Lec 8 Flashcards
Talk about facial nerve in general
• nucleus
1- Motor nucleus: supplied from the motor area of the opposite hemisphere and gives motor supply to facial muscles and stapedius.
2- Superior salivary nucleus: gives secreto-motor fibers to the lacrimal gland by greater superficial petrosal nerve and nasal mucosa and to the submandibular and sublingual salivary glands by chorda tympani.
3- Solitary nucleus: gives taste fibers to anterior ⅔ of tongue by chorda tympani.
• course
1- facial motor nucleus present in pons
2- its fibres turn around abducent nucleus forming facial colliculas
3- it leaves the pons at its lower border within nervous intermedius to CPA along with 8th n
4- it enters IAC within 8 th nerve = labyrinthine segment
5- it forms geniculate ganglia then thrns backwards to form 1st genu
6- it passses horizantly above promontory along medial wall in its fallopian bong canal = tympanic segment
7- it reaches posterior wall , turns downwards above oval window to form 2nd genu
8- it moves vertically downwards through mastoid = mastoid segment
9- it leaves the skull through stylomastoid foramen passing downwards , forwards
10- it passes under the skin 1 cm reaching parotid gland to give its terminal branches
• branches
1-Greater superficial petrosal nerve (GSPN): -from geniculte ganglion
-secretomotor to lacrimal gland and nasal mucosal glands.
2-Nerve to stapedius:
-For stapedius (from mastoid segment).
3-Chorda tympani:
-supplying the anterior / of tongue (taste) -secreto-motor to submandibular and sublingual salivary glands
- (from mastoid segment).
4-Nerve to stylohyoid and posterior belly of digastric:
-at stylomastoid foramen.
5-Nerve to occipital belly of occipito frontails:
-at stylomastoid foramen
6-Five terminal branches Temporal within the parotid gland:
Zygomatic
Buccal.
Mandibular.
Cervical.
7-Sensory fibers to the posterior part of EAC.
Aetiology of facial paralysis
• UMNL ( above the level of nucleus ) : central causes
- Traumatic: Head trauma.
- Inflammatory: Meningitis - encephalitis.
. Vascular. Thrombosis, haemorrhage, or embolism (The).
- Neoplastic: brain tumour.
- Degenerative: Multiple sclerosis.
•Lower motor neuron lesion (LMNL): at or below the level of the nucleus.
1-Pontine lesions: nuclear (central causes)
2-CPA lesions:
- Acoustic neuroma.
- Meningioma.
- Congenital cholesteatoma.
- Arachnoid cyst.
3-Cranial (Otogenic) lesions:
in the temporal bone (TITI)
~idiopathic: Bell’s plasy (the commonest cause).
~Traumatic:
- Surgical: ear operations.
- Accidental: fracture base (transverse or longitudinal).
~Inflammatory:
-AOM (in dehiscent facial bony canal).
-CSOM (in cholesteatoma eroding facial canal).
- Malignant Otitis Externa.
- Ramsay Hunt syndrome.
~Tumour:
- Glomus.
- Squamous cell carcinoma of middle ear.
- Acoustic neuroma.
4-Extracranial (TIT):
~ Traumatic:
- Surgical - parotid surgery.
-Accidental - stab in parotid.
~Inflammatory: Sarcoidosis. (Lymphoid inflammation )
~Tumour: parotid tumour.
5- Miscellaneous:
~ Peripheral neuritis.
~Guilliane- Barre syndrome: ascending polyneuritis.
~Milkersson Rosenthal syndrome: It is a familial facial paralysis with facio-labial oedema, and fissured tongue. ( disease of 4f)
Clinical picture of facial paralysis
3
4
5
Symptoms :
- Inability to close the eye (on affected side)
- Deviation of mouth towards the healthy side
- Accumulation of food behind cheek (on affected side)
Signs:
* Inspection:
- Loss of corrugation of forehead (on affected side).
- Obliteration of nasolabial fold (on affected side).
- Deviation of Mouth towards healthy side
- Drippling of saliva (on affected side).
- Motor power:
- Inability to elevate eye brow (Frontalis).
- Inability to close the eye (orbicularis oculi).
- Inability to whistle ( orbicularis oris)
- inability to blow (Buccinator).
- Inability to show the teeth (Retractor anguli).
Compare between UMNL- LMNL
1- UMNL
•Site of paralysis: contralateral lower1/2 of face
• emotional movement : present
• muscle tone / reflex : increased
• hemiplagia
2- LMNL
•Site of paralysis: ipsilateral upper , lower 1/2 of face
• emotional movement : absent
• muscle tone / reflex : decreases
• no hemiplagia
Detection of level of facial paralysis ( topogragh diagnosis)
1- UMNL ~> contralateral lower 1/2 of face with hemiplegia.
2- LMNL~>ipsilateral upper, lower 1/2 facial paralysis (no hemiplegia) according to lesion site:-
a) Pontine (nuclear) :
-6th nerve paralysis (squint).
- Stapedial reflex is lost (motor nucleus).
- Pontine manifestations.
- Lacrimation, taste and salivation are normal (all are other nuclei)
b) CPA and (IAC):
- 8th nerve paralysis (SNHL+vertigo)
- Lacrimation, taste, salivation and stapedial reflex are lost.
c) Geniculate ganglion:
Lacrimation, taste, salivation and stapedial reflex are lost.
d) Below the Geniculate:
- Lacrimation is normal.
- Taste, salivation and stapedial reflex are lost.
e) Extacranial:
Lacrimation, taste, salivation and stapedial reflex are normal.
Investigations of facial paralysis
•Radiological investigations:
CT: shows fracture line in traumatic cases.
MRI: shows a mass in tumour cases.
• Audiological investigations:
PTA : if there is ear lesion.
• Leveling investigations: (4s)
Schirmer’s test: to detect lacrimation.
Taste sensation: from anterior 2 of tongue
Stapedial reflex.
Submandibular salivary flow test for salivation
• Electrophysiological tests: to detect the degeneration early.
(a) Nerve excitability test (NET): stimulation of nerve ,If the difference between both sides exceeds 3 mAmp ~> Bad prognosis. (The muscle contraction is detected by the eye).
b) Electroneurography (ENOG): stimulation of nerve , detection of muscle contraction , if difference on both side exceeds 3mAMP ~> bad prognosis
(NET and ENOG are of no value in the first 3 days of)
(c) Electromyography (EMG): normally, when muscle contracts it shows action potentials If the muscle is degenerated ~> fibrillation potentials, and if the muscle is reinnervated ~> polyphasic potentials (it occurs 2 months before clinical recovery, so it is a prognostic test).
(EMG is of no value in the first 3 weeks of paralysis)
Result of facial paralysis
1-Contracture: fibrosis of muscles.
2-Cross innervations: due to disarrangement of the regenerating fibers lead to:
(a) Crocodile tears: lacrimation during eating.
(b) Synkinesis: voluntary movement of a muscle will be accompanied with involuntary movement of another muscle.
Pathology of facial injury
-Neuropraxia: just compression of the nerve (Reversible conduction block).
- Axonotemesis: interruption of the axon with still intact end-neurium.
- Neurotemesis: interruption of the axon and endo-neurium.
General treatment of facial paralysis
1-Psychological reassurance:
Especially in cases of Bell’s palsy.
2- Care of the eye: to prevent keratitis:
-Eye drops and artificial tears by day.
- Dark glasses in outdoors.
- Eye ointment by night.
- Lateral tarsorraphy in prolonged cases.
3- Care of facial muscles:
Massage of facial muscles. (+ vascularity)
- Physiotherapy.
- Facial exercise on mirror when the movements start to reappear.
4- Treatment of the cause.
5- Rehabilitation:
-Dynamic: The muscles are still viable.
*End to End anastomosis: if there is narrow gap.
*Nerve graft: if there is wide gap, the graft is taken from greater auricular nerve or sural nerve.
*Hypoglosso facial anastomosis.
-Static:
The muscles are fibrosed so treatment is cosmetic by temporalis muscle transposition.
Talk about bell’s palsy
(6)
• It is the commonest cause (90%)
• Aetiology : unknown but different theories.
- Vascular theory: Exposure to cold air ~> spasm of vasa nervosa ~>ischaemia of the nerve ~> edema (due to metabolite accumulation) and compression of the nerve in its canal
- Viral theory: Herpes simplex or zoster without vesicles
- Auto immune
• CLINICAL PICTURE:
- Diagnosed by exclusion of all other causes.
- [LMNL (symptoms + signs), of sudden onset, partial or complete.
- Pain behind the ear(30%) : hours before paralysis.
- Red chorda tympani (rare)(10%) : seen through the drum
• Investigations: as discussed before.
•If there is no recovery within 6 months, we should do MRI to exclude any tumour
• TREATMENT:
- General: Reassurance, Care of the eye, Care of facial muscles
- Medical:
Steroids : 60-80m/day decreased gradually to avoid adreno-cortical insufficiency, it is called medical decompression (anti- oedematous) - Surgical:
Decompression of facial nerve by deroofing of the facial canal (– oedema). It is indicated if the degeneration is more than 90% within 2 weeks
Talk about traumatic facial paralysis
(3)
1- types
Surgical :-
-CPA surgery: during removal of CPA lesions.
-Ear surgery:
•Post auricular incision: especially in children (small mastoid and superficial nerve), so we do high oblique incision (wild’s incision) in children
•Cortical mastoidectomy.
•Tympanoplasty.
•Radical mastoidectomy.
•Stapedectomy (if the facial canal is dehiscent).
-Parotid surgery: during removal of parotid tumour.
Accidental :-
fracture base of the skull
1- Longitudinal: the paralysis is partial and delayed (due to compression of the nerve by oedema). Associated with CHL.
2- Transverse: the paralysis is complete and immediate (due to cutting of the nerve).
Associated with SNHL and vertigo.
2-Investigations: CT to detect fracture line.
3-Treatment:
~ If the paralysis is immediate and complete: end to end anastomosis (for narrow gap), or nerve graft (for wide gap)
~ If the paralysis is delayed and partial: Conservative treatment (antibiotics + steroids), if there is no improvement within 2 weeks - Surgical exploration ( ممكن تمون عظمة هي السبب)
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