0% found this document useful (0 votes)
111 views53 pages

7th Cranial Nerve

The facial nerve originates from the pons and medulla and has motor, parasympathetic, and sensory nuclei. It exits the skull through the stylomastoid foramen and innervates muscles of the face. Bell's palsy is an idiopathic paralysis of the facial nerve that affects 20 per 100,000 people annually. It is diagnosed by exclusion and typically resolves within 6-9 months with corticosteroids and antivirals, though some permanent damage can occur. Other causes of facial paralysis include Lyme disease, Ramsay Hunt syndrome, tumors, and trauma.

Uploaded by

Beauty
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
0% found this document useful (0 votes)
111 views53 pages

7th Cranial Nerve

The facial nerve originates from the pons and medulla and has motor, parasympathetic, and sensory nuclei. It exits the skull through the stylomastoid foramen and innervates muscles of the face. Bell's palsy is an idiopathic paralysis of the facial nerve that affects 20 per 100,000 people annually. It is diagnosed by exclusion and typically resolves within 6-9 months with corticosteroids and antivirals, though some permanent damage can occur. Other causes of facial paralysis include Lyme disease, Ramsay Hunt syndrome, tumors, and trauma.

Uploaded by

Beauty
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
You are on page 1/ 53

7 TH

CRANIAL NERVE
LECTURE TAKEN BY :
DR. HEMANGI PARMAR
FACIAL NERVE ANATOMY :

▪ The facial nerve originates from the junction of the


pons and the medulla .
▪ It is a mixed nerve
▪ 3 nuclei
– Motor nucleus
– Parasympathetic nucleus
– Sensory nucleus
MOTOR NUCLEUS

▪ Motor nucleus is situated in the pons


▪ Has 2 parts
– Upper part which innervates the forehead muscles receive
fibers from both the cerebral hemisphere
– Lower part which supplies the lower face receives fibers
from one the contralateral hemisphere

▪ Also receives fibers from thalamus by alternate


routes and thus and provide involuntary control of
facial muscles
PARASYMPATHETIC NUCLEUS

▪ Parasympathetic nuclei lies postero lateral to the


motor nucleus
▪ The 2 nuclei are
▪ Superior salivary nucleus receives afferent from
the hypothalamus for information concerning
taste
▪ Lacrimal nucleus receives afferent fibers from
hypothalamus for emotional responses
SENSORY NUCLEUS

▪ Sensory nucleus forms the upper part of the


nucleus of the tractus solitary
▪ Lies close to the motor nucleus
▪ Sensation of taste travels the peripheral axons of
cells situated in the geniculate ganglion
PATHWAY :

▪ From pons, facial nerve travels anterolateral with


the VIII nerve, enters facial canal, traverses
temporal bone & comes out of stylomastoid
foramen
▪ As it runs to the stylomastoid foramen, facial nerve
is divided into 3 parts by the changes of direction:
– horizontal part (a few mm) at the bottom of internal
acoustic meatus
– transverse part (1 cm) located between the two bends
– vertical part (1 cm+) where it descends to reach
stylomastoid foramen.
▪ Course of the nerve can thus be divided into
– Intracranial part: from pons to internal acoustic meatus
(15-17mm)
– Intra temporal part: internal acoustic meatus to the
stylomastoid foramen
– Extra cranial part: from stylomastoid to pes anserinus (15-
20 mm). On emerging from the foramen, facial nerve
innervates the digastric & stylohyoid muscles and divides
into:
▪ Temporalfacial branch:
– Temporal
– Zygomatic
▪ Cervicofacial
– Cervical
– Mandibular
▪ Buccal branch formed by joining temperofacial and
cervicofacial branch
▪ Within the facial canal, it gives rise to intrapetrous
branches
– Greater petrosal nerve: innervates the lacrimal glands
– Nerve to stapedius: motor to stapedius
– Chorda tympani nerve: carries taste, supplies sub lingual
and sub mandibular glands
– Posterior auricular nerve: supplies occipitalis
FUNCTIONS :

▪ Facial expression
▪ Innervates muscles of face & scalp.
▪ Voluntary motor signals derive from the motor cortex.
▪ Large part of facial expression is involuntary and
controlled by the hypothalamus
▪ Anger, pain and disgust, attention, contempt, fear, joy, sadness,
surprise or astonishment.

▪ Even people who are blind from birth produce the


same expressions. These emotional manifestations
are not simply acquired, but are innate.
▪ Stapedius muscle
▪ Innervats the stapedius muscle
▪ This muscle diminishes the oscillation of the
ossicles of the middle ear, thereby diminishing the
vibrations caused by loud noises.
– Consequently, a lesion of the nerve branch to the
stapedius muscle results in hyperacusis
▪ Reflexes – E.g.
▪ The corneal reflex depends on the facial nerve by
its motor arc.
▪ The nasopalpebral reflex consists of bilateral
contraction of the orbicularis oculi muscles when
the bridge of the nose is percussed.
▪ However, a preferable way to evaluate this reflex is
to hold the patient’s eyes closed.
▪ Sensitivity function
▪ The facial nerve conveys general sensation from a
small area around the external acoustic meatus,
from the eardrum and the concha
▪ Sensory function
▪ The sensory root (nervus intermedius) conveys the
taste fibers for the anterior two thirds of the
tongue.
▪ Visceromotor function
▪ Controls lacrimal, submandibular & sublingual
salivary glands, as well as the pharyngeal, nasal
and palatine glands.
▪ Innervates all major glands of face, except skin glands & the
parotid.

▪ This nucleus is connected to the hypothalamus and


are able to evoke reflex activities like salivation or
tears in response to certain smells or emotional
states.
FACIAL NERVE PARALYSIS

▪ It is a common problem that causes paralysis of the


structures innervated by facial nerve
▪ The most common is Bell's palsy, an idiopathic
disease that may only be diagnosed by exclusion.
CLASSIFICATION :

▪ Facial nerve paralysis may be divided into


– Supranuclear lesions (UMN)
– Infranuclear lesions (LMN)
▪ Supranuclear:
– Central facial palsy caused by lacunar infarct affecting
fibers in internal capsule going to the nucleus.
– The facial nucleus itself can be affected by infarcts of
pontine arteries.

▪ Infranuclear:
– Injury to facial nerve
– Refer to the majority of causes of facial palsy
Causes

▪ Bells palsy
▪ Ramsay hunt syndrome: occurrence of facial
paralysis, herpetiform vesicular eruptions, &
vestibulocochlear dysfunction (H. Zoster)
▪ Lyme disease: Infection with Borrelia burgdorferi
via tick bites presenting along with all other
symptoms of disease
– 10% develop facial paralysis, with 25% of these patients
presenting with bilateral palsy
▪ Bacterial infection: acute otitis media or externa,
mastoiditis
▪ Trauma: fractures of the temporal bone, forceps
delivery
▪ Tumors: compressing the nerve e.g. facial
neuromas, hemangiomas, acoustic neuromas,
parotid gland neoplasms, or metastases of other
tumours
▪ Stroke: Central facial palsy caused by lacunar
infarct affecting internal capsule or facial nucleus
Other causes
▪ Diabetes mellitus
▪ Sarcoidosis of the nervous system, neurosarcoidosis
▪ GBS: Bilateral facial nerve paralysis
▪ Botulism: acute paralysis of muscles
▪ Pregnancy
▪ Arsenic intoxication
▪ Iatrogenic: mandibular block anaesthesia, post immunization,
dental extraction
▪ Myesthenia gravis
▪ Parkinsonism
▪ Moebius syndrome: bilateral facial paralysis
resulting from underdevelopment of VII nerve
which is present at birth.
– The VI cranial nerve, which controls lateral eye movement,
is also affected, so people with Moebius syndrome cannot
form facial expression or move their eyes from side to
side.
– Moebius syndrome is extremely rare, and its cause or
causes are not known.
Bells palsy

▪ Bell's palsy is an idiopathic form of facial palsy


resulting from a dysfunction of the cranial nerve VII
▪ It is diagnosed by exclusion , if no specific cause
can be identified, the condition is known as Bell's
palsy
▪ It is named after Scottish anatomist Charles Bell
(1774–1842), who first described it.
incidence

▪ Annual incidence is about 20 per 100,000 population


▪ It affects approximately 1 person in 65 during a
lifetime
▪ Familial inheritance is found in 4–14% of cases
▪ Three times more likely to affect pregnant women
than non-pregnant women
▪ It is more common in adults than children.
▪ The incidence is higher in people with diabetes than
in those without diabetes.
Cause

▪ Idiopathic
▪ Some viruses establish a latent infection without
symptoms e.g. varicella-zoster, Epstein-Barr virus
– Reactivation of an existing (dormant) viral infection has
been suggested as a cause of acute Bell's palsy

▪ New activation could be preceded by trauma,


environmental factors, metabolic or emotional
disorders
Pathology

▪ Inflammation of the nerve compresses the nerve


where it passes in the bony canal and where it exits
from the skull
▪ Latent infection without symptoms e.g. varicella-
zoster, Epstein-Barr virus can be activated due to
trauma, environmental factors, metabolic or
emotional disorders
– Reactivation of an existing (dormant) viral infection may
cause acute Bell's palsy
Signs and symptoms

▪ Sudden onset of paralysis of facials muscles


▪ Post auricular pain
▪ Loss of taste in anterior 2/3 on affected side
▪ Hyperaccusis
▪ Watering of eyes
▪ Loss of wrinkles on the forehead
▪ Bell’s phenomenon
▪ Flattening of nasolabial fold
▪ Angle of mouth deviated on the healthy side
▪ Whistling may not be possible
Other accompanying
features

▪ Facial tingling
▪ Moderate or severe headache
▪ Neck pain
▪ Memory problems
▪ Balance problems
▪ Ipsilateral limb paresthesias & weakness
▪ Sense of clumsiness
▪ Unexplained by facial nerve dysfunction
Differential diagnosis

▪ Stroke
▪ Ramsay Hunt syndrome
▪ Lyme disease
Diagnosis

▪ Electrical testing (SD Curve):


– distinguish degree I from II - V lesions but
cannot distinguish II from V
▪ Serology - Lyme, herpes and zoster (paired
samples 4-6 weeks apart). It may not
influence management but may reveal
etiology
▪ Electrodiagnostic studies – NCV/EMG
(generally a research tool) reveal no
changes in involved muscles for the first 3
days but a steady decline of electrical
activity occurs over the next week
▪ Imaging
– CT scanning and MRI are useful in the
diagnosis of injury to intratemporal or
intracranial affections
– May reveal temporal fracture patterns and
edema formation
▪ For suspected intracranial or infratemporal
injury, a Schirmer test of tearing to assess
lacrimal gland function
Complications

▪ Facial asymmetry
▪ Exposure keratitis
▪ Synkinesis
▪ Crocodile tears
▪ Frey’s syndrome
▪ Psychological and social issues
Prognosis

▪ 60-80% of the cases resolve completely within a


few weeks to months
▪ 15%, recovers in 3–6 months
▪ In few cases it leads to permanent deficits
▪ Approximately 7% of patients have a recurrence.
▪ Recurrent bell’s palsy may not fully recover
Treatment

▪ Pharmacological
▪ Physiotherapy
▪ Surgical
▪ Pharmacological
– Corticosteroid such as prednisone
– Antivirals (such as aciclovir)
– Lubricating eye drops
Surgical

▪ Decompression of facial nerve in the stylomastoid


foramen
▪ In cases which fails to recover
– Anastomosis of facial nerve with accessory (CN-XI) or
hypoglossal (CN-XII) nerve may be considered

▪ In the presence of crocodiles tear, cutting of


tympanic nerve which normally conveys the
glossopharyngeal salivary fibers
▪ In residual weakness and asymmetry, plastic
surgery, tendon transfer
PT assessment

▪ History:
– May not be relevant
– May have h/o viral infection, exposure to cold etc
– Associated with BP or HT
– Family history may not be relevant, some may have
positive family history
– H/o recurrent facial paralysis may be present
▪ Pain:
– Common complains of post auricular pain and earache.
– pulling type of pain in the face may be present

▪ Observation
– Turned out lower eyelid
– Sagging mouth
– Drooping appearance
– Absence of forehead wrinkles and nasolabial fold
– Bell’s phenomenon
▪ Cranial nerve examination
– Trigeminal nerve
– Auditory nerve etc.
– Facial nerve
▪ Refer cranial nerve examination PPT for details
– Motor
– Sensory
– Lacrimal
– Salivary
– Hyperaccusis
▪ Motor examination
– Weakness or paralysis of facial muscle on the affected side
– Hypotonic muscles
– Normal jaw jerk

▪ Sensory function
– Taste sensation in the anterior 2/3 may be lost on the
affected side
– Facial sensations are normal
▪ Reflex integrity
– Corneal reflex: loss of blinking on the affected side
– Nasopalpebral reflex: abnormal

▪ Disease specific scales


– Housebrakeman scale
– Sunny brook scale
– Yanagihara scale
▪ Special test/ investigation
– SD curve
– NCV
Yanagihara facial nerve grading system:
Pt management

▪ Control pain
– IRR to the face in the presence of post auricular and facial
pain
– SWD over face or parotid region
– US with phonophoresis in the post auricular region may
be helpful to control inflammation
▪ Maintain muscle property
– IG current to the facial muscles
▪ 60-90 contractions in each individual muscles
▪ Duration 30, 100 or 300ms
▪ Passive electrode can be placed in the nap of the neck or the
arm
– Massage to improve circulation
▪ For facial lift and reduce sagging
– Taping or S-hook splint from the corner of the mouth to
the ear to avoid facial sagging
▪ Re-education and strengthening of muscle
– Electrical stimulation
– Facial muscle PNF
– Facial exercises with mirror biofeedback
– Quick iceing techniques
– EMG biofeedback
▪ Other treatment modes
– Mime therapy
– Accupuncture
– Dry needling
– Nerve mobilization
– Facial yoga etc.
▪ Home advise
– Cotton plugging of ears while travelling
– Protective glasses for the eyes
– Cleaning of eyes with clean cold water splash frequently
– Facial exercise
▪ Wrinkle forehead
▪ Flare nostrils
▪ Pucker lips
▪ Whistling
▪ Smiling
▪ Blowing and sucking etc
THANK YOU

You might also like