Cranial nerves of 7-12

1. Cranial nerves VII-XII

2. Facial nerve
• The facial nerve is the most frequently
compromised of all the cranial nerves

3. Facial nerve
Anatomically, the course of the facial nerve can be divided into two parts:
Intracranial – the course of the nerve through the cranial cavity, and the cranium itself.
Extracranial – the course of the nerve outside the cranium, through the face and neck.

4. • Within the facial canal, three
important events occur:
• 1. the two roots fuse to form the
facial nerve.
• 2. the nerve forms the geniculate
ganglion (a ganglion is a collection of
nerve cell bodies).
• 3. the nerve gives rise to:
– Greater petrosal nerve –
parasympathetic fibres to mucous
glands and lacrimal gland.
– Nerve to stapedius – motor fibres to
stapedius muscle of the middle ear.
– Chorda tympani – special sensory fibres
to the anterior 2/3 tongue and
parasympathetic fibres to the
submandibular and sublingual glands.
• The facial nerve then exits the facial
canal (and the cranium) via
the stylomastoid foramen.

6. Bell’s palsy
• This most common disorder affecting the
facial nerve arises in about 25 per 100 000
individuals per year. Its cause is still unknown.
It is characterized by flaccid paresis of all
muscles of facial expression(including the
forehead muscles), as well as other
manifestations depending on the site of the
lesion

8. Intracranial lesions
• The muscles of facial expression will be
paralysed or severely weakened. The
other symptoms produced depend on
the location of the lesion, and the
branches that are affected:
• Greater petrosal nerve – ipsilateral
reduced lacrimal fluid production.
• Nerve to stapedius – ipsilateral
hyperacusis (hypersensitive to sound).
• Chorda tympani – reduced salivation and
loss of taste on the ipsilateral 2/3 of the
tongue.
• The most common cause of an
intracranial lesion of the facial nerve is
infection related to the external or
middle ear. If no definitive cause can be
found, the disease is termed Bell’s palsy

9. • Differential diagnosis is important in cases of acutely
arising facial palsy, as not all cases are idiopathic: 10 %
are due to herpes zoster oticus, 4 % to otitis media,
and 2 % to tumors of various types (parotid tumors,
neurinoma, and others)
• A complete recovery occurs without treatment in 6080
% of all patients. The administration of steroids
(prednisolone, 1 mg/kg body weight daily for 5 days), if
it is begun within 10 days of the onset of facial palsy,
speeds recovery and leads to complete recovery in
over 90 % of cases, according to a number of published
studies.

11. • After exiting the skull, the facial nerve turns superiorly to
run just anterior to the outer ear.
• The first extracranial branch to arise is the posterior
auricular nerve. It provides motor innervation to the some
of the muscles around the ear. Immediately distal to this,
motor branches are sent to the posterior belly of
the digastric muscle and to the stylohyoid muscle.
• The main trunk of the nerve, now termed the motor
root of the facial nerve, continues anteriorly and inferiorly
into the parotid gland (note – the facial nerve does not
contribute towards the innervation of the parotid gland,
which is innervated by the glossopharyngeal nerve).

12. • Within the parotid gland, the nerve terminates by splitting into five branches:
• Temporal branch
• Zygomatic branch
• Buccal branch
• Marginal mandibular branch
• Cervical branch
• These branches are responsible for innervating the muscles of facial expression.

14. The muscles of the forehead derive their supranuclear innervation from
both cerebral hemispheres, but the remaining muscles of facial expression
are innervated only unilaterally, i.e., by the contralateral precentral cortex.
If the descending supranuclear pathways are interrupted on one side only
the resulting facial palsy spares the forehead muscles the patient can still
raise his or her eyebrows and close the eyes forcefully. This type of facial
palsy is called central facial palsy.
In a nuclear or peripheral lesion, however, all of the muscles of facial
expression on the side of the lesion are weak

15. https://www.youtube.com/playlist?list=PLO2O9UjkQxLf5eIHtZyosqNoeGRQuTLU2

16. Special Sensory Functions
• The chorda tympani branch of the facial nerve
is responsible for innervating the anterior 2/3
of the tongue with the special sense of taste.

17. Parasympathetic Functions
• The parasympathetic fibres of the facial nerve are carried by
the greater petrosal and chorda tympani branches.
• Greater Petrosal Nerve
• The greater petrosal nerve arises immediately distal to
the geniculate ganglion within the facial canal. It then moves in
anteromedial direction, exiting the temporal bone into the middle
cranial fossa. From here, its travels across (but not through) the
foramen lacerum, combining with the deep petrosal nerve to form
the nerve of the pterygoid canal.
• The nerve of pterygoid canal then passes through the pterygoid
canal (Vidian canal) to enter the pterygopalatine fossa, and
synapses with the pterygopalatine ganglion. Branches from this
ganglion then go on to provide parasympathetic innervation to
the mucous glands of the oral cavity, nose and pharynx, and
the lacrimal gland.

18. Parasympathetic Functions
• Chorda Tympani
• The chorda tympani also carries some
parasympathetic fibres. These combine with
the lingual nerve (a branch of the trigeminal
nerve) in the infratemporal fossa and form
the submandibular ganglion. Branches from
this ganglion travel to the submandibular and
sublingual salivary glands.

20. BULBAR AND PSEUDOBULBAR
PALSY

21. • There are two principal types of bulbar palsy: progressive bulbar palsy
(PBP) and pseudobulbar palsy. In both, the outstanding symptoms are
dysphagia and dysarthria.
• PBP is a form of motor neuron disease involving bulbar innervated
muscles.
• Pseudobulbar palsy is caused by bilateral supranuclear lesions involving
the corticobulbar pathways.In pseudobulbar palsy, the dysarthria is
generally more spastic in nature. There may be dysphagia, nasal
regurgitation, choking, and drooling. Patients may keep food in the mouth
for prolonged periods. Although the tongue may be strikingly immobile,
atrophy and fasciculations do not develop. There is often an exaggerated
jaw jerk, a hyperactive gag reflex and frontal release signs such as snout
and suck reflexes.
• The video by Dr. Paul D. Larsen from the University of Utah collection
demonstrates severe dysarthria, slow tongue movements (The most
common cause is multiple cerebral infarctions. The syndrome may also
occur in encephalitis, MS, trauma, cerebral anoxia, primary lateral
sclerosis, or other disease processes that cause bilateral corticobulbar
tract lesions).