History

TN has been known since ancient times. Two thousand years ago, Aretaeus of Cappadocia referred to headache with “spasm and distortion of countenance,” and Persian scholar Avicenna described a similar syndrome of facial pain in the 10th century.¹ In the 17th century, Fehr and Schmidt described the syndrome in a eulogy.² John Locke described facial pain of the Countess of Northumberland, wife of the English Ambassador to France, as a “fit of such violent and exquisite torment that it forced her to … cries and shrieks … which extended itself all over the right side of her face and mouth.”¹ In 1756, Nicolas Andre coined the term tic douloureux, and described it as “a cruel and obscure illness, which causes … in the face some violent motions, some hideous grimaces which are an insurmountable obstacle to the reception of food, [and] which put off sleep.”³ The first comprehensive clinical description occurred in 1773 when John Fothergill wrote to the medical society of London about 14 patients with TN, and his descriptions of triggerable lancinating pain are still considered accurate.⁴

Early surgical treatments for TN involved intentional lesioning of the trigeminal nerve. In 1934, Walter Dandy described the retrosigmoid approach to the trigeminal nerve and noted frequent vascular contact in patients with TN. He wrote, “In many instances the nerve is grooved or bent in an angle by the artery. This I believe is the cause of tic douloureux.”⁵ Despite his insight, Dandy did not attempt to decompress the nerve, believing the pathologic process to be irreversible. Microvascular decompression (MVD) was first performed by W. James Gardner in 1959, who described mobilizing a vessel from the trigeminal nerve and placing a piece of Gelfoam between them without any intentional damage to the nerve itself.⁶ The procedure was subsequently refined and popularized by Peter Jannetta, who, with the aid of the operating microscope, performed thousands of MVD operations and demonstrated that long-term relief of pain is possible in most of appropriately selected patients.^7–9

Pathophysiology

The etiology of TN is believed to be related to abnormal conduction within the trigeminal nerve, possibly owing to changes in myelin induced by pulsatile mechanical trauma from an adjacent vessel. At the point just before it enters the brainstem, there is a short segment where nerve axons are still ensheathed in central myelin (produced by oligodendrocytes), but after a few millimeters, there is a transition to peripheral myelin (produced by Schwann cells). The region of this transition is called the Obersteiner-Redlich zone. It is thought that the area of the nerve containing the central form of myelin is especially susceptible to pathologic changes from vascular contact that result in demyelination and altered conduction. Pathologic studies from patients with TN have demonstrated severe damage to myelin as well as axon loss within the nerve adjacent to the site of compression.¹⁰ The resulting conduction abnormality may lead to nerve hyperactivity owing to ectopic impulse discharge, spontaneous and triggered afterdischarge, and cross-excitation among neighboring afferent fibers (ephaptic transmission).^10,11

Separation of the nerve from the offending vessel appears to immediately reverse many of the physiologic changes. In Leandri and colleagues’¹² study of 10 patients undergoing MVD who underwent nerve root and scalp electrode recordings, 7 showed signs of immediate improvement in neurophysiologic parameters after decompression. Others authors have reported improvement in sensory thresholds for touch, pinprick, and temperature sensations after MVD¹³ as well as resolution of asymmetric jaw motion.^14,15 These findings suggest that the changes associated with neurovascular compression are likely to be reversible if the nerve is decompressed, at least in the early stages.

Radiographic and anatomic studies have demonstrated that vascular contact with the trigeminal nerve is common even in asymptomatic individuals but tends to be more severe and more proximal on the nerve ipsilateral to TN symptoms.¹⁶ Patients with TN are more likely to have contralateral arterial compression than asymptomatic people even though bilateral TN is distinctly rare.^16,17 Symptomatic and asymptomatic arterial compression of the trigeminal nerve increases with age because of elongation of cisternal arteries, which explains why it is primarily a disease of older adults.¹⁶

Alternative Treatments

TN symptoms often improve with medications that exert a stabilizing effect on neural conduction such as antiepileptics. Medications that have been successfully used include carbamazepine, phenytoin, valproate, gabapentin, pregabalin, baclofen, and clonazepam. Most patients obtain good pain control initially,^18,19 but the effect tends to diminish over time, and after 10 years about half will no longer respond.²⁰ Because the clinical and pathologic changes associated with TN may be progressive over time, initial failure of pharmacologic therapy may represent an indication to proceed with more aggressive treatment.²¹ Nevertheless, medical therapy is recommended as a first-line treatment for patients with TN because some patients will require no further treatment.

Surgical treatments for TN other than MVD generally involve intentional production of a lesion within the trigeminal nerve. Many commonly performed procedures involve percutaneous access to the nerve through a needle advanced through the face followed by direct creation of a lesion using a radiofrequency generator, glycerol injection, or balloon compression. Stereotactic radiosurgery targeting the nerve root entry zone is also effective, although pain relief is delayed by months, and complete elimination of pain may occur less frequently than with other methods. In general, the success of each of these lesioning techniques requires some degree of facial numbness, with greater numbness associated with a higher rate of pain control but also greater likelihood of complications such as facial dysesthesia and anesthesia dolorosa. Also, all these procedures are associated with a high recurrence rate after a few years as facial sensation returns, suggesting that they work primarily by blocking triggering impulses rather than by treating the cause of the pain itself.

MVD differs from the other treatments in that the primary cause of TN is treated so that long-term pain relief is possible. Also, because there is no intentional damage to the nerve, facial dysesthesia and numbness are rare. Although it is the most invasive and expensive treatment, MVD is associated with the lowest rate of pain recurrence and the highest rate of patient satisfaction among all surgical treatments for TN.²² MVD can also be safely performed after a lesioning procedure and appears to be no less effective so long as there is no evidence of trigeminal neuropathy.²³

Patient Selection and Classification of Facial Pain

MVD is ideal for young healthy patients with TN because no other treatment offers a significant likelihood of long-term pain relief.²⁴ However, advanced age is not by itself a contraindication because there is no difference in complication rate or outcome in elderly patients.^25–27 The operation is in fact technically easier in older patients because cerebellar atrophy leads to less need for retraction and less risk for cerebellar swelling. If life expectancy is very short or general anesthesia cannot be tolerated, a less invasive destructive procedure may be more appropriate.^28,29

A careful history is essential during preoperative evaluation. Patients generally report intense stabbing or electric shock–like sensation, although there may be an overlying constant pain that may be more severe than the stabbing pain. Any distribution within the trigeminal nerve innervation territory may be observed. V2 and V3 branches are more common,⁷ especially radiating out from near the mouth. V1 symptoms are sometimes associated with decreased corneal sensation. The pain is often worse during the day and may be positional with relief when supine, with the affected side up, or during sleep. Trigger points are present in most patients and are activated by light cutaneous stimuli such as wind, eating, talking, and shaving. Often, the triggers lead to guarding of the face and refusal to be touched, wash, apply makeup, shave, or brush the teeth because of fear of an attack. Pain-free intervals lasting weeks to months are common at first but become rare as the syndrome progresses. Initial onset of pain is frequently quite memorable. Many patients undergo dental procedures without relief before a diagnosis is made. If the patient is given antiepileptic medication, pain usually improves dramatically. Physical examination is usually normal, although about one third of patients have some degree of sensory loss in the affected area.

When evaluating a patient for surgery, it is helpful to classify facial pain according to the classification scheme reported by Burchiel.³⁰ Patients with TN type 1 have predominantly shock-like pain, whereas patients with TN type 2 report that at least 50% is constant pain, although there still may be a component of lancinating pain. Pain relief after MVD is more strongly correlated with the lancinating pain component than with any other symptom, so although most patients with either type will have long-term pain control, patients with TN type 1 are more likely to do well than those with TN type 2 (Miller and coworkers, unpublished data). Facial pain diagnoses other than TN are unlikely to improve after MVD. TN with a history of multiple sclerosis (MS) is called symptomatic trigeminal neuralgia (STN). MS is present in 1% to 3% patients with TN, and 2% to 4% of patients with MS have TN, probably due to intrinsic demyelination within the nerve or increased sensitivity to vascular trauma.^31,32 Although MS patients sometimes improve after MVD, the recurrence rate is higher, and long-term elimination of pain is rare,^33,34 so destructive procedures may be more appropriate for these patients.³⁵ Sensory loss with burning pain is a sign of trigeminal neuropathic pain (TNP); if it occurs after a previous destructive procedure, this is called trigeminal deafferentation pain (TDP). Allodynia and dysesthesia with a history of herpes zoster suggest postherpetic neuralgia (PHN). MVD is not a good option for any of these patients. Atypical facial pain (AFP), which refers to pain of psychological onset, requires neuropsychological testing for the diagnosis and is unlikely to improve after MVD.

Pain outside the trigeminal nerve distribution is not TN, although other vascular compression syndromes may be present with throat pain (glossopharyngeal neuralgia) or pain deep in the ear (nervus intermedius neuralgia). Other causes of facial pain include dental disease, orbital disease, sinusitis, cluster headache, temporomandibular joint disease, temporal arteritis, and posttraumatic neuralgias. None of these have the clinical characteristics of TN, nor do they respond to MVD of the trigeminal nerve.

Preoperative Imaging

All patients should undergo magnetic resonance imaging (MRI) before MVD to verify that there is no intracranial mass lesion that may be responsible for the pain, such as a tumor, cyst, aneurysm, or arteriovenous malformation. MRI also can identify evidence of demyelinating disease or inflammatory changes and may reveal anatomic characteristics that would make MVD technically problematic, such as an ectopic basilar artery or bony abnormalities. High-resolution MRI using steady-state precession images can be used to identify neurovascular compression preoperatively with a high degree of accuracy, and fusion with magnetic resonance angiography followed by three-dimensional reconstruction can be used to simulate the intraoperative view for surgical planning (Fig. 163-1).³⁶

FIGURE 163-1 Preoperative magnetic resonance imaging to identify arterial compression of the trigeminal nerve before microvascular decompression. Steady-state precession imaging demonstrates contact of a vessel with the nerve (A), and magnetic resonance angiography reveals that the vessel is an artery (B). Fusion and three-dimensional reconstruction of these sequences produce an image (C) that corresponds well with intraoperative findings (D).

(Adapted from Miller J, Acar F, Hamilton B, et al. Preoperative visualization of neurovascular anatomy in trigeminal neuralgia. J Neurosurg. 2008;108:477, 2008.)

Operative Technique

Standard neuroanesthetic techniques are used, with chemical paralysis and controlled ventilation to prevent motion in the field. Use of diuresis or spinal drainage for brain relaxation is generally not necessary because release of cerebrospinal fluid (CSF) from the trigeminal cistern will relax the cerebellum enough to allow adequate retraction. Intraoperative monitoring is helpful to prevent injury to the brainstem and cranial nerves. Brainstem auditory evoked potentials are very sensitive to stretch-induced injury to the eighth cranial nerve, and a delay over baseline of greater than 20% or shift in interpeak latency of more than 1.5 to 2 milliseconds requires loosening of cerebellar retraction until signals normalize. Facial nerve monitoring may also be used but is less helpful.

A cranial fixation device such as the three-pin Mayfield head holder is applied before positioning. There are several options for patient positioning for MVD. The simplest option is to place the patient in a flat supine position with the head rotated and flexed to the opposite side. Ideally, no shoulder roll should be used so that the ipsilateral shoulder does not obscure the operative approach. This position requires a flexible neck and may not work for obese or short-necked patients. Other options include the lateral decubitus or three-quarter prone position with the shoulder taped caudally and neck flexed, ensuring the chin is at least two fingerbreadths from the sternum. Regardless of the position chosen, it is generally best to place the vertex parallel to the floor so that the seventh and eighth cranial nerves are inferior relative to the trigeminal nerve, simplifying the approach.³⁷ All pressure points are padded, and an axillary roll is used if necessary. The sitting position can also be used, although it is associated with complications such as air embolism and subdural hematoma.

Preoperative MRI is used to evaluate the anatomy of the sinuses, cerebellum, and any anomalous veins. A small posterior fossa or Chiari malformation may necessitate alteration of surgical technique. The position of the transverse and sigmoid sinuses may be estimated from bony landmarks. The transverse sinus generally runs along a line connecting the inion to the external auditory meatus, parallel and posterior to the zygomatic arch. The sigmoid sinus runs along the digastric groove posterior to the mastoid eminence. Alternatively, frameless stereotaxy may be used to accurately define the position of the sinuses. Hair is clipped from the surgical site, and the scalp is sterilized and then infiltrated with local anesthetic with epinephrine to reduce bleeding. The linear incision runs longitudinally two fingerbreadths behind the ear (5 mm behind the hairline) and extends 3 to 5 cm, with one fourth of the incision above the iniomeatal line. Monopolar electrocautery is used to dissect and clear muscle and soft tissue until the bone of the mastoid eminence and digastric groove is seen. The occipital artery is often encountered in the muscular tissue and sacrificed. A large mastoid emissary vein is usually seen at this point, which represents an important landmark because it overlies the junction of the transverse and sigmoid sinuses. The bony exposure is extended to the curving portion of the suboccipital bone at the floor of the posterior fossa. The wound is held open with a self-retaining retractor or with sutures. A dural graft is generally not necessary, but if desired, the periosteum along the superior nuchal line may be harvested, or fascia may be collected if a C-shaped incision was used.

Bone removal is performed with a high-speed drill or perforator, starting at the mastoid emissary vein, which exits the bone just inferior and posterior to the transverse-sigmoid sinus junction. If there is any doubt about the location of the sinuses, it is always better to start more inferior and posterior to avoid unintentional damage to the sinuses. A craniectomy is safe and well tolerated if the defect is filled with artificial bone material at the end of the case. Alternatively, some surgeons advocate elevation of a craniotomy flap inferior and posterior to the initial bur hole that can be replaced after the dura is closed. Using a drill and a periosteal elevator to carefully elevate the dura, the craniectomy is expanded until the junction of the transverse and sigmoid sinuses can be seen. The sigmoid sinus is especially susceptible to injury because of its thin outer wall and curved bony groove. In older patients, the lateral wall of the sinus is adherent to the mastoid bone and may be damaged if not carefully separated from the bone before the craniectomy. Small injuries to the sinus are managed with oxidized cellulose or Gelfoam and tack-up sutures, but large rents may require further bony exposure with a dural patch graft because packing with a large amount of hemostatic material may lead to venous obstruction. The mastoid air cells will be visible at the lateral margin of the bony opening and should be carefully waxed. Hemostasis is important at this point to prevent entry of blood into the subarachnoid space.

The dura is opened in an inverted L shape, parallel to and 3 to 5 mm from the transverse and sigmoid sinuses. A C- or T-shaped incision can be used as well, with T-shaped relaxing incisions as needed, although it should be remembered that watertight closure is desired at the end of the case. If necessary, the dura next to the sigmoid sinus is tacked laterally to slightly rotate the sigmoid sinus and expose the lateral surface of the cerebellum. CSF is then allowed to drain by gently retracting on the cerebellum with a cottonoid. Any adhesions or bridging veins along the superior margin of the cerebellum along the transverse sinus are coagulated and sharply divided.

At this point, the microscope is brought into the field, and the self-retaining retractor system is set up. A flexible self-retaining brain retractor is placed over a cottonoid to gently retract the cerebellum up and medially and slightly elevated toward the surgeon. This allows for penetration of the trigeminal cistern and further drainage of CSF, greatly reducing the need for medial cerebellar retraction for exposure of the trigeminal nerve. Superficial cerebellar veins draining into the tentorial sinus and the superior petrosal vein are easy to tear even with gentle retraction, so the cerebellum should first be retracted medially (as though approaching the seventh and eighth cranial nerves), then inferiorly under direct vision once the lateral extent of the cerebellum is visualized. The angle of approach is changed to follow the petrous bone anteriorly, keeping the retractor blade close to the tentorium along the superior surface of the cerebellum to avoid injury to the seventh and eighth cranial nerves. If bleeding is encountered during retraction, a dorsal bridging vein may have been torn, requiring removal of the retractor and gentle depression of the cerebellum to identify and coagulate the vein.

As the retractor is advanced, the petrosal vein complex is encountered, often appearing as an inverted Y that drains into the superior petrosal sinus. This vein is usually two thirds of the way from the dura to the trigeminal nerve, but there is great variability: the vein may be completely absent, or it may lie on the nerve itself producing venous compression. The petrosal vein is divided sharply after thorough coagulation. It is prudent not to coagulate or divide the nerve all the way to the point of its entry into the bone because it tends to retract with cautery and is difficult to control if it retracts into the petrous bone. Some surgeons recommend preserving all or at least the superior part of the petrosal venous complex if the veins do not obstruct the nerve or are easily mobilizable, but their presence usually prevents full exploration of the nerve, and they nearly always can be taken with impunity.

The arachnoid over the nerve is carefully removed to allow complete inspection of the nerve. Thin, translucent arachnoid can be teased off, but thick, opaque bands must be sharply dissected to avoid injury to the trigeminal nerve, the trochlear nerve (a thin, delicate structure in the arachnoid above the trigeminal nerve), or small vascular branches in the subarachnoid space. Vascular compression is usually seen close to the brainstem, often anterior to the nerve. The site of compression may vary based on symptoms, with symptoms closer to V1 associated with compression of more caudolateral portions of the nerve. The arachnoid anterior to the nerve must be dissected to allow decompression. Endoscopic assistance has been advocated as a method of very thorough evaluation of the nerve with minimal cerebellar retraction.^38–41 Some advocate use of a small mirror to visualize behind the nerve.

The artery that most frequently produces compression is the superior cerebellar artery (SCA), which often compresses the nerve anteromedially from within the axilla. Decompression requires elevation of the artery into a horizontal rather than vertical orientation, displacing it upward and away from the nerve. SCA often divides into two branches as it courses around the midbrain, either or both of which may compress the nerve. The anterior inferior cerebellar artery (AICA) may compress the nerve from below, requiring displacement more inferiorly away from the nerve. Sometimes both SCA and AICA are involved, surrounding the nerve like a pincer, in which case both must be mobilized and decompressed. Less commonly, the vertebral or basilar artery contacts the nerve, usually in hypertensive, elderly, and male patients.⁷ Small arterioles may be seen, more often in younger patients. Compression by a persistent trigeminal artery has also been described.⁴²

Any arterial loops producing compression are carefully dissected, avoiding kinking of arteries at all times. Shredded Teflon is created by grasping and tearing a piece of Teflon to create a soft substance resembling a cotton ball. This material is then placed between the vessel and nerve in a proximal-to-distal manner, held in place by the tension between the artery and nerve root and reinforced if necessary with Gelfoam or fibrin glue. The vessel is flipped onto the dorsal aspect of the nerve with the Teflon separating the nerve from the vessel. If small vessels are pushed into the nerve by the Teflon it must be replaced. Multiple pieces of Teflon can be used to decompress multiple arteries or looping arteries affecting more than one side of the nerve. Small veins may be coagulated, but arteries should always be preserved. The nerve must be explored along its entire length, because the root entry zone may extend many millimeters from the brainstem and even very small vessels may cause compression.

Venous contact is frequently seen, often concomitantly with arterial compression. The vein may be anterior (transverse pontine vein), posterior (petrosal vein), or distal at the entrance to Meckel’s cave (trigeminal vein); frequently, compression is caused by one of the many unnamed veins that run along the brainstem.^43,44 Posterior venous compression may be obscured by the ridge of the petrous bone. Compression from draining veins from a venous angioma or arteriovenous malformation is sometimes observed. If venous compression is identified, the vein is carefully dissected from the nerve and coagulated with low-voltage small bipolar forceps to prevent spread of current into the adjacent nerve, after which the vein is coagulated and divided.

It is uncommon to find no evidence of compression whatsoever, but if after thorough exploration no compression is found, the nerve may be gently manipulated to produce a lesion or the nerve partially sectioned along the anteroinferior aspect. Alternatively, the patient may be treated with a subsequent destructive procedure such as radiofrequency rhizolysis or stereotactic radiosurgery.

After decompression, the vessels are carefully observed, and topical papaverine-soaked Gelfoam is used if there is any evidence of vasospasm. The operative field is liberally irrigated, retractors are removed, and a Valsalva maneuver is performed by anesthesia to ensure there is no bleeding. The dura is closed in a watertight manner using continuous or interrupted braided 4-0 sutures to prevent subsequent leakage of CSF. It is usually possible to close the dura primarily, but if necessary, a graft of cadaveric, synthetic, or autogenous tissue may be used. Fibrin dural sealant is helpful, especially in redo operations. A piece of Gelfoam is placed over the dura, and a cranioplasty of wire mesh and artificial bone material is fashioned, or the bone is replaced if a craniotomy was performed (Fig. 163-2). The fascia, subcutaneous tissue, and skin are closed in standard fashion using absorbable sutures.

FIGURE 163-2 Right-sided retromastoid craniotomy. A, The patient is positioned supine with the head turned 90 degrees toward the opposite shoulder, slightly flexed, and slightly bent toward the floor. The Mayfield head holder apparatus is visible on the extreme upper right and left of the figure, and the right ear has been taped forward (visible to the right of the incision). The 5-cm incision extends just above the iniomeatal line. B, The bone is removed with high-speed drill and rongeurs, starting at the emissary vein and extending anterior and superior to the junction of the transverse and sigmoid sinuses. C, The dura is opened, and a cottonoid patty is placed in the trigeminal cistern to facilitate drainage of cerebrospinal fluid. D, The petrosal vein is visualized and divided after coagulation. E, After dissection of the arachnoid, the right trigeminal nerve is seen to be compressed by a branch of the superior cerebellar artery. F, The artery is decompressed with Teflon. G, The dura is closed, and the bony defect is filled with artificial bone material; the wound is then closed in layers.

Postoperative Care

After the operation, the patient must be observed overnight in the intensive care unit or stepdown unit.⁴⁵ Blood pressure is monitored with an arterial line, and antihypertensives (labetalol or hydralazine) are administered if systolic blood pressure exceeds 160 mm Hg. Mild narcotics may be used for headache, which may persist for several weeks. Severe bifrontal headache warrants computed tomography (CT) to rule out posterior fossa hemorrhage, but postoperative imaging is otherwise not necessary. Nausea is common and usually responds to antiemetics. Steroids are not helpful. The patient is transferred to the ward on the first postoperative day, and diet and activity are gradually increased. Patients are generally discharged by the third postoperative day. After discharge, activity is gradually increased over a week, and most patients are able to return to work within 2 to 4 weeks. Half of all patients undergoing MVD return to baseline activity within 1 month, and 90% by 3 months.⁴⁶

Complications

Complications from MVD are rare in experienced hands,^7,24 and morbidity is lowest at high-volume centers.⁴⁷ Cranial nerve damage is rare, and such complications as facial dysesthesia and anesthesia dolorosa are much less common than with the lesioning procedures. Many patients have a transient conductive hearing loss due to tracking of fluid from the mastoid into the middle ear that clears spontaneously within a few weeks. Sensorineural hearing loss tends to be permanent but can be prevented by gentle retraction, careful technique, and treatment of any AICA vasospasm that occurs. Brainstem auditory evoked potential monitoring is very helpful in preventing this complication and has diminished its incidence from 1.3% to 0.6%.³⁷ Prolonged postoperative vertigo or tinnitus is reported in about 2% of patients,⁴⁸ and some degree of facial nerve palsy occurs in up to 5% of patients.⁷ Both of these tend to improve spontaneously over a few weeks. Injury to the fourth cranial nerve produces a trochlear palsy that usually subsides after a few months.

CSF rhinorrhea, which occurs in 1.5% of cases,⁷ is caused by leakage of CSF through the dural opening, into the mastoid air cells, and through the pharyngotympanic tube into the nasopharynx. This complication occurs more often with reoperations and may be prevented by meticulous waxing of the mastoid, careful dural closure, and application of fibrin glue. CSF rhinorrhea is often successfully treated with 3 days of CSF drainage using a lumbar drain. If leakage continues, it may be necessary to reexplore the wound and close the fistula directly.

Aseptic meningitis with headache and sterile CSF pleocytosis may occur in response to artificial materials such as the Teflon pledget used or dural graft material. This is usually self-limited but often responds to steroids or lumbar puncture to remove CSF. Wound infection presents with swelling of the wound, fever, and purulent drainage and requires reoperation with removal of all foreign materials and 4 to 6 weeks of intravenous antibiotics.

Cerebellar contusion may be caused during the opening and initial retraction and is prevented by avoidance of aggressive cerebellar retraction, initial lateral retraction, and early drainage of CSF. Cerebellar hemorrhagic infarction may occur from arterial damage but more often results from venous insufficiency, so it is important to minimize the number of veins sacrificed. Posterior fossa hemorrhage occurs early in the postoperative course and usually requires immediate evacuation.

Results

Multiple investigators have found MVD to be an effective treatment for TN. In one study of 1204 patients, 75% had complete relief and 9% had partial relief after 1 year. After 10 years, 64% had complete relief, and 4% had partial relief. The annual rate of recurrence was less than 2% by 5 years and less than 1% by 10 years.⁷ Although initial results are similar, MVD offers a much higher likelihood than destructive procedures for a long-term cure. In one study comparing 378 MVD patients with 316 radiofrequency (RF) patients over 20 years, patients undergoing RF rhizotomy had a 75% chance of pain recurrence in the first 5 years. By contrast, 63% of MVD patients were pain free at 20 years.⁴⁸

The most significant predictor of outcome after MVD appears to be type of TN pain. Patients with TN type 1 (mostly episodic, lancinating pain) tend to have much better immediate and long-term results than those with TN type 2 (mostly constant pain). This effect appears to be graded with the amount of lancinating pain, so that a greater proportion of lancinating pain leads to a better outcome.⁴⁹ TN type is more predictive of outcome than any other clinical feature of TN, including duration of symptoms, presence of trigger points, response to antiepileptics, and type of compression (arterial versus venous) found at surgery.⁴⁹ In one large study, 80% of patients with TN type 1 had some degree of pain relief at 5 years, compared with 51% of those with TN type 2.⁵⁰ However, although outcomes for TN type 2 are less satisfactory than for TN type 1, MVD still benefits most patients, and no alternative interventions appear to offer a better chance of long-term relief.

Venous compression appears to predict worse outcome, possibly because of regrowth of veins. In one study of 393 patients treated by MVD for venous compression, the 1-year recurrence rate was 31%, and 28 of 32 undergoing re-exploration had evidence of recurrent venous contact.⁴³ Venous compression is also more common in pediatric patients with TN. In one study, venous contact was found in 86% of pediatric TN patients undergoing MVD, and a vein was the sole offending vessel in 18%. This may explain why pediatric TN patients have worse results after MVD, with 10-year recurrence rates as high as 43%.⁵¹ Other predictors of recurrence include female gender, prolonged preoperative symptoms (>8 years), and failure of immediate postoperative relief.^7,52–58 Severity of compression and focal arachnoiditis have also been associated with worse outcome.⁵⁹

It is unclear whether MVD for recurrent TN after a previous destructive procedure is associated with a worse prognosis. The likelihood of pain relief appears to be similar,²³ but patients who have undergone a lesioning procedure before MVD have a higher likelihood of postoperative trigeminal neuropathic symptoms (burning, aching pain).⁷ Some investigators have noted that lesioning procedures before an initial MVD may increase the likelihood of negative exploration during subsequent MVD operations for recurrent TN.⁶⁰

Recurrent disease after a prolonged postoperative pain-free interval may be effectively treated with medication, but repeat MVD has also been advocated, even though it is associated with a much higher rate of negative exploration. Reoperations are technically more difficult, and if the first MVD was unsuccessful for technical reasons, it is unlikely that repeating the operation will yield better results. When neurovascular compression is seen during a repeat MVD, it is nearly always because of growth of veins or expansion of arteries rather than dislodging of the Teflon felt placed during the first operation, although scarring produced by the felt can produce neural compression. Reports of operative findings during repeat MVD vary widely; most investigators report recurrent vascular compression in about half of patients.^61,62 Outcome after the second operation is generally good.⁵³

Other Neurovascular Facial Pain Syndromes

Conclusion

TN is associated with and is likely to be caused by pulsatile mechanical compression of the trigeminal nerve by a blood vessel near the dorsal root entry zone. MVD differs from other treatments because it fixes the underlying cause to produce long-term relief of symptoms. Careful patient selection is the most important determinant of outcome, and morbidity is rare when the procedure is performed by an experienced surgeon.