ENT power point in facial nerve palsy

1. Done by:
Haneen
Adyan
Rawnaq

2. Anatomy of facial nerve
it`s the seventh cranial nerve and it is very
complex. It has many branches, which transmit
a combination of sensory, motor and
parasympathetic fibres.

3. facial nerve can be divided into
two parts:
Intracranial :
The nerve arises in the pons, an area of
the brainstem. It begins as two roots; a
large motor root, and a small sensory root

4. Extracranial :
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.

5. Facial nerve branches :
Structure supplytypebranches
Post.belly of diagastric
m.
Styloid m.
motorPosterior auricular
Muscle of facial
expression
motorTemporal
Muscle of facial
expression
motorzygomatic
Muscle of facial
expression
motorbuccal
Muscle of facial
expression
motormandibular

6. Muscle of facial
expression
platyama
motorCervical
stapediusmotornerve to stapedius
Lacrimal glandParasympathetic
secretomotor
Greater petrosal
Submandibular and
sublingual gland
Parasympathetic
secretomotor
Taste
Chorda tympani
Area around external
auditory meatus
Somatic sensoryFibers to geniculated
ganglion

7. Facial nerve paralysis

8. Facial nerve paralysis
_ Facial nerve paralysis is a common problem that
involves the paralysis of any structures innervated by
the facial nerve
_Facial paralysis of lower-motor-neuron origin may be
due either to physiological (reversible) block or to
degeneration of the facial nerve. The prognosis
depends on which has occurred, the chances of full
recovery being good in physiological block but poor in
degeneration. The present study demonstrates how
accurately this knowledge may be acquired early in
the course of the paralysis by a simple
electrodiagnostic test

9. Classification
:Supranuclear and nuclear lesion
_ Central facial palsy can be caused by a lacunar
infarct affecting fibers in the internal capsule
going to the nucleus. The facial nucleus itself can
be affected by infarcts of the pontine arteries.
These are corticobulbar fibers travelling in
internal capsule
:Infranuclear lesions
_ Infranuclear lesions refer to the majority of
causes of facial palsy.

10. signs :
_ facial asymmetry
_eyebrow droop
_ loss of forehead &nasolabial folds
_ dropping of corner of mouth
_ uncontrolled tearing
_ inability to close eye
_lips cann`t be held tightly together (difficult
to keep food in mouth )
_facial muscle atrophy (late)

11. causes
_ congenital :birth trauma ,mytonic dystrophy,
occulo-auriculo-vertebral syndrome
_ infection : bell`s palsy ,Reactivation of herpes zoster
virus or
Ramsay Hunt syndrome symptoms may include ear pain
and vesicles, sensorineural hearing loss, and vertigo
Otitis media is an infection in the middle ear, which can
spread to the facial nerve and inflame it,
_ Trauma
Physical trauma, especially fractures of the temporal bone
_ Tumors
facial neuromas, congenital cholesteatomas,
hemangiomas, acoustic neuromas, parotid gland
neoplasms, or metastases of other tumours
_ Stroke
_ others

12. Facial nerve paralysis

13. There are five classes of injury:
Class I. Pressure on a nerve trunk, provided that it
is not too severe, caused conduction block
Class II. A more severe lesion, whether caused by
pressure or some other insult, such as viral
inflammation
Class III. If the lesion disrupts the endoneurium,
Class IV. Perineural disruption obviously implies an
even more severe injury
Class V. A complete transection of a nerve,
including its epineurial sheath

14. Prognostic
test

15. Assessment
/outcome
Technique
consideration
Nerve branch
assessed
Topodiagnostic
test
>75% unilateral
decrease in
lacrimation or a
bilateral decrease in
lacrimation (less
than 10 mm for both
sides at five
minutes)
Strips of paper are
placed in the inferior
conjunctival fornix
for five minutes and
the length of paper
moistened is
compared between
eyes
Great superficial
petrosal nerve
Schirmer test
Present or absentPsychoacoustic
audiometry
Nerve to stapedius
muscle
Stapedial reflex

16. Threshold of the
test is compared
between sides
The tongue is
stimulated
electrically to
produce a metallic
taste and the two
sides are
compared
Chorda tympanielectrogustometry
A reduction of 25%
is considered
abnormal
warthin`s ducts are
cannulated and
salivary flow is
measured over time
following a
gustatory stimulus
(6% citric acid on
anterior part of
tongue)
Chorda tympaniSalivary flow
testing

21. Compare between ENG &EMG
Use in long –
standing
paralysis
Use in acute
onset
paralysis
When to
measure
measurementstudy
Not useful
because of
desynchronizatio
n
>90%of
degenerated
fibers suggests
poor prognosis
Between three
days and three
weeks
Evoked CMAP
compared to
normal size
ENG
Defibrillation
potentials
suggest
wallerian
Degeneration
Polyphasic
potentials
suggest
reinnervation
Presence of
active motor
potentials in
response to
voluntary
contractions
indicate good
prognosis
Complementar
y
To ENoG after
2 weeks
In long
standing
paralysis
Active motor
unit potentials
after voluntary
forceful
contraction
EMG

22. ENG :

23. EMG :

24. Compare between NET&MST :
Prognostic
value
Outcome
measure
techniquetest
Indicates poor
recovery
>3.5 mA
difference is
considered
significant
Compares
transcutaneous
current
threshold
required to elicit
minimal muscle
contraction
between two
sides
NET
Loss of
response within
ten days is
associated with
incomplete
recovery
Equal response,
reduced
response or
absent
response
Compares
muscle
contraction at
maximal nerve
stimulation
(~5mA) between
two sides
MST

25. MST :

26. !Thank you