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.

The vagus nerve (Xth cranial nerve) has motor, sensory, and parasympathetic components [1]. Its intracranial portion is formed from multiple (5–6) smaller rootlets which join lateral to the medulla and then exit the skull through the jugular foramen [2]. Understanding the nerve’s regional anatomy, its variations, and its relationship to the glossopharyngeal nerve are crucial for neurosurgeons operating on patients with glossopharyngeal neuralgia, hemi-laryngopharyngeal spasm [3], and Vagus Associated Neurogenic Cough due to Unilateral Vascular Encroachment of the Root (VANCOUVER syndrome) [4].

This case report demonstrates, for the first time in humans, the location of the parasympathetic fibres within the vagus nerve rootlets. The results shed light on the pathophysiology of bradycardia in rare cases of vago-glossopharyngeal neuralgia and may also guide surgical exploration for cases with one of the vagal rhizopathies.

A 47-year-old woman presented with a 1-year history of medically refractory left-sided glossopharyngeal neuralgia. She reported swallowing-induced, excruciating, sharp or electrical pain radiating from her posterior tongue down her left throat. The pain was eased but not eliminated by nortriptyline, and she refused other anti-neuralgia medications. More recently, she developed an intermittent tightness in her throat “like a noose strangling her” with coughing. These additional symptoms (hemi-laryngopharyngeal spasm) could be triggered by prolonged talking and often left her voice hoarse. Investigations revealed no pharyngeal cancer, Eagle’s syndrome, or acid reflux. Magnetic resonance imaging with fluid attenuated inversion recovery sequence showed no demyelinating lesions, and constructive interface in a steady state sequence showed her left posterior inferior cerebellar artery (PICA) distorting the lower cranial nerves on the affected left side (with a normal right 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.

Intraoperative Findings

The patient underwent a left retrosigmoid approach to expose the lower cranial nerves. At the beginning of the exposure, the patient had a loop of the PICA compressing the IXth and most rostral rootlets of the Xth cranial nerve (Fig. 1a). Our a priori goal for these operations is to decompress the IXth and Xth cranial nerves, but if that is not possible, we will sacrifice the IXth nerve and any purely sensory upper rootlets of the Xth nerve. In order to determine if a vagus rootlet has a motor component, we routinely monitor the motor response of the vagus nerve with endotracheal EMG electrodes (i.e., laryngeal contraction) [5]. Direct vagus rootlet stimulation can then determine if the rootlet has a motor function (and must therefore be preserved) or has no motor response and can potentially be sacrificed as a sensory rootlet. This is done in collaboration with our neurophysiologist using a bipolar nerve stimulator (Medtronic Xomed) stimulating at 0.2 mA and 2.75 Hz with pulse duration of 100 µs. The patient had five vagus nerve rootlets on her left side (Fig. 1b, c). These were arbitrarily named vagus rootlets A (most rostral), B, C, D, and E (most caudal). Rootlets C, D, and E had motor responses.

Fig. 1.

Operative microscope view of left lower cranial nerves. a A loop of the PICA (arrow) can be seen distorting the upper rootlets of the Xth nerve, with the IXth nerve more rostral and the XIth nerve more caudal. b The individual rootlets of the vagus nerve have been exposed, with the most rostral rootlet, XA, being stimulated. c The more caudal rootlets of the vagus are exposed, with the most caudal rootlet, XE, being stimulated. d The PICA (arrow) has been displaced anterocaudally.

Fig. 1.

Operative microscope view of left lower cranial nerves. a A loop of the PICA (arrow) can be seen distorting the upper rootlets of the Xth nerve, with the IXth nerve more rostral and the XIth nerve more caudal. b The individual rootlets of the vagus nerve have been exposed, with the most rostral rootlet, XA, being stimulated. c The more caudal rootlets of the vagus are exposed, with the most caudal rootlet, XE, being stimulated. d The PICA (arrow) has been displaced anterocaudally.

Close modal

When the stimulation was increased to 0.2 mA at 50 Hz, there was a profound bradycardia when vagus rootlet E was stimulated (Fig. 2) but no similar response from any of the other rootlets. At the conclusion of the operation, a loop of the PICA was mobilized anteroinferiorly, allowing complete decompression of the lower cranial nerves without the need to sacrifice any nerve rootlets (Fig. 1d). Post-operatively, the patient had temporary dysphagia (7 days), temporary hoarseness (1 month), and complete resolution of her glossopharyngeal neuralgia and hemi-layngopharyngeal spasm.

Fig. 2.

Video of the anaesthetic monitor during stimulation of the most caudal rootlet of the left vagus nerve, XE. The upper trace, ECG, demonstrates profound bradycardia when the stimulation (2.0 mA, 100 μs, 50 Hz) is turned “on.”

Fig. 2.

Video of the anaesthetic monitor during stimulation of the most caudal rootlet of the left vagus nerve, XE. The upper trace, ECG, demonstrates profound bradycardia when the stimulation (2.0 mA, 100 μs, 50 Hz) is turned “on.”

Close modal

It is well known that the vagus nerve can slow the heart [6]. Otto Loewi received the 1936 Nobel Prize for demonstrating the first neurotransmitter (acetylcholine), collected after electrical stimulation of the vagus, could slow another frog’s heart [7]. We now know that the cardiac vagal preganglionic neurons arise from two nuclei within the caudal medulla oblongata. The larger group (80%) lies within the nucleus ambiguous and has faster conduction (β fibres). The smaller group (20%) lies within the dorsal motor nucleus and has slower conduction (unmyelinated C fibres) [8, 9]. The rapid onset of bradycardia following vagus nerve stimulation is due to the former. The cardiac fibres within the two vagus nerves (left and right) travel caudally from the skull base through the carotid sheath and end in ganglia located in fat pads around the heart. The cardiac vagal post-ganglionic neurons then innervate the atria, sinoatrial, and atrioventricular nodes, as well as the ventricles [2]. Although the origin and termination of the vagal parasympathetic cardiac fibres are well described, their location within the vagus nerve rootlets has not been described in humans.

This is the first demonstration, to our knowledge, of the location of the cardiac parasympathetic fibres within the human vagus nerve rootlets. In our patient, only stimulation of the most caudal rootlet caused bradycardia. The only other study in the literature on this topic reported a similar conclusion in dogs. In this study, published by Professor Okinaka in 1952, dogs under sedation had immediate bradycardia when their caudal but not rostral vagus rootlets were electrically stimulated [10].

Approximately 10% of patients with glossopharyngeal neuralgia have neuralgia-induced syncope [11]. This rare condition is sometimes called “vago-glossopharyngeal neuralgia,” and there has been some debate as to its cause since it was first described by Riley in 1942 [12]. One hypothesis is that vascular compression of the IXth nerve causes the neuralgia, and a simultaneous compression of the Xth nerve triggers a direct parasympathetic outflow to the heart [13]. The other hypothesis is that the compression of the IXth nerve causes the neuralgia but also triggers impulses from what would be Hering’s nerve to travel up to the brainstem (to the nucleus tractus solitarius) which then senses a false hypertension and triggers a reflexive bradycardia down the vagus nerve [14, 15]. Our results support the second hypothesis for two reasons. First, the most caudal rootlet of the vagus nerve, with its parasympathetic fibres, is typically unaffected during the vascular compression of glossopharyngeal neuralgia. In fact, it is the farthest vagal rootlet from the IXth nerve, and any compression of the intervening rootlets would cause symptoms of hemi-laryngopharyngeal spasm. Second, we also had 1 patient (unreported) with vago-glossopharyngeal neuralgia, whose pain and syncope stopped following sectioning of just the IXth nerve. If there was any direct stimulation of vagal parasympathetic fibres in that patient, it would still be present after cutting only the IXth nerve.

This new understanding of the distribution of the pure sensory (most rostral), motor/sensory (more caudal), and parasympathetic (most caudal) fibres within the vagus nerve rootlets may lead to better diagnoses of the vagal rhizopathies. VANCOUVER syndrome, for example, is a neurogenic cough triggered by a vascular compression of the vagus nerve [4]. It is a purely sensory problem, much like trigeminal neuralgia [3]. The sensory fibres of the vagus carry a tickling sensation, not pain, from the tracheobronchial tree. The result is an irresistible cough [4]. One would postulate that the location of the compression would be the more rostral rootlets of the vagus nerve. This anatomical juxtaposition may also explain why cough can be present in up to 20% of patients with glossopharyngeal neuralgia [9]. Hemi-laryngopharyngeal spasm, on the other hand, has both a motor component – intermittent contractions of the larynx and/or pharynx much like hemifacial spasm affects the face – as well as coughing [3]. One would postulate that the location of the compression would be the more caudal rootlets of the vagus nerve. 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.

Ethical approval is not required for this study in accordance with local or national guidelines. Written informed consent was obtained from the patient for publication of the details of their medical case and any accompanying images.

The authors have no personal or institutional interest to declare.

No funding was obtained for the publication of the article. Open Access funding was provided by the Qatar National library.

Conception and design of work: Aisha Alkubaisi and Christopher R. Honey. Acquisition of data, drafting the article, and approval for the final version of the manuscript on behalf of all authors: Aisha Alkubaisi. Analysis and interpretation of data: Charles C.J. Dong. Reviews submitted version of the manuscript: Christopher R Honey.

All data generated or analysed during this study are included in this article. Further enquiries can be directed to the corresponding.

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