Authors: Campbell, William W.
Title: Pocket Guide and Toolkit to DeJong’s Neurologic Examination, 1st Edition
Copyright ©2008 Lippincott Williams & Wilkins
> Table of Contents > Section D – The Cranial Nerves > Chapter 14 – The Glossopharyngeal and Vagus Nerves
Chapter 14
The Glossopharyngeal and Vagus Nerves
The glossopharyngeal (CN IX)
and vagus (CN X) nerves are intimately related and similar in function.
Both have motor and autonomic branches with nuclei of origin in the
medulla. Both conduct general somatic afferents as well as general
visceral afferents fibers to related or identical fiber tracts and
nuclei in the brainstem and both have a parasympathetic, or general
visceral efferent and a branchiomotor, or special visceral efferent
component. The two nerves leave the skull together, remain close in
their course through the neck, and supply some of the same structures.
They are often involved in the same disease processes, and involvement
of one may be difficult to differentiate from involvement of the other.
For these reasons the two nerves are discussed together.
and vagus (CN X) nerves are intimately related and similar in function.
Both have motor and autonomic branches with nuclei of origin in the
medulla. Both conduct general somatic afferents as well as general
visceral afferents fibers to related or identical fiber tracts and
nuclei in the brainstem and both have a parasympathetic, or general
visceral efferent and a branchiomotor, or special visceral efferent
component. The two nerves leave the skull together, remain close in
their course through the neck, and supply some of the same structures.
They are often involved in the same disease processes, and involvement
of one may be difficult to differentiate from involvement of the other.
For these reasons the two nerves are discussed together.
THE GLOSSOPHARYNGEAL NERVE
Cranial nerve IX is difficult to examine because most or
all of its functions are shared by other nerves and because many of the
structures it supplies are inaccessible. It is possible to examine pain
and touch sensation of the pharynx, tonsilar region, and soft palate,
and the gag reflex. The only muscle to receive its motor innervation
purely from CN IX is the stylopharyngeus. The only deficit that might
be detectable is a slight lowering of the palatal arch at rest on the
involved side. Other palatal motor functions are subserved either by CN
X, or the two nerves working together.
all of its functions are shared by other nerves and because many of the
structures it supplies are inaccessible. It is possible to examine pain
and touch sensation of the pharynx, tonsilar region, and soft palate,
and the gag reflex. The only muscle to receive its motor innervation
purely from CN IX is the stylopharyngeus. The only deficit that might
be detectable is a slight lowering of the palatal arch at rest on the
involved side. Other palatal motor functions are subserved either by CN
X, or the two nerves working together.
The gag reflex is elicited by touching the lateral
oropharynx in the region of the anterior faucial pillar, or by touching
one side of the soft palate or uvula, with a tongue blade, applicator
stick, or similar object. The afferent limb of the reflex is mediated
by CN IX and the efferent limb through CNs IX and X. The reflex center
is in the medulla. The motor response is constriction and elevation of
the oropharynx. This causes the midline raphe of the palate and the
uvula to elevate, and the pharyngeal constrictors to contract. The
activity on the two sides is compared. The gag reflex is protective; it
is designed to prevent noxious substances or foreign objects from going
beyond the oral cavity. There are three motor components: elevation of
the soft palate to seal off the nasopharynx, closure of the glottis to
protect the airway, and constriction of the pharynx to prevent entry of
the substance.
oropharynx in the region of the anterior faucial pillar, or by touching
one side of the soft palate or uvula, with a tongue blade, applicator
stick, or similar object. The afferent limb of the reflex is mediated
by CN IX and the efferent limb through CNs IX and X. The reflex center
is in the medulla. The motor response is constriction and elevation of
the oropharynx. This causes the midline raphe of the palate and the
uvula to elevate, and the pharyngeal constrictors to contract. The
activity on the two sides is compared. The gag reflex is protective; it
is designed to prevent noxious substances or foreign objects from going
beyond the oral cavity. There are three motor components: elevation of
the soft palate to seal off the nasopharynx, closure of the glottis to
protect the airway, and constriction of the pharynx to prevent entry of
the substance.
When unilateral pharyngeal weakness is present, the
midline raphe will deviate away from the weak side and toward the
normal side. This movement is usually dramatic. Minor movements of the
uvula and trivial deviations of the raphe are not of clinical
significance. There is variation in the intensity of the stimulus
required. The gag reflex may be bilaterally absent in some normal
individuals. Unilateral absence signifies a lower motor neuron lesion.
Like most bulbar muscles
midline raphe will deviate away from the weak side and toward the
normal side. This movement is usually dramatic. Minor movements of the
uvula and trivial deviations of the raphe are not of clinical
significance. There is variation in the intensity of the stimulus
required. The gag reflex may be bilaterally absent in some normal
individuals. Unilateral absence signifies a lower motor neuron lesion.
Like most bulbar muscles
P.141
the pharynx receives bilateral supranuclear innervation, and a unilateral cerebral lesion does not cause detectable weakness.
The gag reflex is often used to predict whether or not a
patient will be able to swallow or guard the airway. A decreased gag
reflex may portend inadequate guarding of the airway and increased
aspiration risk, but the status of the gag reflex is not a completely
reliable indicator. Patients with an apparently intact gag reflex may
still aspirate, and a patient with a depressed gag reflex may not. The
clinical assessment of swallowing, a major component of which is the
status of the gag reflex, underestimates the probability of aspiration
in patients who are at risk, and overestimates it in patients who are
not. The gag reflex may be hyperactive in some normal individuals, even
to the point of causing retching and vomiting. A hyperactive gag reflex
may occur with bilateral cerebral lesions, as in pseudobulbar palsy and
amyotrophic lateral sclerosis (ALS).
patient will be able to swallow or guard the airway. A decreased gag
reflex may portend inadequate guarding of the airway and increased
aspiration risk, but the status of the gag reflex is not a completely
reliable indicator. Patients with an apparently intact gag reflex may
still aspirate, and a patient with a depressed gag reflex may not. The
clinical assessment of swallowing, a major component of which is the
status of the gag reflex, underestimates the probability of aspiration
in patients who are at risk, and overestimates it in patients who are
not. The gag reflex may be hyperactive in some normal individuals, even
to the point of causing retching and vomiting. A hyperactive gag reflex
may occur with bilateral cerebral lesions, as in pseudobulbar palsy and
amyotrophic lateral sclerosis (ALS).
Disorders of Function
Isolated lesions of CN IX are extremely rare if they
ever occur. In all instances, the nerve is involved along with other
cranial nerves, especially CN X. In glossopharyngeal neuralgia or “tic
douloureux of the ninth nerve,” the patient experiences attacks of
severe lancinating pain originating in one side of the throat or
tonsilar region and radiating along the course of the eustachian tube
to the tympanic membrane, external auditory canal, behind the angle of
the jaw and adjacent portion of the ear. There may be trigger zones,
usually in the pharyngeal wall, fauces, tonsilar regions, or base of
the tongue. The pain may be brought on by talking, eating, swallowing,
or coughing. It can lead to syncope, convulsions, and rarely to cardiac
arrest because of stimulation of the carotid sinus reflex.
Glossopharyngeal neuralgia must be differentiated from other
craniofacial neuralgias, and from pain due to a structural lesion of
the nerve.
ever occur. In all instances, the nerve is involved along with other
cranial nerves, especially CN X. In glossopharyngeal neuralgia or “tic
douloureux of the ninth nerve,” the patient experiences attacks of
severe lancinating pain originating in one side of the throat or
tonsilar region and radiating along the course of the eustachian tube
to the tympanic membrane, external auditory canal, behind the angle of
the jaw and adjacent portion of the ear. There may be trigger zones,
usually in the pharyngeal wall, fauces, tonsilar regions, or base of
the tongue. The pain may be brought on by talking, eating, swallowing,
or coughing. It can lead to syncope, convulsions, and rarely to cardiac
arrest because of stimulation of the carotid sinus reflex.
Glossopharyngeal neuralgia must be differentiated from other
craniofacial neuralgias, and from pain due to a structural lesion of
the nerve.
THE VAGUS NERVE
Despite its size and importance, CN X is difficult to
evaluate at the bedside. Formal autonomic function assessment can
sometimes provide useful information.
evaluate at the bedside. Formal autonomic function assessment can
sometimes provide useful information.
Examination of the Motor Functions
The motor branches of CN X supply the soft palate,
pharynx, and larynx in the same distribution as for CN IX, and are
examined in the same manner. The gag reflex is discussed in the section
on CN IX.
pharynx, and larynx in the same distribution as for CN IX, and are
examined in the same manner. The gag reflex is discussed in the section
on CN IX.
The character of the voice and the ability to swallow
provide information about the branchiomotor functions of the vagus.
With acute unilateral lesions the speech may have a nasal quality and
dysphagia is often present; this is more marked for liquids than solids
with a tendency to nasal regurgitation. Examination of the soft palate
includes observation of the position of the palate and uvula at rest,
and during quiet breathing and phonation. The median raphe of the
palate rises in the midline on phonation. With a unilateral lesion of
the vagus there is weakness of the levator veli palatini and musculus
uvulae, which causes a droop of the palate and flattening of the
palatal arch. Preserved function of the tensor veli palatini
(innervated by CN V) may prevent marked drooping of the palate. On
phonation, the medial raphe deviates toward the normal side. The gag
reflex may be lost on the involved side because of interruption of the
motor rather than sensory path.
provide information about the branchiomotor functions of the vagus.
With acute unilateral lesions the speech may have a nasal quality and
dysphagia is often present; this is more marked for liquids than solids
with a tendency to nasal regurgitation. Examination of the soft palate
includes observation of the position of the palate and uvula at rest,
and during quiet breathing and phonation. The median raphe of the
palate rises in the midline on phonation. With a unilateral lesion of
the vagus there is weakness of the levator veli palatini and musculus
uvulae, which causes a droop of the palate and flattening of the
palatal arch. Preserved function of the tensor veli palatini
(innervated by CN V) may prevent marked drooping of the palate. On
phonation, the medial raphe deviates toward the normal side. The gag
reflex may be lost on the involved side because of interruption of the
motor rather than sensory path.
With bilateral vagus involvement the palate cannot
elevate on phonation; it may or may not droop depending on the function
of the tensor veli palatini. The gag reflex is absent bilaterally. The
tendency toward nasal speech and nasal regurgitation of liquids is
pronounced. The speech is similar to that of a patient with cleft
palate.
elevate on phonation; it may or may not droop depending on the function
of the tensor veli palatini. The gag reflex is absent bilaterally. The
tendency toward nasal speech and nasal regurgitation of liquids is
pronounced. The speech is similar to that of a patient with cleft
palate.
Weakness of the pharynx may also produce abnormalities
of speech and swallowing. With pharyngeal weakness, dysarthria is
usually minimal unless there is also weakness of the soft palate or
larynx. Spontaneous coughing and the cough reflex may be impaired.
Dysphagia may occur but without the tendency to greater difficulty with
liquids and to nasal regurgitation that occurs with
of speech and swallowing. With pharyngeal weakness, dysarthria is
usually minimal unless there is also weakness of the soft palate or
larynx. Spontaneous coughing and the cough reflex may be impaired.
Dysphagia may occur but without the tendency to greater difficulty with
liquids and to nasal regurgitation that occurs with
P.142
palatal
weakness. Dysphagia is marked only in acute unilateral or in bilateral
lesions. Examination of the pharynx includes observation of the
contraction of the pharyngeal muscles on phonation, notation of the
elevation of the larynx on swallowing, and testing the gag reflex.
Unilateral weakness of the superior pharyngeal constrictor may cause a
“curtain movement,” with motion of the pharyngeal wall toward the
nonparalyzed side on testing the gag reflex or at the beginning of
phonation. The normal elevation of the larynx may be absent on one side
in unilateral lesions, and on both sides in bilateral lesions.
Cranial nerve X innervates the vocal cords. Normal
movement of the vocal cords is necessary for three vital functions:
breathing, coughing, and talking. During inspiration and expiration,
the cords abduct to allow for free air flow; when speaking the cords
adduct and vibrate to accomplish phonation. The cords are also adducted
when coughing. Movements of the myriad small muscles that control the
larynx are complex and have different effects on laryngeal function. A
unilateral lesion of the vagus may cause cord weakness or paralysis.
Vocal cord dysfunction alters the character and quality of the voice,
and may produce abnormalities of articulation, difficulty with
respiration, and impairment of coughing.
movement of the vocal cords is necessary for three vital functions:
breathing, coughing, and talking. During inspiration and expiration,
the cords abduct to allow for free air flow; when speaking the cords
adduct and vibrate to accomplish phonation. The cords are also adducted
when coughing. Movements of the myriad small muscles that control the
larynx are complex and have different effects on laryngeal function. A
unilateral lesion of the vagus may cause cord weakness or paralysis.
Vocal cord dysfunction alters the character and quality of the voice,
and may produce abnormalities of articulation, difficulty with
respiration, and impairment of coughing.
Spasmodic dysphonia is a common focal dystonia that
involves the vocal cords and causes characteristic voice changes.
Spasmodic dysphonia most often causes abnormal adduction spasms of both
vocal cords, and the voice is strained and high-pitched. Abductor
dysphonia is due to spasmodic contraction of the posterior
cricoarytenoid, which causes a failure of normal adduction on
phonation; the voice is breathy and hoarse. This type of spasmodic
dysphonia is most likely to be confused with a lesion of CN X.
involves the vocal cords and causes characteristic voice changes.
Spasmodic dysphonia most often causes abnormal adduction spasms of both
vocal cords, and the voice is strained and high-pitched. Abductor
dysphonia is due to spasmodic contraction of the posterior
cricoarytenoid, which causes a failure of normal adduction on
phonation; the voice is breathy and hoarse. This type of spasmodic
dysphonia is most likely to be confused with a lesion of CN X.
The most common cause of vocal cord paralysis is a
lesion of one recurrent laryngeal nerve. The paralysis may evolve from
mild abduction impairment due to isolated involvement of the posterior
cricoarytenoid to complete paralysis with the cord in the cadaveric
position. With slight weakness of the vocal cords or pharynx,
hoarseness and dysphagia may be apparent only when the head is turned
to either side. Occasionally, even severe weakness of a vocal cord
causes little appreciable effect on the voice because of preserved
movement of the normal cord.
lesion of one recurrent laryngeal nerve. The paralysis may evolve from
mild abduction impairment due to isolated involvement of the posterior
cricoarytenoid to complete paralysis with the cord in the cadaveric
position. With slight weakness of the vocal cords or pharynx,
hoarseness and dysphagia may be apparent only when the head is turned
to either side. Occasionally, even severe weakness of a vocal cord
causes little appreciable effect on the voice because of preserved
movement of the normal cord.
Disorders of Function
Nuclear and infranuclear processes that may affect CN IX
and X include intramedullary and extramedullary neoplasms and other
mass lesions (e.g., glomus jugulare tumor), trauma (e.g., basilar skull
fracture or surgical dissection), motor neuron disease, syringobulbia,
retropharyngeal abscess, demyelinating disease, birth injury, and
brainstem ischemia. Extramedullary, intracranial involvement can occur
in processes involving the meninges, extramedullary tumors, aneurysms,
and skull fractures. Lesions at the jugular foramen or in the
retroparotid space usually involve some combination of IX, X, XI, XII,
and the cervical sympathetics. Isolated or multiple lower cranial nerve
palsies can be a manifestation of dissecting aneurysm of the cervical
internal carotid artery or occur as a complication of carotid
endarterectomy. Surgical section or other trauma to the carotid branch
of CN IX may cause transient or sustained hypertension. Involvement of
CN IX may be related to the cardiovascular dysautonomia that sometimes
accompanies Guillain-Barré syndrome.
and X include intramedullary and extramedullary neoplasms and other
mass lesions (e.g., glomus jugulare tumor), trauma (e.g., basilar skull
fracture or surgical dissection), motor neuron disease, syringobulbia,
retropharyngeal abscess, demyelinating disease, birth injury, and
brainstem ischemia. Extramedullary, intracranial involvement can occur
in processes involving the meninges, extramedullary tumors, aneurysms,
and skull fractures. Lesions at the jugular foramen or in the
retroparotid space usually involve some combination of IX, X, XI, XII,
and the cervical sympathetics. Isolated or multiple lower cranial nerve
palsies can be a manifestation of dissecting aneurysm of the cervical
internal carotid artery or occur as a complication of carotid
endarterectomy. Surgical section or other trauma to the carotid branch
of CN IX may cause transient or sustained hypertension. Involvement of
CN IX may be related to the cardiovascular dysautonomia that sometimes
accompanies Guillain-Barré syndrome.
A unilateral vagal lesion causes weakness of the soft
palate, pharynx, and larynx. Acute lesions may produce difficulty
swallowing both liquids and solids and hoarseness or a nasal quality to
the voice. The only definite sensory change is anesthesia of the larynx
due to involvement of the superior laryngeal nerve. It is seldom
possible to demonstrate loss of sensation behind the pinna and in the
external auditory canal. The gag reflex is absent on the involved side.
Autonomic reflexes (vomiting, coughing, sneezing) are not usually
affected. Tachycardia and loss of the oculocardiac reflex on the
involved side may occur, but usually there are no cardiac symptoms.
Gastrointestinal disturbances are inconspicuous. Bilateral complete
vagal paralysis is incompatible with life. It causes complete paralysis
of the palate, pharynx, and larynx, with marked dysphagia and
dysarthria;
palate, pharynx, and larynx. Acute lesions may produce difficulty
swallowing both liquids and solids and hoarseness or a nasal quality to
the voice. The only definite sensory change is anesthesia of the larynx
due to involvement of the superior laryngeal nerve. It is seldom
possible to demonstrate loss of sensation behind the pinna and in the
external auditory canal. The gag reflex is absent on the involved side.
Autonomic reflexes (vomiting, coughing, sneezing) are not usually
affected. Tachycardia and loss of the oculocardiac reflex on the
involved side may occur, but usually there are no cardiac symptoms.
Gastrointestinal disturbances are inconspicuous. Bilateral complete
vagal paralysis is incompatible with life. It causes complete paralysis
of the palate, pharynx, and larynx, with marked dysphagia and
dysarthria;
P.143
tachycardia;
slow, irregular, respiration; vomiting; and gastrointestinal atonia.
Lesions of individual vagal branches are rare except for involvement of
the recurrent laryngeal nerve.
The primary effect of increased vagal activity is
bradycardia. The term vasovagal refers to the effects of the vagus
nerve on the blood vessels. Vasovagal attacks (fainting, syncope) are
characterized by bradycardia, hypotension, peripheral vasoconstriction,
and faintness, sometimes with loss of consciousness. Vasovagal attacks
are typically induced by strong emotion or pain. The bradycardia and
projectile vomiting that occur with increased intracranial pressure may
be vagally mediated. Cheyne-Stokes, Biot, and Kussmaul breathing,
respiratory tics, forced yawning, and other abnormalities of breathing
may be vagally mediated as well.
bradycardia. The term vasovagal refers to the effects of the vagus
nerve on the blood vessels. Vasovagal attacks (fainting, syncope) are
characterized by bradycardia, hypotension, peripheral vasoconstriction,
and faintness, sometimes with loss of consciousness. Vasovagal attacks
are typically induced by strong emotion or pain. The bradycardia and
projectile vomiting that occur with increased intracranial pressure may
be vagally mediated. Cheyne-Stokes, Biot, and Kussmaul breathing,
respiratory tics, forced yawning, and other abnormalities of breathing
may be vagally mediated as well.
Rhythmic movements of the palate (palatal myoclonus,
palatal microtremor, or palatal nystagmus) can occur with a lesion of
the brainstem, usually vascular. The movements are mediated by CN X.
Bilateral supranuclear lesions, as from pseudobulbar palsy, cause
dysphagia and dysarthria. Extrapyramidal disorders may produce
difficulty with swallowing and talking. Laryngeal spasm with stridor
may occur in Parkinson disease and other extrapyramidal disorders.
Nuclear lesions of the nucleus ambiguus can occur with any intrinsic
brainstem disease. A slowly progressive nuclear lesion, such as in
bulbar ALS, syringomyelia, and some neoplasms, may cause fasciculations
in the palatal, pharyngeal, and laryngeal muscles.
palatal microtremor, or palatal nystagmus) can occur with a lesion of
the brainstem, usually vascular. The movements are mediated by CN X.
Bilateral supranuclear lesions, as from pseudobulbar palsy, cause
dysphagia and dysarthria. Extrapyramidal disorders may produce
difficulty with swallowing and talking. Laryngeal spasm with stridor
may occur in Parkinson disease and other extrapyramidal disorders.
Nuclear lesions of the nucleus ambiguus can occur with any intrinsic
brainstem disease. A slowly progressive nuclear lesion, such as in
bulbar ALS, syringomyelia, and some neoplasms, may cause fasciculations
in the palatal, pharyngeal, and laryngeal muscles.
Individual vagal branches may be involved by disease
processes in the neck, upper mediastinum, thorax, and abdomen. The
recurrent laryngeal nerve is the most frequently affected. This may be
damaged by tumors in the neck, aortic aneurysms, mediastinal and apical
tumors, stab wounds in the neck, or accidental trauma during a
thyroidectomy or other surgical procedure. The superior laryngeal and
pharyngeal branches may be involved in trauma, or in neoplasms or
abscesses in the neck.
processes in the neck, upper mediastinum, thorax, and abdomen. The
recurrent laryngeal nerve is the most frequently affected. This may be
damaged by tumors in the neck, aortic aneurysms, mediastinal and apical
tumors, stab wounds in the neck, or accidental trauma during a
thyroidectomy or other surgical procedure. The superior laryngeal and
pharyngeal branches may be involved in trauma, or in neoplasms or
abscesses in the neck.