Cranial nerves Flashcards

1
Q

How many functions does a cranial nerve commonly have? what is a brainstem nuclei?

A

Cranial nerves commonly have more than one function- each function can be tested independently.

A brainstem nucleus is a cluster of neurones within the brainstem associated with one of the cranial nerves. Brainstem nuclei can be purely motor, sensory or both, projecting motor fibres and receiving sensory fibres that synapse here.

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2
Q

What would loss of all functions of a cranial nerve indicate? what would partial loss of cranial nerves indicate?

A

Loss of all functions indicates peripheral damage to the cranial nerve (LMN lesion)

Partial loss indicates damage to one part of the brainstem nucleus:

E.g Trigeminal has three regions that perceive different sensations- proprioception/light touch/ pain and temperature. Intranuclear damage i.e by a small infarct could knock out one particular function (pain sensation in the opthalmic region of the face), whereas loss of all these functions would indicate LMN damage.

Loss of one function could also occur if there was damage to the cerebral cortex involved in the perception of that sensory modality (i.e infarct in primary somator sensory cortex involved in pain reception from the face).

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3
Q

What is the anterior cranial fossa?

What is it made up of?

What travels through it?

what is the clinical relevance?

A
  • Anterior cranial fossa made up of the frontal bone, ethmoid bone (the cribriform plate) and the lesser wing of the sphenoid bone
  • Bony landmarks -
    • frontal crest of frontal bone= point of attachment for the falx cerebri
    • Crista galli of ethmoid bone = point of attachment of the falx cerebri
    • Cribriform plate supports olfactory bulb, contains multiple foramina for transmiting olfactory nerve fibres into nasal cavity.
  • Clinical aspects: ethmoid bone thinnest bone in anterior cranial fossa, most likely to fracture.
    • fracture can cause CSF rhinorrhoea where meningeal covering are ripped
    • Anosmia - where shearing of olfactory neve fibres occurs
    • Can also introduce air into the cranial cavity
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4
Q

What is the middle cranial fossa formed of?

A
  • Formed of the sphenoid bone (after the lesser wings marking boundary of anterior cranial fossa) and temporal bone- posterior boundary marked by petrous portion.
  • Bony landmarks- sella turcica of sphenoid bone- pituitary gland sits here.
  • Foramina of sphenoid bone:
    • Optic canals situated anteriorly in middle cranial fossa, transmit optic nerve (CNII) (and opthalmic arteries)
    • Superior orbital fissure - transmits CN III, IV, Va/V1, VI. (and opthalmic veins)
    • Foramen rotundum- CN V2 (maxillary branch- max is very rotund).
    • Foramen ovale - CN V3 (mandibular branch - mandy affects your mandible).
    • Foramen spinosum - middle meningeal artery/ vein and meningeal branch CN V3.
  • Foramen of temporal bone:
    • ​Carotid canal - internal carotid artery enters here
    • Foramen lacerum - filled with cartilage and small blood vessels
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5
Q

What is the posterior cranial fossa?

What is it made up of?

What foramina are there/ what structures pass through?

A
  • Posterior cranial fossa formed of the temporal bones and occipital bone. Bound anteriorly by superior petrous portion of the temporal bone. Floor formed by occipital bone.
  • Houses the brainstem (midbrain/pons/medulla) and cerebellum, contines out foramen magnum as the spinal cord
  • Foramina /Bony landmarks:
    • Temporal bone- Internal acoustic meatus:
      • transmits CN VII and CNVIII (facial and vestibulochoclear). (and labyrinthine artery)>
    • Occipital bone- Foramen magnum:
      • transmits medulla/meninges/vertebral arteries/ ascending accessory nerve (CN XI), dural veins and posterior spinal arteries.
    • Occipital bone- jugular foramen:
      • Transmits CN IX, X , XI ( glossopharyngeal, vagus, descending portion spinal accessory nerve)
      • Internal jugular vein, sigmoid sinus
    • Hypoglossal canal:
      • Transmits CN XII
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6
Q

What is the clinical relevance of the foramen magnum?

A
  • Cerebellar tonsilar herniation also known as coning
  • Cause : increased intracranial pressure - could be due to hydrocephalus, space occupying lesion
  • Results in: compression of pons and medulla which contain cardiac and respiratory centres- leads to death from cardiorespiratory arrest.
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7
Q

What pathology can affect CN II?

What pathology can particulary affect CN IV?

A
  • Pituitary adenoma can compress the optic chiasm causing a distubrance in visual acuity, visual field and accomodation
  • Cranial N IV - trochlear nerve - is the only nerve to come off the back of the dorsal surface of the brainstem- therefore particularly susceptible to increases in intracranial pressure.
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8
Q

What pathology can affect CN’s VII and VIII?

A
  • An acoustic neuroma = tumour on cranial nerve 8, facial nerve is very close to this nerve
  • Often presents with facial paralysis/ loss of sensation
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9
Q

Fill out the table

A
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10
Q

Describe the pathway of CN I:

What is the structure of its place of origin?

A
  • CN I= Olfactory nerve which allows sense of smell.
  • Projects from the olfactory mucosa in the superior portion of the nasal cavity:
    • Olfactory mucosa formed of:
      • 1) basal cells from which new olfactory cells can develop
      • 2) sustentacular cells - structural support
      • 3) olfactory receptor cells- bipolar neurons with dendritic processes projecting out to surface of olfactory epithelium into the mucous membrane and central porcesses that enter through the basement membrane- once through the cribriform plate they enter the olfactory bulb.
      • 4) also bowmans glands which secrete mucus
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11
Q

What is special about olfactory neurons?

What could unilateral anosmia be caused by?

What would bilateral anosmia indicate?

A
  • Olfactory neurons can regenerate (basal cells in the olfactory epithelium)
  • Unilateral anosmia is likely due to a perihpheral cause 1) anterior cranial fossa trauma 2) meningioma - which is a slow growing brain tumout in the arachnoid layer
  • Bilateral anosmia more likely caused by trauma to the olfacotory bulb- closer to the brain itself.
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12
Q

How would you test CN I function?

What are some common causes of anosmia?

A
  • Patient asked if there has been any change in their taste or sense of smell
  • Each nostril testing by asking patient to identify a certain well known smell (orange/ coffee/ peppermint) whilst eyes are closed.
  • Anosmia causes:
    • Anterior cranial fossa trauma (CSF Rhinorrhoea)
    • meningioma
    • Neurodegenerative conditions - Parkinson’s and alzheimers. Often progressive loss, precedes motor symptoms. Not often noticed by patient.
    • Viral infection
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13
Q

What is phantosmia?

What is cacosmia?

A
  • Phantosmia = smelling an odor that is not actually there (olfactory hallucination)
  • Cacosmia= Brain unable to properly identify a certain smell. Cacosmia smell often described as similar to faeces or burning.
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14
Q

Cranial nerve II:

Where does it run from/ to?

What sense does this allow?

A
  • CN II formed by convergence of axons from retinal ganglion cells
  • These cells have received impulses from rod and cone photoreceptor cells
  • Leave via optic canal, enter cranial cavity and unite to form optic chiasm.
  • Fibres enter lateral geniculate nucleus then projects to the primary visual cortex in the occipital lobe.
  • Allows sight!
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15
Q

How can you test CN ii function?

A
  • Visual acuity (Snellen chart)
  • Visual fields - fibres from temporal visual fields cross over at the optic chiasm
  • Pupil light reflex - pupillary constriction in both eyes from shining light into one
  • Accomodation - ability of the eye to change its focus from distant to near object, achieved by the lens changing shape
  • Fundoscopy - exam that uses magnifying lens and light ot check retina at back of the eye
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16
Q

What is the pupillary light reflex?

A
  • The pupillary light reflex tests the functioning of the retina, the midbrain and CN III.
  • Shining light in ONE eye should make BOTH pupils contraact (Consensual light reflex).
  • Light hits the back of the retina, excites the photosensitive ganglion cells, impulse sent to the midbrain via the optic nerve.
  • The two optic nerves (R and L) come together at the optic chiasm. In the optic chiasm, nasal/medial fibres cross over. The left optic tract contains lateral/temporal fibres from the left eye, the right optic tract contains right temporal/lateral fibres and left medial/ nasal fibres.
  • Light in one eye (R eye) excites right optic nerve, the temporal/ lateral fibres synapse with ipsilateral PTN and the medial/ nasal fibres cross over and synapse with the contralateral PTN.
  • PTN also interconnected by the posterior commissure.
  • PTN then sends both ipsilateral and contralateral fibres to the Erdinger- Westphal nuclei. The Erdinger Westphal nuclei contain parasympathetic nerve cell bodies for cranial nerve iii.
  • Cranial nerve iii then carries PS innervation to the ciliary ganglion.
  • Post ganglionic parasympathetic fibres in short ciliary nerves enter iris and contract the sphincter pupillae muscles - bilateral constriction of both pupils.
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17
Q

What is cranial nerve iii?

What fibres does it contain?

What does it innervate?

What is its action?

A
  • Cranial nerve iii = oculomotor nerve, is both motor and parasympathetic
  • Motor - 4/6 extraocular muscles
  • Parasympathetic - sphincter pupillae and ciliary muscles of the eye
    • travels with sympathetic fibres to innervate levator palpebrae superioris (raise eyelid)
  • Actions: move eyeball, raise eyelid, constrict pupils
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18
Q

Describe the course of the oculomotor nerve to its targets

Describe the action on the targets

A
  • Originates in the oculomotor nucleus in the midbrain near to its parasympathetic nuclei in Erdinger Westphal
  • Enters the cavernous sinus
  • Exits via the superior orbital fissure
  • Innervates 4/6 extraocular eye muscles, levator palpabrae superioris and sphincter pupillae ( lens accomodation) and cililary muscles of the eye (constrict the pupils).
  • once nerve leaves the superior orbital fissue it divides into superior and inferior branches.
  • Superior branches innervate superior rectus and levator palpabrae superiosis (elevates eyeball and elevates eyelid respectively).
  • inferior branches innervate inferior rectus, medial rectus and inferior oblique.
  • Inferior rectus depresses eyeball, medial rectus adducts eyeball, inferior oblique elevates, abducts and laterally rotates eyeball.
  • ​Parasympathetic fibres run with inferior branch of oculomotor nerve and innervates 1) sphincter pupillae - pupil constriction 2) ciliary muscles- contract to make lens more convex, more adapated for short range vision.
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19
Q

What is the cavernous sinus?

What structures pass through it?

What is the clinical relevance of the cavernous sinus?

A
  • Cavernous sinus is a paired dural venous sinus either side of the sella turcica.
  • Mutiple structures travel through the sinus: O TOM CAt:
    • Lateral wall of cavernous sinus:
      • Oculomotor nerve
      • Trochlear nerve
      • Opthalmic division V1
      • Maxillary division V2
    • Medial portion cavernous sinus:
      • Carotid artery
      • Abducens (CN VI)
  • As multiple structures pass through, they are at risk of compression and bacterial infection which can track back into the sinus from the facial veins/ opthalmic veins
  • Infection in the carotid sinus can cause cavernous sinus thrombosis in an attempt to block further infection spread.
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20
Q

Where can lesions to the oculomotor nerve occur?

A

Oculomotor nerve motor and parasympathetic fibres exit the brainstem together via the interpeduncular fossa, passes below the posterior cerebral artery, pierces dura mater and travels through the cavernous sinus, through the superior orbital fissure and into the orbit.

Damage can occur:

  1. Midbrain (near its parasympathetic nuclei)
  2. Interpeduncular fossa
  3. posterior cerebral artery
  4. Cavernous sinus
  5. superior orbital fissue
  6. general ischaemia
21
Q

How might a cranial nerve iii lesion present?

A

1) Ptosis - drooping upper eyelid due to paralysis of levator palpabrae superioris
2) “down and out” eye- exotropia: due to unopposed action of the abducens and trochlear nerve. Loss of ability to adduct, elevate or depress eyeball.
3) Dilated pupil- loss of consensual light reflex
4) Diplopia- double vision both horizontally and vertically.

22
Q

What fibres does CN IV carry?

What is its route from its origin to its targets?

What is its action?

A
  • CN IV= Trochlear nerve
  • Route from trochlear nucleus (midbrain). Decussates before its fibres leave the brainstem and is the only CN to emerge from the dorsal side of the brainstem.
  • Enters the cavernous sinus goes through the superior orbital fissure to innervate the superior oblique muscle of the eye.
  • This muscle depresses the eye down and in
23
Q

What extraocular muscle does the trochlear nerve innervate?

what does a lesion to the trochlear nerve result in?

A
  • Trochlear nerve innervates the superior oblique muscle which travels through a pully (trochlea) hence name of the CN.
  • Pulls eye down and in
  • Lesion of CNIV can lead to eye being deviated upwards and out (extorsion).
  • Leads to vertical diplopia/ double vision
24
Q

What is cranial nerve VI?

Describe its course from its point of origin to its target

A
  • Cranial nerve VI - Abducens nerve
  • Motor supply to the lateral rectus muscle
  • Abducts the eye - moves eyeball laterally
  • Abducens nucleus in pons, nerve emerges at the pontomedullary junction
  • Travels across the base of the skull and into the cavernous sinus, immediately below the carotid artery
  • travels through the superior orbital fissure and reaches the lateral rectus muscle
25
Q

What would happen if CN VI (abducens) is lesioned?

A
  • Loss of innervation to lacteral rectus muscle
  • Loss of ability to abduct the eye/ look laterally
  • Eye rests in adducted position (convergent squint)
  • Leads to horizontal diplopia worse on affected side
26
Q

What would horizontal diplopia indicate?

What would vertical diplopia indicate?

A
  • Horizontal diplopia inidicates inability to to move the eye laterally - i.e abducens nerve trauma
  • Vertical diploplia inidicates inability to elevate/ depress the eye- i.e due to trauma of CN III or CNIV. CNIV innervates the superior oblique (depress eye down and in), CN III 4/ 6 that also elevate, depress and adduct.
27
Q

What is CN V?

Describe it origins, its targets and route of travel

A
  • CN V= Trigeminal nerve - motor and sensory
  • Origins - large sensory nucleus that spans the entire brainstem (midbrain/pons/medulla). Motor nucleus that originates in the pons
  • Sensory nuclei converge at the trigeminal ganglion which then splits into 3 divisions:
    • V1 -Opthalmic
    • V2- Maxillary
    • V3- Mandibular
    • Motor portion from the pons joins mandibular division, exits skull with it.
  • V1/V2/V3 allows sensory innervation to the face. Innervates the skin/mucuous membranes/sinuses. Motor portion of V3 does the motor innervation to all the muscles of mastication.
  • V1- opthalmic travels through cavernous sinus, exits via superior orbital fissure. Allows sensory innervation to the forehead/ scalp, cornea. (Also down to upper eyelid and dorsum of nose).
  • V2 - maxillary travels through the cavernous sinus, exits via foramen rotundum to allow sensory innervation from the maxillary region of the face. (From lower eyelid onto lateral nose, upper lip, upper teeth and gums, superior palate).
  • V3- Mandibular division exits via foramen ovale and travels onward to allow sensory innervation of the external ear/ lower lip and chin/ anterior 2/3 tongue/ oral cavity/ lower teeth and gums. Provides motor innervation to muscles of mastication, tensor veli palatini, tensor tympani.
28
Q

Describe the sensory innervation regions of the three divisions of CV 5

A
  • V1- opthalmic : forehead/ scalp/ dorsum of nose/ upper eyelid/ cornea/ frontal and ethmoid sinuses
  • V2- Maxillary - from lower eyelid, lateral nose, upper lip, upper teeth and gums, superior palate, maxillary sinus
  • V3- Mandibular - from lower lip and chin/ oral cavity/ lower teeth and gums/ anterior 2/3rds of the tongue/ portion of external ear
29
Q

Describe exit of the motor component of CN V

How would we test this function?

A
  • CN V motor division comes from a small motor nucleus in the pons
  • Fibres exit next to sensory trigeminal nerve fibres from lateral pons and accompany manidbular division towards muscles of mastication.
  • Testing CN V:
  • Ask patient to clench jaw whilst feeling for the contraction of temproalis and inferiorly for the masseter. Ask patient to open mouth a deviate mandible from R to L to check medial and lateral pterygoid function. Mandible will deviate towards weak side
  • Test jaw jerk reflex- stretch reflex of the masseter that will close the jaw.
  • Exaggerated in upper motor neurone lesion.
30
Q

What is cranial nerve VII?

What fibres does it contain?

Where does its fibres originate?

Where do they travel to?

What is the main route taken by the facial nerve?

A
  • Cranial nerve VII = Facial nerve
  • Contains motor (muscles of facial expression), special sense (taste to anterior 2/3rds of the tongue) and parasympathetic fibres (salivary glands (submandibular and sublingual) , lacrimal glands)
  • Originates in nuclei within the pons. The facial nucleus (with motor and small sensory branch) and superior salivatory nucleus (neurones innervate salivary glands)
  • Travels through the internal acoustic meatus, through the facial canal and exits via the stylomastoid foramen
  • Enters the parotid gland where it splits into 5 branches that innervate the muscles of facial expression.
31
Q

What are the branches of the facial nerve and when/ where do they split off?

A
  • Arises in the pons, beginning as two routes- a large motor root and small sensory root
  • Exits lateral pontomedullary junction and with CN VIII travels through internal acoustic meatus, then enter the facial canal. Within the facial canal:
    • two roots fuse to form facial nerve
    • Nerve gives rise to greater petrosal nerve - parasympathetic supply to mucuous glands and lacrimal glands
    • nerve to stapedius in middle ear
    • chorda tympani- special sensory fibres to anterior 2/3 tongue and parasympathetic fibres to submandibular and sublingual glands.
  • Facial nerve then exits facial canal via stylomastoid foramen, located just posteior to styloid process on temporal bone.
  • Enters parotid gland where it splits into 5 branches.
32
Q

What are the 5 branches of the facial nerve that split in the parotid gland?

A

Two Zebras Best Mates Cute

Temporal

Zygomatic

Buccal

Mandibular

Cervical

33
Q

How do the corticobulbar tracts innervate the muscles of the face?

What would this mean in the case of a lower motor neuron lesion?

What would this mean in the case of an upper motor neurone lesion?

A
  • Cells of the facial motor nucleus receive input from upper motor neurons in the primary motor cortex. These descend through the internal capsule to synapse with LMN’s in the facial motor nucleus.
  • This pathway from the cortex to the brainstem is called the corticoculbar tract.
  • The facial motor nucleus has two regions- one that has LMN’s that innervate the upper quadrants of the face and another with LMN’s that innervate the lower quadrants of the face.
  • The LMN’S that innervate the upper quadrants of the face receive cortical input from both sides of the cortex- both the ipsilateral and contralateral side.
  • The LMN’s that innervate the lower quadrants of the face only receive motor cortical input from the contralateral side of the cortex.
  • Therefore a LMN of the facial nerve leads to total paralysis of that side of the face.
  • An upper MN lesion of the cortex (say the R side) will only lead to paralysis of the lower L quadrant of the face. This is because the upper L quadrant will still receive cortical input from the L cortex, whereas the lower L quadrant relies wholly on the R motor cortex.
34
Q

Damage to the facial nerve can present with?

A
  • Facial asymmetry, loss of facial expression
  • Hyperacusis- particularly sensitive to loud noises due to loss of innervation of stapedius.
  • loss of anterior 2/3rds taste sensation
  • loss of tears/ nasal mucosa and saliva (exluding parotid).
35
Q

What is cranial nerve VIII?

Where does it originate?

what is its route of travel?

What does it allow?

A
  • VIII = Vestibulocochlear nerve
  • Originates in the cochlear and vestibular nuclei of the pons
  • Travels via internal acoustic meatus to the cochlea and vestibular organs of the inner ear
  • Allows hearing and balance
36
Q

How do you test the functions of CN VIII?

A
  • Hearing and balance are tested separately.
  • Vestibular portion of the nerve is tested it the patient complains of vertigo.
  • Uses the hallpike manouvre where the patient’s head is rapidly lowered below the level of the bed from a sitting position and head rotates side to side whilst looking for nystagmus (rapid, involuntary movements of the eyes).
  • Positive test produces nystagmus towards affected side
  • To test hearing the Rinne and Webers tests are used.
  • Rinne’s - tuning fork on mastoid then by external acoustic meatus. Patient should hear sound for longer by air conduction. If not- conductive hearing loss.
  • Webers- tuning fork held on forehead, if sound lateralises suggests either conductive hearing loss (where sound lateralises to affected ear) or sensorineural loss (sound lateralises to unaffected ear).
37
Q

What is cranial nerve IX?

What is its origin?

What does it travel through?

What fibres does it carry and to what structures?

A
  • CN IX = Glossopharyngeal nerve
  • Origin: Medulla oblongata- Inferior salivatory nucleus, nucleus ambiguus, nucleus solitarius
  • Travels via the jugular foramen
  • Sensory: innervates all of the pharynx, carotid body and sinus, posterior 1/3 tongue, middle ear cavity and eustachian tube
  • Special sensory: provides taste sensation to posterior 1/3 tongue
  • Parasympathetic: to parotid gland
  • Motor: innervates stylopharyngeus muscle of pharynx.
38
Q

What structures pass through the jugular foramen?

A
  • Internal jugular vein, CN IX, X, XI (spinous portion)
39
Q

What structures does the glossopharyngeal nerve pass between after it has exited the skull?

A
  • Glossopharyngeal nerve emerges as multiple roots that exit the lateral medulla and join together to leave via the jugular foramen
  • CN IX then passes inbetween the internal and external carotid arteries. ( innervates the carotid bodies (chemoreceptors) and carotid sinus (baroreceptors) located here).
40
Q

What might be absent in CN IX damage?

A
  • The glosspharyngeal nerve supplies sensory innervation to the posterior 1/3 of the tongue and oropharynx, forming the sensory component of the gag reflex. The efferent portion of motor innervation via CN X
  • absent gag reflex may signify damage to CN IX
41
Q

What is cranial nerve X?

Where does it originate?

What fibres does it carry? What are its targets?

A
  • CN X= Vagus nerve
  • Originates in the medulla - nucleus tractus solitarius, nucleus ambiguus
  • Sensory - external acoustic meatus, laryngopharynx, larynx, visceral sensation to thoracic and abdominal viscera
  • Special sensory- taste to the anterior 2/3 on tongue (along with CNIX)
  • parasympathetic- innervation to smooth muscles of trachea, bronchi, GI tract and regulates heart rhythm.
  • Motor- muscles of the pharynx, larynx, soft palate.
    *
42
Q

Describe the route of CN X from its point of origin to its exit via the skull

A
  • CN X originates at medulla (nucleus tractus solitarius, nucleus ambiguus)
  • Exits via jugular foramen
43
Q

What are the motor targets of the Vagus nerve?

A
  • The constrictor muscles of the pharynx - superior, middle and inferior constrictor muscles
  • palatopharyngeus
  • Palatoglossus
  • Levator veli palatini
  • Salpingopharyngeus
  • All the muscles of the larynx and cricothyroid- gives off recurrent larygeal nerve (all intrinsic muscle of the larynx except cricothyroid) and the superior laryngeal nerve. Superior laryngeal nerve splits into internal (sensory above vocal fold) and external (cricothyroid).
  • Muscles of upper oesophagus
44
Q

Describe how CNIX and X may be tested together?

A
  • Eliciting the gag reflex and inspection of the oropharynx and soft palate.
  • If one sided damage has occured, soft palate/ uvula will hang towards the unaffected side.
  • Touch pharynx to elicit gag reflex- if no reflex occurs on one side there is a CNIX lesion
  • If sensation is felt but not muscular contraction occurs there is CN X damage.
45
Q

What is cranial nerve XI?

Where does it originate?

Describe its route of travel to its targets

What effect does it have on its targets?

A
  • CN XI =accessory nerve
  • Motor function
  • Spinous portion- Originates from nucleus in cervical spinal cord
  • enters cranium via foramen magnum
  • exits cranium via jugular foramen alongside CN IX, X, and internal jugular vein
  • innervates sternocleidomastoid and trapezius muscles, allows turning of the head and shrugging of the shoulders.
46
Q

How would you test the function CN XI? (Spinal portion)

What could damage CN XI?

A

Ask patient to shrug their shoulders and turn their head from side to side whilst you feel for the contraction of the sternocleidomastoid.

Trauma, surgery, traction injury (stretch injury).

47
Q

What is cranial nerve xii?

Where does it originate?

How does it pass to its targets?

A
  • CN XII- hypoglossal nerve
  • originates in the medulla (hypoglossal nucleus)
  • passes to tongue muscles via the hypoglossal canal
  • all tongue muscles except palatoglossus - CN X
  • Allows movement of the tongue
48
Q

How would you test CN XII function?

what sign would show if there was damage?

A
  • Ask patient to stick out their tongue
  • If lesioned it will deviate towards the weak side.
  • Look for tongue muscle wasting and fasciculation