SUPERIOR COLLICULUS
CEREBRAL
AQUEDUCT
SUBSTANTIA
NIGRA
RED
NUCLEUS
BASIS
CEREBRAL PEDUNCULI
PEDUNCLE
1
INFERIOR COLLICULUS
SUBS.
NIGRA
CEREBRAL
PEDUNCLE
BASIS
PEDUNCULI
4th V.
PONS
Middle cerebellar
peduncle
Transverse pontine
fibers Corticospinal fibers
2
4TH VENTRICLE
MIDDLE
CEREBELLAR
PEDUNCLE
TRANSVERSE
PONTINE FIBERS
CORTICOSPINAL
FIBERS
Medulla Oblongata
The medulla oblongata is directly continuous with the cervical spinal cord. As such, its more
caudal regions are similar in appearance to the spinal cord. More cranially the medulla
oblongata has its own distinctive appearance.
3
4TH VENTRICLE
Inferior
cerebellar
peduncle
INFERIOR
OLIVARY
NUCLEUS
PYRAMID
4
NUCLEI
GRACILIS & CUNEATUS
DECUSSATION OF MEDIAL
LEMNISCUS
CAUDAL MEDULLA
LEVEL OF DECUSSATION OF MEDIAL LEMNISCUS
LATERAL CORTICOSPINALTRACT
DECUSSATION
OF PYRAMIDS
Six longitudinal columns of nuclei within the brain stem control the seven functional
categories of cranial nerves. Separate columns exist for five of these functions: GSA, GSE,
5
SSA, GVE, and SVE. Two of the functions, SVA and GVA, are represented in a single
column. Each of these columns is subdivided into nuclei subserving specific cranial nerves
or their functional subcomponents. Concomitantly, each cranial nerve is associated with one
or more brain stem nuclei depending on its functions: i.e., if a cranial nerve has an SVE
component it will be associated with a nucleus in the SVE column, if it has a GSA
component as well, it will also be associated with a nucleus in the GSA column. (Table I lists
nuclei, functions, and associated cranial nerves. These are also discussed in detail
below.)
6
Brainstem cranial nerve nuclei
Eventually, you will be required to recognize all of the nuclei and columns on brainstem cross
sections. One key to locating these columns is to remember their positions with respect to each
other. Remember that in the spinal cord the columns were located in the following dorsal to
ventral order: GSA, GVA, GVE, GSE.
GSA
GVA
GVE
GSE
The brainstem folds in such a way that the columns which are dorsal in the spinal cord (GSA,
GVA) become lateral in the brainstem giving the following relative positions of the columns.
7
Lower motor neuron nuclei cranial nerves.
Muscles of the head, like those of the body, are controlled by both upper and lower motor
neurons. Lower motor neurons lie within the brainstem and send their axons directly to
muscles. Upper motor neurons lie in higher neural processing centers including the neocortex
and influence the functions of the lower motor neurons.
In the spinal cord, lower motor neurons for the cranial nerves are found within the GSE column.
In the brainstem, they are found both within the GSE and the SVE columns.
Within the general somatic efferent (GSE) column are four nuclei.
1. The motor nucleus of the IIIrd nerve (oculomotor nucleus) contains lower motor
neurons for the medial, superior, and inferior rectus muscles, the inferior oblique muscle
and the levator levator palpebrae superioris.
2. The motor nucleus of the IVth nerve (troclear nucleus) contains lower motor neurons
for the superior oblique muscle of the eye.
3. The motor nucleus of the VIth nerve (abducens nucleus) contains lower motor
neurons for the lateral rectus muscle.
4. The hypoglossal nucleus contains lower motor neurons which innervate all extrinsic
and intrinsiic muscles of the tongue except for the palatoglossus.
8
The special visceral efferent (SVE) column contains lower motor neurons to all of the muscles
derived from the branchial arches.
1. The motor nucleus of the trigeminal (V) nerve innervates the muscles of mastication, the
tensor tympani, the tensor veli palatini, the anterior digastric muscle, and the mylohyoid.
2. The motor nucleus of the facial nerve innervates the muscles of facial expression, the
stapedius muscle, the stylohyoid and the posterior digastric muscles.
3. The nucleus ambiguus contains lower motor neuron nuclei for the branchial arch
components of nerves (IX, X, and XI). This nucleus innervates the majority of the
muscles of the palate, the pharynx, and the larynx.
The special somatic afferent column contains cochlear and vestibular nuclei which are
second order afferent nuclei for the VIIIth cranial nerve.
The general somatic afferent column contains the second order afferent nuclei for all
general somatic sensation.
1. The mesencephalic nucleus of the trigeminal nerve contains first order afferent
nuclei for proprioceptive sensation of the face. This nucleus is the only first order
afferent nucleus within the central nervous system.
2. The main sensory nucleus of the trigeminal nerve contains second order afferent
neurons for fine touch and proprioception in the face.
3. The spinal nucleus of the trigeminal nerve contains second order afferent neurons for
pain, temperature, and light touch of the face. Most of these fibers are carried in nerve
V, but some fibers from VII, IX, and X which are sensory to the outer and middle ear also
9
reach this nucleus. This nucleus is directly continuous with the substantia gelatinosa of
the spinal cord.
The general visceral efferent (GVE) column contains preganglionic parasympathetic motor
nuclei.
1. The nucleus of Edinger-Westphal supplies preganglionic parasympathetic fibers to the
IIIrd nerve. These fibers mediate pupillary constriction.
3. The inferior salivatory nucleus supplies preganglionic parasympathetic fibers via the
IXth cranial nerve to the otic ganglion and parotid gland.
4. The dorsal motor nucleus of the vagus supplies preganglionic parasympathetic fibers
via the Xth cranial nerve to thoracic and abdominal viscera.
At this point, you should study the atlas and make sure that you can identify each of these
nuclei on brain stem sections.
10
CRANIAL NERVES AND ASSOCIATED BRAIN STEM NUCLEI
SUMMARY TABLE
11
TABLE (Continued)
12
ipsilateral side. The corneal reflex will be absent on the ipsilateral side. Damage to the
nucleus ambiguus will result in paralysis of the vocal cord and an accompanying hoarse voice
and deviation of the uvula away from the side of the lesion. The cough and gag reflexes will be
lost. Damage to the oculomotor nucleus will result in lateral strabismus, diplopia, ptosis, and
poverty of eye movement. Damage to the abducens nucleus will cause medial strabismus.
Damage to the hypoglossal nucleus will produce paralysis of the tongue on the ipsilateral side.
The ipsilateral tongue will be shrunken and wrinkled and will deviate to the side of the lesion.
Upper motor neuron fibers for the head and neck lie in descending corticobulbar,
corticopontine and corticomesencephalic tracts. These tracts which are comparable in
function to the corticospinal tracts, all arise in the cortex or other higher brain centers and are
named according to the brain stem level at which they terminate. Those fibers providing upper
motor neuron control for mesencephalic nuclei terminate in the mesencephalon and are named
corticomesencephalic tracts; those providing upper motor neuron control for pontine nuclei are
termed corticopontine tracts; and those for the nuclei of the medulla are termed corticobulbar
tracts. These longitudinally running fiber tracts are part of one continuous system which
descends from the cortex via the internal capsule to the basis pedunculi of the mesencephalon.
When they reach the pons, the fibers are separated by the transverse pontine fibers into
bundles of corticopontine, corticobulbar and corticospinal tracts. The corticospinal fibers again
coalesce into one bundle, the pyramids, in the medulla oblongata. Some fibers then cross in
the decussation of the pyramids to become the lateral corticospinal tracts, while others remain
the uncrossed ventral corticospinal tracts.
13
Corticomesencephalic tract
Corticopontine tract
Corticobulbar tract
One of the most difficult problems in diagnosis is that of differentiating between upper motor neuron
and lower motor neuron lesions of the cranial nerves. As each muscle receives only ipsilateral (same
sided) innervation from the lower motor neurons in the cranial nerves, lesions of lower motor neurons
in both cranial and spinal nerves always cause paralysis on the same side as the lesion. Lower
motor neuron lesions in cranial nerve motor nuclei are also usually ipsilateral.
Upper motor neuron innervation is more complicated. Examine, for a moment, voluntary
movements in your own body. Note that it is extremely easy to move the right hand without
moving the left hand or to move one foot without the other. Now attempt to contract only one
side of your diaphragm or one side of your anal sphincter. You will probably find this extremely
difficult, if not impossible. In general, muscle groups that move independently of similar
muscles on the opposite side of the body have unilateral innervation from the contralateral
cortex only. Muscles that always work in unison with the similar muscles of the opposite body
side receive bilateral innervation from both the contralateral and the ipsilateral cortex. Those
muscles which receive innervation only from the contralateral cortex will suffer severe upper
14
motor neuron symptoms if these upper motor neurons are disrupted at any portion of the upper
motor neuron pathway. Those muscles which are innervated by both cortical hemispheres will
suffer only temporary weakness if the upper motor neuron pathway is disrupted on one side.
The lesion must be bilateral to cause permanent damage to these muscles.
Now examine the muscles of your head. Try to move one eye at a time. Very few people can do
this. The extrinsic eye muscles work in unison and are bilaterally innervated. Upper motor
neuron paralyses of the extrinsic eye muscles are rare. Most paralyses of the eye muscles are
lower motor neuron in type. However, damage to the frontal eye fields or the horizontal gaze
center in the pons will produce a paralysis of conjugate gaze, that is, a loss of the ability to
move both eyes simultaneously towards the opposite side of the lesion. The muscles of
mastication fall between the two extremes of bilateral, symmetrical movement and unilateral,
asymmetrical action. Thus, the muscles of mastication are bilaterally innervated by the upper
motor neurons. Unilateral upper motor neuron lesions will not cause permanent paralysis, only
temporary weakness. All unilateral permanent paralyses of the muscles of mastication are
lower motor neuron in type.
Now test the muscles innervated by nerve VII. Raise one eyebrow. Many people find this
difficult. The frontalis muscle is bilaterally innervated. Close one eye. People vary in their
ability to do this. The orbicularis oculi muscles are bilaterally innervated, but not to the same
extent as the frontalis. Retract one corner of your mouth. The muscles which retract the lips
are unilaterally innervated. Upper motor neuron lesions of nerve VII may be readily
differentiated from lower motor neuron lesions of that nerve by remembering the above facts.
Lower motor neuron paralysis will affect all muscles innervated by nerve VII on the ipsilateral
side of the face. The patient will be unable to raise his eyebrow, close his eye, or retract his lip
on that side. In upper motor neuron lesions, the ability to raise the eyebrow will be unaffected
on the side of the lesion. The eye may close, but weakly. Major effects will be below the orbit in
the mouth region. The lip will not retract on the affected side, the mouth will droop toward the
affected side and the nasolabial fold will be diminished on that side. Most upper motor neurons
of cranial nerve VII are contralateral.
Can you contract of your palate, of your pharynx, or of your vocal cords? The muscles
innervated by nerves IX and X are bilaterally innervated. Unilateral paralysis of the muscles
innervated by these nerves is nearly always lower motor neuron in type.
15
The tongue is intermediate between the extremes of unilateral and bilateral innervation. A
unilateral upper motor neuron lesion will cause a mild, transient paresis of tongue.
Lesions in certain parts of the brainstem can affect both upper motor neurons to the limbs and
lower motor neurons associated with specific cranial nerves. For example, a lesion in the
ventral medulla oblongata can affect both the pyramids and the emerging hypoglossal nerve. In
this case, the patient will have an ipsilateral lower motor neuron paralysis of the tongue and an
upper motor neuron paralysis of the contralateral arm and leg. Lesions that produce lower
motor symptoms of a cranial nerve of one side combined with contralateral upper neuron
lesions of the extremities are termed alternating hemiplegias. Lesions in the pons can
produce alternating hemiplegias affecting the trigeminal or facial nerves. Lesions in the
mesencephalon can produce an alternating hemiplegia of the oculomotor nerve resulting in
ipsilateral lateral strabismus, ptosis, inability to constrict the pupil, loss of corneal reflex and
contralateral hemiplegia. This constellation of symptoms is termed Webers syndrome.
16
primary auditory cortex. Vestibular impulses synapse with vestibular nuclei of the medulla.
Ascending pathways to the cortex are poorly understood. Definitive vestibular connections are
made with the brain stem motor nuclei of the extraocular muscles. These connections permit
the eyes to remain focused on a visual stimulus when the head and body are moving. The
vestibular system also sends fibers to the cerebellum for aid in control of body posture.
17
Second
order fibers
emerge from
the spinal
SPINAL
nucleus,
NUCLEUS OF
TRIGEMINAL
cross to the
opposite side
of the brainSKIN
ONION
PATTERN
stem and ascend to the thalamus in the trigeminal lemniscus (ventral trigeminothalamic tract). As
is the case for the spinal nerves, cranial nerves mediate both fast and slow pain. Slow pain pathways
terminate in the thalamus. Third order afferents for the fast pain system ascend from the thalamus to
the somatosensory cortex. Descending fibers from higher brain centers are apparently able to control
the intensity of pain perception in the facial region just as they do for the remainder of the body.
18
Lesions in the peripheral nerves, spinal nucleus of the trigeminal or spinal tract of the trigeminal
produce ipsilateral loss of pain, temperature, and light touch. Lesions in the trigeminal
lemniscus, somatosensory portion of the internal capsule or somatosensory cortex produce
contralateral loss. Lesions in the dorsolateral medulla can damage the spinal nucleus and
tract of the trigeminal and the lateral spinothalamic tract simultaneously. In this case, the patient
will have an alternating analgesia. There will be an ipsilateral loss of pain and temperature
sensation in the face and a contralateral loss on the opposite body.
ALTERNATING
ANALGESIA
Fine Touch
Fine touch of the face and oral cavity is mediated primarily by the trigeminal nerve. Cell bodies
of the first order afferent neurons lie in the trigeminal ganglion and synapse in the main
sensory nucleus of the trigeminal nerve. From here most second order afferent fibers cross to
the contralateral side and travel in the trigeminal lemniscus (ventral trigeminothalamic tract)
to the thalamus. Others travel to the thalamus ipsilaterally in the dorsal trigeminothalamic
tract. Third order afferents pass from the thalamus to the somatosensory cortex. Lesions in the
trigeminal nerve or main sensory nucleus produce ipsilateral loss of fine touch sensation.
Lesions in the trigeminal lemniscus, thalamus, internal capsule or cortex produce contralateral
loss.
19
Proprioception
A peculiarity of the proprioceptive system of the head and neck is that the first order afferent cell
bodies lie within the brain rather than within the peripheral ganglia. First order afferent
proprioceptive fibers, (presumably from all cranial nerves carrying motor impulses), travel in the
mesencephalic tract of the trigeminal nerve. Their cell bodies lie in the mesencephalic
nucleus. This is the only brain stem nucleus containing first order afferent cell bodies. From the
mesencephalic nucleus, fibers travel to the main sensory nucleus of the trigeminal. Second
order afferents of the proprioceptive system emerge from this nucleus. Some cross to the
opposite side and travel to the thalamus in the trigeminal lemniscus (ventral
trigeminothalamic tract). Others travel to the thalamus in the ipsilateral dorsal
trigeminothalamic tract. Pure proprioceptive defects of the head and neck region are rare.
Note that the trigeminal lemniscus carries contralateral second order fibers for fine touch,
proprioception, pain, temperature and light touch.
20
PROPRIOCEPTION
HEAD
Taste and General Visceral Sensation Cranial Nerves VII, IX, and X
Taste sensation (SVA) for the anterior two thirds of the tongue is carried by the seventh nerve,
for the posterior one third by the ninth nerve and for the epiglottis by the tenth. General visceral
sensation (GVA) for the posterior palate, posterior one third of the tongue and oral pharynx is
provided by cranial nerve nine; that for the laryngopharynx, larynx, thoracic and abdominal
viscera by nerve X. Cell bodies for both SVA and GVA functions lie in the peripheral ganglia of
21
the superficial nerves. Within the brain, all SVA and GVA fibers from nerves VII, IX, and X follow
the same pathways. All first order afferents for either taste or general visceral sensation
descend in the tractus solitarius to the nucleus solitarius. The pathways for second order
afferents are uncertain but are thought to emerge from the nucleus solitarius and then travel in
close association with the ipsilateral trigeminal lemniscus, possibly in the central tegmental
tract, to synapse in the thalamus. Third order afferents travel from the thalamus to the
neocortex, including the insula.
22
Level of Cranial Nerve IX
GVA nucleus solitarius GSA spinal nucleus of V
GVE inferior salivatory nucleus SVE nucleus ambiguus
Nerve IX
Inferior cerebellar peduncle
Nerve VIII
23
CRANIAL NERVE REFLEXES
Two types of reflexes found in the spinal cord are also found in the cranial nerves: stretch
reflexes and superficial reflexes. In addition, the cranial nerves mediate many visceral and
special reflexes.
Superficial Reflexes
The corneal reflex is the primary superficial reflex of the facial region. With the patient staring
straight ahead, cotton is applied to the lateral cornea in such a manner that the patient cannot
see it. A blink results in both eyes. The sensory limb of this reflex is carried by the ophthalmic
division of V and synapses in the spinal nucleus. From the spinal nucleus, fibers are sent to the
motor nucleus of the seventh nerve on both sides. Absence of blinking in both eyes
24
subsequent to corneal stimulation usually indicates damage to the ophthalmic division of V. If
blinking occurs in one eye, but not the other, the seventh nerve or nucleus is lesioned on the
side of the absent reflex.
Cough Reflex Irritation of the larynx, trachea or bronchi results in coughing. Both sensory
and motor limbs of the cough reflex are carried by the vagus nerve. Afferent impulses travel to
the nucleus solitarius. From there, special connections are made to the respiratory center of the
reticular formation of the medulla to bring about forced expiration. The nucleus ambiguus
provides motor innervation to laryngeal muscles; spinal motor nuclei provide it to the diaphragm.
A loss of the cough reflex usually reflects damage to the vagus nerve, but may result from
damage to the medulla.
Vomiting Reflex Both sensory and motor limbs of the vomiting reflex are mediated by cranial
nerve X. In addition to the muscles of the gastrointestinal tract and glottis, the diaphragm and
abdominal muscles also function during vomiting. Hence, spinal nerves also mediate this reflex.
Consequently, a vomiting center is located in the reticular formation of the medulla to coordinate
this response. Loss of the vomiting reflex may signify damage to the vagus nerve or brain stem.
Salivary Reflexes Salivation occurs as a reflex response to taste. Usually the facial nerve
and nucleus solitarius serve as the afferent limb of this reflex. The superior and inferior
salivatory nuclei and cranial nerves VII and IX are the motor limb. Loss of salivation can
indicate damage to any of these structures.
Pupillary Light Reflex When light is flashed in the eye, the pupils of both eyes constrict. The
afferent limb of this reflex passes from the optic nerve to the pretectal region of the midbrain (a
region just rostral to the superior colliculus). From here fibers are sent to the Edinger-Westphal
nucleus. This nucleus sends preganglionic parasympathetic fibers via nerve III to the ciliary
25
ganglion. From the ganglion, postganglionic fibers pass to the pupil. The response in the
directly stimulated eye is the direct reflex. The response in the opposite eye is the
consensual reflex. In lesions of the optic nerve the direct reflex is abolished in the blind eye
and the consensual in the opposite eye. Lesions of the oculomotor nerve abolish both direct
and consensual responses on the side of the lesion (paralyzed eye). Response in the opposite
eye remains normal. Absence of light reflexes can also indicate malfunction of the midbrain.
Pupillary Accommodation Reflex When the eyes focus on a near object, the pupils constrict.
This complex reflex requires participation of the occipital cortex. Sensory fibers ascend from the optic
nerve to the lateral geniculate body to the visual cortex and from there to visual association cortex.
Descending fibers proceed to the superior colliculus which sends impulses to the Edinger-Westphal
nucleus. The final limb of the reflex travels with the oculomotor nerve to the ciliary ganglion and from
there to the pupil. Lesions at any point in this pathway destroy the accommodation reflex.
26
Argyll-Robertson Pupil The pupil constricts in response to accommodation but not in response
to light. This results from a midbrain lesion and is usually symptomatic of neurosyphillis.
Trigeminal Neuralgia Consists of very severe lightning-like pains in one or more branches of
nerve V. These begin abruptly and stop suddenly. The pains are usually initiated by touching a
trigger zone, which may be located on the lip, face, gum or tongue. Trigeminal neuralagia
usually affects adults over age 40. In most cases the cause is unknown. Trigeminal neuralgia,
however, may be symptomatic of multiple sclerosis, neurosyphillis or other neurologic disease,
particularly if it is bilateral, occurs in a young patient, or in conjunction with other neurologic
signs. Histologic examination generally reveals preferential destruction of large type A fibers in
the trigeminal nerve or roots. Hence, the lesions somewhat resemble those of tabes dorsalis in
that large tactile fibers which may exert an inhibitory role in pain perception are degenerated.
Trigeminal neuralgia may be treated by drugs including diphenylhydantoin and
carbamazepine.
Bells Palsy is a lower motor neuron lesion of the VIIth nerve which produces symptoms of VIIth
nerve paralysis on one side of the face. It may result from chilling of the face, middle ear
infections, tumors, fractures, infectious diseases or, occasionally, a misplaced dental injection.
27
Usually the palsy clears spontaneously. Bells palsy must be differentiated from upper motor
lesions of cranial nerve VII which result from stroke, tumor, or other cranial diseases. In upper
motor neuron lesions, only the muscles of the lower half of the face are afflicted. Whereas in
lower motor lesions, the forehead and eye muscles are affected as well as those of the mouth. A
special type of Bells palsy results from the Ramsey-Hunt Syndrome. This is a Herpes zoster
infection of the geniculate ganglion (sensory ganglion of nerve VII). It is signified by a vesicular
eruption of the external ear, Bells palsy, and loss of taste in anterior 2/3 of the tongue.
Glossopharyngeal Neuralgia consists of severe lightning-like pains which start in the throat
and radiate to the auditory tube. Pain may be initiated by coughing, swallowing, or clearing the
throat.
Herpes Zoster of the Vth Nerve is usually limited to one division of the Vth nerve, most
commonly, the ophthalmic. The first symptom is pain followed by vesicular eruptions. The
greatest danger is that the cornea may be seriously damaged. Sometimes, Herpes zoster is
followed by trigeminal neuralgia.
Trismus refers to spasm of the masseter muscle resulting in pain accompanied by difficulty in
opening the jaw. In extreme cases it may lead to lock-jaw. Although bilateral trismus can
indicate tetanus if accompanied by other muscle spasms, trismus most often is a reflex spasm
resulting from pain or disease in the region of the teeth.
Amyotrophic lateral sclerosis is a systemic disease which often first manifests itself in the
head and neck region. The patient may experience difficulty in chewing or swallowing
secondary to muscular atrophy or paralysis.
Horners Syndrome Lesions of the sympathetic trunk, often subsequent to lung cancer, result
in Horners syndrome. The ipsilateral pupil is constricted, ptosis occurs; the skin is reddened
and exhibits loss of sweat.
CASE HISTORIES
1. A 46 year old man complained to his dentist that he was having trouble chewing.
Examination disclosed atrophy and complete paralysis of the left temporal and masseter
muscles. When he opened his jaw, it deviated to the left. He could not move it forcefully to the
right. He had no motor or sensory deficits involving other cranial or spinal nerves. The jaw jerk
reflex was absent.
28
a. What nerve is involved?
b. What side?
2. A 42 year old man visited a dentist complaining of difficulty in chewing and articulating his
dentures. The dentist readjusted the dentures and sent the patient on his way.
Unbeknownst to the dentist, the patient also suffered from back pain and weakness and
fasciculations of the muscles of the limbs. These symptoms had been diagnosed as nervous
tension. The patients problems persisted, and several months later, he again visited the
dentist. This time marked fasciculations and atrophy of the tongue were noted. The patients
bite was extremely weak and his mouth tended to hang open. The dentist referred the patient to
a neurologist who noted that the patient had many hyperactive reflexes, coupled with marked
degeneration and weakness of muscles throughout the body.
3. A 46 year old woman awakened one morning with her face drawn to one side. Examination
disclosed that on the right side she could not wrinkle her forehead, close her eye, smile, or
wrinkle the skin of her neck. The left side of her face moved normally. There was no problem
with hearing or taste.
4. A 76 year old patient complains of severe pain in his face. His symptoms have existed for
four months. His wife claims that he is irascible and impossible to live with. He has very brief,
shock-like episodes of unbearable pain which run from the side of his cheek down to the tip of
the jaw on the right side only. All motor and sensory functions of the cranial nerves are normal,
but the patient will not allow the examiner to test sensation over the right lower jaw because he
29
fears pain. He neither brushes his right mandibular teeth, nor attempts to chew on the right
side, because to do so causes unbearable pain.
b. What side?
c. What branch?
5. A patient awakes one morning to find the left half of his face paralyzed. Painful vesicles are
also found in the left external ear. Testing reveals loss of taste in the anterior two thirds of the
tongue on the left.
6. When the dentist inadvertently touches the patients posterior palate, the patient suffers
paroxysms of pain in the throat.
7. A patient awakes one morning to find painful vesicular eruptions over his forehead and
cornea.
8. A patient bothered by persistet cough and loss of weight exhibits the following symptoms. 1)
constriction of the left pupil 2) ptosis of the left eye 3) reddening and loss of sweat in the left
face.
9. A patient has the following symptoms: his left shoulder droops and his chin is deviated to the
left and cannot be turned toward the right. The left tongue is wrinkled and exhibits
fasciculations. When protruded his tongue deviates to the left.
b. On what side?
10. A patient exhibits shortness of breath and hoarseness. When asked to say Ah his uvula
deviates to the right.
b. On what side?
30
11. An elderly woman awakens one morning to find she cannot smile or purse her lips on the
left. Movements of the forehead and eye, however, are normal.
b. Is this malfunctioning likely to be upper motor neuron or lower motor neuron in type?
12. A patient slowly develops deafness in the left ear, vertigo, and nystagmus. What nerve is
diseased?
13. A patient develops blindness in the left eye accompanied by loss of both direct and
consensual light reflexes. What nerve is damaged?
14. A patient has a slowly developing bitemporal hemianopsia. Where is the lesion?
15. A patient has a ptosis, a lateral strabismus, a dilated pupil, and a general lack of movement
in the left eye. Both direct and consensual light reflexes are absent in the left eye. What nerve
is damaged?
16. A patient suffers from vertigo and from deafness in the left ear. What nerve is damaged?
1. Lesions of motor division of left trigeminal nerve. Lower motor neuron lesion.
2. Upper neuron lesion, lower motor neuron lesion. Amyotrophic lateral sclerosis.
6. Glossopharyngeal neuralgia.
31
10. Vagus on left.
32