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.