Operations for Vascular Compressive Syndromes

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Chapter 44 Operations for Vascular Compressive Syndromes

Peter J. Jannetta, Raymond F. Sekula, Jr.

In recent years, microvascular decompression (MVD) has become the operative treatment of choice for many disorders of the cranial nerves, augmenting and replacing ablative procedures. These cranial rhizopathies have long defied categorization, clarification of pathophysiology, and definitive treatment despite efforts by clinicians in several disciplines. Although the clinical presentations of disorders such as trigeminal neuralgia, hemifacial spasm, glossopharyngeal neuralgia, tinnitus, spasmodic torticollis, disabling positional vertigo, and Meniere’s disease are quite different, these problems all share a common underlying pathology: vascular compression of the respective cranial nerve in the proximal nonfascicular region. Several studies have shown improved blood pressure control in medically refractory, severely hypertensive patients after MVD of the left lateral medulla oblongata.^1,²

Beginning in 1966, a patient with trigeminal neuralgia was noted at operation to have compression of the trigeminal nerve by a small artery near the brainstem.³ The same year, a patient with hemifacial spasm was cured after coagulation of a vein that was distorting the facial nerve at the brainstem. As we performed operations to relieve vascular compression of the trigeminal and facial nerves, it became apparent that pulsatile, mechanical forces from a blood vessel were the pathophysiologic mechanism responsible for these cranial hyperactive syndromes. These syndromes later included glossopharyngeal neuralgia, tinnitus, and vertigo. All the cranial nerves are subject to the forces of vascular compression with arteriosclerosis, elongation, and brain sag as operant factors. This chapter describes the patient selection criteria, operative technique, perioperative management, results, and complications after more than 8000 MVDs for the aforementioned cranial rhizopathies.

PREOPERATIVE EVALUATION

Before MVD for any cranial rhizopathy, all patients at our institution give a detailed history and undergo a physical examination. Preoperative testing for every patient involves audiometry (pure tone and speech), acoustic middle ear reflexes, and brainstem auditory evoked potentials (BAEPs). All patients have preoperative magnetic resonance imaging (MRI) to rule out tumors, cysts, vascular anomalies (arteriovenous malformation), aneurysms, and congenital abnormalities, especially Chiari malformation.

The audiometric tests are performed preoperatively to obtain a baseline for quantitatively determining deteriorations or improvement in hearing function. The pure tone audiogram often shows anomalies represented by small dips in the frequency range of 1500 to 2000 Hz.⁴ Additionally, preoperative BAEPs provide baseline information for the clinical neurophysiology team so that they may warn the surgeon of any deviations during monitoring of the intraoperative auditory evoked potentials. Typical changes observed in the BAEP are an increased interpeak latency between peaks I and III ipsilaterally or prolongation of interpeak latency between III and V contralaterally (Figs. 44-1 to 44-4). These findings are based on our knowledge of the neural generators of BAEPs.⁵^–⁸

FIGURE 44-1 Brainstem auditory evoked potential recordings from a patient with normal hearing and with hemifacial spasm of 8 years’ duration on the right side. Recordings from the left ear (LE) show a normal response, whereas recordings from the right ear (RE) show an increased interpeak latency I-III and a double-peak II.

FIGURE 44-2 Brainstem auditory evoked potential recordings preoperatively and 6 days postoperatively from the left ear (LE) in a patient with trigeminal neuralgia on the right side. Preoperatively, peak V fluctuates in latencies, indicating changes at the level of the contralateral lateral lemniscus. Postoperatively, peak V is normal.

FIGURE 44-3 Results of audiometry and recordings of brainstem auditory evoked potentials in a patient with a 10 year history of disabling positional vertigo (DPV) on the right side. There is a slight decrease in pure tone threshold in the right ear (RE), and bilateral increased thresholds of acoustic middle ear reflex responses. Brainstem auditory evoked potentials show low amplitude and increased interpeak latency I-III for the right ear. Initial vestibular tests showed canal paresis on the right side, and 4 years later directional preponderance to the right; tests before operation show normal electronystagmographic result. LE, left ear.

(From Møller MB: Results of microvascular decompression of the eighth nerve as treatment for disabling positional vertigo. Ann Otol Rhinol Laryngol 99:724-729, 1990.)

FIGURE 44-4 Results of audiometry and recordings of brainstem auditory evoked potentials in a patient with severe tinnitus, such as that occurring after trauma. Increased interpeak latency I-III occurs on the left side and there is a double-peak II. LE, left ear; RE, right ear.

If there is any question of hearing loss, at operation, audiometric tests are repeated in late in the operative procedure. Some patients may experience transient conductive hearing loss because of middle ear effusions. They resolve spontaneously within 6 weeks. Audiometry should be repeated 3 months postoperatively in such cases.

TRIGEMINAL NEURALGIA

Patient Selection

Patients with trigeminal neuralgia refractory to medical management are selected for MVD on the basis of their symptoms, history, and ability to undergo a general anesthetic. Patients with contraindications to general anesthetics or intracranial procedures may be treated with ablation procedures, including percutaneous glycerol rhizotomy, percutaneous radiofrequency rhizotomy, trigeminal balloon microcompression, stereotactic radiosurgery, and peripheral neurectomy.^9,¹⁰ A discussion of these other surgical techniques is imperative for understanding why surgeons in many centers consider MVD to be the operative procedure of choice for most patients.

Peripheral neurectomy, although less invasive, typically has a short duration of tic relief, and may be indicated for patients with a shortened life expectancy.¹¹ Radiofrequency lesions, created by percutaneous passage of a needle into the gasserian ganglion, have an initial success rate of 90% or greater, with long-term pain relief ranging from 20% to 78% of patients.¹²^–¹⁵ Approximately 20% of patients have facial dysesthesias after radiofrequency rhizotomy. The greater the sensory loss, the more likely the trigeminal neuralgia will be relieved, but it is also more likely that dysesthesias leading to frank anesthesia dolorosa will supervene. Percutaneous glycerol rhizotomy rarely causes facial dysesthesias or sensory loss when performed strictly according to the technique introduced by Hakanson in 1981.¹⁶ Although glycerol rhizotomies have initial success rates of 80% to 90%,¹⁷ median time to recurrence varies from 16 to 36 months.¹⁸^–²¹ Balloon microcompression of the trigeminal ganglion has initial pain relief ranging from 78% to 100%,^17,²² with mean time to recurrence of 3.5 years.²³ Minor dysesthesias occur in approximately 20% of patients,²³ and mild temporary masseter weakness is seen in most patients treated with balloon microcompression.²² The corneal reflex is usually present.

Patients who have undergone radiofrequency lesions and balloon compression are initially satisfied because the trigeminal neuralgia is gone, but the side effects of numbness gradually become bothersome. In large series, new or worsening numbness or paresthesias after stereotactic radiosurgery (i.e., Gamma Knife) for trigeminal neuralgia occurred in 10%,²⁴ 10%,²⁵ and 19%²⁶ of patients, and complete pain relief (without medication) was achieved in 40% (2-year median follow-up),²⁴ 48% (1-year follow-up),²⁵ and 34% (3-year follow-up).²⁶ Median time to response (achievement of at least 50% pain relief) after stereotactic radiosurgery was 60 days,²⁴ 10 days,²⁵ and 24 days.²⁶ In another series of patients undergoing repeat stereotactic radiosurgery for trigeminal neuralgia, the authors concluded that most patients (85%) achieved more than 50% pain relief. New or worsening paresthesias occurred in 13% of patients, however, and complete pain relief (without medication) was achieved in only 19% of patients.²⁷

Too often, advocates of stereotactic radiosurgery for trigeminal neuralgia report high rates of “success” in patients despite continued medication use. Particularly in elderly patients, medication side effects, including imbalance, confusion, and lethargy, are debilitating. The goal of all treatments for trigeminal neuralgia should be complete pain relief without medication. Pain relief with medication is not a good result. To our knowledge, follow-up of patients after stereotactic radiosurgery has been frequently inadequate. Of the first 15 patients we operated on who had failed gamma irradiation, only 1 had been followed.

The choice between MVD and other procedures should be governed by patient preference and ability to tolerate a craniotomy under general anesthesia. Advantages of MVD include consistently higher long-term success rates with a minimal chance of facial sensory loss or dysesthesias. These advantages are quite substantial in that the average life expectancy of the patients treated by the authors was 32 years from the initial onset of symptoms.²⁸

The classic symptom of typical trigeminal neuralgia is lancinating pain in one or more distributions of the trigeminal nerve. Talking, eating, shaving, and feeling the wind blowing often precipitate symptoms. Patients typically have an abrupt and memorable onset of symptoms, with a variable duration of remission. A burning, aching pain without specific trigger points characterizes atypical trigeminal neuralgia,²⁹ in contrast to typical trigeminal neuralgia. Although surgical success with these patients is less than with patients with typical symptoms, no other reasonable alternative treatments currently exist. Many patients have initial success with medical management using agents such carbamazepine, phenytoin, baclofen, valproic acid, clonazepam, and gabapentin. Carbamazepine historically has been most effective, but only 56% of patients maintain satisfactory pain relief after 10 years.³⁰ Often, side effects, allergies, and the development of refractory symptoms to medications necessitate the need for early surgical intervention.

Operative Technique for Microvascular Trigeminal Decompression

As in any operation, patient positioning is important. The patient is placed on the operating table with the head at the foot of the bed, providing maximal room for the surgeon during the microscopic portion of the case. A three-point head holder is applied and the patient is placed in the lateral decubitus position. An axillary roll and padding to other pressure points are placed. The neck is minimally put on stretch and slightly flexed, always maintaining at least two fingerbreadths between the patient’s chin and sternum. The patient is secured to the bed using straps and adhesive tape across the hips. The head holder is fastened into position. The patient’s shoulder is taped caudally for maximal working room (Fig. 44-5).^31,³²

FIGURE 44-5 Three-point head fixation device is applied to the patient’s head, and the patient is placed in a lateral park bench position with affected side up. An axillary roll is placed to prevent brachial plexus injury, and all other pressure points are padded appropriately. The head is elevated and distracted, then rotated 10 degrees away from the surgeon. The head is locked into place, and the ipsilateral shoulder is distracted caudally and rotated medially, giving the surgeon maximal working area. The patient is taped securely at the hips and chest to allow rotation of the table during surgery.

FIGURE 44-6. Junction of the transverse and sigmoid sinuses must be exposed at superior margin of the craniectomy. Edge of the sigmoid sinus must be identified along the lateral margin of the craniectomy. To minimize cerebellar retraction, craniectomy is extended caudally and laterally for procedures involving lower cranial nerves.

FIGURE 44-7. Intraoperative view of superior cerebellar artery (SCA) and a vein causing compression of the trigeminal nerve in a patient with trigeminal neuralgia.

FIGURE 44-8. Intraoperative view of CN VII compressed by posterior inferior cerebellar artery (PICA) in a patient with hemifacial spasm. VA, vertebral artery.

FIGURE 44-9. Intraoperative view of left lateral medulla and fascicles of CN IX and X compressed by left posterior inferior cerebellar artery (PICA) and left vertebral artery (VA).

After satisfactory positioning, a 2 cm strip of hair behind the ear is shaved and prepared. The incision, approximately 3 to 5 cm long (longer in a large man, shorter in a small woman), is placed 0.5 cm posterior to the hairline, extending one fourth above the iniomeatal line and three fourths below.^31,³² Electrocautery is used to dissect and clear soft tissue until the mastoid eminence is adequately visualized.

Before beginning the craniectomy, the digastric groove should be visualized (5 cm behind the ear canal [4 cm in women] and 1 cm caudal to the lateral canthus, external ear canal line). The mastoid emissary vein, which is a good landmark for the junction between the sigmoid and transverse sinuses, may bleed. It should be waxed. The craniectomy is expanded until the junction of the transverse and sigmoid sinuses is definitively appreciated, with the apex of the triangular craniectomy pointed at this junction (variations are discussed with other cranial nerve syndromes) (Fig. 44-6). All air cells are waxed diligently, after which a curvilinear or T-shaped durotomy is performed, exposing a direct corridor along the petrotentorial bone down to the brainstem.^31,³²

When the dura is sutured back, the operating microscope is used to “turn the corner,” or expose the cerebellopontine angle. While gently retracting on the cerebellum with a Cottonoid on a sterile piece of latex (rubber dam), the surgeon must allow adequate cerebrospinal fluid to drain so that the cerebellum falls away, minimizing the need for much cerebellar retraction. Penetration of the trigeminal cistern and sharp dissection of arachnoid adhesions greatly reduce the need for significant cerebellar retraction medially. The Cottonoid and a precisely flexible, self-retaining brain retractor are placed on the supralateral portion of the cerebellum for trigeminal exposures. The cerebellum is retracted up and medially. Often, the first vessels encountered are the petrosal vein complex, which are coagulated and divided after evaluating relationships to the nerve.^31,³²

Before performing MVD of the trigeminal nerve, the surgeon must be aware that the dorsal root exit zone of the trigeminal nerve (the junctional area of myelin) extends to the distal portion of the nerve. The nerve must be meticulously inspected from the brainstem to Meckel’s cave, and all offending vessels must be decompressed. When performing the actual decompression, all arachnoid over the nerve must be dissected away. Shredded polytef (Teflon®) felt is placed between the vessel and the nerve. The most frequent vessel found is the superior cerebellar artery. Often multiple pieces of shredded Teflon felt are used to decompress looping arteries affecting more than one side of the trigeminal nerve.^31,³²

Before closing, a Valsalva maneuver is performed to ensure hemostasis. The dural opening is closed carefully with a watertight closure over a strip of absorbable gelatin sponge (Gelfoam) to prevent cerebrospinal fluid leakage. If a watertight closure cannot be obtained, cadaveric tissue, synthetic material, or muscle (if the leak is small) is used to patch the leak. The bone edges are waxed for a second time, and a cranioplasty is performed using titanium wire mesh placed over a piece of Gelfoam. Fascia, subcutaneous tissue, and skin are closed in standard manner.

Results for Trigeminal Microvascular Decompression

The most frequent operative finding was trigeminal compression by the superior cerebellar artery in 76% of the patients (Fig. 44-7). Veins were causing neural compression in 68% of patients, but were the sole offending vessel in only 13%.^38,³⁹ In a report³⁸ of 1204 patients who underwent initial MVD, 80% were pain-free at 1 year, and an additional 8% had greater than 75% relief, for a total success rate of 88%.³⁸ At 10 years, 70% remained pain-free, and 4% had greater than 75% relief. Persistent mild postoperative facial numbness was noted in 17%, of which only 1% was severe. Repeat MVD was performed in 11% of patients for persistent or recurrent pain.³⁸ Of these, 96% were pain-free or had greater than 75% pain relief 1 year after surgery (89% at 10 years).

MVD for pediatric-onset trigeminal neuralgia has a lower success rate than MVD for adults. At the time of discharge, 73% of patients had complete pain relief, with an additional 18% having greater than 75% diminution of pain.⁴⁰ At last follow-up (mean 105 months), 57% of patients had either complete pain relief or greater than 75% relief of pain. The lower therapeutic response is likely due to the fact that the pathophysiology of the disease is different in pediatric patients. Venous compression was noted in 86% of the cases and was the sole offending vessel in 48%; this is markedly greater than for the adult patients. Additionally, venous compression often results in recurrence of pain because of revascularization. In 393 cases of trigeminal neuralgia caused by veins, 31% developed recurrence (most within 1 year of initial operation) after initial improvement of pain.

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