When arachnoid thickening (Figure 3A) surrounding the trigeminal nerve was discerned, adhesiolysis (Figure 3B) was performed. In cases where only veins were in contact with the trigeminal nerve, the veins were not touched, whereas arteries in proximity judged likely to potentially contact or compress the TN (Figure 4A) were separated from the trigeminal nerve during cerebellar retraction and transposed with a square Teflon with a cleft on one side (Figure 4B). The degree of cross compression was classified into two categories: (1) vascular contact, denoting the crossing of a vessel into the nerve entry zone, and (2) nerve distortion, denoting grooves, notches, or indentations in the trigeminal nerve root. The brain stem-evoked potential was routinely monitored intraoperatively during MVD.
Results Between June 2000 and April 2015, 27 patients (17 females and 10 males) with TN admitted for MVD were enrolled; one patient was lost to follow-up. The mean age at operation of the remaining 26 patients was 57.4±11.4 years (38–79 years), whereas the average duration of postoperative symptoms was 5.9 years (0.5–30 years). TN was localized to the right and left sides of the face in 18 and eight patients, respectively. One patient experienced facial pain in the ophthalmic branch (V1), 10 in the maxillary branch (V2), five in the mandibular branch (V3), and 10 in both the V2 and the V3 branch (Table 1). All patients had been treated with carbamazepine or other drugs that were discontinued because of side effects or gradual recurrence of facial pain. Three patients had undergone trigeminal ablative or decompressive procedures that had failed to relieve TN symptoms. One patient had undergone radiofrequency thermal rhizotomy, but the facial pain persisted. Another patient, treated through Gamma Knife surgery, reported only 6 months of pain relief. A third patient who had undergone MVD 10 years earlier was admitted because of recurrent TN on the same side. Arterial cross compression was detected in 22 patients (85%), with the superior cerebellar artery (SCA) identified as the predominantly involved blood vessel. Other structures potentially involved with nerve compression, including the arachnoid and vein, were found in four patients (Table 2). Twelve cases of arterial contact with the trigeminal nerve and 10 of trigeminal nerve distortions (vascular cross compression) were observed. Venous contact with the trigeminal nerve was observed in two patients, whereas arachnoid thickening was observed in two patients (Table 3).