Cranial nerve dysfunction Associate professor Elitsa Deliverska, PhD Department of Dental, Oral and Maxillofacial surgery, FDM, MU-Sofia Classification of cranial nerves Sensory cranial nerves: contain only afferent (sensory) fibers

ⅠOlfactory nerves

ⅡOptic nerve

Ⅷ Vestibulocochlear nerve Motor cranial nerves: contain only efferent (motor) fibers

Ⅲ Oculomotor nerve

Ⅳ Trochlear nerve

ⅥAbducent nerve

Ⅺ Accessory nerve

Ⅻ Hypoglossal nerve Mixed nerves: contain both sensory and motor fibers

ⅤTrigeminal nerve,

Ⅶ Facial nerve,

ⅨGlossopharyngeal nerve

ⅩVagus nerve neuroanatomy review consider:

• position of cranial nerve nuclei in the brainstem • central pathways of CN’s

• brainstem; cerebral peduncles; diencephalon; internal capsule; corona radiata; cerebral cortex

• intracranial & extracerebral course • exit foramina • extracranial (peripheral) course

Cranial nerve pathologies: • Tumours

- Schwannoma (Neurilemoma, neurinoma) - Neurofibroma

• Infections Infectious meningitis results from viral, bacterial, fungal, or parasitic infection. Tuberculosis – Leptomeningitis is the most common form of intracranial tuberculosis, particularly in the pediatric population. Nerve impairment has been attributed to ischemia of the nerve or entrapment of the nerve in basal exudates Lyme disease • Multisystem inflammatory disorder caused by a spirochete (Borrelia burgdorferi). Cranial neuritis in Lyme disease may involve any of cranial nerves III through VII, with the facial nerve most frequently affected and often associated with cochleovestibular nerve abnormalities • Post-infectious and Demyelinating Disorders • Post-radiation Neuritis

Viral infections • related to herpes simplex virus type 1, cytomegalovirus, and Varicella zoster virus • manifest with cranial nerve involvement and show abnormal enhancement on MRI. Fungal • Cryptococcus neoformans is the most common fungus to involve the CNS. • Optic neuropathy is a rare complication of cryptococcal meningitis and usually

occurs in non-AIDS patients. • Necrosis of the optic nerves and infiltration of the meninges around the optic tracts,

nerves, and chiasm by cryptococcal organisms have been observed. In clinical examination the clinician should methodically and systematically examine each cranial nerve • from olfactory nerve to ---> hypoglossal nerve • consider fiber types in each cranial nerve:

• somatic motor; visceral motor; special motor; general sensory; special sensory; visceral sensory

Trigeminal Neuralgia (TN) is neuropathic facial pain arising from the trigeminal nerve. • Incidence 4-5 cases: 100.000 • TN or Tic douloureux occur patients > 50 years. • Male: Female ratio 2: 3 • Unilateral (97%). Most affected V2 and V3. • The pain is intense, usually sharp, electric shock like pain in face, lasting

periods of seconds to 2 minutes • The disorder affects the right side of the face 5 times more frequently than

the left

Trigeminal neuralgia is divided into classic [idiopathic] and symptomatic types

The classic form includes the cases that are due to a normal artery present in contact with the nerve, such as the SCA- superior cerebellar artery or even a primitive trigeminal artery

Symptomatic forms can have multiple origins: Aneurysms, tumours, chronic meningeal inflammation. An abnormal vascular course of the superior cerebellar artery is often cited as the cause

Uncommonly, an area of demyelination from multiple sclerosis may be the precipitant ETIOLOGY - Tumour-related causes : (most commonly in the cerebello-pontine angle) include

acoustic neurinoma, chordoma at the level of the clivus, pontine glioma or glioblastoma, metastases, and lymphoma and paraneoplastic etiologies- traumatic compression of the trigeminal nerve by neoplastic (cerebellopontine angle tumor).

- vascular anomalies eg arteriovenous malformations- vascular causes include a pontine infarct and arteriovenous malformation or aneurysm in the vicinity.

- Infections- varicella virus, Lyme disease neuropathy ; granulomatous and non granulomatous,postherpetic and infections involving 5th cranial nerve.

- foci of abscesses

- bone resorption with irritation of the trigeminal nerve in the maxilla or mandible - MS(multiple sclerosis)-Myelin gone…. signals blend….nerves may sense light

touch as pain , sarcoidosis, LAS

Pulsation of vessels upon the trigeminal nerve root do not visibly damage the nerve. However, irritation from repeated pulsations may lead to changes of nerve function, and delivery of abnormal signals to the trigeminal nerve nucleus. Over time, this is thought to cause hyperactivity of the trigeminal nerve nucleus, resulting in the generation of TN pain.

“Neurovascular conflict(NVC)” i.e. vascular compression of nerve most commonly its entry into pons

Significant NVC= an artery (not a vein), crossing (not parallel to) the nerve and provoking displacement/grooving of it (Casselman,2000)

Amplifying

compression results in focal trigeminal nerve demyelination

leads to ephaptic transmission [action potentials jump from one fibre to another]

A lack of inhibitory inputs from large myelinated nerve fibres plays a role.

a re-entry mechanism causes an amplification of sensory inputs Multiple Sclerosis-Related Trigeminal Neuralgia

• The symptoms and characteristics identical è Typical TN • 2 - 4% patients with TN have multiple sclerosis (MS) • MS is associated with formation of demyelinating plaques within the brain • First attack of pain in most of cases is in younger patients, bilateral

Patients with multiple sclerosis (MS) and trigeminal neuralgia have similar complaints to those with the idiopathic variety, except that these individuals present at a much younger age (often < 40 years). In some cases, it is present with atypical facial pain, without trigger zones, and without the lancinating brief paroxysms of discomfort. Atypical facial pain is characterized by persistent pain in the facial region and can be further divided into pain with demonstrable organic disease and conditions in which no pathology can be found. As previously noted, trigeminal neuralgia is not unusual in multiple sclerosis, but it is rarely the first manifestation. Typically, it occurs in the advanced stage. Post-Traumatic Trigeminal Neuralgia

• Develop following cranio-facial trauma, dental trauma, sinus trauma, destructive procedures (rhizotomies)

• It is associated with severe pain, constant, triggers such as wind and cold, start immediately or days to years following injury

Clinical characteristics PAIN Sudden Unilateral Intermittent paroxysmal Lancinating shock like pain elected by slight touching Superficial trigger points which radiates across the distribution of one or more branches of the trigeminal nerve Pain rarely crosses the midline Pain is of short duration and last for few seconds to minutes In extreme cases patient has a motionless face called the frozen or mask like face Presence of intraoral or extraoral trigger points During attacks, patients may grimace, wince, or make an aversive head movement, as if trying to escape the pain, thus producing an obvious movement, or tic; hence the term "tic douloureux.” Provocated by obvious stimuli like Touching face at particular site Chewing Speaking Brushing Shaving Washing the face The characteristic of the disorder being that the attacks do not occur during sleep. The number of attacks may vary from less than 1 per day, to a 12 or more per hour, up to hundreds per day. Outbursts fully abate between attacks, even when they are severe and frequent. DIAGNOSIS

• Anamnesis • Clinical examination • CT scan • MRI

Strict criteria for trigeminal neuralgia as defined by the International Headache Society (IHS) (International Classification of Headache Disorders, 2nd ed) in 2004 are as follows

- Paroxysmal attacks of pain lasting from a fraction of a second to 2 minutes, affecting 1 or more divisions of the trigeminal nerve and fulfilling criteria B and C

- Pain has at least 1 of the following characteristics: (1) intense, sharp, superficial or stabbing; or (2) precipitated from trigger areas or by trigger factors

- Attacks stereotyped in the individual patient - No clinically evident neurologic deficit - Not attributed to another disorder

The criteria for symptomatic trigeminal neuralgia vary slightly from the strict criteria above and include the following

- Paroxysmal attacks of pain lasting from a fraction of a second to 2 minutes, with or without persistence of aching between paroxysms, affecting 1 or more divisions of the trigeminal nerve and fulfilling criteria B and C

- Pain has at least 1 of the following characteristics: (1) intense, sharp, superficial or stabbing; or (2) precipitated from trigger areas or by trigger factors

- Attacks stereotyped in the individual patient - Causative lesion, other than vascular compression, demonstrated by special

investigations and/or posterior fossa exploration

Keep a low threshold for MRI in….. - younger patients - atypical clinical features - sensory loss - dull burning pain between paroxysms - patients who do not respond to initial medical therapy

DIAGNOSIS: CLINICAL EXAMINATION with HISTORY is mandatory Response to treatment with tablet of carbamazepine is universal Injections of local anaesthetic agents into patients trigger zone gives temporarily relief Differential diagnosis

1. Glossopharyngeal neuralgia 2. Occipital neuralgia 3. Paroxysmal hemicrania syndromes 4. Migraine and cluster headaches 5. Dental pathology- pulpitis, periodontitis, dentocle, osteomyelitis 6. Glaucoma 7. Ramsey- Hunt syndrome 8. Sphenopalatine ganglion neuralgia 9. Temporal arteritis(Horton) 10. Temporomandibular dysfunction 11. Atypical facial pain

Variety of tumours and other lesions involving, or impinging on, the trigeminal nerve, ganglion or sensory root tumours of the C-P angle, MCF, cranium or extracranial tissues (often metastatic), and from the envelopes of the Gasserian ganglion Surgical treatment: Peripheral injections Peripheral neurectomy Cryotherapy Peripheral radiofrequency Neurolysis(thermocoagulation) Gasserian ganglion procedures Medication

Carbamazepine

Oxycarbazepine (Trileptal)

Phenytoin is the second treatment of choice

3 weeks over, adequate serum levels obtained…..but no relief DISCONTINUE

because higher doses may lead to toxicity.

The short-term efficacy rate is 60%; decreases to 30% after 2 years

Lamotrigene useful in failure/intolerance with Carbamazepine

Gabapentin: benign adverse effect profile, can be used as adjuvant also

Topiramate: proved to be effective where combination therapy fails Carbamazapine and phenytoin are the traditional anticonvulsants given primarily. The dosage of the drug used initially should be kept small to minimum especially in elderly patients to avoid nausea, vomiting and gastric irritation. Dosage should be taken at night so that adequate serum concentration is present early morning. Complete blood count, liver function, platelet count should be done prior to treatment. Once the pain remission has being achieved the drug dose should be kept at maintenance level or withdrawn and restarted if symptoms reappear When carbamazepine is contraindicated clonazepam can be given Co-administration of phenytion or baclofen is also advocated. As peripheral nerve block the anaesthetic agent without adrenaline with or without corticosteroids is injected. Surgical Procedures For patients who’s medical therapy has failed, surgery is a viable and effective option. Microvascular decompression- Microvascular decompression (MVD)

- non-destructive technique - Under general anesthesia, incising the skin behind the ear (Craniotomy) - Identify an arterial loop compressing the nerve è pad the vascular structure with

Teflon felt - Complication: CSF leaks, hearing loss, permanent anesthesia over the face

Risks higher: in patients who have an ecstatic (atherosclerotic) and a tortuous vertebrobasilar arterial tree

the risk for perioperative mortality [around 0.4%], serious morbidity (eg, stroke, hemorrhage, venous occlussion, M.I.,HCP), permanent hearing loss, and facial palsy is higher after MVD than after percutaneous procedures.

But ablative procedures are less effective in the long term and more likely to produce facial numbness and other minor complications than MVD

Nerve Injury/ Destructive Procedure (Rhizotomy)

1. Percutaneus Glycerol Rhizotomy 2. Percutaneus Balloon Compression Rhizotomy 3. Radiofrequency Rhizotomy 4. Stereotactic Radiosurgery (Gamma Knife) 5. Microsurgical Rhizotomy

CRYOTHERAPY FOR PERIPHERAL NERVE: Direct application of cryotherapy probe (nitrous oxide probe) Temperature colder than -60 degree C, for 2-3 minutes Repeated three times PERIPHERAL RADIOFREQUENCY NEUROLYSIS THERMOCOAGULATION: Radiofrequency electrode that has the capacity to destroy the pain fibres is used in this procedure. Temperature being 65 to 75 degree Centigrade for 1 to 2 minutes. Shown to induce pain remissions in 20%of cases. THERMOCOAGULATION- A radiofrequency electrode that has the capacity to destroy pain fibres is used. Alternating currents of high frequency is passed through the electrode. It produces ionization in the biological tissues leads to coagulation of tissues. GASSERIAN GANGLION PROCEDURS: Includes various procedures: - Glycerol injection - Thermocoagulation - Balloon compression Trigeminal Neuralgia (TN) is neuropathic facial pain arising from the trigeminal nerve. Treatment for TN: medication is the initial therapy if pharmacologic treatment fails the treatment of choice are surgical procedures. GLOSSOPHARYNGEAL NEVRALGIA

• BRANCHIAL MOTOR COMPONENT:(SVE ) supplies the stylopharyngeus muscle. • VISCERAL MOTOR COMPONENT: (GVE)parasympathetic innervation of smooth

muscles and glands of pharynx and secretomotor to the parotid gland . • VISCERAL SENSORY COMPONENT:(GVA)This innervates the baroreceptors of the

carotid sinus, and the chemoreceptors of the carotid body • GENERAL SENSORY COMPONENT:(GSA)carries pain, temp, and touch from skin of

external ear ,internal surface of tympanic membrane, upper pharynx and post.1/3rd of tongue.

• SPECIAL SENSORY COMPONENT:(SA) carries taste sensation from the posterior 1/3rd of the tongue .

• The Tympanic branch- to the tympanic plexus in the middle ear. • Important branches • Lesser petrosal N arises from this plexus and passes to the parotid gland. • Carotid branch, which carries sensory fibers. • Nerve to the Stylopharyngeus • Pharyngeal branches • Lingual branch, which supplies the post 1/3rd of the tongue. GN is characterized by severe, sharp, lancinating pain in the region of the tonsil, radiating to the ear. It is similar to trigeminal neuralgia in its timing and its ability to be

triggered by various stimuli. Pain may be initiated by yawning, swallowing, or contact with food in the tonsillar region. In rare instances, the pain may be associated with syncope(a fall in heart rate and blood pressure resulting in fainting). • Typically, GFN is idiopathic • Occasionally GFN is secondary to the compression of the nerve by carotid aneurism,

oropharyngeal malignancies, peritonsillar infections, or lesions at the base of the skull

The general sensory component mediates the afferent limb of pharyngeal reflex in which touching the back of the pharynx elicits the gag reflex. This is used to test the Glossopharyngeal nerve clinically. Facial palsy • Facial nerve is the VII CN. • Facial mimic muscles develop from the mesoderm of second branchial arch. Intracranial course 1. Central segment (tegmentum pontis). 2. Cisternal segment (CPA). 3. Canalicular segment (IAC). 4. Labyrinthine segment (Fallopian canal). 5. Geniculate ganglion. 6. Tympanic segment. 7. Stylomastoid segment.

Muscle action • Frontalis –wrinkling • Corrugator supercili — frowning,vertical wrinkles of forehead • Orbicularis oculi—closure of eyes • Orbicularis oris—whistling • Buccinator –puffing the mouth • Dilator of the mouth –showing the teeth • Platysma-forcibly pulling the angle of mouth downwards and backwards.

Examination of facial nerve

• Show the teeth • Open his mouth—compare nasolabial folds • Close his eyes • Frown • Wrinkle forehead • Raise eyebrows • Bare his teeth and open his mouth • Blowing out cheeks • Pursuing the lips –strength and weakness Facial nerve pathology Idiopathic (Bell’s palsy) Congenital Traumatic Inflammatory Neoplastic Vascular

Bell’s palsy Acute onset of non-suppurative inflammation of the facial nerve above the stylomastoid foramen, producing a unilateral LMN FACIAL PALSY. Main cause of Bell's palsy is latent herpes viruses which are reactivated from cranial nerve ganglia.

• IDIOPATHIC LMN (lower motor neuron) FACIAL PALSY • HERPES SIMPLEX FACIAL PARALYSIS • HERPETIC FACIAL PARALYSIS

• Most common form of lower motor neuron facial palsy. • Sudden onset of LMN facial palsy. • No other neurologic abnormalities. • Incidence is 23/1,00,000 • Affects men and women equally, all ages, all times of the year. • Increased occurrence in the elderly diabetics, hypertensives than in the common

people. • Increased incidence in women during the third trimester of pregnancy 2 weeks

preceding delivery, first two weeks postpartum. • 1 in 6o life time occurrence of single episode • Facial palsy recurs with each pregnancy

Clinical features • Onset of bell’s palsy is acute. • ½ of the cases attain maximum paralysis in 48 hours. • All cases are clinically prominent by 5 days. • Pain behind the ear may precede the paralysis by a day or two. • Impairment of taste is present to some degree in all cases –rarely beyond second

week of paralysis. • Hyperacusis or distortion of sound in ipsilateral ear ---paralysis of stapedius muscle. • Paralysis is partial in 30%, complete in 70%cases. • Emotional fibers are affected • Jaw jerk is normal • Corneal reflex is absent • These differentiate it from Upper Motor Neuron (UMN) palsy Clinically….. • Corner of mouth droops • Crease and skin folds effaces • Forehead is unfrowned • Eyelids will not close • Eye on the paralyzed side rolls upward –BELL’S PHENOMENON • Lower lid sags and falls away from conjunctiva • Tears spill over cheek • Food collects between the teeth and lips • Saliva may dribble from the corner of the mouth • Heaviness or numbness of the face • Sensory loss rarely demonstrable Patient’s complaints

• Patient feels stiffness of face pulled to one side. • Ipsilateral restriction of eye closure, difficulty with eating , fine facial movements. • Disturbance of taste –chorda tympani fibres • Hyperacusis—fibers to stapedius

Paraclinical tests • Serology - Lyme, herpes and zoster (paired samples 4-6 weeks apart). • Check Blood Pressure in children with Bell's palsy (2 case reports of aortic

coarctation). • Schirmer tear test (reveals reduced flow of tears from an affected greater palatine

nerve). • Stapedial reflex (an audiological test absent if stapedius muscle is affected). • Electrodiagnostic studies (generally a research tool) reveal no changes in involved

facial muscles for the first three days, but a steady decline of electrical activity often occurs over the next week, and will identify the 15% with axonal degeneration.

• Enhancement of the facial nerve on gadolinium enhanced MRI • Increased lymphocytes, mononuclear cells in CSF. • Blood glucose levels Differential diagnosis should be made to exclude malignancies in parotid gland!!! • Lyme disease • Ramsay-Hunt syndrome • Sarcoidosis • Guillain -Barre syndrome • Leprosy • Amyloidosis • Melkerson-Rosenthal syndrome • Acoustic neuroma • Multiple sclerosis • Middle ear infections • Carotid body tumors • Cholesteatoma MELKERSON ROSENTHAL SYNDROME • recurrent facial paralysis • labial edema • plication of tongue

Post-traumatic facial paralysis. A fracture line may be seen to cross the facial nerve canal with or without any associated nerve dysfunction.

Management

• Eye care focuses on protecting the cornea from drying and abrasion due to problems with lid closure and the tearing mechanism.

• Lubricating drops should be applied Treatment of facial palsy is controversial • Symptomatic

• Protection of eye during the sleep- patch • Massage of the weakened muscles • Lubricating eye drops

• Prednisolone 60-80 mg/day in divided doses initial 4-5 days, then taper over next 7-10 days.

• Decreases the possibility of permanent paralysis • From swelling of facial nerve in facial canal. • Decreases the severe pain. • Mannitol- osmotic diuretic • Vit B complex

• Acyclovir /Valacyclovir alone is not useful. • No evidence that surgical decompression of facial nerve is effective ---may be

harmful Complications

• Contracture develops in the paralyzed muscles and is evident when patient smiles. • Incomplete recovery • Crocodile tears • Jaw winking • Synkinesis • hemifacial spasms

- Painless - Irregular contractions on one side of the face. - As a sequelae to bell’s palsy or irritative lesion of facial nerve.---acoustic

neuroma,aberrant artery.,basilar aneurysm • Treatment – carbamazepine, gabapentin • Resistant cases – baclofen • Local injection of botulinum toxin • Surgical decompression

Prognosis • 80% patients recover within a few weeks- 2-12 weeks. • 10%--permanent disfigurement. Long term sequelae. • 8%--recurrence • Best clinical guide to progress is the severity of the palsy during the first few days

after presentation. • Recovery of taste precedes motor function. • Clinically complete palsy when first seen are less likely to make a full recovery—than

incomplete one • Advanced age • Hyperacusis—persistent • Severe initial pain. • If recovery of taste occurs in first week –good prognostic sign. • Early recovery of motor function in the first 5-7 days— most favorable prognosis. • Recurrence is due to reactivation of virus, pregnancy and interval between periods is

not predictable

The HYPOGLOSSAL NERVE dysfunction

• The hypoglossal nerve is the twelfth CN (XII), leading to the tongue.

• The nerve arises from the hypoglossal nucleus and emerges from the medulla oblongata in the preolivary sulcus separating the olive and the pyramid. It then passes through the hypoglossal canal.

• It arises in the medulla. • It leaves the skull through the hypoglossal canal. • Descends in the neck with structures like the ICA, IJV, and Vagus nerve. • It then passes forwards on the side of the tongue • It is joined in the upper part of its course by C1 fibers. • It supplies motor fibers to all of the muscles of the tongue, except the

palatoglossal muscle, which is innervated by the vagus (cranial nerve X) or, according to some classifications, by fibers from the glossopharyngeal (cranial nerve IX) that "hitchhike" within the vagus. Important branches

• The meningeal branch. • The descending branch. • Nerve to the Thyrohyoid muscle. • Muscular branches to the muscles of the tongue. • Nerve to the Geniohyoid muscle.

• To test the function of the nerve, a person is asked to poke out his/her tongue. If

there is a loss of function on one side- unilateral paralysis, the tongue will point toward the affected side.

• The strength of the tongue can be tested by getting the person to poke the inside of his/her cheek, and feeling how strongly he/she can push a finger pushed against the cheek - a more elegant way of testing than directly touching the tongue.

• The tongue can also be looked at for signs of LMN disease, such as fasciculation and atrophy.

• Paralysis/paresis of one side of the tongue results in ipsilateral curvature of the tongue (apex toward the impaired side of the mouth); i.e., the tongue will move toward the affected side.

• Cranial Nerve XII is innervated by the contralateral cortex, so a purely upper motor neuron lesion will cause the tongue to deviate away from the cortical lesion.

• The causes may be central or peripheral and include cerebrovascular accidents, brain stem tumours, multiple sclerosis, syringomyelia, and infectious poly neuritis. Injury to this nerve causes dysarthria and dysphagia Clinical assessment

• In peripheral lesion there is deviation of the tongue towards the affected side, during protrusion. When in tongue rest on the floor of the mouth, a mild deviation towards the unaffected side may be observed.

• In central lesion, involvement is often bilateral. The patient cannot protrude the tongue, and attempt movement of tongue posteriorly is defective and un co-ordination. The tongue is also small and firm.

• These individuals will also have problem in swallowing. There is no control over tongue that results in swallowing problems

SPEECH CHARACTERISTICS • The abnormality of tongue will lead to misarticulation.

• The individuals will have problem in producing /t/, /d/,/t∫/,/l/,/n/,/i/,/j/,/k/ and /g/. • Due to dysarthria these individuals may have distorted vowel and word flow without

pauses • Severity ranges from occasional articulation difficulties to verbal speech that is

completely unintelligible

Management • Speech therapy should be given • Exercise for the treatment of dysarthria may help to improve tongue co-ordination

and strength. • Treatment of hypoglossal nerve injuries due to penetrating wounds is surgical and

the nerve tend to recover quite well Reference:

• Лицевочелюстна и орална хирургия, Угринов и кол., София, 2006г • Peterson’s principles in OMFS, 4-th edition • Fonseca and Walker Maxillofacial trauma, 2-nd edition • Gray's Atlas of Anatomy (Gray's Anatomy) 2nd Edition • Atlas of Human Anatomy (Netter Basic Science) 7th Edition • Lee and MacGregors surgical anatomy • Oral and Maxillofacial Pathology, 4th Edition Neville et all. • Shafer's Textbook of Oral Pathology, 2012 • Cole CD, Liu JK, Apfelbaum RI 2005. Historical Perspectives on the Diagnosis and

Treatment of Trigeminal Neuralgia. Neurosurg Focus. 18(5) • Dixon J, Chan L, Olmedo R, Talavera F, Ungar J, 2005. Tic Douloureux.

emedicinehealth.1-13. • Janetta P, 2011. Trigeminal Neuralgia. Oxford University Press. 2-10 • Office of Communications and Public Liaison, 2014. Trigeminal Neuralgia. National

Institute of Neurological Disorders and Stroke • Towne EB, 1927. Neurosurgery: Tic Douloureux. Cal West Med. v27(6): 814. • Zakrzewska JM, Linskey ME, 2014. Trigeminal Neuralgia. Clin Evid. pII: 1207 • Love S, Coakham HB, 2001. Trigeminal Neuralgia: Pathology and Pathogenesis. Brain.

v124(12): 2347-2360. • Diagnostic and imaging anatomy- Head, neck and brain- Harnsbergen, Osborn at al. • Bell's Palsy Handbook Facial Nerve Palsy or Bell's Palsy facial paralysis causes,

symptoms, treatment, face exercises & recovery all covered by Alan Mc Donald | Alan Mc Donald

• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5652082/