martes, 22 de noviembre de 2016

Physiology of Oculomotor Nerve, Trochlear Nerve and Abducens Nerve

Physiology of Oculomotor Nerve, Trochlear Nerve and Abducens Nerve




Physiology of
oculomotor, trochlear and abducens nerves.
Physiology of
trigeminal nerve.Physiology of facial nerve.
Physiology of
Vestibulocochlear
nerve.
Physiology of Glossopharyngeal
 Nerve
. Physiology of Vagus nerve. Physiology of Accessory
Nerve.
Physiology of Hypoglossal Nerve.

There
are 12 pairs of cranial nerves.
·       
Olfactory I
·       
Optic II
·       
Oculomotor III
·       
Trochlear IV
·       
Trigeminal V
·       
Abducens VI
·       
Facial VII
·       
Auditory (vestibulocochlear) VIII
·       
Glossopharyngeal IX
·       
Vagus X
·       
Spinal Accessory XI
·       
Hypoglossal XII
The cranial nerves:
The
cranial nerves (with the exception of I and II) originate in the brainstem,
which includes the midbrain, the pons, and the medulla. The 12 cranial nerves
can be divided into sensory, motor, or mixed nerves. Overall, sensory nerve
nuclei tend to be located in the lateral brainstem, while motor nuclei tend to
be located medially. Nerves with mixed sensory and motor fibers must have more
than one nucleus of origin - at least one sensory (afferent) and one motor
(efferent). Sometimes more than one nerve will originate from a single nucleus:
for example, the sense of taste is spread across at least two nerves but merges
into a single nucleus. Finally, keep in mind that any sensory nucleus is receiving
input from the periphery, but the sensory receptor cell bodies are never in the
nucleus itself. They will always be located just outside the CNS in a ganglion.

Here is a dorsal view of the
brainstem, looking down through it as though it were transparent, so you can
see the relative positions of the cranial nerve nuclei. Motor or efferent
nuclei are blue, sensory or afferent nuclei are yellow. Note that this is a
schematic to give you the big picture - some of these nuclei would technically
overlap if you could really see through the brainstem.      
Abbreviations:
EW: Edinger-Westphal nuc.
III: oculomotor nuc.
IV: trochlear nuc.
meV:
mesencephalic nuc. of V
V: trigeminal
moV:
motor nuc. of V
senV:
main sensory nuc. of V
spV: spinal nuc. of V
VI: abducens nuc.
VII: facial nuc.
VIIIc: cochlear nuc.
VIIIv: vestibular nuc.
IX: glossopharyngeal
X: vagus
amb:
nuc. ambiguus
dnv:
dorsal nuc. of the vagus
sol:
solitary nucleus
XII: hypoglossal nuc.

Not shown:
-cranial nerve I
-cranial nerve II
-cranial nerve XI
-salivatory nuclei


The next sections describe the
functions and features of the nerves and nuclei

B. Nerves that innervate the eye muscles:
Nerves
III, IV, and VI are pure motor nerves that innervate the extrinsic eye muscles.
All are located very close to the midline.
III - the oculomotor nerve -
This nerve innervates the bulk
of the eye muscles: superior and inferior recti, medial rectus, and inferior
oblique. If this nerve is damaged, the action of the remaining two muscles
(superior oblique and lateral rectus) pulls the eye "down and out".
The nucleus is located medially in the midbrain, and the nerve fibers exit
ventrally, just inside the peduncles.
Edinger Westphal nucleus –
This nucleus is the source of
the parasympathetics to the eye, which constrict the pupil and accommodate the
lens. It is located just inside the oculomotor nuclei, like nested
"V"s. The fibers travel in the IIIrd nerve, so damage to that nerve
will also produce a dilated pupil.
Note: the eye drops that you
are given at the ophthomologist's office are an acetylcholine antagonist
(blocker) so they inhibit the actions of the parasympathetic system. As a
result your eyes are dilated, so the physician can look inside clearly. As a
side effect, you cannot accommodate your lens (focus on close objects) which is
why you can't read while you are sitting in the waiting room.
IV - the trochlear nerve -
"Trochlea"
is from the Latin word for pulley. If you remember from gross anatomy, the
superior oblique muscle loops through a pulley-like sling on its way to the
back of the eye. Hence the IVth nerve innervates the superior oblique. This
nucleus is also located near the midline. It is very small, and hard to find in
sections. It looks like a crescent-notch taken out of a dark fiber bundle in
the rostral pons. The fiber bundle is the MLF, which carries eye movement
signals between brainstem nuclei.
The
trochlear nerve is unique for two reasons: 1) it exits the brainstem dorsally,
and 2) it crosses on the way out. The fibers cross over each other just like a
half-tied shoelace in the roof of the fourth ventricle.
VI - the abducens nerve -
"Abducens"
comes from "abduct". To abduct a part is generally to move it
laterally, and the muscle that abducts the eye is the lateral rectus. It is the
only muscle innervated by VI. The nucleus is again near the midline, but this
one is in the pons. The key landmark for finding the abducens is actually the
facial nerve. The facial nerve fibers come up to the floor of the fourth
ventricle, loop around in a hairpin turn, and dive back into the pons. The bump
that they loop over is the abducens nucleus.
The
abducens fibers exit the pons medially and ventrally. Often you can see the
facial fibers exiting in the same section; the facial fibers will always be lateral.

C. The trigeminal nerve:
All
sensation from the face and mouth is covered by the mixed trigeminal nerve. A
branch of the trigeminal is injected by your dentist when you have a cavity
filled. The trigeminal also carries motor fibers to the muscles of mastication
(chewing). The most prominent of these is the masseter muscle, the hard knot in
your cheek when you clench your teeth. The functions of the different
trigeminal nuclei are extensively covered in the "Somatosensory pathways
from the face" section, so they will not be repeated here.
The mesencephalic nucleus is a thin ribbon of cells
that runs along the fourth ventricle and cerebral aqueduct, just outside the
periaqueductal grey.  
The motor nucleus is
located in the mid-pons, and is often hard to see. The best landmark is the
presence of trigeminal nerve fibers streaking through the adjacent middle
cerebellar peduncles (MCP). The fibers appear as a hand gripping a pale egg.
The pale egg is the motor nucleus.    
Once you have found the motor
nucleus, look immediately lateral to find the main sensory nucleus. It is a faint
collection of cells tucked just inside the middle cerebellar peduncle.
The spinal nucleus of V is easiest to see in the caudal
medulla, although it extends throughout the entire medulla. Here it bears some
resemblance to the dorsal horn of the spinal cord, both functionally and
anatomically. Just like the dorsal horn, it receives pain afferents. The
adjacent spinal tract of V is analogous to Lissauer's tract, as it is carrying
those same pain afferents before they synapse.     

D. The facial nerve:
All
of the muscles of facial expression are innervated by the facial nerve. It is
considered a mixed cranial nerve, however, since it also carries the sensation
of taste. The facial nerve also carries some parasympathetic fibers to the
salivary glands.
Recall
that the facial nerve fibers loop over the abducens nucleus in the pons. The
facial nucleus itself is hard to see in a myelin stain. The fibers of the
facial nerve do not acquire their myelin (and become dark) until they arrive at
the hairpin turn, so you cannot even trace them back to the nucleus. The
approximate location is shown below, however.

E. Taste:
Taste fibers, from the taste
buds, are predominantly (from the front 2/3 of the tongue, anyway) carried by
the facial nerve. (Keep in mind that touch and pain
sensation from the tongue is V, and motor to the tongue is XII.) Taste from the
back of the tongue and palate is carried by the glossopharyngeal nerve. Regardless of their origin, the taste
fibers enter the solitary tract of the medulla, and synapse in the surrounding solitary nucleus.

Taste and touch sensation at the
back of the throat are carried by the glossopharyngeal nerve, and also synapse
in the solitary nucleus. These sensations can trigger the gag reflex.

F. Hearing and balance:
The
VIIIth nerve carries auditory information from the cochlea and vestibular
information from the semicircular canals, utricle, and saccule. It is really
two nerves running together, the auditory (cochlear) nerve and the vestibular
nerve. The VIIIth nerve is very important clinically because a common type of
tumor, the acoustic neuroma, can arise from the nerve as it exits the
brainstem.
The
cochlear nuclei are like small hands draped over the inferior cerebellar
peduncles (ICP), and are fairly small in primates. The vestibular nuclei have
several subdivisions, however, and extend throughout a large fraction of the
pons.

G. The glossopharyngeal nerve:
The
IXth nerve has no real nucleus to itself. Instead it shares nuclei with VII and
X. The sensory information in IX goes to the solitary nucleus, a nucleus it
shares with VII and X. All motor information, essentially the innervation of
the stylopharyngeus muscle, comes from the nucleus ambiguus, also shared with
X. Finally, like VII, there are some parasympathetic fibers in IX that
innervate the salivary glands.

H. Salivation:
The salivation center is a
pair of nuclei located just rostral to the dorsal nucleus of the vagus, the
superior and inferior salivatory nuclei. They supply the parasympathetic
innervation of the various salivary glands, and send their axons through the facial
and glossopharyngeal nerves.
I. The various and sundry
nuclei of the vagus:
When you think vagus, you tend
to think parasympathetic - this is a flashback to your gross anatomy days.
However, the vagus has dozens of functions. They can be grouped into about
three categories, and each category is associated with a medullary nucleus. The
first is the nucleus ambiguus, which is a motor nucleus. Cells in the nucleus
ambiguus are very difficult to see (hence the name), and innervate striated
muscle throughout the neck and thorax. This includes some muscles of the palate
and pharynx, muscles of the larynx, and the parasympathetic innervation of the
heart. Problems with the vagus can show up as hoarseness, or a deviated uvula:
X elevates the palate when you open up and say "AH". An asymmetrical
uvula would indicate that X is not working on one side.
The second is the dorsal
nucleus of the vagus, which is the secretomotor parasympathetic nucleus. Secretomotor
primarily means that it stimulates glands - including mucus glands of the
pharynx, lungs, and gut, as well as gastric glands in the stomach.
(Incidentally, it is fair-inks, not far-nicks.)
The third is the sensory
nucleus of the vagus, the solitary nucleus. As we have seen, it receives taste
information, sensation from the back of the throat, and also visceral
sensation. Visceral sensation includes blood pressure receptors, blood-oxygen
receptors, sensation in the larynx and trachea, and stretch receptors in the
gut.

J. The spinal accessory nerve:

The
XIth nerve actually originates in the cervical spinal cord. Were it not for the
fact that it sneaks up along side the medulla and exits the skull with IX and
X, it might not even be a cranial nerve. It is a motor nerve that innervates
two muscles: the trapezius and the sternocleidomastoid.

K. The hypoglossal nerve:
The
XIIth nerve innervates the muscles of the tongue. Like most pure motor nuclei,
the XII nucleus is located along the midline, and can be found throughout most
of medulla. The tongue muscles actually push the tongue forward, so a problem
with the hypoglossal nerve can be detected by asking the patient to stick out
his tongue. The tongue will deviate towards the weak side, towards the side of
the lesion.

L. Information overload!!
If your head is spinning, it
could be your vestibular nerve, but it could also be the sheer volume of
information. This is a fairly superficial look at the cranial nerves; the
details and subtleties could fill a book (and has, many times - an excellent
one is Cranial Nerves, by Wilson-Pauwels, Akesson, and Stewart). For now, you
should know a single phrase or two that describes the main function of each
cranial nerve - just enough to be able to effectively test each nerve. Evidence
of nerve damage could mean a peripheral lesion in the nerve, or a central
lesion in the brainstem. Draft a sheet of paper for yourself, including main
functions and easy ways to test the nerves. Classification of the Cranial Nerves
It is possible to describe a
cranial nerve in terms of its function and embryological origin,
initially cranial nerves can be subdivided into being either:
Motor (efferent)
Sensory (afferent)
And
from there further categorization can occur.
Motor (efferent) Cranial nerves
-Somatic
motor (general somatic efferent)
(III,
IV, VI, XII)
These
cranial nerves are so called because they innervate muscles derived from the
occipital somites, such as the extra ocular and extrinsic tongue muscles.
-Branchial
motor (special visceral efferent)
(V,
VII, IX, X, XI)
These
are described as branchial because they specifically innervate muscles which
are derived from the branchial arches during development (muscles of
mastication, larynx, facial expression, pharynx and middle ear)
-
Parasympatheic (general visceral efferent)
(III,
VII, IX, X)
These
nuclei do not innervate striated muscle like the branchial and somatic, they
instead provide preganglionic parasympathetic fibers to innervate glands, smooth
muscle and cardiac muscle within the head, heart, lungs and digestive tract
above the splenic flexure.

Sensory (afferent) cranial nerves
-Visceral
sensory
special visceral
afferent- (VII, IX, X)
general visceral
afferent- (IX, X)
The name is related to the
fact that it detects sensation from visceral organs.
They are divided into special
visceral, referring to the rostral portion of the nucleus which contributes to
the special sensation of taste. Whilst the general visceral portion is named as
such due to this caudal portion receiving general sensory impulses such as
cardiac, respiratory and GI inputs.
- General somatic sensory
(general somatic afferent)
(V, VII, IX, X)
These nuclei detect general
sensation, such as touch, pain, vibration from the face, sinuses and meninges
- Special somatic sensory
(special somatic)
(VIII)
This carries information from
the special sensation of hearing and balance.
 Overview of the Functions of the Cranial
Nerves
1)
CN I (Olfactory nerve)
Special
somatic sensory - Olfaction (sense of smell)
2)
CN II (Optic nerve)
Special
somatic sensory - Vision
3)
CN III (Oculomotor nerve)
Somatic
motor - Control of levator palpebrae superioris and the medial rectus, inferior
oblique, superior and inferior rectus muscles for eye movement.
Parasympathetic
- innervation of the ciliary ganglion controlling the sphincter pupillae and
ciliary muscles.
 4) CN IV (Trochlear nerve)
Somatic motor - Control of the superior oblique muscle
leading to depression and intorsion (inward rotation of the upper pole) of the
eye.
 5) CN V (Trigeminal nerve)
General
somatic sensory - Sensation of touch, pain, proprioception and temperature for
the face, mouth, nasal passages, anterior 2/3s of the tongue and part of the
meninges (supratentorial dura mater).
Branchial
motor - It also innervates the muscles of mastication (masseter, temporalis,
lateral pterygoid, medial pterygoid) and tensor
tympani.
 6) CN VI (Abducens nerve)
Somatic
motor - Controls the lateral rectus, leading to abduction of the eye.
7)
CN VII (Facial nerve)
Branchial
motor - Innervates the muscles of facial expression as well as the stapedius
and digastric muscle.
Parasympathetic
- Stimulates the lacrimal, sublingual, submandibular and other salivary glands
(except parotid).
Special
visceral sensory - Senses taste on the anterior 2/3 of the tongue.
 8) CN VIII (Vestibulocochlear nerve)
Special
somatic sensory - Controls the sensation of hearing and balance
 9) CN IX (Glossopharyngeal Nerve)
Branchial
motor - innervates the stylopharyngeus
Parasympathetic
- stimulates the parotid gland
General
somatic sensory - detects sensation from the middle ear, near the External
acoustic meatus (EAM), pharynx and posterior 1/3 of the tongue.
Special visceral sensory - sensation of taste on the
posterior 1/3 of the tongue.
General
visceral sensory - innervates chemo and baroreceptors on the carotid bodies.
 10) CN X (Vagus nerve)
Branchial
motor - Innervates the muscles of the pharynx and larynx for swallowing and
speech.
Parasympathetic
- innervation of the heart, lungs and digestive tract down to the splenic
flexure.
General
somatic sensory - provides general sensation to the pharynx, meninges
(posterior fossa) and a small region around the EAM.
Special
visceral sensory - taste from the epiglottis and pharynx
General
visceral sensory - chemo and baroreceptors of the aortic arch
 11) CN XI (Spinal Accessory nerve)
Branchial
motor - innervation of the sternocleidomastoid and upper part of trapezius
muscle
12)
CN XII (Hypoglossal nerve)
Somatic
motor - The intrinsic muscles of the tongue

Brainstem Nuclei
The cranial nerves originate
from pairs of nuclei (motor or sensory) within the brainstem, where like in the
spinal cord, the motor nuclei are located ventrally
whilst sensory nuclei are found dorsally along the brainstem. 3 motor and 3
sensory columns run the length of the brainstem.

Brainstem
Nuclei Overview


Cranial
nerve foramina
 Abbreviations Explaination
S.O.F- Superior Orbital
Fissure
F.-
Foramen
I.A.M- Internal Acoustic
Meatus

CN I Course


Cranial
nerve exit foramen: Cribriform plate of the Ethmoid bone
CNI
is the only cranial nerve to enter the cerebrum directly. The olfactory bulbs
and tracts called CNI are actually tracts of the CNS not nerves.
Olfactory
receptor neurones are found in the roof of the nasal cavity, the nasal septum
and medial wall of superior nasal concha. These ciliated neurones are
stimulated by aerosolised odour molecules dissolved in the surrounding mucus.
On either side of the nasal septum, these receptor neurones pass through the
cribriform plate of the ethmoid bone by forming 20 olfactory nerves to reach
the olfactory bulb found on the orbital surface of the frontal lobe, within the
anterior cranial fossa.
These
olfactory nerves synapse onto mitral and tufted cells at the glomerulus of the
olfactory bulb, which form the olfactory tract. These tracts form the anterior
olfactory nucleus along its route, which can then form medial and lateral
striae.
The lateral striae projects to
the primary olfactory cortex, formed of the piriform
cortex and periamygdaloid cortex which is found near the medial tip of the
temporal lobe. From here connections to the amygdala (involved in emotional
olfaction) and entorhinal cortex (memory aspect of olfaction) exist.
The medial striae projects
through the anterior commissure to the contralateral olfactory bulb and cortex.
 Clinical Correlation of CN I
Clinical Correlation - Anosmia
Usually patients with
unilateral anosmia are unaware of their condition due to the contralateral
nostril compensating. This is why each nostril must be tested individually.
An important sign of bilateral
anosmia is a loss of taste, due to the importance of olfaction to the sensation
of flavour.
Differential diagnosis of
Anosmia:
Head trauma - These can damage
the olfactory nerves as they pass through the cribriform plate.
Viruses - damage the olfactory
neuroepithelium
Obstruction
Parkinson's/Alzheimer's - this
is believed to be due to atrophy of the anterior olfactory nucleus.
Intracranial lesions such as
meningioma, metastases, meningitis or sarcoidosis when manifested on the
frontal lobe cause anosmia. This is important, as frontal lobe lesions are
usually difficult to detect and may produce no symptom other than anosmia.
Temporal lobe epilepsy
sometimes manifests with olfactory hallucinations, due to irritation of the
lateral olfactory area.

CN II Course

Cranial
nerve exit foramen: Optic canal
Embryologically
CNII is derived from the diencephalon, so is formed of oligodendrocytes rather
than schwann cells, hence CNII is considered a tract
of the CNS not a nerve. CNII is unique in that it is covered with meninges.
CNII
begins where the unmyelinated axons of the retinal ganglion cells pierce the
sclera and form the optic disc.
These
nerves enter the middle cranial fossa, by exiting the optic canal
posteromedially where the optic chiasm is formed. Here decussation occurs,
whereby the nasal (medial) fibres of the retina cross to join the uncrossed
temporal (lateral) fibres to form the optic tract.
Most of these fibres terminate
in the lateral geniculate body of the thalamus, whereby the axons pass through
two seperate loops (Baum & Meyer) to enter the occipital cortex, the part
of the cerebral hemisphere involved in visual processing.
Some fibres enter the
pre-tectal nucleus, through the brachium of the superior colliculus, and act as
the afferent limb of the pupillary light reflex and control eye movements.
Some other fibres enter the
suprachiasmatic nucleus controlling circadian rhythmns.
Clinical Correlation of CNII
Multiple sclerosis, which
normally spares the PNS, affects the optic nerve, due to the fact it is a CNS
tract rather than a PNS nerve. This results in optic neuritis, leading to loss
of visual acuity/peripheral vision. Toxic substances such as alcohol or other
inflammatory disorders may also precipitate this condition.
Visual field defects can occur
due to different lesions that occur along the length of the visual pathway.
These lesions can obstruct the transfer of retinal information along the
pathway and lead to a loss of a portion of the respective visual field that it
was transmitting. This can commonly occur due to berry aneurysms or pituitary
gland tumours.
Quite commonly during a
transient ischaemic attack, occlusion of the retinal artery can occur by an emboli from a carotid stenosis which causes loss of
vision in one eye for a brief period of time. This is a warning sign for
impending retinal or cerebral infarcts.

CN III course
Cranial
Nerve Exit Foramen: Superior orbital fissure
CNIII
leaves the midbrain between the posterior cerebral and superior cerebellar
arteries and pierces the sellar diaphragm over the hypophysis. Subsequently
upon piercing the cavernous sinus, it enters the superior orbital fissure.
CNII
then forms two divisions:
Superior
division - innervates the superior rectus and levator palpebrae superioris.
Inferior
division - innervates the inferior and medial rectus and inferior oblique.
Within
the inferior division the ciliary ganglion is formed from parasympathetic
fibres; these form short ciliary nerves to innervate the ciliary body and
sphincter pupillae. This pre-ganglionic parasympathetic branch is derived from
the Edinger-Westphall nucleus, and serves as the efferent (motor) limb of the
pupillary light reflex.
Clinical
Correlation of CNIII
Due
to the close proximity of CNIII with the superior cerebellar, posterior
cerebral and posterior communicating artery, any aneurysms here can lead to
CNIII palsy. However due to the more medial and superficial aspects of CNIII
carrying the parasympathetics, these are more likely to be compressed.
Fractures
of the cavernous sinus and a herniating uncus can also lead to CNIII palsy.
Any
loss of CNIII manifests with dilated pupils due to loss of parasympathetic
constriction and absence of pupillary light reflex will be observed as the
efferent limb is carried by CNIII. Ptosis may occur due to loss of levator
palpebrae superioris. The eye will turn down and out due to overaction of CN IV
and VI.

CN
IV Course
Cranial
nerve exit foramen: Superior orbital fissure
CN
IV is unique in that it is the only cranial nerve to arise from the dorsal
brain stem. It loops around the brainstem and passes anteriorly within the
subarachnoid space. It, like CNIII, passes between the superior cerebellar and
posterior cerebral arteries, and pierces the dura at the tentorium cerebelli
and enters the cavernous sinus. After it does this, it passes through the
superior orbital fissure into the orbital fissure to innervate the trochlear
nerve.
Clinical correlation
Due to its crossed method of
exiting the brainstem, CNIV is susceptible to cerebellar tumour compression.
Due to CNIV being thin and
having such a long intracranial course it is easily damaged by the shear injury
of head trauma.
Symptoms manifest as vertical
diplopia, which worsens when the patient looks down and medially, due to the
superior oblique normally depressing the pupil and causing intorsion. However
the inferior oblique is unopposed in causing extorsion due to CN IV paralysis,
which can also cause the eye to drift upward.

CN V course



Cranial nerve exit foramen:
V1: Superior orbital fissure
V2: Foramen rotundum
V3: Foramen ovale

CN
V is called trigeminal nerve due to it having 3 major branches.
Sensory:
Upon
leaving the ventrolateral pons it enters a small fossa posterior and
inferolateral to the cavernous sinus called Meckel's (trigeminal) cave. Here
the trigeminal ganglion (sometimes known as the semilunar or gasserian
ganglion) is found and sensory innervation is derived. Here the trigeminal
nerve splits into its 3 characteristic branches:
1)
Ophthalmic nerve (V1)- this branch travels through the
cavernous sinus and exits via the superior orbital fissure.
2)
Maxillary nerve (V2)- Leaves via the foramen rotundum
3)
Mandibular nerve (V3)- leaves via the formen ovale.
Motor:
The
trigeminal motor nucleus is found near the trigeminal nerve. This branchial
motor root runs inferomedial to the trigeminal ganglion and joins V3 to exit
via the foramen ovale, to supply the muscles of mastication.
 Though CNV has no preganglionic
parasympathetic fibers, all parasympathetic ganglia are associated with its
divisions, and join CNV branches.
 Clinical Correlation of CN V
Due to its bilateral upper
motor neurone control, jaw movement is not usually affected by unilateral
corticobulbar or motor cortex lesions. However when they do occur, they result
in hyper reflexia and a brisk jaw jerk reflex.
 Usually trigeminal nerve disorders are
relatively uncommon, however Trigeminal neuralgia can
cause pain which follows the distribution of V2 and V3. Usually the cause is
idiopathic, however an MRI scan needs to be performed to rule out tumours or
other lesions.
Due to the fact that part of
the trigeminal nucleus enters the spinal cord, it is therefore vulnerable to
demyelination due to MS, which can manifest as neuralgia.
Herpes Zoster, metastatic
disease, trauma and aneurysms of the petrous portion of the internal carotid
can all lead to damage to CNV and loss of sensory function. Due to the
uncrossed nature of CN V sensory fibers, any lesions in the brain stem cause
ipsilateral loss of pain/temperature/sensation. Any lesions can also affect the
spinothalamic tract leading to a common clinical manifestion of loss of pain
and temperature sensation ipsilateral to the lesion in the face, and
contralateral to the lesion in the limbs.

CN
VI course
Cranial
nerve exit foramen: Superior orbital fissure
Upon
leaving the brainstem at the pontomedullary junction of the pons, these fibres
travel within the subarachnoid space between the pons and clivus straddling the
basilar artery. Upon exiting the dura, CNVI enters Dorello's canal, where it
runs between the skull and dura. It makes a sharp bend as it passes over the
petrous temporal bone tip to enter the cavernous sinus. Through this it enters
the superior orbital fissure to innervate the lateral rectus.
Clinical correlation of CN VI
Due to its long vertical
course, CNVI is affected by raised intracranial pressures which act downward
especially as it bends over the crest of the petrous tip of the temporal bone.
Therefore CNVI palsy is an important sign of hydrocephalus, brain tumours,
basilar artery aneurysm and intracranial lesions. Diabetes may cause this due
to microvascular complications.
Lesions lead to horizontal
dipolpia, which causes improper abduction of the eye, and unopposed constant
adduction.

CN VII course


Cranial
nerve exit foramen: Stylomastoid foramen
CN
VII leaves the pontomedullary junction ventrally adjacent to the abducens
nerve.
It
traverses the subarachnoid space to enter the internal acoustic meatus within
the petrous part of the temporal bone, alongside CNVIII. Within the auditory
canal it forms the geniculate ganglion, a sharp bend occurs from which a branch
travels inferiorly past the middle ear to exit via the stylomastoid foramen.
Upon
exiting, it passes through the parotid gland, within which it forms its 5
branches which innervate the muscles of facial expression:
temporal
zygomatic
buccal
mandibular
cervical
Parasympathetics
are carried by the geniculate ganglion along the greater petrosal nerve to
synapse with the sphenopalatine ganglion. From here they stimulate the lacrimal
glands and nasal mucosa.
The chorda tympani is a branch just proximal to the stylomastoid foramen. This
travels upward past the middle ear, leaving via the petrotympanic fissure. This
joins the lingual nerve, V3, to reach the submandibular ganglion, which
innervates the salivary glands.
CN VII is involved in
mediating taste for the anterior 2/3's of the tongue as part of its special
visceral sensory role. These fibers have their cell bodies in the geniculate
ganglion, which synapse with neurons which go to the rostral nucleus
solitarius.
There is a minor general
somatic sensory role as the CN VII provides the sensation for a small area near
the external acoustic meatus, which eventually synapses to the trigeminal
(chief) nucleus.
 Clinical Correlation of CN VII
Amongst motor nerves, CN VII
is the most frequently damaged. A lesion may lead to loss of facial muscle
movement, loss of taste and altered secretions.
Unilateral UMN lesions in the
cortex or corticobulbar tract cause contralateral facial weakness, however they
usually spare the forehead due to bilateral motor cortices contributing to
muscles of the forehead. However LMN damage to the facial nucleus/nerves
themselves leads to ipsilateral facial weakness, and the forehead is not
spared, such as seen in Bell's palsy. Hence observing the forehead is a useful
diagnostic marker for motor neurone damage.
Hyperacusis can occur in
patients with CN VII damage, due to stapedius muscle weakness, which usually
dampens incoming sound though this finding is variable amongst patients.
Dry eyes are noticed, as lack
of lacrimal stimulation occurs from insufficient parasympathetic stimulation.
Trauma is a common cause of CN
VII injury due to how superficial its branches are. Trauma itself to the
petrous temporal bone, can lead to LMN type facial weakness. Likewise it is
common for a viral infection to lead to viral neuritis which causes
inflammation and swelling of the nerve whilst it is within the facial canal
before it exits the stylomastoid foramen.

  CN VIII Course
Cranial
nerve exit foramen: Auditory canal (Internal acoustic meatus)
CN
VIII leaves at the pontomedullary junction, lateral to
the facial nerve. Upon traversing the subarachnoid space it enters the internal
acoustic meatus alongside the facial nerve and labyrinthine artery, where it
travels within the auditory canal of the petrous temporal bone. Within this it
splits into the vestibular nerve and the cochlear nerve.
Vestibular
nerve - formed of the vestibular ganglion. This nerve attaches to the utricle
and saccule and cristae of the ampullae, thereby sensing movement.
Cochlear
nerve - formed of the spiral ganglion. This extends around the cochlea to sense
hearing.

 Clinical Correlation of CN VIII
Due
to the close relationship of the vestibular nerve and cochlear nerve, lesions
of one usually affect the other, leading to both tinnitus, vertigo and impaired
hearing. Infact usually the cause of vertigo after head trauma is a peripheral
vestibular nerve lesion.

There are two forms of hearing
loss:
Conductive hearing loss -
CNVIII is working but bone conduction of sound is impaired, due to the external
auditory canal/middle ear not transmitting soundwaves.
Sensorineural hearing loss -
physical ear structures are preserved, however there
is damage to the cochlea or neurone that is impairing hearing.
Acoustic neuromas are the most
common tumours of this region and grow within the auditory canal on the
surrounding schwann cells of CNVIII. This tumour can
lead to loss of hearing and commonly dysequilibrium and tinnitus. This can
eventually affect CN V, leading to facial pain and sensory loss and CNVII
damage causing facial weakness.

 CN IX course


Cranial
nerve exit foramen: Jugular foramen
Also
called "a poor man's facial nerve", it is very similar to CN VII.
Upon
leaving the ventrolateral medulla below CN VIII, it traverses the subarachnoid
space to exit via the jugular foramen.
Upon
exiting, it forms two sensory ganglions, where afferent general sensation,
touch and pain of the tongue, pharynx and middle ear are relayed, alongside
taste.
The
only muscle it innervates is the stylopharyngeus, and so it follows its course
eventually reaching the tongue. It passes further inferiorly to convey inputs
to the baro and chemoreceptors in the carotid body.
Parasympathetic
fibres leave via the tympanic nerve to join the lesser petrosal to synapse with
the otic ganglion (associated with CNV3), innervating the parotid gland.


Clinical Correlation of CN IX
Usually isolated lesions of CN
IX are fairly uncommon. However when they occur, taste is absent on the
posterior 1/3 of the tongue, alongside an absence of the gag reflex (as the
afferent limb is derived from CN IX). However, due to roughly 25% of the
population having an absent gag reflex, this is usually not alone a diagnostic
marker.
Due to the fact that CN IX, X
and XI all exit via the jugular foramen, it is common for tumours, infection or
trauma to involve these adjacent cranial nerves. Infact tumours in this region
cause "jugular foramen syndrome" leading to cranial nerve palsies.
  Glossopharyngeal neuralgia is very similar to
trigeminal neuralgia, but limited to the throat and ear and worsens during
eating by sensory stimulation, usually initiated by swallowing.

CN X course


Cranial
nerve exit foramen: Jugular foramen
The
vagus nerve is named after the latin for wanderer, due
to it having the longest course and extensive distribution.
CN
X leaves as several rootlets below CN IX on the ventrolateral medulla, crossing
the subarachnoid space and exiting the cranium through the jugular foramen
between CN IX and XI.
Upon
exiting, CN X forms 2 ganglions:
the superior ganglion of vagus
nerve- synapses with CN IX and the superior cervical ganglion. It is
responsible for general sensation.
the inferior ganglion of the
vagus nerve- responsible for taste and chemoreceptors from aortic arch.
As it descends CN X supplies
all pharyngeal, laryngeal and upper oesophageal muscles.
CN X continues inferiorly
within the carotid sheath; from here it extends into the thorax, supplying
parasympathetic sensation to the heart, lungs and bronchi.
Upon reaching the eosophageal
hiatus, it passes through with the eosophagus entering the abdomen. From here
it innervates the oesophagus, stomach and intestines up to the colic flexure.
 Clinical Correlation of CN X
Isolated lesions are very
uncommon, however CNX damage to the pharyngeal branches can lead to dysphagia,
and aphonia can develop due to paralysis of the laryngeal muscles.
The recurrent laryngeal nerve
(CNX branch) commonly occurs with surgery of the neck, eg. thyroid
surgery and carotid endarterectomy, or cardiac surgery due to the recurrent
laryngeal looping around the arch of aorta on the left side. Aortic aneurysms
and apical lung cancers can also damage the recurrent laryngeal. Damage to the
recurrent laryngeal leads to loss of voice and inspiratory stridor.
An abnormal gravelly voice is
common in Parkinson's disease due to interference of basal ganglia dysfunction
with articulation.
Usually dysphagia and
dysarthria occur together and can be caused by MS, infarcts,
cerebellar/brainstem lesions and alcohol. Commonly any dysphagia can lead to
aspiration pneumonia due to impaired swallowing in an individual, and is
frequently a cause of death.

  CN XI course
Cranial
nerve exit foramen: Jugular foramen (however it enters the skull via the
foramen magnum)
This
cranial nerve does not arise from the brainstem, rather from C1-5. These
rootlets leave the spinal accessory nucleus between the dorsal and ventral
nerve roots and ascend through the foramen magnum. Upon entering the cranium it
exits the cranium via the jugular foramen by descending alongside the internal
carotid artery. It eventually supplies the sternocleidomastoid (SCM) and the
upper portion of the trapezius muscle. As it is leaving the cranium, some
rootlet fibres from the nucleus ambiguus in the medulla join CN XI briefly
before leaving immediately and rejoining CN X to form the recurrent laryngeal
nerve. It is mentioned within literature that there are cranial contributions
from the medulla, these fibers however do not connect with the spinal component
and only travel with CN XI for a few cm, so functionally these fibers can be
assumed still part of CN X.
Clinical correllation of CN XI
LMN/UMN lesions of CN XI cause
ipsilateral weakness of the shoulder shrug due to trapezius damage and a
weakness of the head turning away from the lesion, this is due to the left SCM
turning the head right (and vice versa).
Due to a tendency of other
neck muscles to compensate for the SCM, it is essential to palpate the SCM to
detect its contraction.
Due to its very superficial
course through the cervical region, it is very commonly damaged in surgery,
especially lymph node biopsies, internal jugular vein cannulation and carotid
endarterectomy.

CN
XII course
Cranial
nerve exit foramen: Hypoglossal canal
Arising
from several rootlets from the ventral medulla it leaves the cranium via the
hypoglossal canal. Upon leaving the hypoglossal canal, it is joined by branches
of the cervical plexus which use CN XII to reach the hyoid muscles. Upon
reaching the angle of the mandible it travels anteriorly to innervate all
intrinsic and extrinsic muscles of the tongue (except the palatoglossus).

Clinical
correlation of CN XII
Upper
motor neurones that control tongue movement decussate within the corticobulbar
tracts before arriving at the hypoglossal nuclei. This means UMN lesions of the
primary motor cortex/internal capsule cause contralateral weakness of the
tongue, whereas LMN lesions of the hypoglossal nuclei cause ipsilateral
weakness of the tongue.
Tongue
weakness causes the tongue upon protrusion to deviate towards the weak side due
to overactive compensatory action of the other hypoglossal nerve. CN XII damage
also causes tongue muscles to atrophy.

1. Cranial Nerve III - Oculomotor Nerve consists
of two components with distinct functions: somatic and motor. Ggeneral somatic
efferent supplies four of the six extraocular muscles of the eye and the
levator palpebrae superioris muscle of the upper eyelid. Visceral motor
(general visceral efferent) provides parasympathetic innervation of the constrictor
pupillae and ciliary muscles.
There are six
extraocular muscles in each orbit. The
somatic motor component
of CN III innervates the following four extraocular
muscles of the eyes: ipsilateral inferior rectus muscle, ipsilateral inferior
oblique muscle, ipsilateral medial rectus muscle, contralateral superior rectus
muscle. The remaining extraocular muscles, the superior oblique and lateral
rectus muscles, are innervated by the trochlear nerve (CN IV) and abducens
nerve (CN VI), respectively. The somatic motor component of CN III also
innervates the levator palpebrae superioris muscles bilaterally. These muscles
elevate the upper eyelids.
The
somatic motor component of CN III originates from the oculomotor nucleus
located in the rostral midbrain at the level of the superior colliculus. Like
other somatic motor nuclei, the oculomotor nucleus is located near the midline
just ventral to the cerebral aqueduct. In a coronal cross-section of the
brainstem the oculomotor nucleus is "V-shaped" and is bordered
medially by the Edinger-Westphal nucleus and laterally and inferiorly by the
medial longitudinal fasciculus which allows communication between various
brainstem nuclei.
Upon
emerging from the brainstem the oculomotor nerve passes between the posterior
cerebral and superior cerebellar arteries and pierces the dura mater to enter
the cavernous sinus. The nerve runs along the lateral wall of the cavernous
sinus just superior to the trochlear nerve and enters the orbit via the
superior orbital fissure.
Within
the orbit CN III fibers pass through the tendinous ring of the extraocular
muscles and divide into superior and inferior divisions. The superior division
ascends lateral to the optic nerve to innervate the superior rectus and and
levator palpebrae superioris muscles on their deep surfaces.
The visceral motor component provides
parasympathetic innervation of the constrictor pupillae and ciliary muscles of
the eye. The visceral motor component of CN III is involved in the pupillary
light and accommodation reflexes. The visceral motor component originates from
the Edinger-Westphal nucleus located in the rostral midbrain at the level of
the superior colliculus. In a coronal cross-section of the brainstem the
Edinger-Westphal nucleus sit within the "V-shaped" oculomotor nuclei
just ventral to the cerebral aqueduct. Preganglionic parasympathetic fibers
course ventrally through the midbrain, interpeduncular fossa, cavernous sinus,
and superior orbital fissure along with the somatic motor fibers of CN III.
Once within the orbit the preganglionic parasympathetic fibers leave the
nerve to the inferior oblique muscle to synapse in the ciliary ganglion which
lies deep to the superior rectus muscle near the tendinous ring of the
extraocular muscles. Postganglionic fibers exit the ciliary ganglion in the
short ciliary nerves which enter the posterior aspect of the eye near the point
of exit of the optic nerve. Within the eye these fibers travel forward between
the choroid and sclera to innervate the ciliary muscles (which control the
shape and therefore the refractive power of the lens) and the constrictor
pupillae muscle of the iris (which constricts the pupil).
2. Cranial Nerve IV - Trochlear Nerve
The trochlear nerve has only a somatic motor
component (general somatic efferent). Somatic motor innervates the superior
oblique muscle of the contralateral orbit.
Origin
and central course
.
The fibers
of the trochlear nerve originate from the trochlear nucleus located in the
tegmentum of the midbrain at the level of the inferior colliculus. The nucleus
is located just ventral to the cerebral aqueduct. It is readily identifiable by
its close association with the myelinated medial longitudinal fasciculus that
allows communication between various brainstem nuclei. Fibers leaving the
trochlear nucleus travel dorsally to wrap around the cerebral aqueduct. All
fibers of the two trochlear nerves decussate (i.e. cross) in the superior
medullary velum and exit the dorsal surface of the brainstem just below the
contralateral inferior colliculus.
Intracranial
course
.
Upon emerging from the dorsal
surface of the brainstem the trochlear nerve curves around the brainstem in the
subarachnoid space and emerges between the posterior cerebral and superior
cerebellar arteries (along with CN III fibers). The trochlear nerve then enters
and runs along the lateral wall of the cavernous sinus with CNS III, V, and VI.
From the cavernous sinus the trochlear nerve enters the orbit through
the superior orbital fissure. CN IV does not pass through the tendinous ring of
the extraocular muscles, rather it passes above the
ring. The trochlear nerve then crosses medially along the roof of the orbit
above the levator palpebrae and superior rectus muscles to innervate the
superior oblique muscle along its proximal one-third:
Clinical
correlation.
The
superior oblique muscle normally depresses, intorts, and abducts the eye. Extorsion (outward rotation) of the affected eye due to the
unopposed action of the inferior oblique muscle.
Vertical
diplopia (double vision) due to the extorted eye.
Weakness
of downward gaze most noticeable on medially-directed eye.
This is often
reported as difficulty in descending stairs.
The trochlear nerve has several features that make it unique from the other
cranial nerves. The trochlear nerve is the only nerve to exit from the dorsal
surface of the brain; is the only nerve in which all the lower motor neuron
fibers decussate. The trochlear nerve has the longest intracranial course and
the smallest number of axons.
3. Cranial Nerve VI - Abducens Nerve has
only a somatic motor (general somatic efferent) component. Somatic motor:
innervates the lateral rectus muscle of the ipsilateral orbit. The lateral
rectus muscle is one of the six extraocular muscles responsible for the precise
movement of the eye for visual tracking or fixation on an object. See the CN
III section (occulomotor nerve) for a discussion of eye movements and the
interaction between the three nuclei and nerves that innervate the extraocular
muscles.
Origin
and central course.
The
fibers of the abducens nerve originate from the abducens nucleus located in the
caudal pons at the level of the facial colliculus. The nucleus is located just
ventral to the fourth ventricle near the midline. Axons of CN VII (facial
nerve) loop around the abducens nucleus and give rise to a bulge in the floor
of the fourth ventricle - the facial colliculus. Fibers leaving the abducens
nucleus travel ventrally to exit the brainstem at the border of the pons and
medullary pyramids.
Intracranial
course.
Upon
exiting the brainstem the abducens nerve climbs superiorly along the ventral
surface of the pons. On reaching the apex of the petrous portion of the
temporal bone the nerve makes a sharp turn anteriorly to enter the cavernous
sinus. The abducens nerve travels along the lateral wall of the cavernous sinus
with CNS III, IV, and V. From the cavernous sinus the abducens nerve enters the
orbit through the superior orbital fissure. CN VI passes through the tendinous
ring of the extraocular muscles and innervates the lateral rectus muscle on its
deep surface.
Coordination
of lateral rectus and medial rectus muscles.
The exact
control of eye movements requires input from integration centers in the brain
that coordinate the output from the occulomotor, trochlear, and abducens nuclei
which control the six extraocular muscles. For eye movements in the horizontal
plane, the lateral rectus muscle of one eye and the medial rectus muscle of the
other eye must work precisely together. The actions of these
muscles is
coordinated by the lateral gaze center located in the pontine
reticular formation. Inputs from higher centers of the brain synapse in the
lateral gaze center, which then sends simultaneous signals to the ipsilateral
abducens nucleus and to the contralateral occulomotor nucleus via the medial
longitudinal fasciculus. The abducens nucleus sends signals via CN VI to the
lateral rectus muscle of the ipsilateral orbit to command that eye to be
abducted. Simultaneously, the occulomotor nucleus generates a command via CN
III to contract the medial rectus muscle of the contralateral orbit resulting
in adduction of that eye. The end result is that both eyes precisely fixate on
or track the same object.
Clinical correlation -
lower motor neuron (LMN) lesion. Damage to the abducens nucleus or its axons
results in weakness or paralysis of the ipsilateral lateral rectus muscle.This
is indicated by: 1) medially directed eye on the affected side due to the
unopposed action of the medial rectus muscle; 2) inability to abduct the
affected eye beyond the midline of gaze (up to approximately the midline, the
superior and inferior oblique muscles can abduct the eye).
Strabismus - the inability to direct both eyes to the same object. When
asked to look at an object located laterally to the side of the lesion, the
patient's affected eye will be unable to be abducted beyond the midline of
gaze. The opposite normal eye will be adducted to effectively fixate on the
object. Horizontal diplopia (double vision) due to the
strabismus.
Patients may compensate by turning their head so that the
affected eye is focused on an object and then moving the normal eye so as to
fixate on the object. CN VI paralysis is the most common isolated palsy due to
the long peripheral course of the nerve.
Damage to the pontine lateral gaze center may result in conjugate
paralysis of lateral gaze to the affected side. This is indicated by an
inability of the patient to fixate on an object placed laterally to the
affected side. Specifically it is: 1) inability to abduct the eye on the
affected side past approximate midline gaze; 2) inability to adduct the eye
opposite the lesion past midline gaze. The end result is that neither eye is
moved to effectively fixate on the target object.
Assuming the lateral gaze center is intact, damage to the medial
longitudinal fasciculus (MLF) between the pons and occulomotor nucleus will
result in a defect in lateral gaze. On attempting lateral gaze due to loss of
input to the occulomotor nucleus from the lateral gaze center, the adducting
eye is unable to move medially past approximately the midline of gaze.
Monocular horizontal nystagmus is observed for the abducting eye. The abducting
eye moves smoothly laterally followed by a rapid movement (saccade) back to
midline gaze. MLF syndrome is most often seen in patients with multiple
sclerosis due to demyelination of the MLF tract.

Key words and phrases: oculomotor
nerve, trochlear nerve and abducens nerve, oculomotor muscles.

Inspection of
oculomotor nerve (III) function
a) Check the pupillary response (oculomotor
nerve): look at the diameter of your partner's eyes in dim light and also in
bright light. Check for differences in the sizes of the right and left pupils.
b) Hold up a neurological hammer (or finger) in
front of your partner. Tell your partner to hold his or her head still and to
follow neurological hammer (or finger), then move your finger forward towards
your partner's nose. Put attention on converging of eyeballs and pupillary
diameter. What is reaction of the healthy persone?
c) Hold up a neurological hammer (or finger) in
front of your partner's eyes. Tell your partner to hold his or her head still
and to follow neurological hammer (or finger), then move your
it
up and down, right and left. Do your partner's eyes follow
neurological hammer (or finger)?
In conclusion describe mechanisms of observed
results.

Physiology trigeminal nerve
1. General characteristic of
trigeminal nerve.
The
trigeminal nerve (V) has somatic motor,
proprioceptive,
and cutaneous sensory functions. It supplies motor
innervation
to the muscles of mastication, one middle ear muscle,
one
palatine muscle, and two throat muscles. In addition to proprioception
associated
with its somatic motor functions, the trigeminal nerve also carries
proprioception from the temporomandibular
joint.
Damage to the trigeminal nerve may impede chewing.
The
trigeminal nerve has the greatest general sensory function
of
all the cranial nerves and is the only cranial nerve involved
in
sensory cutaneous innervation. All other cutaneous innervation
comes
from spinal nerves. Trigeminal means
three twins,
and the sensory distribution of the trigeminal nerve
in
the face is divided into three regions, each supplied by a branch
of
the nerve. The three branches—ophthalmic, maxillary, and
mandibular—arise
directly from the trigeminal ganglion, which serves the same function as the
dorsal root ganglia of the spinal
nerves. Only
the mandibular branch has motor axons, which
bypass
the trigeminal ganglion, much like the ventral root of a
spinal
nerve bypasses a dorsal root ganglion.
Conveys sensations
(touch, pain, pressure etc.) from  skin of the head (face and scalp) and
mucosa of cavities in the head.
Responsible for consciously perceived pain emanating from the head:
toothache, headache and sinus pain.
Provides sensory input
for for 2 reflexes often tested during a neurologic examination: corneal reflex
& jaw jerk
Does
not contain preganglionic parasympathetic axons.
Gives attachment to 3  parasympathetic
ganglia.
Helps distribute
postganglionic parasympathetic fibers to lacrimal and two salivary glands.


2. Sensory Branches of the Trigeminal
Nerve
The ophthalmic, maxillary and mandibular branches
leave the skull through three separate
foramina:
the
superior orbital fissure,
the
foramen rotundum and the foramen ovale.
The
mnemonic
standing room only can be used to remember that V1 passes through the superior
orbital
fissure, V2 through the foramen rotundum, and V3
through the foramen ovale.
Dermatome Distribution of the Trigeminal Nerve
Dermatome
Distribution of the Trigeminal Nerve

The ophthalmic nerve carries sensory information from the scalp and
forehead, the upper eyelid, the conjunctiva and cornea of the eye, the nose
(including the tip of the nose), the nasal mucosa, the frontal sinuses and
parts of the
meninges
(the
dura
and blood vessels).
The maxillary nerve caries sensory information from the lower eyelid and
cheek, the nares and upper lip, the upper teeth and gums, the nasal mucosa, the
palate and roof of the pharynx, the maxillary, ethmoid and sphenoid sinuses,
and parts of the meninges.
The mandibular nerve carries sensory information from the lower lip, the
lower teeth and gums, the floor of the mouth, the anterior ⅔ of the
tongue, the chin and jaw (except the angle of the jaw, which is supplied by
C2-C3), parts of the external ear, and parts of the meninges.
The mandibular nerve carries touch/position and pain/temperature
sensation from the mouth. It does not carry taste sensation, but one of its
branches, the
lingual nerve carries multiple types of nerve
fibers that do not originate in the
mandibular nerve.
Taste fibers from the anterior 2/3 of the tongue are initially carried in the
lingual nerve
(which is anatomically a branch of V3) but then enter the
chorda tympani,
a branch of
cranial nerve VII.
3. Motor
Branches of the Trigeminal Nerve
Motor branches of the trigeminal nerve are distributed in the mandibular
nerve. These fibers originate in the motor nucleus of the fifth nerve, which is
located near the main trigeminal nucleus in the pons. Motor nerves are
functionally quite different from sensory nerves, and their association in the
peripheral branches of the mandibular nerve is more a matter of convenience
than of necessity.
In classical anatomy, the trigeminal nerve is said to have general
somatic afferent (sensory) components, as well as special visceral efferent
(motor) components. The motor branches of the trigeminal nerve control the
movement of eight muscles, including the four
muscles of mastication. The
other muscles are
masseter, temporalis, medial pterygoid, lateral pterygoid, tensor veli palatini, mylohyoid,
anterior belly of
digastric, tensor tympani.
With the exception of tensor tympani, all of these muscles are involved
in biting, chewing and swallowing. All have bilateral cortical representation.
A central lesion (e.g., a
stroke),
no matter how large, is unlikely to produce any observable deficit. However,
injury to the peripheral nerve can cause paralysis of muscles on one side of
the jaw. The jaw deviates to the paralyzed side when it opens.
4. Central
Anatomy
The fifth nerve is primarily a sensory nerve. The
anatomy of sensation in the face and mouth is the subject of the remainder of
this article. Background information on sensation is reviewed, followed by a
summary of central sensory pathways. The central anatomy of the fifth nerve is
then discussed in detail.
There are two
basic types of sensation: touch/position and pain/temperature. They are
distinguished, roughly speaking, by the fact that touch/position input comes to
attention immediately, whereas pain/temperature input reaches the level of
consciousness only after a perceptible delay. Think of stepping on a pin. There
is immediate awareness of stepping on something, but it takes a moment before
it starts to hurt.
In general, touch/position information is carried
by myelinated (fast-conducting) nerve fibers, while pain/temperature
information is carried by unmyelinated (slow-conducting) nerve fibers. The
primary sensory receptors for touch/position (Meissner’s corpuscles, Merkel’s
receptors, Pacinian corpuscles, Ruffini’s corpuscles, hair receptors, muscle
spindle organs, Golgi tendon organs) are structurally more complex than the
primitive receptors for pain/temperature, which are bare nerve endings.
The term “sensation” refers to the conscious
perception of touch/position and pain/temperature information. It does not
refer to the so-called “special senses” (smell, sight, taste, hearing and
balance), which are processed by different cranial nerves and sent to the
cerebral cortex through different pathways. The perception of magnetic fields,
electrical fields, low-frequency vibrations and infrared radiation by certain
nonhuman vertebrates is processed by the equivalent of the fifth cranial nerve
in these animals.
The term “touch,” refers to the perception of
detailed, localized tactile information, such as two-point discrimination (the
difference between touching one point and two closely-spaced points) or the
difference between grades of sandpaper (corse, medium and fine). People who
lack touch/position perception can still “feel” the surface of their bodies,
and can therefore perceive “touch” in a crude, yes-or-no way, but they lack the
rich perceptual detail that we normally experience.
The term “position” refers to conscious proprioception.
Proprioceptors (muscle spindle organs and Golgi tendon organs) provide
information about joint position and muscle movement. Much of this information
is processed at an unconscious level (mainly by the
cerebellum
and the
vestibular nuclei). Obviously, however, some of
this information is available at a conscious level.
The two types of sensation in humans, touch/position and
pain/temperature, are processed by different pathways in the central nervous
system. The distinction is hard-wired, and it is maintained all the way to the
cerebral cortex. Within the cerebral cortex, sensations are further hard-wired
to (associated with) other cortical areas. Roughly speaking, touch/position
sensation is associated with planning your next move, while pain/temperature
sensation is associated with your emotions and memories.
5. Sensory Pathways
Sensory pathways from the periphery to the cortex are summarized below.
There are separate pathways for touch/position sensation and pain/temperature
sensation. All sensory information is sent to specific nuclei in the
thalamus.
Thalamic nuclei, in turn, send information to specific areas in the
cerebral cortex.
Anatomically, each pathway consists of three bundles of nerve fibers,
connected together in series:
Remarkably, the secondary neurons in each pathway
decussate (cross to the other side of the spinal cord or brainstem).

The reason for this is unknown.
Sensory pathways are often depicted as chains of individual neurons
connected in series. This is an oversimplification. Sensory information is
processed and modified at each level in the chain by interneurons and by input
from other areas of the nervous system. For example, cells in the main
trigeminal nucleus (“Main V” in the diagram) receive input (not shown) from the
reticular formation and from the cerebral cortex. This information contributes
to the final output of the cells in Main V to the thalamus.
Touch/position information from the body is carried to the thalamus by
the medial lemniscus; touch/position information from the face is carried to
the thalamus by the trigeminal lemniscus. Pain/temperature information from the
body is carried to the thalamus by the spinothalamic tract; pain/temperature
information from the face is carried to the thalamus by the trigeminothalamic
tract (also called the quintothalamic tract).
Anatomically, pathways for touch/position sensation from the face and
body merge together in the brainstem. A single touch/position sensory map of
the entire body is projected onto the thalamus. Likewise, pathways for
pain/temperature sensation from the face and body merge together in the
brainstem. A single pain/temperature sensory map of the entire body is
projected onto the thalamus.
From the thalamus, touch/position and pain/temperature information is
projected onto various areas of the cerebral cortex. Exactly where, when and
how this information becomes conscious is entirely beyond our understanding at
the present time. The explanation of consciousness is one of the great,
unsolved, “hard” problems in science.
6. Trigeminal
Nucleus
Brainstem Nuclei: Red = Motor; Blue = Sensory; Dark Blue = Trigeminal Nucleus
Brainstem
Nuclei: Red = Motor; Blue = Sensory; Dark Blue = Trigeminal Nucleus
It is not widely appreciated that all sensory
information from the face (all touch/position information and all
pain/temperature information) is sent to the trigeminal nucleus. In classical
anatomy, most sensory information from the face is carried by the fifth nerve,
but sensation from certain parts of the mouth, certain parts of the ear and
certain parts of the meninges is carried by “general somatic afferent” fibers
in cranial nerves VII (the
facial nerve), IX (the glossopharyngeal
nerve
) and X (the vagus nerve).
Without exception, however, all sensory fibers
from these nerves terminate in the trigeminal nucleus. On entering the
brainstem, sensory fibers from V, VII, IX and X are
sorted out and sent to the trigeminal nucleus, which thus contains a complete
sensory map of the face and mouth. The spinal counterparts of the trigeminal
nucleus (cells in the
dorsal horn
and
dorsal column nuclei of
the spinal cord) contain a complete sensory map of the rest of the body.
The trigeminal nucleus extends throughout the
entire brainstem, from the midbrain to the medulla, and continues into the
cervical cord, where it merges with the dorsal horn cells of the spinal cord.
The nucleus is divided anatomically into three parts, visible in microscopic
sections of the brainstem. From caudal to rostral (i.e. going up from the
medulla to the midbrain) they are the spinal trigeminal nucleus, the main
trigeminal nucleus and the mesencephalic trigeminal nucleus.
The three parts of the trigeminal nucleus receive
different types of sensory information. The spinal trigeminal nucleus receives
pain/temperature fibers. The main trigeminal nucleus receives touch/position
fibers. The mesencephalic nucleus receives proprioceptor and mechanoreceptor
fibers from the jaws and teeth.
7. Spinal
Trigeminal Nucleus
The spinal trigeminal nucleus represents pain/temperature sensation from
the face. Pain/temperature fibers from peripheral
nociceptors
are carried in cranial nerves V, VII, IX and X. On entering the brainstem,
sensory fibers are grouped together and sent to the spinal trigeminal nucleus.
This bundle of incoming fibers can be identified in cross sections of the pons
and medulla as the spinal tract of the trigeminal nucleus, which parallels the
spinal trigeminal nucleus itself. The spinal tract of V is analogous to, and
continuous with, Lissauer’s tract in the spinal cord.
The spinal trigeminal nucleus contains a pain/temperature sensory map of
the face and mouth. From the spinal trigeminal nucleus, secondary fibers cross
the midline and ascend in the trigeminothalamic tract to the contralateral
thalamus. The trigeminothalamic tract runs parallel to the spinothalamic tract,
which carries pain/temperature information from the rest of the body.
Pain/temperature fibers are sent to multiple thalamic nuclei. As discussed
below, the central processing of pain/temperature information is markedly
different from the central processing of touch/position information.
8.
Somatotopic Representation
Exactly how pain/temperature fibers from the face are distributed to the
spinal trigeminal nucleus has been a subject of considerable controversy. The
present understanding is that all pain/temperature information from all areas
of the human body is represented (in the spinal cord and brainstem) in an
ascending, caudal-to-rostral fashion. Information from the lower extremities is
represented in the lumbar cord. Information from the upper extremities is
represented in the thoracic cord. Information from the neck and the back of the
head is represented in the cervical cord. Information from the face and mouth
is represented in the spinal trigeminal nucleus.
Onion Skin Distribution of the Trigeminal Nerve
Onion
Skin Distribution of the Trigeminal Nerve
Within the spinal trigeminal nucleus, information
is represented in an onion skin fashion. The lowest levels of the nucleus (in
the upper cervical cord and lower medulla) represent peripheral areas of the
face (the scalp, ears and chin). Higher levels (in the
upper medulla) represent more central areas (nose, cheeks, lips). The highest
levels (in the pons) represent the mouth, teeth, and pharyngeal cavity.
The onion skin distribution is entirely different
from the dermatome distribution of the peripheral branches of the fifth nerve.
Lesions that destroy lower areas of the spinal trigeminal nucleus (but which
spare higher areas) preserve pain/temperature sensation in the nose (V1), upper
lip (V2) and mouth (V3) while removing pain/temperature sensation from the
forehead (V1), cheeks (V2) and chin (V3). Analgesia in this distribution is
“nonphysiologic” in the traditional sense, because it crosses over several
dermatomes. Nevertheless, analgesia in exactly this distribution is found in
humans after surgical sectioning of the spinal tract of the trigeminal nucleus.
The spinal trigeminal nucleus sends
pain/temperature information to the
thalamus. It also
sends information to the
mesencephalon and the reticular
formation
of the brainstem. The latter pathways are
analogous to the spinomesencephalic and spinoreticular tracts of spinal cord,
which send pain/temperature information from the rest of the body to the same
areas. The mesencephalon modulates painful input before it reaches the level of
consciousness. The reticular formation is responsible for the automatic
(unconscious) orientation of the body to painful stimuli.
9. Main Trigeminal Nucleus
The main trigeminal nucleus represents touch/position sensation from the
face. It is located in the pons, close to the entry site of the fifth nerve. Fibers
carrying carry touch/position information from the face and mouth (via cranial
nerves V, VII, IX and X) are sent to the main trigeminal nucleus when they
enter the brainstem.
The main trigeminal nucleus contains a touch/position sensory map of the
face and mouth, just as the spinal trigeminal nucleus contains a complete
pain/temperature map. The main nucleus is analogous to the
dorsal column nuclei (the gracile and cuneate nuclei) of
the spinal cord, which contain a touch/position map of the rest of the body.
From the main trigeminal nucleus, secondary fibers cross the midline and
ascend in the trigeminal leminiscus to the contralateral
thalamus. The
trigeminal lemniscus runs parallel to the medial leminscus, which carries
touch/position information from the rest of the body to the thalamus.
Some sensory information from the teeth and jaws is sent from the main trigeminal nucleus to the ipsilateral thalamus, via the
small dorsal trigeminal tract. Thus touch/position information from the teeth
and jaws is represented bilaterally in the thalamus (and hence in the cortex).
The reason for this special processing is discussed below.
10.
Mesencephalic Trigeminal Nucleus
The mesencephalic trigeminal nucleus is not
really a “nucleus.” Rather, it is a sensory ganglion (like the trigeminal
ganglion) that happens to be imbedded in the brainstem. The mesencephalic
“nucleus” is the sole exception to the general rule that sensory information
passes through peripheral sensory ganglia before entering the central nervous
system.
Only certain types of sensory fibers have cell
bodies in the mesencephalic nucleus:
proprioceptor
fibers from the jaw and mechanoreceptor fibers from the teeth. Some of these
incoming fibers go to the motor nucleus of V, thus entirely bypassing the
pathways for conscious perception. The
jaw jerk reflex is an
example. Tapping the jaw elicits a reflex closure of the jaw, in exactly the
same way that tapping the knee elicits a reflex kick of the lower leg. Other
incoming fibers from the teeth and jaws go to the main nucleus of V. As noted
above, this information is projected bilaterally to the thalamus. It is
available for conscious perception.
Activities like biting, chewing and swallowing
require symmetrical, simultaneous coordination of both sides of the body. They
are essentially automatic activities, to which we pay little conscious
attention. They involve a sensory component (feedback about touch/position)
that is processed at a largely unconscious level.
The unusual anatomy of “mesencephalic V” has been
found in all
vertebrates,
with the exception of
lampreys
and
hagfishes. Lampreys
and hagfishes are the only vertebrates without jaws. Evidently, information
about biting, chewing and swallowing is singled out for special processing in
the vertebrate brainstem, specifically in the mesencephalic nucleus.
Lampreys and hagfishes have cells in their
brainstems that can be identified as the evoutionary precursors of the
mesencephalic nucleus. These “internal ganglion” cells were discovered in the
latter part of the 19th century by a young medical student named
Sigmund Freud.
11. Clinical aspect. In addition to these
cutaneous functions, the maxillary and
mandibular
branches are important in dentistry. The maxillary nerve
supplies
sensory innervation to the maxillary teeth, palate, and gingiva. The mandibular
branch supplies sensory innervation
to the
mandibular teeth, tongue, and gingiva. The various nerves innervating the teeth
are referred to as alveolar (refers to the sockets in which the teeth are located).
The superior alveolar nerves
to the
maxillary teeth are derived from the maxillary branch of the
trigeminal
nerve, and the inferior alveolar nerves to the mandibular
teeth
are derived from the mandibular branch of the trigeminal nerve.
Trigeminal neuralgia and glossopharyngeal neuralgia are
extremely painful conditions that typically afflict an older population.
Distinct clinical characteristics guide the diagnosis of these unique
syndromes. Treatment involves medication first and then surgical
procedures if a patient is
refractory to medicinal therapy.
Antiepileptic medications are the most effective agents for these disorders.
Trigeminal neuralgia, also called tic douloureux,
involves one or more of the
trigeminal
nerve branches and consists of
sharp bursts
of pain in the face. This disorder
often has a
trigger point in or around
the mouth,
which, when touched, elicits the
pain response
in some other part of the
face. The
cause of trigeminal neuralgia is
unknown. 
The most sensitive tactile areas of the posterior mouth and pharynx for
initiation of the pharyngeal stage of swallowing lie in a ring around the
pharyngeal opening, with greatest sensitivity on the tonsillar pillars.
Impulses are transmitted from these areas through the sensory portions of the
trigeminal and glossopharyngeal nerves into the medulla oblongata either in or
closely associated with the tractus solitarius, which receives essentially all
sensory impulses from the mouth. The successive stages of the swallowing
process are then automatically controlled in orderly sequence by neuronal areas
of the brain stem distributed throughout the reticular substance of the medulla
and lower portion of the ports. The sequence of the swallowing reflex is the
same from one swallow to the next, and the timing of the entire cycle also
remains constant from one swallow to the next. The areas in the medulla and
lower ports that control swallowing are collectively called the deglutition or
swallowing center. The motor impulses from the swallowing center to the pharynx
and upper esophagus that cause swallowing are transmitted successively by the
5th, 9th, 10th, and 12th cranial nerves and even a few of the superior cervical
nerves. In summary, the pharyngeal stage of swallowing is principally a reflex
act. It is almost always initiated by voluntary movement of food into the back
of the mouth, which in turn excites involuntary pharyngeal sensory receptors to
elicit the swallowing reflex.
Inspection of trigeminal nerve
1. Inspection of skin sensitivity. Have the
patient recognize touch and pain from the skin territories by each division.
The sensory function may be tested by using cotton and a pin over each area of
the face supplied by the divisions of the trigeminal nerve. Note that there is
very little overlap of the dermatomes and that the skin covering the angle of
the jaw is innervated by branches from the cervical plexus (C2 and C3),
In a lesion of the ophthalmic division, the cornea and
conjunctiva will be insensitive to touch.
Compare the two sides for equal responses.
2. Cornea reflex. The patient looks to one side,  the opposite cornea
is gently stimulated by a wisp of cotton. The normal response is a bilateral
closure of the eyes. V1 is the afferent limb of the reflex and the efferent is
the VII.
3.
The motor function may be tested by asking the patient to clench his or
her teeth. The masseter and the temporalis muscles can be palpated and felt to
harden as they contract
.
Have the patient clench her teeth?
Palpate the contraction of the masseter and temporalis muscles.
Have
the patient move mandible
? Look for
normal movements without any deviation to either side
.
4. Jaw jerk. Keep the jaw relaxed and the mouth
slightly open. Tap the chin to stretch the temporalis and masseter. Jaw closure
in response normally weak or absent, exaggerated in some motor neuron diseases
.

Physiology of facial nerve
1. Cranial Nerve VII - Facial Nerve. Visceral motor (general visceral efferent) component. The
facial nerve has four components with distinct functions:
Brancial motor (special visceral efferent)
component supplies the muscles of facial expression; posterior belly of
digastric muscle; stylohyoid, and stapedius.
Visceral motor (general visceral efferent) component
gives parasympathetic innervation of the lcrimal, submandibular, and sublingual
glands, as well as mucous membranes of nasopharynx, hard and soft palate.
Visceral motor
component is the parasympathetic component of the facial nerve. Consists of efferent fibers which stimulate secretion from the
submandibular, sublingual, and lacrimal glands, as well as the mucous membranes
of the nasopharynx and hard and soft palates.
The motor part of the facial nerve arises from
the
facial nerve nucleus
in the
pons
while the sensory part of the facial nerve arises from the
nervus intermedius.
The motor part of the facial nerve enters the petrous temporal bone
into the
internal auditory meatus
(intimately close to the
inner ear)
then runs a tortuous course (including two tight turns) through the
facial canal,
emerges from the
stylomastoid foramen
and passes through the
parotid gland, where it divides into five major
branches. Though it passes through the parotid gland, it does not innervate the
gland. This action is the responsibility of cranial nerve IX, the
glossopharyngeal
nerve
.
Inside one of the tight turns in the facial
canal, the facial nerve forms the
geniculate ganglion. No other
nerve in the body travels such a long distance through a bony canal. Branches
inside
the facial canal:
1) Greater petrosal nerve -
provides parasympathetic innervation to lacrimal gland, as well as special
taste sensory fibers to the palate via the
nerve of pterygoid canal;
2)
Nerve to stapedius - provides motor innervation
for
stapedius
muscle in middle ear; 3)
Chorda tympani -
provides parasympathetic innervation to submandibular and sublingual glands and
special sensory taste fibers for the anterior 2/3 of the tongue; 4) Outside skull (distal to
stylomastoid foramen): Posterior auricular nerve -
controls movements of some of the scalp muscles around the ear

Testing the facial nerve
1. As the facial nerve supplies: the muscles of
facial expression, the anterior two-thirds of the tongue with taste fibers, is
secretomotor to the lacrimal, submandibular, and sublingual glands, so to test
the facial nerve the patient is asked  to
show his teeth by separating the lips with the teeth clenched.
Normally, equal areas of the upper and lower
teeth are revealed on both sides
.
If a lesion of the facial nerve is present on one
side, the mouth is distorted.
A greater area of teeth is revealed on the side
of the intact nerve, since the mouth is pulled up on that side.
2. Voluntary facial movements, such as wrinkling
the brow, showing teeth, frowning, closing the eyes tightly, pursing the lips
and puffing out the cheeks, all test the facial nerve. Ask the patient to close
both eyes firmly. The examiner then attempts to open the eyes by gently raising
the patient’s upper eyelids. There should be no noticeable asymmetry.
3. Taste can be tested on the anterior of the tongue, this can be tested with a swab dipped in a flavoured
solution, or with electronic stimulation (similar to putting your tongue on a
battery).
The sensation of taste can be tested by placing
small amounts of sugar, salt, vinegar, and quinine on the tongue for the sweet,
salt, sour, and bitter sensations.
In conclusion explain functional mechanism,
causing the result.
Physiology of Vestibulocochlear
nerve
 1.
General information about vestibulocochlear nerve. The vestibulocochlear nerve
is the
nerve along which
the sensory cells (the
hair cells)
of the
inner ear
transmit information to the
brain. It consists of the cochlear nerve, carrying
information about
hearing, and the vestibular nerve, carrying
information about
balance.
It emerges from the
medulla oblongata and enters
the inner
skull via the internal
acoustic meatus
(or internal
auditory meatus
) in the temporal bone, along with
the
facial nerve. The eighth
cranial nerve has two prime roles. It is needed to convey information of
vestibular sensation - that is, the position and movement of the
head. Secondly, it is used for
hearing. The eighth cranial nerve has two prime roles. It is needed to convey
information of vestibular sensation - that is, the position and movement of the
head. Secondly, it is used for
hearing.
2.
Nerve endings of
vestibulocochlear nerve. The auditory
hair cells are located within the
organ of Corti on a thin basilar membrane in the cochlea of the inner
ear. They derive their name from
the tufts of
stereocilia
that protrude from the apical surface of the cell, a structure known as the
hair bundle, into the
scala media,
a fluid-filled tube within the cochlea.
Mammalian cochlear
hair cells come in two anatomically and functionally distinct types: the outer
and inner hair cells. Damage to these hair cells results in decreased hearing
sensitivity, i.e. sensorineural hearing loss. The inner
ear is the bony
labyrinth
, a system of passages comprising two main
functional parts: the organ of hearing, or
cochlea and the
vestibular apparatus, the organ of balance that consists of three
semicircular canals and
the
vestibule.
Auditory
nerve fibres provide a direct synaptic connection between the hair cells of the
cochlea and the cochlear nucleus. The
cochlear nerve fibres originate in the
spiral ganglion of the
cochlea, which in turn connect to the hair cells. In humans, there are about
30,000 ganglion cells in each cochlea. It was once believed that most of the
cochlear nerve fibres were directed to the
outer hair cells,
but it is now understood that at least 90% of the cochlear ganglion cells
terminate on inner hair cells, the rest terminating on the outer hair cells.
Each axon innervates only a single hair cell, but each hair cell directs its
output to an average of 10 nerve fibres.
The
transmission between the inner hair cells and the neurons is chemical, using
glutamate as a
neurotransmitter. The cochlear neurons can be divided into two groups: Type I
and Type II. Type I neurons make up 90-95% of the neurons and innervate the
inner hair cells. They have a relatively large diameter, and are bipolar and
myelinated. Type II cells, which have a relatively small
diameter, connect with the outer hair cells, are monopolar and are not
myelinated.
3.
The cochlear nuclear complex. The axons from each cochlear nerve terminate in
the cochlear nuclear complex which are ipsilaterally
located in the medulla of the brainstem. The cochlear nucleus is the first
'relay station' of the auditory nervous system and receives mainly ipsilateral
afferent input.
The
three major components of the cochlear nuclear complex are: the dorsal cochlear
nucleus (DCN), the anteroventral cochlear nucleus (AVCN), the posteroventral
cochlear nucleus (PVCN).
Each
of the three cochlear nuclei are tonotopically
organised. The axons from the lower frequency area of the cochlea innervate the
ventral portion of the dorsal cochlear nucleus and the ventrolateral portions
of the anteroventral cochlear nucleus, while the higher frequency axons project
into the dorsal portion of the anteroventral cochlear nucleus and the uppermost
dorsal portions of the dorsal cochlear nucleus. The mid frequency projections
end up in between the two extremes, in this way the frequency spectrum is
preserved.
4. Human
hearing. Humans can generally hear sounds with frequencies between 20 Hz and 20 kHz.
Human hearing is able to discriminate small differences in loudness (intensity)
and pitch (frequency) over that large range of audible sound. This healthy
human range of frequency detection varies significantly with age, occupational
hearing damage, and gender; some individuals are able to hear pitches up to 22
kHz and perhaps beyond, while others are limited to about 16 kHz. The ability
of most adults to hear sounds above about 8000 Hz begins to deteriorate
in early middle age.
5.
The cochlea is the auditory branch of the
inner ear. Its core
component is the
Organ of Corti,
the sensory organ of hearing, which is distributed along the partition
separating fluid chambers in the coiled tapered tube of the cochlea.
The
name is from the Latin for snail, which is from the Greek kokhlias "snail,
screw," from kokhlos "spiral shell,"
[1] in reference
to its coiled shape, though the cochlea is only coiled in non-
monotreme mammals.

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