Perspectives

Gerardo Guinto Balanzar, M.D.

President, Mexican Society of Neurological Surgery
Professor and Chairman, Department of Neurological Surgery
Hospital de Especialidades Centro Medico Nacional Siglo XXI
Member of the Centro Medico ABC
Nervus Intermedius
Gerardo Guinto
1
and Yoshiaki Guinto
2
T
he facial nerve is undoubtedly one of the cranial nerves
with a high interest for the practice of neurosurgery. Its
complex anatomy, the high frequency with which it is
affected by lesions (particularly tumors of the skull base) and
surgery, and the consequences that facial paralysis generates in
patients, have originated a day by day increased interest in the
integral study of this nerve.
The facial nerve has four functional components and can be fully
identied from the anatomic viewpoint. The most important
component, from which its name is derived, is the general
somatic efferent and it is responsible for carrying motor innerva-
tions to most of the muscles controlling facial expression. It is
originated in the so-called facial motor nucleus located on the
pons. From this nucleus, bers follow a dorsal direction toward
the nucleus of the sixth cranial nerve, which is surrounded to
form the internal genu, and exits the brainstem in the pontomed-
ullary groove between the abducens and vestibulocochlear
nerves. It then travels through the subarachnoid space to enter
the temporal bone through the internal auditory canal and tra-
verses the labyrinth. Once it crosses the labyrinth, it presents
another outward bend, thus forming the external genu where
the geniculate ganglion is located. The nerve then reaches the
tympanic region, nally emerging from the skull through the
stylomastoid foramen. Exiting the skull, its rst muscular branch
originates, directed toward the posterior belly of the digastric
muscle. The facial nerve then crosses the parotid gland where it
is divided into ve terminal branches through which it provides
innervations to most of the facial muscles.
The facial nerve has three additional functional components that,
even if considered part of this nerve, actually travel together in a
separate branch, the nervus intermedius (NI). The name of this
nerve was suggested by Wrisberg because it is located between
the motor component of the facial nerve and the superior vestibular
nerve. NI may be considered, both anatomically and functionally, as
an independent cranial nerve. However, due to its small size as well
as to its close relationship in most of its trajectory with the motor
component, it is considered as part of the seventh cranial nerve.
The functional components of the NI are as follows.
The general visceral efferent consists of preganglionic parasym-
pathetic bers originating from the superior salivary nucleus
traveling in contact with the motor component to the geniculate
ganglion where, without synapses, it is divided into two branches:
the greater petrosal nerve, which runs forward, crossing the base
of the pterygoid process of the sphenoid (through the vidian or
pterygoid canal) to reach the pterygopalatine fossa where it
synapses with the ganglion of the same name. Thus, the
postganglionic bers are responsible for the parasympathetic
innervation of the main and ancillary lacrimal glands. The rest of
the parasympathetic preganglionic bers of the NI traverse
through the geniculate ganglion and continue with the facial
motor component. After reaching the tympanic portion, they join
the chorda tympani nerve, which emerges from the skull through
the petrotympanic ssure to form the lingual nerve. This nerve
travels rostrally to the submandibular region where it synapses in
a ganglion of the same name and from which emerge postgan-
glionic bers that carry the parasympathetic innervation of the
sublingual and submandibular salivary glands.
Key words
Anterior inferior cerebellar artery
Cranial nerve
Facial nerve
Intermediate nerve
Microvascular decompression
Neuralgia
Nervus intermedius
Vestibulocochlear nerve
Wrisberg nerve
Abbreviations and Acronyms
GN: Geniculate neuralgia
NI: Nervus intermedius
From the
1
Department of Neurosurgery, Hospital de Especialidades Centro
Mdico Nacional Siglo XXI, Mexico City; and
2
Universidad Panamericana School
of Medicine, Mexico City, Mexico
To whom correspondence should be addressed: Gerardo Guinto, M.D.
[Email: gguinto@prodigy.net.mx]
Citation: World Neurosurg. (2013) 79, 5/6:653-654.
http://dx.doi.org/10.1016/j.wneu.2012.05.011
Commentary on:
The Nervus Intermedius: A Review of Its
Anatomy, Function, Pathology, and Role in
Neurosurgery
by Tubbs et al. pp. 763-767.
WORLD NEUROSURGERY 79 [5/6]: 653-654, MAY/JUNE 2013 www.WORLDNEUROSURGERY.org 653
The general somatic afferent originates from the sensory recep-
tors located in the concha of the auricle, a small area behind the
ear, the outer layer of the tympanic membrane and part of the
wall of the external auditory canal. The bers thus originated
travel through the NI in parallel, but in retrograde direction, with
the motor component of the facial nerve and synapse in the
geniculate ganglion, traveling through the cisternal portion to
penetrate the brainstem and terminate in the tract and the
trigeminal nucleus.
The special visceral afferent originates from the taste receptors
located in the anterior two thirds of the tongue, oor of the
mouth, and part of the palate from where the bers join the
lingual nerve and then the chorda tympani nerve through which
they run with the facial motor component and synapse in the
geniculate ganglion. The bers originating here are projected to
the brainstem and end in the tract and nucleus solitarius.
One of the entities that, in an isolated form, most often affect the
NI is neuralgia. This syndrome is also known as geniculate
neuralgia (GN) because it primarily affects pathways that synapse
in this ganglion, especially the general somatic afferent compo-
nent. GN is characterized by paroxysms of severe pain located
deep in the auditory canal and may be accompanied by symp-
toms related to involvement of other components of the NI such
as salivation, lacrimation, and alterations in taste perception.
Although the precise pathophysiology of this syndrome is not
known, it is assumed that the most common cause is similar to
other cranial nerve neuralgias: vascular compression of the NI in
its entry zone to the brainstem. In addition, a viral infection
(herpes) at the geniculate ganglion has also been described as a
cause. This entity is also known as Ramsay Hunt syndrome in
which, in addition to the already described neuralgia, the patient
has characteristic vesicles of herpes infection located in the
external auditory canal.
The differential diagnosis of GN includes painful syndromes
affecting other cranial nerves, mainly glossopharyngeal and vagal
neuralgia. However, there are also some forms of trigeminal
neuralgia where pain is referred to the auditory region that may
cause diagnostic confusion. Treatment is similar to other neural-
gias and includes antineuritic medications, such as gabapentin,
pregabalin, or carbamazepine in association with antidepressants
or anxiolytics. If there is no response, surgical management
should be attempted. At present, it is not possible to carry out
percutaneous geniculate ganglion ablation because it is com-
pletely surrounded by bone and intimately related to the internal
carotid artery and the cochlea, which would represent a high
functional risk. For this reason, when medical management has
failed, surgical exploration of the cerebellopontine angle is nec-
essary. Initially, a vascular compression in the entry zone of the
NI must be searched. If a vessel is found in this area, a standard
microvascular decompression should be carried out. It is also
important to explore entry zones of the IX, X, and even the V
cranial nerves due to their clinical similarity that may occur with
other painful syndromes. The problem arises when there is no
vessel as a possible cause of pain because a section of the NI
must be considered as the next step. Section of this nerve is
complex and results in some functional consequences that may
be uncomfortable for the patient. Surgical identication of the NI
is technically difcult because it is often rmly attached to the
rest of the VIIVIII nerves complex and separation represents a
high risk of facial paralysis or deafness. The best area to identify
the NI is in its cisternal portion as closely as possible to the
brainstem because in this area the nerve is frequently found
separated from the other components. Finally, it must be recog-
nized that sectioning of this nerve does not always relieve pain.
Most cases of surgical failure are due to diagnostic error because
of the possibility of confusing the different syndromes associated
with otalgia.
In this issue of WORLD NEUROSURGERY, Tubbs et al. present an
excellent study on the NI and GN. They begin by presenting a
review of the functional and microsurgical anatomy of the NI,
which demonstrates to the reader the sense of the complexity of
this nerve and its anatomic variability. This is followed by a
comprehensive clinical description of GN based on case reports
in the international literature. Here the reader will note that a
classic syndrome cannot be dened, making this condition easily
confused with other painful syndromes of this region. The study
also emphasizes the importance of reaching a correct differential
diagnosis because this will be the core of the management
response, especially surgical. Tubbs et al. analyze various surgical
treatment options, which draw attention to the diverse results
reported. Although some patients clearly showed postoperative
improvement, other patients demonstrated no change, pointing
to establishing an accurate diagnosis. It also draws attention to
such diverse functional outcomes that have been reported after
sectioning the NI, as there are some cases where, even if the
nerve was totally cut, the patients did not completely lose
functions such as lacrimation, salivation, and/or the gustatory
sensation of the anterior two thirds of the tongue. There are only
three explanations for this situation: 1) the nerve was not
properly identied during surgery, 2) the nerve was identied but
not completely sectioned, or 3) patients had a combined inner-
vation with other cranial nerves (IX or X). At the conclusion of the
article, Tubbs et al. present a surgical case where clearly there is
vascular compression on the NI entry zone, probably caused by
the anterior inferior cerebellar artery. Excellent intraoperative
images are shown where one can see not only the vascular
compression but also the NI clearly separated from the rest of
the VIIVIII complex.
Articles such as this help us to further understand the anatomy of
the NI along with clinical characteristics, treatment options, and
surgical outcomes of GN. Currently there are few reports,
increasing the importance of this study. At the end of the article,
the conclusion is that we need further (preferably prospective)
studies to more accurately dene the true extent that both
microvascular decompression as well as NI sectioning, to offer
patients surgical alternatives more objectively and explain the
possible consequences of the procedures. The problem, how-
ever, is that these are very rare cases. Reports such as the one
presented are certainly very encouraging in attempting to seek a
correlation among clinical ndings, functional microanatomy, and
therapeutic options in syndromes affecting the cranial nerves.
Citation: World Neurosurg. (2013) 79, 5/6:653-654.
http://dx.doi.org/10.1016/j.wneu.2012.05.011
Journal homepage: www.WORLDNEUROSURGERY.org
Available online: www.sciencedirect.com
1878-8750/$ - see front matter 2013 Elsevier Inc. All rights reserved.
PERSPECTIVES
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