Fully endoscopic vascular decompression of the glossopharyngeal nerve
By Reza Jarrahy, M.D., Sung Tae Cha, M.D., George Berci, M.D., F.A.C.S., Hrayr K. Shahinian, M.D., FACS
Microvascular decompression of the glossopharyngeal nerve is an effective treatment for patients with glossopharyngeal neuralgia in whom compression of the nerve by a blood vessel is implicated in the pathogenesis of the disease. The standard surgical technique uses the binocular operating microscope for all intraoperative visualization. Growing experience with posterior fossa endoscopy, however, has demonstrated that endoscopes provide equal if not more comprehensive anatomical views of cerebellopontine angle. Our objective was to demonstrate that endoscopy can be used as the sole imaging modality for vascular decompression of the glossopharyngeal nerve.
Case report of an innovative surgical technique with review of the relevant medical literature.
We performed a fully endoscopic vascular decompression of the glossopharyngeal nerve in a patient with glossopharyngeal neuralgia. The endoscope was used to survey the posterior fossa, guide the placement of insulating sponges, and conduct a final assessment of the intervention.
Endoscopes provided detailed images of the posterior fossa and the pathological vascular conflict. Despite the constricted operating space, the offending vessel was successfully separated from the nerve without prolonged brain retraction or damage to surrounding structures. The patient awoke free of his presenting symptoms.
The versatility of endoscopy allows for superior visual appreciation of neurovascular conflicts in the posterior fossa. Although endoscopy has only been used to supplement microscopy in cranial nerve decompression surgery to date, this report demonstrates how it can be used as the sole imaging modality in glossopharyngeal nerve decompression with an excellent outcome.
endoscopy, posterior fossa, microvascular decompression, glossopharyngeal neuralgia, trigeminal neuralgia
Glossopharyngeal neuralgia (GN) is a disease characterized by severe paroxysmal attacks of sharp, lancinating pain effecting the sensory distribution of the glossopharyngeal nerve, including the base of the tongue, soft palate, tonsils, pharyngeal pillars, posterior pharyngeal wall, and the inner ear. 1-3 Attacks may be associated with vagally-mediated cardiovascular and hemodynamic compromise: bradycardia, hypotension, cardiac syncope, and asystole have been reported to occur in conjunction with episodes of neuralgia.4,5
Based upon the original gross observations made by Dandy 6 and the microscopic correlates described by Jannetta 7 with respect to trigeminal neuralgia, aberrant neurovascular conflicts causing vascular compression of the roots of the glossopharyngeal and vagus nerves in the posterior fossa have been implicated in the pathogenesis of GN. Surgical decompression has resulted in excellent results and has gained wide acceptance as the preferred choice of surgical therapy. 2,8,9
Microvascular decompression (MVD) of the glossopharyngeal nerve makes use of the operating microscope as the sole imaging modality during surgery. Recent implementation of rigid endoscopy in posterior fossa surgery, however, has revealed it to be an equal if not superior imaging tool in this region of the anatomy. Although its use has been described as an adjunctive imaging modality in cranial nerve decompression surgery, 10,11 the use of endoscopy as the sole means of intraoperative imaging in this setting has not been reported. We present the case of a patient with glossopharyngeal neuralgia who underwent a fully endoscopic vascular decompression of the glossopharyngeal and vagus nerves with complete postoperative resolution of his symptoms.
Materials and methods: History
This 35-year-old man presented to our service reporting a 4-year history of periodic left-sided attacks of sharp pains affecting the base of the tongue and back of the oral cavity. The pains had the quality of electric shocks and radiated to the inner ear. He described an associated numbness at the posterior base of the tongue and a perceived decrease in his ability to taste, but could not identify any particular trigger points that initiated the symptoms. There were no associated cardiovascular manifestations and the patient was otherwise in excellent health. His neuralgia was poorly controlled on a medical regimen that included carbamazepine and baclofen.
After consultation regarding surgical options in the management of his disease, the patient consented to a fully endoscopic approach to vascular decompression of the glossopharyngeal nerve.
Following the induction of general anesthesia, the patient was placed in the left lateral decubitus position. The neck was flexed and the head was slightly rotated toward the surgeon before being fixed in a three-pin head clamp. A curvilinear 3-cm incision was made behind the ear and subperiosteal musculocutaneous flaps were elevated anteriorly and posteriorly. Retraction of these flaps allowed for a 2-cm diameter craniectomy to be made at the confluence of the transverse and sigmoid sinuses. Dura was exposed and incised and cerebrospinal fluid (CSF) was drained. A 4.0 mm 0° rigid endoscope (Karl Storz of America, Culver City, CA) was introduced into the posterior fossa and was stabilized in place with the use of a pneumatically powered holding arm (Mitaka Kohki Co., Tokyo). It was advanced to the level of the lower cranial nerves and a survey of the regional neurovascular anatomy was performed, revealing a looping branch of the vertebral artery compressing the inferior surface of the lower cranial nerves at their ingress to the jugular foramen. Dissecting instruments were used to liberate the nerves from the vessel. (Figure 1) Teflon pads were then interposed between the nerves and blood vessel to maintain the separation. (Figure 2) A final survey was conducted to evaluate the adequacy of the decompression and a fibrin-based sealant (Hemaseel APR™, Haemacure Co., Sarasota, FL) was liberally applied over the field. The dura was closed, the bone flap repositioned, and the skin flaps reapproximated.
Endoscopic views of the posterior fossa were facilitated by the ability to advance the endoscopes directly to the level of dissection. This allowed detailed inspection of the neurovascular structures of the cerebellopontine angle (CPA) and accurate determination of the pathological anatomical relationship. Endoscopes of varying angles of view (0° and 30°) provided different perspectives of the region and minimized the obscuring effects of the petrous temporal bone.
The patient awoke from surgery free of his preoperative glossopharyngeal neuralgia symptoms. He was monitored in the intensive care unit overnight and transferred to the floor on the morning following surgery. Following complaints of having difficulty swallowing, a swallow study was obtained which showed a slight weakness of the palate and posterior pharyngeal muscles on the side of surgery. Otherwise, no other neurological deficits were noted. The patient was discharged home on the second postoperative day with instructions for outpatient follow up with a speech and swallow therapist.
Six months postoperatively the patient remains pain free and reports significant improvement of his dysphagia following a regimen of speech therapy.
Glossopharyngeal neuralgia is a rare clinical entity, with a reported incidence of approximately 0.8 per 100,000 people. 12,13 Compared to trigeminal neuralgia, GN occurs with a relative frequency of 0.2 to 1.3%. 8,14 The disease is characterized by unilateral, self-limited, episodic, paroxysmal attacks of sharp, lancinating, stabbing, or burning pain affecting the sensory distribution of the glossopharyngeal nerve. The base and back of the tongue, the tonsil, the pharyngeal pillars, the posterior pharyngeal wall, and the soft palate may all be involved on the affected side. In some patients, attacks can be triggered by stimulation of well-defined trigger zones located anywhere in this intraoral distribution; stimuli may include hot or cold liquids, swallowing, coughing, or shouting. 1,4,15
Many patients also experience radiation of pain to the ipsilateral ear; this is due to branches of the glossopharyngeal nerve that send sensory axons to the middle ear, Eustachian tube, tympanic plexus, and the mastoid air cells. 1,2,3,16-18
Some cases of GN are associated with cardiovascular compromise. Bradycardia, arrhythmia, hypotension, cardiac syncope, and asystole have all been related to attacks of neuralgia. 4,5 In addition to the inhibition of peripheral vasomotor activity, the central mechanism behind these cardiac manifestations involves vagus nerve irritation resulting from the proximity of the dorsal motor nuclei to the nucleus of Solitar, which receives afferent signals from the glossopharyngeal nerve. 2,19-21
Widely recognized as the author of the first clinical description of GN, 1,15,17,18,22 Weisenberg 23 in 1910 reported the case of a patient with paroxysms of intraoral pain in the distribution of the glossopharyngeal nerve. The source of nerve irritation was found, postmortem, to be a tumor of CPA. Although there is some debate as to whether or not this was the first true report on GN, 4,13 Weisenberg's experience drew attention to this relatively rare disorder and helped establish GN as a clinical entity distinct from trigeminal neuralgia, with which it had often been confused. During the years following his report numerous additional cases of GN were described. 24-28
In his original review of these cases, Dandy 15 concluded that the symptoms of GN were either attributable to tumors involving the ninth and tenth cranial nerves or to idiopathic causes. He believed the treatment of GN to be "purely surgical." Aside from resection of intracranial tumor in appropriate cases, early surgical techniques employed in the management of GN focused on intracranial section of the root of the glossopharyngeal nerve and the upper rootlets of the vagus nerve, extracranial avulsion of glossopharyngeal branches, and percutaneous neurolytic injections. 15,17,29 Protocols for additional percutaneous ablative therapies have been elaborated. 30-38 Vagal nerve paresis, manifested as dysphagia and hoarseness, has been reported as a complication of these procedures. 3,31-33,37,39 Anticonvulsant medical regimens have also been described. 1,3,4,40 Carbamazepine has generally been reported to be less effective in patients with GN than in those with trigeminal neuralgia.
In his later observations, Dandy 6 identified aberrant vascular structures as pathogenic factors in the etiology of trigeminal and glossopharyngeal neuralgia, providing gross descriptions of how arterial and venous structures impinged upon and distorted the normal anatomy of the root of the trigeminal nerve. His conclusions were consistent with those of Pope, 41 who earlier reported the case of a patient with glossopharyngeal sensory deficit due to a vascular compression of the glossopharyngeal root in the posterior fossa that was discovered at autopsy.
The gross observations made by Dandy were verified microscopically by Jannetta, 7 to whom the use of the binocular operating microscope was available. Intraoperative microscopic imaging greatly facilitated accurate identification of nerve-vessel conflicts involving the cranial nerves at the CPA. 7,8,42 Jannetta's confirmation of an anatomical basis for trigeminal neuralgia provided the rationale for microvascular decompression surgery, in which decompression of the trigeminal nerve was accomplished by separating it from the blood vessel by means of cautery (for veins) or interposition of a physical barrier (for arteries). Success with MVD in patients with trigeminal neuralgia led to the adaptation of the same strategy to the surgical management of GN. 8,43,44
Several factors have been considered in the etiology of GN, including trauma, infection, elongated styloid process, ossified stylohyoid ligament, vascular lesions, and malignancies. 1,4,14,8,45,46 Following Jannetta's initial contributions, however, vascular compression has gained acceptance as the primary causative factor in the majority of cases of GN. 1,4,8,43 Numerous authors have since described their success with MVD in the setting of GN. 1,2,9,22,44,47,48 Excellent long-term relief of pain has been observed in 75-80% of patients. 9,22
As originally described and currently practiced, MVD of the cranial nerves at the CPA is performed under microscopic visualization via a retrosigmoid craniectomy. 7 In recent years, however, increasing interest in posterior fossa endoscopy has generated numerous observations on the merits of the rigid endoscope as an operative imaging tool for surgery at the CPA. 49-55
The concept of using endoscopes to visualize the anatomy of the posterior fossa is not new. In 1917, Doyen 56 described a technique for trigeminal root neurectomy under endoscopic guidance via an occipital craniotomy. Since then, however, published experience with posterior fossa endoscopy has been scarce. Isolated reports detailing endoscopic exploration of the posterior fossa for diagnostic purposes and for selective trigeminal nerve root sectioning were published in the 1970s, 57,58 but only during the past decade has interest in the application of endoscopic imaging to this region been renewed in earnest.
This resurgence has coincided with the recent development of advanced endoscopic equipment and accessory instruments. These include Hopkins rod telescopes of varying lengths and diameters, lens systems that allow viewing over a wide range of angles, various illumination devices, digital video recorders and processors, sturdy endoscope holding arms, and endoscope irrigation sheaths. 59-62
The flexibility of endoscopy as a surgical imaging tool makes it particularly well suited to cranial nerve vascular decompression surgery, in which the confined dimensions of working space between the brainstem and the petrous apex severely limit viewing angles and surgical maneuverability. Magnan 10 used the endoscope in addition to the microscope in patients receiving MVD of the facial nerve for hemifacial spasm. He observed that the use of endoscopy added an additional 72% accuracy rate in identifying nerve-vessel conflicts. In a study of patients who underwent endoscope-assisted microvascular decompression of the trigeminal nerve we found that endoscopic surveys were required to identify 27% of the total number of nerve-vessel conflicts observed. Final endoscopic examinations additionally revealed persistent nerve compression in 24% of cases in this series, despite microscopic evidence to the contrary. 11 The use of endoscopy as the sole imaging modality in vascular decompression surgery is an outgrowth of these observations.
Reported results in series of MVD for trigeminal neuralgia describe variable rates of postoperative persistence and recurrence of facial pain. 63-68 These outcomes have been attributed to incomplete identification of nerve-vessel conflicts and to incomplete decompression of the nerve at the time of surgery. 67,69,70 The strength of the endoscope in this setting is its ability to impart to the surgeon more comprehensive views of the relevant anatomy than those that are obtainable under the microscope. As the surgical anatomy of the lower cranial nerves can be more intricate than that of the trigeminal nerve, 22 improved visualization has direct implications for better identification of nerve-vessel conflicts and more complete surgical therapy.
In the case we present, the rigid endoscope provided an effective means of accurately identifying all implicated nerve-vessel conflicts with minimal disturbance of the surrounding structures. Following the placement of insulating pads, a panoramic perspective of the surgical site confirmed the completion of the decompression. Our experience emphasizes the effectiveness of posterior fossa endoscopy in the treatment of cranial nerve vascular compression syndromes.
Although rare, glossopharyngeal neuralgia is a potentially debilitating clinical entity that calls for accurate diagnosis and definitive therapy. The advent of operative microscopy helped surgeons confirm an anatomical basis for this disease and develop a new approach to surgical management. Similarly, current progress in endoscopic medical technology has yielded tools that can further improve the outcome of surgical therapy.
We present the first reported case of vascular decompression of the glossopharyngeal nerve performed entirely endoscopically. All neurovascular conflicts were identified and decompression of the nerve was successfully performed with minimal disturbance to surrounding structures. The adequacy of the therapy was readily assessed at the completion of the operation.
The use of endoscopy in the surgical management of glossopharyngeal neuralgia is ideal due to the maneuverability of the endoscope within the posterior fossa. The versatility of endoscopes of varying angles of view makes endoscopy an invaluable tool in cranial nerve vascular decompression surgery.
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