1. CRANIAL NERVES
Bundles of sensory or motor fibers that innervate muscles or glands,
Carry impulses from sensory receptors, or
Have a combo of motor and sensory fibers.
Called cranial nerves because they emerge through foramen/ fissures in the cranium, but individual names reflect either their location, distribution or their function.

2. Spinal Cord CN XI Brain Forebrain Cerebral hemispheres CN I
Diencephalon (epithalamus, thalamus, hypothalamus
CN II
Midbrain ( brainstem)
CN III, CN IV
Hindbrain
Pons (brainstem)
CN V
Medulla oblongata (brainstem)
CN IX, CN X, XII
Cerebellum
Spinal Cord CN XI

3. 2 prs of CNs [CNI, II]originate from the forebrain.
The remaining 10 prs [CN III- XII] originate from the brainstem (incl midbrain, pons & medullla).
They pass through skull foramina, fissures or canals to exit the cranial vault and then distribute their innovation to their respective structures in the head and neck. CNs are designated Roman Numerals I-XII, derived by their position along the brain [rostrally to caudally], ↑ toward the back of the brain.
The names indicate structures innervated by these nerves (e.g. facial) or the principal function of the nerves (e.g. occulomotor).
Other than the Vagus N. which extend into the abdmn, the names indicate structures innervated by these nerves (e.g. facial) or the principal function of the nerves (e.g. occulomotor). to the abdomen; the 11 other CNs serve only H&N structures.

4. Cranial nerves can have: 1. Motor (efferent) fibers
Voluntary (striated) muscle
Involuntary(smooth) muscle or glands – by parasympathetic division of ANS: CN III, VII, IX, and X.
Preganglionic fibers emerge from brain and synapse in a parasympathetic ganglion outside CNS.
Postganglionic fibers continue to smooth muscle/glands.
2. Sensory (afferent) fibers
General sensation – touch, heat, pressure, etc.
Sensation from viscera (heart, GI tract, etc.)
Unique sensations – taste, smell, and those for vision, hearing, balance
Overall, sensory nerve nuclei tend to be located in the lateral brainstem, while motor nuclei tend to be located medially.
Nerves w/ mixed sensory and motor fibers must have more than one nucleus of origin – at least one sensory (afferent) and one motor (efferent).

5. Cranial Parasympathetic ganglia
Each has three roots entering the ganglion.
The motor root carries presynaptic parasympathetic nerve fibers that terminate in the ganglion by synapsing with the postsynaptic fibers traveling to target organs.
The sympathetic root carries postsynaptic sympathetic fibers that traverse the ganglion without synapsing.
The sensory root carries general sensory fibers that also do not synapse in the ganglion.

6. GENERAL ORGANIZATION OF CRANIAL NERVES

7. Cranial nerves: cranial base, foramina

8. Midbrain, Diencephalon, Cerebral Aqueduct, Pons, Medula Oblongata

9. Slide: Ventral view of brain depicting the CNs
Most cranial nerves are classified as mixed nerves. This term indicates that the nerve contains both sensory and motor fibers.
Those cranial nerves associated with the special senses (e.g. olfactory, optic), however, consist of sensory fibers only. The cell bodies of these sensory neurons are not located in the brain, but instead are found in ganglia near the sensory organ.
CNs … possess ‘gen’l’ functional fiber types found in spinal n. but are supplemented by ‘special’ afferent or efferent fibers, fibers conveying olfaction (CNI) and taste (CN VII, IX, and X) are classified as special visceral afferent, while the designation of special somatic afferent is applied to fibers conveying vision (CNII) and equilibrium and hearing (CN VIII).
Skeletal m. that arise from the brachial (pharyngeal) arches are innervated by fibers of CN V, VII, IX and X; these are classified as special visceral efferent fibers.

10. Olfactory Nerve : CN I Exits the nose →
cribiform plate in ethmoid bone → olfactory bulb in anterior cranial fossa → olfactory tracts → cerebral cortex
∙sense of smell
CNI: Olfactory N (sp sensory/ sp afferent) Olfaction = sense of smell.
Only cranial n to enter the cerebrum directly.
Bipolar cells in the nasal mucosa ↑axons → enter cranium through foramina in the cribiform plate of the ethmoid bone. These cells and their axons, totalling in #, make up the Olfactory N..
Inhaled aromatic molecules dissolve in the moisture lining the olfactory epithelium and stimulate its chemoreceptors.
Olfactory receptor cells initiate action potentials in response to these chemical stimuli.
Once in the cranial cavity, the fibers terminate in a sm oval structure resting on the cribiform plate called the olfactory bulb. The functional component of olfactory fibers is special visceral afferent.
Cell bodies in nasal mucosa/septum > Olfactory tracts are formed from secondary neurons created by the synapse in the ant cranial fossa > Go on to temporal lobe.
Clinical testing: Person asked to sniff aromatic substances (i.e., vanilla, instant coffee) and identify each.
Homeostatic imbalance: anosmia

11. OLFACTORY NERVE: CLINICALLY SPEAKING
Fracture of ethmoid bone/ leisons of olfactory fibers may result in partial or totat loss of smell, anosmia [an-oz-me-ah]= an inability to detect odors) this may also dull the sense of taste.
Anosmia may also be caused by the common cold, allergic rhinitis, frontal lobe tumors, trauma, aging.
After head trauma, patient complains of runny nose (rhinnorhea): test nasal drip with dextrose or urine test strips --- WHY?
anosmia [an-oz-me-ah]= an inability to detect odors)

12. Optic Nerve: CN II Fibers arise from retina
exit orbit via optic canals
optic chiasm
optic tracts
thalamus (synapse)
primary visual cortex of occipital lobe
∙sense of
vision
B/C this sensory n. of vision develops as an outgrowth of the brain, it is really a brain tract.
Fibers arise from retina of eye to form Optic N, which passes through optic canal of orbit. The Optic N converge to form the optic chiasma where fibers partially cross over, continue on as optic tracts, enter thalmus, and synapse here. Thalamic fibers run (as the optic radiation) to occipital (visual) coretex, where visual interpretation occurs.
Rods & cones in the retina of the eye rec info from the visual fields, and through intermediary cells, convey this input to retinal ganglion cells. Ganglion cell axons converge at the optic disc, pass through the sclera, and form the optic n. The optic n. from ea eye enters the skull via the optic foramen and joins its opposite to form the optic chiasm. At the chiasm, fibers from the nasal halves of ea retina cross, while those from the temporal halves remain uncrossed. In this way the optici tracts, which extend from the chiasm to the thalmus, contain fibers conveying information from both eyes. Injury to one optic n. therefore results in total blindness in that eye, while damage to the optic tract on one side results in partial blindness in both eyes. Optic fibers also participate in accommodation in the lens and in the pupillary light reflex. Since the subarachnoid space around the brain is continuous w/ that around the optic n., incr in intracranial pressure can result in papilledema, or damage to the opic n., as it exits the bulb of the eye.
FXN: purely sensory; carry afferent impulses for vision

13. Nasal fibers cross at chiasm.
Fibers from nasal half of retina relay info from temporal field of that eye.
Fibers from temporal half of the retina relay info from the nasal field of that eye.
Nasal fibers cross at chiasm.
ONLY THE FIBRES FROM THE MEDIAL HALF OF EA RETINA CROSS IN OPTIC CHIASM.
Hemianopsia: blindness in one half of the visual field of one or both eyes.
Each optic nerve carries fibers from the nerve cells of the retina and leaves the back of the orbit as the stalk of the eyeball through the optic foramen to enter the middle cranial fossa. The two optic nerves for an X-shaped crossing or chiasma under the frontal lobes, in front of the pituitary stalk, the hind limbs of the X being the optic tracts. The effect of this is that fibers from the outer half of each retina remain in the optic tract of the same side, while those from the inner halves cross into the opposite tract. Thus the right tract carries all the fibers from the right halves of both retinas, and, therefore, all the sensation from the left half of the visual field, and vice versa for the left tract. This separation is essential to maintain one-sided representation of function in each half of the brain. The eye is a one-sided organ, but sees on both sides of the body, and what is needed for coordination is that each side of the visual field should be represented as such in the cerebral cortex. The impulses are relayed to the visual area of the occipital cortex, and are connected with the nucleus of the third nerve (the oculomotor nerve), which controls eye movements.

14. OPTIC NERVE: CLINICALLY SPEAKING
Clinical testing: vision and visual field are determined w/ eye chart and by testing the point at which the person first sees and object (finger) moving into the visual field. Fundus of eye viewed w/ opthalmoscope to detect papilledema (swelling of optic disc, the site where the optic n leaves the eyeball) as well as for routine exam of the optic disc and retinal blood vessels.
Homeostatic imbalance: damage to optic n results in blindess in eye served by n.; damage to visual pathway beyond the optic chiasma results in partial visual losses; visual defects are called anopsias (ah-nop-se-ahz). The nerve that transmits visual information from the retina to the brain. Also known as the second cranial nerve, it is a purely sensory nerve consisting of about 1.2 million nerve fibers.
visual_fields.php
Visual Field Defects: result from leisons of different parts of the optic pathway – complete section of optic n, chiasm or tract; also pituitary gland tumors, berry aneursyms of ICA.
If section of optic n affected .. Ipsilateral blindness
If ‘ ‘ optic chiasm …….Bitemporal hemianopsia
If “ “ optic tract ………..Contraleral homonymous Hemianopsia *m.c. visual field loss and seen in stroke patient.
MS: can affect optic n since it is susceptible to demyelination. Other CNs not involved here.

15. Cranial Nerves to the Eye

16. LR is supplied by CN VI, SO by IV and rest by CNIII

17. Oculomotor Nerve: CN III
Emerges from midbrain enters orbit thru superior orbital fissure branches into superior division and inferior division Motor(efferent) control of all eye muscles except sup oblique and lateral rectus. Parasympathetic innervation via ciliary ganglion. This produces accommodation via the ciliary muscle and pupillary constriction via the sphincter pupillae
Ganglion= collection of nerve cell bodies outside of CNS .
Fibers extend from ventral midbrain (near its junc w/ pons) and pass through bony orbit, via superior orbital fissure, to eye.
FXN: Chiefly motor n (Oculomotor = motor to the eye); contain a few proprioceptive afferents. Ea n incl the following:
SOMATIC motor fibers to 4/6 extrinsic eye musc (inf oblique & supr, inf, and med’l rectus musc) that help direct eyeball, and to levator palpebrae supeioris musc, which raises upper eyelid.
PARASYMPATHETIC (autonomic) motor fibers to sphincter pupillae (circ musc of iris), which cz pupil to constrict, and to ciliary musc, controlling lens shape for visual focusing. Some parasympathetic cell bodies are in the ciliary ganglia.
SENSORY (proprioceptor) afferents, which run from same 4 extrinsic eye musc to midbrain.
The Oculomotor N exists the ventral midbrain, pierces the dura, course through the lat’l wall of the cavernous sinus, and exits the cranial cavity via the superior orbital fissure. The third cranial nerve. The oculomotor nerve stimulates only motor functions. This nerve controls all the muscles that move the eye, except for two – the superior oblique muscle (which rotates the eyeball downward and outward and is controlled by the trochlear nerve) and the lateral rectus muscle (which moves the eye outward and is controlled by the abducens nerve). The oculomotor nerve also carries parasympathetic fibers to the muscles that constrict the pupil (sphincter pupilae), the ciliary muscle (which focuses the eye), and the muscle that raises the upper eyelid. The oculomotor nerve arises from the brainstem and enters the dura mater to lie on the side wall of the cavernous sinus. The nerve enters the orbit through the superior orbital fissure.

18. OCULOMOTOR NERVE: CLINICALLY SPEAKING
Pupil Involvement with CN3:
Oculomotor palsies often have pupillary involvement because the parasympathetic nerves innervating the iris travel with the third nerve.
Pupillary involvement is a crucial diagnostic sign — compressive lesions tend to involve the pupil, while vascular lesions actually spare it!
Homestatic imbalance: in Oculomotor n paralysis, eye can not be moved up, down, or inward and at rest, eye rotates laterally (ext’l strabismus) b/c the actions of the 2 extrinsic eye musc not served by CNs III are unopposed; upper evelids droop (ptsosis) and the person has dbl vision and trouple focusing on objects.
Majority of the extraocular muscles are innervated by CN3, so when knocked-out the eye deviates down and out because of the still functioning abducens and superior oblique muscles. In addition, the levator palpebrae (the main lid retractor) is innervated by CN3 and its paralysis gives you a severe eyelid ptosis. Finally, the parasympathetic pupil-constrictor fibers from the Edinger-Westphal nucleus travel within CN3, and their loss gives you a “blown pupil.”
These aneurysms occur at the junction of the posterior communicating artery and the internal carotid artery.
Most third nerve palsies are caused by ischemic events at the nerve secondary to hypertension or diabetes. The one thing you really need to worry about in these patients is a compressive aneurysm pushing on the nerve. These aneurysms occur at the junction of the posterior communicating artery and the internal carotid artery. Compressive lesions usually affect the parasympathetic nerve component: a blown pupil is a potential emergency. Whenever you have pupillary involvement, you need an MRI and angiography to rule out a dangerous aneurysm or tumor
CN III palsy

19. Trochlear Nerve: CN IV
Smallest CN, but longest intracranial (subarachnoid) course
Emerges from post midbrain →
passes to orbit via superior orbital
fissures →
superior oblique m.
(abducts, depresses,
medially rotates).
The fourth and thinnest cranial nerve.
Each of the two trochlear nerves controls just one of the small muscles (ocular muscles) which moves each eyeball, and is purely motor. Like the oculomotor nerve, the trochlear nerve arises in the midbrain, issues through the back of it, curves forward round the side of it, and appears at the front of the brain between the posterior cerebral and superior cerebral arteries. It enters the dura mater through a small aperture hidden under the free margin of the tentorium at or immediately behind the point where the two margins cross. The nerve then runs forward in the lateral wall of the cavernous sinus below the oculomotor nerve and above the ophthalmic nerve. It next runs obliquely upward across the lateral side of the oculomotor nerve, and passes through the superior orbital fissure into the orbit,
FXN: Primarily motor n.; supply somatic motor fibers to (and carry proprioceptor fibers from) one of the extrinsic eye musc, the supr obliq musc.
Damage to the trochlear n. will result in a loss of this eye mvmt and may produce diplopia (dbl vision).

20. CN III & CN IV LEISONS: CLINICALLY SPEAKING
Oculomotor N. compression: from increasing intracranial pressure(extradural hematoma) can compress the autonomic part of CNIII against the temporal bone(petrous)ipsilateral dilated pupil; slowness of pupillary response to light
Trochlear N. palsy: can be caused by trauma or ischemic event. Due to long intracranial passage, susceptible to damage if brain sloshes around or bounces against tentorium. Patients have an upward deviation of the affected eye and ‘cyclotorsion’ twisting of the eye that makes them turn away from the lesion.
Pupillary reflex: afferent-optic n; efferent – oculomotor n
Clinical testing: Tested in common w/ CN III.
Homeostatic imbalance: Trauma to, or paralysis of, a trochlear N results in dbl vision and reduced ability to rotate eye inferolaterally.

21. Trigeminal Nerve: CN V
This is the largest of the CNs. It has both motor and sensory components: sensory fibers being gen’l somatic afferent and the motor fibers being spec visc’l efferent. Most of the cell bodies of sensory fibers are loc in the trigeminal ganglion, which is attached to the pons by the trigeminal root. These convey pain and thermal sensations from the face, oral and nasal cavities, and parts of the dura and nasal sinuses, sensations of deep pressure, and inf from sensory endings in m.. Trigeminal motor fibers, projecting from nuclei in the pons, serve the m. of mastication. Lesions of the trigeminal n. result in sensory losses over the face or in the oral cavity. Damage to motor fibers results in paralysis of the masticatory m; as a result, the jaw may hang open or deviate toward the uninjuried side when opened. Trigeminal neuralgia, or tic douloureux, is an intense idiopathic pain originating mainly from areas supplied by sensory fibers of the maxillary and mandibular branches of this n. The trigeminal ganglion gives rise to 3 lg n.: the opthalmic, maxillary and mandibular.
The maxillary nerve courses through the cavernous sinus below the ophthalmic nerve and passes through the foramen rotundum into the orbital cavity. Branches of the maxillary nerve are (1) the meningeal branches, which serve the dura of the middle cranial fossa; (2) the alveolar nerves, serving the upper teeth and gingiva and the lining of the maxillary sinus; (3) the nasal and palatine nerves, which serve portions of the nasal cavity and the mucosa of the hard and soft palate; and (4) the infraorbital, zygomaticotemporal, and zygomaticofacial nerves, serving the upper lip, the lateral surfaces of the nose, the lower eyelid and conjunctiva, and skin on the cheek and the side of the head behind the eye.

22. Trigeminal Nerve: CN V Largest cranial nerve
Principal somatic sensory nerve to the face
Emerges from lateral pons by a large sensory and small motor rootsensory root leads to trigeminal ganglion. Motor root bypasses ganglion to become part of CN V3.
Sensory Root:
Ophthalmic (V1)– exits by sup orbital fissure to give sensation to cornea, skin of forehead, scalp, eyelids, nose.
Ciliary ganglion associated with V1. Corneal reflex tests V1.
Maxillary (V2)– exits by foramen rotundum to give sensation over maxilla, upper lip and teeth. Pterygopalatine (parasymatetic ) ganglion is associated with V2 lacrimal glands, glands of nose and palate.
Mandibular (V3)– exits by foramen ovale to give sensation over mandible and lower lip and teeth, ant 2/3 of tongue.
Otic and submandibular (parasymp) ganglia associated with V3.
Motor Root: exits with V3 via foramen ovale to supply m. of mastication, mylohyoid, ant belly of digastric, tensor tympani and tensor veli palatini m.
The mandibular nerve exits the cranial cavity via the foramen ovale and serves (1) the meninges of middle and parts of the anterior cranial fossae (meningeal branches); (2) the temporomandibular joint, skin over part of the ear, and skin over the sides of the head above the ears (auriculotemporal nerve); (3) oral mucosa, the anterior two-thirds of the tongue, gingiva adjacent to the tongue, and the floor of the mouth (lingual nerve); and (4) the mandibular teeth (inferior alveolar nerve). Skin over the lateral and anterior surfaces of the mandible and the lower lip is served by cutaneous branches of the mandibular nerve.
Trigeminal motor fibers exit the cranial cavity via the foramen ovale along with the mandibular nerve. They serve the muscles of mastication (temporalis, masseter, medial and lateral pterygoid), three muscles involved in aspects of swallowing (anterior portions of the digastric muscle, the mylohyoid muscle, and the tensor veli palatini), and a muscle that has a damping effect on loud noises by stabilizing the tympanic membrane (tensor tympani).
Corneal reflex: afferent – trigeminal; efferent – facial(orbicularis oculi).
**The fibers from the branches of CN V carry only POSTsynaptic parasympathetic fibers from the various ganglia(ciliary etc)

23. TRIGEMINAL NERVE LEISONS: CLINICALLY SPEAKING
Injury : by trauma (dental, cranial), tumors, aneurysms, infection (herpes zoster ophthalmicus) can all cause numbness
Paralysis of m of mastication with deviation of mandible toward side of lesion-
Motor branch of V3
Ophthalmic N passes through the wall of the cavernous sinus, enters the orbit via the superior orbital fissure. Branches in the orbit are (1) the lacrimal nerve, serving the lacrimal gland, part of the upper eyelid, and the conjunctiva; (2) the nasociliary nerve, serving the mucosal lining of part of the nasal cavity, the tentorium cerebelli and some of the dura of the anterior cranial fossa, and skin on the dorsum and tip of the nose; and (3) the frontal nerve, serving the skin on the upper eyelid and the forehead and scalp above the eyes up to the vertex of the head.
The trigeminal pathway for touch and pressure. Touch and pressure sensation from the orofacial structures transmitted to the brainstem trigeminal nuclei, the main sensory nucleus, & spinal nucleus via the central processes of first order
pseudounipolar neurons whose cell bodies are located in the trigeminal ganglion. Second order neurons in these nuclei form the post & ant trigeminal
lemnisci which terminate in the ventral posterior medial nucleus of the thalamus (VPM). Third order neurons in the thalamus project to the postcentral
gyrus. PCG, postcentral gyrus; Sc, subnucleus caudalis; Si, subnucleus interpolaris; So, subnucleus oralis; V1, ophthalmic division of the trigeminal nerve; V2,
maxillary division of the trigeminal nerve; V3, mandibular division of the trigeminal nerve.
The trigeminal pathway for pain and temperature. Pain and temperature sensation from the orofacial structures is transmitted to the brainstem subnucleus caudalis
Branchiomotor innervation of the trigeminal nerve. The motor nucleus of the trigeminal nerve contains the motoneurons whose axons assemble to form the motor root of the trigeminal nerve. The motor root exits the pons and joins the mandibular division of the trigeminal nerve anddistributes to the muscles of mastication, the mylohyoid, the anterior belly of the digastric, the tensor tympani, and the tensor veli palatini muscles to provide them with motor innervation.

24. Abducens Nerve: CN VI Emerges from between pons and medulla
exits through sup orbital fissure to enter the eye
Supply motor fibers to lateral rectus m of eyeball
(abducts eye)
From its nucleus in the caudal pons, the abducens nerve exits the brain stem at the pons-medulla junction, pierces the dura, passes through the cavernous sinus close to the internal carotid artery, and exits the cranial vault via the superior orbital fissure. In the orbit the abducens nerve innervates the lateral rectus muscle, which turns the eye outward. Damage to the abducens nerve results in a tendency for the eye to deviate medially, or “cross.” Double vision may result on attempted lateral gaze.

25. CN VI PALSEY: CLINICALLY SPEAKING
supplies LR6: unable to look LATERALLY (OUTWARDS)
develop double vision when looking to the side of the lesion
medial deviation of eye
Most commonly caused by increased intracranial pressure or vasculopathic etiologies (Diabetes, Hypertension).
Sixth cranial nerve (abducens) palsy is a common cause of acquired horizontal diplopia. Note the lack of abduction of the right eye.
The abducens nerve controls the lateral rectus muscle. Loss of CN6 renders the eye unable to abduct (turn out). Patients will go cross-eyed, so to compensate they may turn their head to avoid double vision.
If you look back in that drawing of the brainstem, you’ll see that the abducens nerve is located further down the brainstem, “all by its lonesome” down in the pons. The nerve root exits the brainstem even further down at the ponto-medulary junction and has to run up the floor of the skull to get to the cavernous sinus and into the orbit. Where the nerve enters the cavernous sinus, it makes an abrupt 90-degree bend. Something about this abrupt turn makes the 6th nerve susceptible to high intracranial pressure. Patients with high ICP from pseudotumor cerebri commonly have their 6th nerve(s) knocked out – an abducens palsy is actually incorporated into the Dandy criteria for diagnosing PTC

26. Facial Nerve: CN VII Emerges from junction between pons and medulla
traverses post cranial fossa runs through internal acoustic meatus and facial canal
in petrous part of temporal bone exits via stylomastoid foramen (gives post auricular)forms parotid plexus
gives rise to terminal br: temporal, zygomatic, buccal, marginal mandibular, cervical.
When in facial canal it gives rise to:
Greater petrosal n.presyn parasym fibers for pterygopalatine ganglia
N. to stapedius motor fibers to stapedius
Chordae typmani n.  presyn parasympathetic fibers to submandibular ganglia
Somatic Motor fibers: to m of facial expression, stylohyoid, post belly of digastric,stapedius
Presynaptic Parasympathetic motor fibers: pterygopalatine ganglion(lacrimal glands), and submandibular ganglion(sublingual and submandibular salivary glands)
Special Sensory fibers: taste to ant 2/3 of tongue and soft palate

27. Main motor root: innervates m of facial expression
Intermediate n: taste, parasympathetic, somatic sensory fibers

28. FACIAL NERVE LESIONS: CLINICALLY SPEAKING
With a peripheral(LMN) 7th n lesion:
paralysis of ALL facial muscles on IPSILATERAL side:
pt cannot close eye, wrinkle that side of forehead or raise that corner of mouth = Bell’s Palsy
The facial nerve is composed of a large root that innervates facial muscles and a small root (known as the intermediate nerve) that contains sensory and autonomic fibers. Other signs of 7th N lesions: Also loss of taste to anterior 2/3 of tongue; dry cornea
If damage occurs at the stylomastoid foramen, facial muscles will be paralyzed but taste will be intact.
From the facial nucleus in the pons, facial motor fibers enter the internal auditory meatus, pass through the temporal bone, exit the skull via the stylomastoid foramen, and fan out over each side of the face forward of the ear. fibers of the facial nerve are special visceral efferent; they innervate small muscles of the external ear, the platysma, the stapedius, the occipitofrontalis, the stylohyoid posterior belly of the digastric, the buccinator, and the muscles of facial expression.
The intermediate nerve contains autonomic (parasympathetic) as well as general and special sensory fibers. Preganglionic autonomic fibers, classified as general visceral efferent, project from the superior salivatory nucleus in the pons. Exiting with the facial nerve, they pass to the pterygopalatine ganglion via the greater petrosal nerve (a branch of the facial nerve) and to the submandibular ganglion by way of the chorda tympani nerve (another branch of the facial nerve, which joins the lingual branch of the mandibular nerve). Postganglionic fibers from the pterygopalatine ganglion innervate nasal and palatine glands and the lacrimal gland, while those from the submandibular ganglion serve submandibular and sublingual salivary glands. Among the sensory components of the intermediate nerve, general somatic afferent fibers relay sensation from the caudal surface of the ear, while special visceral afferent fibers originate from taste buds in the anterior two-thirds of the tongue, course in the lingual branch of the mandibular nerve, and then join the facial nerve via the chorda tympani branch. Both somatic and visceral afferent fibers have cell bodies in the geniculate ganglion, which is located on the facial nerve as it passes through the facial canal in the temporal bone.
With central (UMN) 7th n lesions:
paralysis of LOWER facial muscles on CONTRALATERAL side
(forehead wrinkling possible)--- ex common in stroke
Other signs of 7th n lesions: loss of taste to anterior 2/3 of tongue; dry cornea

29. Vestibulocochlear Nerve: CN VIII
This cranial nerve has a vestibular part, which functions in balance, equilibrium, and orientation in three-dimensional space, and a cochlear part, which functions in hearing. The functional component of these fibers is special somatic afferent; they originate from receptors located in the temporal bone.
Vestibular receptors are located in the semicircular canals, which provide input on rotatory movements (angular acceleration), and in the utricle and saccule, which generate information on linear acceleration and the influence of gravitational pull. This information is relayed by the vestibular fibers, whose bipolar cell bodies are located in the vestibular (Scarpa's) ganglion. The central processes of these neurons exit the temporal bone via the internal acoustic meatus and enter the brain stem alongside the facial nerve.

30. Vestibulocochlear Nerve: CN VIII
Originate between pons and medullainternal acoustic meatus where it divides into the vestibular n. and the cochlear n.
Vestibular n. : sensory to semicircular ducts and saccule and utricle, for equilibrium and motion
Cochlear n : sensory to spiral organ for hearing
Auditory receptors of the cochlear division are in the organ of Corti and follow the spiral shape (about 2.5 turns) of the cochlea. Air movement against the eardrum produces mechanical actions by the ossicles of the ear, which, in turn, cause movement of fluid in the spiral cochlea. This fluid movement is transduced by the organ of Corti into nerve impulses interpreted as auditory information. The bipolar cells of the spiral (Corti's) ganglion give rise to central processes that course with the vestibular nerve. At the brain stem, cochlear fibers separate from vestibular fibers to end in the dorsal and ventral cochlear nuclei.
Lesions of the vestibular root result in eye movement disorders (nystagmus), unsteady gait with a tendency to fall toward the side of the lesion, nausea, and vertigo. Damage to the cochlea or cochlear nerve results in complete deafness, ringing in the ear (tinnitus), or both.

31. CLINICALLY SPEAKING: VESTIBULOCOCHLEAR NERVE LEISONS
Lesions of CN VIII may cause: tinnitus (ringing of ears), vertigo (dizziness), loss of hearing.
Lesions may involve either vestibular or cochlear or both divisions of CN VIII.

33. Glossopharyngeal Nerve: CN IX
Emerges from medulla jugular foramen
Motor(efferent) fibers to stylopharyngeus, and presynaptic parasym fibers to Otic ganglion for parotid gland innervation.
Sensory fibers to post 1/3 tongue for taste and general sensation, and sensory to pharynx, carotid sinus and body
Lesions of CN IX:
gag reflex absent on side of lesion or loss of taste on post 1/3 of tongue (i.e., infection/tumors).
Tumors usually involve IX, X, XI –jugular foramen syndrome
The glossopharyngeal nerve provides parasympathetic innervation to the
parotid gland
CLINICALLY SPEAKING A unilateral lesion to the glossopharyngeal nerve near its exit from
the brainstem, damaging all of its fibers, will result in damage to the SVA
fibers relaying taste sensation and will cause ipsilateral loss of taste
sensation from the posterior one-third of the tongue. Damage to the GVE
parasympathetic fibers will cause a reduction in salivary secretion of
the parotid gland; and damage to the GVA fibers will result in diminished
visceral sensation from the pharyngeal mucous membrane, loss of the
gag reflex (due to damage of the afferent limb of the reflex arc), and loss
of the carotid sinus reflex. The stylopharyngeus muscle, which elevates
the pharynx during swallowing, will be paralyzed.

34. Vagus Nerve: CN X Emerge as rootlets from the lateral medulla
exit skull via jugular foramen
traverses down neck in carotid sheath
enters superior mediastinum and gives rise to recurrent laryngeal nerves
then reforms as vagal trunks into the abdomen
Motor: voluntary m of larynx and esophagus; pharynx; mediates motor limb of gag reflex; parasympathtic to involuntary m of heart, tracheobronchial tree, esophagus and GI tract
Sensory: pharynx, larynx
The vagus nerve has the most extensive distribution in the body, innervating
structures in the head but also the neck, thorax, and abdomen
Longest course and most extensive distribution of all cranial n.

35. CLINICALLY SPEAKING:
Unilateral damage of the vagus nerve near its emergence from the brainstem results in a number of deficiencies on the ipsilateral side. Damage to the SVE branchio otor fibers will cause flaccid paralysis or weakness of: (i) the pharyngeal muscles and levator veli palatini of the soft palate, resulting in dysphagia (difficulty swallowing); (ii) the laryngeal muscles, resulting in dysphonia (hoarseness) and dyspnea (difficulty breathing); and (iii) loss of the gag reflex (efferent limb). Damage to the GVA fibers
will cause loss of general sensation from the soft palate, pharynx, larynx, esophagus, and trachea. Damage to the GVE fibers will cause cardiac arrhythmias.
A bilateral lesion of the vagus nerve is incompatible with life, due to the interruption of parasympathetic innervation to the heart.

36. Pharyngeal Plexus of CN X
Pharyngeal Plexus of Vagus Nerve: network of nerve fibers innervating most of palate, larynx, and pharynx.
Located on the surface of the middle pharyngeal constrictor muscle. Composed of fibers from CN IX, X, XI
(all leave jugular foramen together)
Sensory Innervation:
Oropharynx and laryngopharynx
Motor Innervation:
all muscles of pharynx(except stylopharyngeus (direct IX))
all muscles of soft palate(except tensor veli palatini(V3))
pharyngeal constrictors
Palatoglossus (extrinsic tongue and palatine m)

37. Spinal Accessory: CN XI
Arise as rootlets from the sides of the spinal cord
pass through jugular foramen.
Motor fibers to SCM and trapezius
The spinal accessory nerve supplies motor innervation to the sternocleidomastoid, trapezius, and many of the intrinsic laryngeal muscles.
CLINICALLY SPEAKING
A unilateral lesion confined to the spinal accessory nucleus or the nerve proximal to its muscular distribution results in an ipsilateral flaccid paralysis and subsequent atrophy of the sternocleidomastoid and upper part of the trapezius muscles. An individual with such a lesion is unable to turn his or her head away from the lesion. Normally, unilateral contraction of the sternocleidomastoid muscle draws the mastoid process inferiorly, bending the head sideways (approximating the ear to the shoulder), which
is accompanied by an upward turning of the chin towards the opposite side. If the upper part of the trapezius is paralyzed, the upper border of the scapula is rotated laterally and inferiorly with its inferior angle pointing towards the spine. This results in slight drooping of the ipsilateral shoulder, accompanied by a weakening of the shoulder when attempting to raise it.

38. Hypoglossal Nerve: CN XII
Arise from the medulla by rootlets
exits cranium via hypoglossal canal 
runs inferiorly and anteriorly to tongue
Motor fibers supply all extrinsic and intrinsic muscles of tongue except palatoglossus
The hypoglossal nerve provides motor innervation to the muscles of the tongue
CLINICALLY SPEAKING
A unilateral lesion of the hypoglossal nerve will cause the tongue to deviate toward the side of the lesion (impaired side)
A lesion in the hypoglossal nucleus or nerve results in flaccid paralysis and subsequent atrophy of the ipsilateral tongue musculature.
Hemiparalysis of the tongue causes creasing (wrinkling) of the dorsal surface of the tongue ipsilateral to the lesion. Normally, the simultaneous contraction of the paired genioglossi muscles causes the tongue to protrude straightforward. During examination of the patient it is important to remember that a unilateral lesion of the hypoglossal nerve will cause the tongue to deviate towards the side of the lesion (impaired side) since the functional genioglossus on the intact side is unopposed by the paralyzed,
inactive genioglossus on the lesion side.

39. CRANIAL NERVE LESIONS X, XI AND XII
CN X: isolated lesions uncommon; paralysis of recurrent laryngeal n
(cancer of larynx or thyroid gland; surgery)
Injury of the recurrent laryngeal n: hoarseness, dysphonia due to paralysis of vocal cords
Deviation of uvula to normal side
CN XI: injury causes drooping of shoulder
CNXII: injury causes paralysis to ipsilateral side of tongue—tongue deviates toward affected side
Hypoglossal N Palsey: Isolated left LMN leison

41. Anatomy of Cranial Nerves and foramina of skull: http://www. youtube
Cranial Nerve and foramina quizzes/tutorials: