The Location of the Parasympathetic Fibres within the Vagus Nerve Rootlets: A Case Report and a Review of the Literature.

The vagus nerve has motor, sensory, and parasympathetic components. Understanding the nerve's internal anatomy, its variations, and relationship to the glossopharyngeal nerve are crucial for neurosurgeons decompressing the lower cranial nerves. We present a case report demonstrating the location of the parasympathetic fibres within the vagus nerve rootlets. A 47-year-old woman presented with a 1-year history of medically refractory left-sided glossopharyngeal neuralgia and a more recent history of left-sided hemi-laryngopharyngeal spasm. magnetic resonance imaging showed her left posterior inferior cerebellar artery distorting the lower cranial nerves on the affected left side. The patient consented to microvascular decompression of the lower cranial nerves with possible sectioning of the glossopharyngeal and upper sensory rootlets of the vagus nerve. During surgery, electrical stimulation of the most caudal rootlet of the vagus nerve triggered profound bradycardia. None of the more rostral rootlets had a similar parasympathetic response. This case is the first demonstration, to our knowledge, of the location of the cardiac parasympathetic fibres within the human vagus nerve rootlets. This new understanding of the vagus nerve rootlets' distribution of pure sensory (most rostral), motor/sensory (more caudal), and parasympathetic (most caudal) fibres may lead to a better understanding and diagnosis of the vagal rhizopathies. Approximately 20% of patients with glossopharyngeal neuralgia also have paroxysmal cough. This could be due to the anatomical juxtaposition of the IXth cranial nerve with the rostral vagal rootlets with pure sensory fibres (which mediate a tickling sensation in the lungs). A subgroup of patients with glossopharyngeal neuralgia have neuralgia-induced syncope. The cause of this rare condition, "vago-glossopharyngeal neuralgia," has been debated since it was first described by Riley in 1942. Our case supports the theory that this neuralgia-induced bradycardia is reflexively mediated through the brainstem with afferent impulses in the IXth and efferent impulses in the Xth cranial nerve. The rarer co-occurrence of glossopharyngeal neuralgia with hemi-laryngopharyngeal spasm (as seen in this case) may be explained by the proximity of the IXth nerve with the more caudal vagus rootlets which have motor (and probably sensory) supply to the throat. Finally, if there is a vagal rhizopathy related to compression of its parasympathetic fibres, one would expect it to be at the most caudal rootlet of the vagus nerve.

Defining the Anatomy of the Vagus Nerve and Its Clinical Relevance for the Neurosurgical Treatment of Glossopharyngeal Neuralgia.

The neurosurgical treatment of glossopharyngeal neuralgia includes microvascular decompression or rhizotomy of the nerve. When considering open section of the glossopharyngeal nerve, numerous authors have recommended additional sectioning of the 'upper rootlets' of the vagus nerve because these fibers can occasionally carry the pain fibers causing the patient's symptoms. Sacrifice of vagus nerve rootlets, however, carries the potential risk of dysphagia and dysphonia. In this study, the anatomy and physiology of the vagus nerve rootlets are characterized to provide guidance for surgical decision-making. Twelve patients who underwent posterior fossa craniotomy with intraoperative electrophysiological monitoring of the vagus nerve rootlets were included in this study. In the 7 patients with glossopharyngeal neuralgia, the clinical outcomes and complications were further analyzed. In half of the patients, electrophysiological data demonstrated pure sensory function in the rostral rootlet(s) of the vagus nerve and motor responses in its caudal rootlets. This orientation of the vagus nerve, with some pure sensory function in its most rostral rootlet(s), was defined as Type A. In the other half of patients, all vagus nerve rootlets (including the most rostral) had motor responses. This was defined as Type B. The surgical strategy was guided by whether the patient had a Type A or Type B vagus nerve. For those with Type B, no vagus nerve rootlets were sacrificed. None of the patients with glossopharyngeal neuralgia developed any permanent neurological deficits. We recommend intraoperative electrophysiological testing of the vagus nerve rootlets. If the testing reveals motor innervation in the rostral vagal rootlet (Type B), that rootlet may be decompressed but should not be sectioned to avoid a motor complication. Patients with pure sensory innervation of the rostral rootlet(s) (Type A) can have decompression or section of those rootlets without complication.

Use of endotracheal tube electrodes in treating glossopharyngeal neuralgia: technical note.

BACKGROUND/AIMS: This paper describes the use of endotracheal tube surface electrodes to help delineate the sensory and motor vagal rootlets which may be sacrificed during the surgical treatment of glossopharyngeal neuralgia. METHODS: Three patients with glossopharyngeal neuralgia were studied. All patients had their procedure under general anesthesia and a nerve integrity monitor electromyography endotracheal tube (Medtronic Xomed, Jacksonville, Fla., USA) was inserted under direct vision by the anesthesiologist. A bipolar stimulating electrode identified which, if any, of the upper rootlets of the vagus nerve caused a motor contraction near the vocal cords (i.e. motor branch) and which did not cause contractions (i.e. sensory branch). Sectioning of the glossopharyngeal and any purely sensory rootlets of the vagus nerve was subsequently performed. RESULTS: All patients had immediate and long-lasting relief of their glossopharyngeal neuralgia. In all 3 patients, use of the bipolar stimulating electrode on the lower vagal rootlets induced a recordable muscle action potential in the region of the vocal cords with low current (<0.2 mA). There were no complications consequent to placement of the nerve integrity monitor endotracheal tube. CONCLUSION: Due to the ease of use and reduced trauma, compared to needle electrodes, we would advocate endotracheal tube surface electrode monitoring in all patients undergoing surgical treatment of their glossopharyngeal neuralgia or any intracranial procedure where the integrity of the vagal nerve is in jeopardy.

Localized transcranial electrical motor evoked potentials for monitoring cranial nerves in cranial base surgery.

OBJECTIVE: To describe a novel monitoring technique that allows "functional" assessment of cranial nerve continuity during cranial base surgery. METHODS: Facial motor evoked potentials (MEP) in 71 consecutive patients were obtained by localized transcranial electrical stimulation in all patients requiring facial nerve monitoring during the period from November 2002 to August 2004. With transcranial electrical stimulation localized to the contralateral cortex, facial nerve MEPs are obtained through stimulation of more proximal intracranial structures. RESULTS: Logistic regression revealed that the final-to-baseline facial MEP ratio predicted satisfactory (House-Brackmann Grade 1 and 2 function) immediate postoperative facial function (0.005 > P > 0.0005). Contingency table analysis showed high correlation (chi2, P < or = 2 x 10(8)) and acceptable test characteristics using a 50% final-to-baseline MEP ratio. CONCLUSION: Facial nerve MEPs recorded intraoperatively during cranial base surgery using the proposed technique predicts immediate postoperative facial nerve outcome. This technique can also be used to monitor other motor cranial nerves in cranial base surgery.

Intraoperative facial motor evoked potential monitoring with transcranial electrical stimulation during skull base surgery.

OBJECTIVE: To address the limitations of standard electromyography (EMG) facial nerve monitoring techniques by exploring the novel application of multi-pulse transcranial electrical stimulation (mpTES) to myogenic facial motor evoked potential (MEP) monitoring. METHODS: In 76 patients undergoing skull base surgery, mpTES was delivered through electrodes 1cm anterior to C1 and C2 (M1-M2), C3 and C4 (M3-M4) or C3 or C4 and Cz (M3/M4-Mz), with the anode contralateral to the operative side. Facial MEPs were monitored from the orbicularis oris muscle on the operative side. Distal facial nerve excitation was excluded by the absence of single pulse responses and by onset latency consistent with a central origin. RESULTS: M3/M4-Mz mpTES (n=50) reliably produced facial MEPs while M1-M2 (n=18) or M3-M4 (n=8) stimulation produced 6 technical failures. Facial MEPs could be successfully monitored in 21 of 22 patients whose proximal facial nerves were inaccessible to direct stimulation. Using 50, 35 and 0% of baseline amplitude criteria, significant facial deficits were predicted with a sensitivity/specificity of 1.00/0.88, 0.91/0.97 and 0.64/1.00, respectively. CONCLUSIONS: Facial MEPs can provide an ongoing surgeon-independent assessment of facial nerve function and predict facial nerve outcome with sufficiently useful accuracy. SIGNIFICANCE: This method substantially improves facial nerve monitoring during skull base surgery.

Intraoperative spinal cord monitoring during descending thoracic and thoracoabdominal aneurysm surgery.

BACKGROUND: Postoperative paraplegia is one of the most dreaded complications after descending thoracic and thoracoabdominal aneurysm surgery. In this study, intraoperative monitoring was applied during resection of descending thoracic and thoracoabdominal aneurysms to detect spinal cord ischemia and help prevent paraplegia. METHODS: Fifty-six patients (descending thoracic, 25; thoracoabdominal, 31) were monitored intraoperatively with both motor- (MEP) and somatosensory- (SSEP) evoked potentials. MEPs were elicited with transcranial electrical stimulation and recorded from the spinal epidural space (D wave) or peripheral muscles (myogenic MEP). SSEPs were obtained with median and tibial nerve stimulation. RESULTS: A total of 16 patients (28.6%) showed MEP evidence of spinal cord ischemia, only 4 of whom had delayed congruent SSEP changes. In 13 patients (23.2%), ischemic changes in MEPs were reversed by reimplanting segmental arteries or increasing blood flow or blood pressure. None of these 13 patients suffered acute paraplegia regardless of the status of SSEP at the end of the procedure, but 1 of them developed delayed postoperative paraplegia after multisystem failure. Three patients (5.4%) who had persistent loss of MEPs despite of recovery of SSEPs awoke paraplegic. CONCLUSIONS: The results demonstrate that compared with SSEP, MEP, especially myogenic MEP, is more sensitive and specific in detection of spinal cord ischemia, and that intraoperative monitoring can indeed help prevent paraplegia.