Cranial Nerves Summary

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Name Anatomy Motor Sensory Clinical correlations

Olfactory S ● Has receptors ● Info runs posteriorly ● Trauma to nose 🡪 loss of CSF via nose 🡪
within mucous along olfactory tract potential route for meningococcal infection
membrane of nose and through olfactory
● Most common trauma resulting in loss of
bulb of temporal lobe
● The only sense not smell and taste (anosmia), is an injury
where it is processed
mediated by involving frontal impact
thalamus

● One of the few CN


that go directly into
brain without going
into relay station
like pons and
medulla

Optic S ● Presence of optic ● Visual info from ● Site of lesion has direct effect on severity of
chiasma periphery to retina injury – damage could occur from blunt
primarily carried back trauma or lesion/ tumour which compresses
to LGN/ LGB (nuclei in nerve
thalamus) via optic
● Compression/ shearing injuries from traumatic
tract
brain injury
● From LGN, info sent to
● Central processing injuries in occipital lobe
visual cortex for
processing (occipital ● If damage thalamus, loss of peripheral vision
lobe) on left lateral side and right medial cos of
wiring.

Oculomoto M ● Nucleus in ● Mediates movements ● Most susceptible to compression e.g. from


r midbrain of eyeball, eyelid and tumour / aneurysm (lack of blood supply)
constriction and
● Bc it innervates so many of the muscles of the
dilation of pupil
eye, tricky to work out what could go wrong.
● Major role in Damage to 1 or more branches 🡪 diff set of
controlling muscles clinical symptoms
responsible for
● Ipsilateral LMN lesion (i.e. damage to single
precise movement of
side) 🡪 ipsilateral paralysis causing 🡪
eyes for visual
downward and outward deviation. Drooping
tracking/ fixation on
eyelids. Abnormal dilation of pupils.
object

Trochlear M ● Nucleus in ● Innervates the ● Damage can cause double vision


midbrain superior oblique
● Inability to pull the eye down when rotated
muscle of the eye
medially. Upward deviation of affected eye
(responsible for
downward and
outward movement,
and precise
movement of eye for
visual tracking/
fixation on object.
One of six ocular
muscles)

Trigeminal B ● Originates in the ● Muscles of ● Head Motor


pons mastication
● Jaw/ Mandible ● LMN: atrophy and weakening on affected side
(temporalis, masseter,
● Three branches: V1
medial and lateral ● Face ● Bilateral LMN 🡪 jaw hangs open 🡪 extreme
Ophthalmic, V2
pterygoid) effect on speech
Maxillary, V3 ● Mouth
Mandibular ● Anterior belly of ● UMN 🡪 minimal motor deficit due to strong
digastric ● Some sinuses
bilateral innervation by each hem
● Soft palate (tensor veli ● Tactile sensations from
Sensory
palatini) anterior 2/3 of tongue
(via lingual nerve) – ● Loss of tactile sensation to anterior 2/3 of
● Tensor tympani BUT NOT TASTE tongue
(important for
● Loss of corneal blink reflex (ophthalmic
chewing; protects division)
ears)
● Altered sensation (pins and needles)
● Assists CN9
● Loss of sensation to respective areas of face
glossopharyngeal in
innervated by various branches
raising larynx and
pulling it forward
during swallowing

Abducens M ● Nucleus in pons ● Innervation for lateral ● Damage causes inability to hold eye in lateral
movement of eyeball aspect. Causes inward deviation of affected
(lateral rectus muscle) eye 🡪 causes double vision. Inability to look L
or R

Facial B ● Junction of pons ● Muscles of facial ● Taste, anterior 2/3 of ● Affects articulatory function, by causing
and medulla expression: temporal, tongue weakness/ paralysis of muscles of facial
zygomatic, buccal, expression on side of injury
● Communicates ● Hard and soft palates
mandibular, cervical
with trigeminal (V), ● Cannot close eye on affected side, wrinkle
● General sensation from
vestibulocochlear ● Posterior belly of forehead (frontalis) or pucker lips
skin of concha of
(VIII), digastric
auricle (mastoid part of ● Upper face is bilaterally innervated (ipsilateral
glossopharyngeal
● Stylohyoid temporal bone)and and contralateral) from UMN tracts. Unilateral
(IX) and vague (X)
from small area behind UMN damage will NOT result in upper face
nerves ● Lacrimal (tear)/
ear paralysis, but may affect muscles below eyes
submandibular/
● Efferent branches: (e.g. left hem damage) 🡪 right facial paralysis
sublingual (salivary)
Temporal, of mouth but not eye
glands
Zygomatic, Buccal,
● Lower part of face receives only unilateral
Mandibular, ● Stapedius muscle of
innervation (arising from contralateral hem).
Cervical middle ear (protective
Unilateral LMN lesions will cause BOTH upper
reflex to loud sound)
and lower face paralysis on side of lesion.
● Mucous membranes Symptoms: inability to close eyelid, muscle
of nasopharynx, hard sagging and loss of tone, affected corners of
and soft palate mouth drawn toward unaffected side if
● Ear (e.g. wiggling ears) attempting to smile

● Bell’s palsy 🡪 can result from any compression


of VII nerve

Vestibuloco S ● Aka auditory nerve ● Mediates auditory info ● Because of diff relays, not too much damage
chlear and sense of to hearing. Bilateral innervation. Get input
● Two branches
movement in space from second ear.
which carry info
from cochlea and ● Lesions on cell bodies in medulla will not
from vestibular result in total hearing loss because of bilateral
organs in inner ear auditory projections.
(hearing/ balance
● Lesions to VIII nerve will result in ipsilateral
sensation)
hearing impairment, reflecting degree of
● Originates in trauma
medulla
● Primary prob: localisation of sound.
● Auditory fibres
project to
midbrain, then
medial geniculate
bodies of thalamus,
and finally project
bilaterally to
temporal cortex

● Bilateral
innervation

Glossophar B ● Originates in ● Stylopharyngeus ● General sensory info ● Paralysis of stylopharyngeus muscle and may
yngeal medulla muscle (important for from posterior 1/3 of result in general loss of sensation in posterior
swallowing) and tongue 1/3 of tongue and pharynx
● Works with vague
middle/ superior
nerve, making its ● Velum/ palate ● May contribute to reduced / absent gag reflex
pharyngeal constrictor
independent (although absence of reflex does not
muscle (works with ● Oral pharynx (including
function difficult to guarantee lesion exists – not everyone has gag
determine CN10 – vagus) tonsils) reflex)

● Parasympathetic ● Middle ear ● Premature spillage of bolus (cos soft palate


regulation of not working properly, spillage through nose bc
● Eustachian tube
secretion of parotid no closing of pharynx)
gland ● Carotid sinus

● Taste sensation from


posterior 1/3 of tongue
and oral pharynx (the
one nerve that has
both tactile and taste
sensation within it)

Vagus B ● Originates from Focus: pharynx, larynx, lungs ● Pharynx ● Can have damage to either glossopharyngeal
medulla or vagus nerve but can still swallow
● One motor nucleus: ● Larynx
● Extensive, Majority of viscera of ● CN 9 and 10 are evaluated by testing patient’s
● Oesophagus
‘wandering’ nerve thorax and abdomen sensitivity to touch on the posterior wall of
– wanders all the (i.e. internal organs in ● Trachea the pharynx and presence of gag and
way down main cavities of body, swallowing reflexes when posterior tongue
esp in abdomen e.g. ● Abdominal and thoracic and pharynx are stimulated
● Consists of cranial, viscera
intestines), incl heart,
cervical, thoracic ● Pharyngeal branch: deficits in swallowing and
respiratory system, ● Stretch receptors of
and abdominal potential loss of gag reflex (via interaction
digestive system lungs (relevance to
parts with CN9 glossopharyngeal nerve). Loss of
● Another motor controlling breathing) taste sensation to posterior 1/3 of tongue but
nucleus: pharyngeal ● Chemoreceptors of more important in airway safety. If loss of
constrictor muscles, aortic bodies function of swallowing muscles, fluid could
intrinsic musculature enter airways.
of larynx ● Very minor component:
provides taste ● Pharyngeal branch: unilateral lesion 🡪 failure
Branches sensation from to elevate soft palate on involved side
epiglottic region (asymmetry)
● Superior branch:
cricothyroid muscle Bilateral lesion 🡪 absent/ reduced (but
(involved in pitch symmetrical) movement of soft palate, nasal
changes) regurgitation (bc can’t close off soft palate),
hypernasality, and paralysis of pharyngeal
● Recurrent branch: all
musculature
other intrinsic
laryngeal ● Superior laryngeal nerve branch: loss of
musculature. sensation in upper larynx, paralysis of
cricothyroid muscle (thus changes to pitch.
● Pharyngeal branch:
Depends whether unilateral/ bilateral – if non-
palatoglossus (aka
functional VF even on one side then there’s
glossopalatine),
aspiration. Reduced ability to cough – through
levator veli palatini,
VF adduction/ pressure build-up/ release)
making it primarily
responsible for palatal ● Recurrent laryngeal nerve: altered sensation
functioning below VF.
Unilateral recurrent laryngeal nerve lesion
typically results in flaccid VF and
hoarse/breathy voice.
Bilateral recurrent laryngeal nerve lesion VF
can be paralysed in adducted position (rare,
life threatening). More commonly paralysed in
paramedian position (risk of aspiration to
airways)

Accessory M ● Originates in the ● Trapezius and Damage to spinal root of CN 11


medulla sternocleidomastoid
● LMN lesion. Results in ipsilateral weakness or
muscles of the neck
● Has cranial and flaccid paralysis of sternocleidomastoid and/
(stabilise scapulae,
spinal components or trapezius muscles
shrug shoulders)
(but bc has cranial
● Test function by ability to turn head, resist
components and ● Works with vagus
attempts to turn head, shrug shoulders,
nucleus in medulla, nerve to innervate
elevate shoulders against resistance.
it’s a CN) muscles of larynx
(intrinsic), pharynx ● Injury causes shoulder on affected side to
● Fibres contribute
and soft palate 🡪 droop, interfered with arm movements above
to function of sends motor shoulder on affected side, turning head away
vagus messages to uvula from side of injured nerve (nb. Left
and levator veli sternocleidomastoid rotates head right)
palatine (raises
velum)

Hypoglossal M ● Originates in the ● Supplies musculature ● Unilateral LMN lesion 🡪 loss of movement on
medulla of tongue side of lesion. Muscular weakness/ atrophy on
this side 🡪 deviation of tongue toward side of
● Controls tongue
lesion
movement by
innervating both ● If there is damage to hypoglossal nerve itself,
intrinsic and extrinsic tongue may reveal presence of LMN lesion by
tongue muscles fasciculation (twitching)
(except palatoglossus)
● UMN lesion 🡪 muscle weakness, impaired
volitional movements with accompanying
spasticity

● Inaccuracy of articulation and poorly


controlled swallowing

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