Branches of the facial nerve leaving the facial motor nucleus (FMN) for the muscles do so via both left and right posterior (dorsal) and anterior (ventral) routes.  In other words, this means lower motor neurons of the facial nerve can leave either from the left anterior, left posterior, right anterior or right posterior facial motor nucleus.  The temporal branch travels out from the left and right posterior components.  The inferior four branches do so via the left and right anterior components.  The left and right branches supply their respective sides of the face (ipsilateral innervation).  Accordingly, the posterior components receive motor input from both hemispheres of the cerebral cortex (bilaterally), whereas the anterior components receive strictly contralateral input.  This means that the temporal branch of the facial nerve receives motor input from both hemispheres of the cerebral cortex whereas the zygomatic, buccal, mandibular and cervical branches receive information from only contralateral hemispheres.


Now, because the anterior FMN receives only contralateral cortical input whereas the posterior receives that which is bilateral, a corticobulbar lesion (UMN lesion) occurring in the left hemisphere would eliminate motor input to the right anterior FMN component, thus removing signaling to the inferior four facial nerve branches, thereby paralyzing the right mid- and lower-face.  The posterior component, however, although now only receiving input from the right hemisphere, is still able to allow the temporal branch to sufficiently innervate the entire forehead.  This means that the forehead will not be paralyzed.


The same mechanism applies for an upper motor neuron lesion in the right hemisphere.  The left anterior FMN component no longer receives cortical motor input due to its strict contralateral innervation, whereas the posterior component is still sufficiently supplied by the left hemisphere.  The result is paralysis of the left mid- and lower-face with an unaffected forehead.


On the other hand, a lower motor neuron lesion is a bit different.


A lesion on either the left or right side would affect both the anterior and posterior routes on that side because of their close physical proximity to one another.  So, a lesion on the left side would inhibit muscle innervation from both the left posterior and anterior routes, thus paralyzing the whole left side of the face ( Bell’s palsy ).  With this type of lesion, the bilateral and contralateral inputs of the posterior and anterior routes, respectively, become irrelevant because the lesion is below the level of the medulla and the facial motor nucleus.  Whereas at a level above the medulla a lesion occurring in one hemisphere would mean that the other hemisphere could still sufficiently innervate the posterior facial motor nucleus, a lesion affecting a lower motor neuron would eliminate innervation altogether because the nerves no longer have a means to receive compensatory contralateral input at a downstream decussation.


Thus, the main distinction between an UMN and LMN lesion is that in the former, there is hemiplegia of the contralateral mid- and lower-face, whereas in the latter, there is complete hemiplegia of the ipsilateral face.


2° ( Spinomesencephalic tract  →  Superior colliculus  of  Midbrain tectum )


The  facial muscles  are a group of striated  skeletal muscles  supplied by the  facial nerve  (cranial nerve VII) that, among other things, control facial expression.  These muscles are also called  mimetic muscles . They are only found in  mammals , although they derive from  neural crest  cells found in all vertebrates. They are the only muscles that attach to the  dermis . [ 1 ]


The facial muscles are just under the skin ( subcutaneous ) muscles that control facial expression.  They generally  originate  from the surface of the  skull  bone (rarely the fascia), and insert on the skin of the face. When they contract, the skin moves. These muscles also cause wrinkles at right angles to the muscles’ action line. [ 2 ]


The facial muscles are supplied by the facial nerve (cranial nerve VII), with each nerve serving one side of the face. [ 2 ]   In contrast, the nearby  masticatory muscles  are supplied by the  mandibular nerve , a branch of the  trigeminal nerve  (cranial nerve V).


The facial muscles include: [ 3 ]


The  platysma  is supplied by the facial nerve. Although it is mostly in the neck and can be grouped with the neck muscles by location, it can be considered a muscle of facial expression due to its common nerve supply.


The  stylohyoid muscle ,  stapedius  and posterior belly of the  digastric muscle  are also supplied by the facial nerve, but are not considered muscles of facial expression.


The facial muscles are derived from the second branchial/ pharyngeal arch . They, like the branchial arches, originally derive from neural crest cells. In humans, they typically begin forming around the eighth week of embryonic development. [ 1 ]


An inability to form facial expressions on one side of the face may be the first sign of damage to the nerve of these muscles. Damage to the facial nerve results in  facial paralysis  of the muscles of facial expression on the involved side. Paralysis is the loss of voluntary muscle action; the facial nerve has become damaged permanently or temporarily. This damage can occur with a  stroke ,  Bell palsy , or parotid salivary gland cancer (malignant neoplasm) because the facial nerve travels through the gland. The  parotid gland  can also be damaged permanently by surgery or temporarily by trauma. These situations of paralysis not only inhibit facial expression but also seriously impair the patient’s ability to speak, either permanently or temporarily. [ 2 ]


The  facial nerve , also known as the  seventh cranial nerve ,  cranial nerve VII , or simply  CN VII , is a  cranial nerve  that emerges from the  pons  of the  brainstem , controls the  muscles of facial expression , and functions in the conveyance of  taste  sensations from the anterior two-thirds of the  tongue . [ 1 ] [ 2 ]  The nerve typically travels from the pons through the  facial canal  in the  temporal bone  and exits the skull at the  stylomastoid foramen . [ 3 ]  It arises from the brainstem from an area posterior to the  cranial nerve VI  (abducens nerve) and anterior to  cranial nerve VIII  (vestibulocochlear nerve).


The facial nerve also supplies preganglionic  parasympathetic  fibers to several head and neck  ganglia .


The facial and  intermediate nerves  can be collectively referred to as the  nervus intermediofacialis. [ citation needed ]


The path of the facial nerve can be divided into six segments:


The motor part of the facial nerve arises from the  facial nerve nucleus  in the  pons , while the sensory and parasympathetic parts of the facial nerve arise from the  intermediate nerve .


From the brain stem, the motor and sensory parts of the facial nerve join and traverse the  posterior cranial fossa  before entering the  petrous temporal bone  via the  internal auditory meatus .  Upon exiting the internal auditory meatus, the nerve then runs a tortuous course through the  facial canal , which is divided into the labyrinthine, tympanic, and mastoid segments.


The labyrinthine segment is the shortest and narrowest segment of the facial nerve and ends where the facial nerve forms a bend known as the geniculum of the facial nerve ( genu  meaning knee), which contains the  geniculate ganglion  for sensory nerve bodies.  The first branch of the facial nerve, the  greater petrosal nerve , arises here from the geniculate ganglion. The greater petrosal nerve runs through the  pterygoid canal  and synapses at the  pterygopalatine ganglion .  Postsynaptic fibers of the greater petrosal nerve innervate the  lacrimal gland .


In the tympanic segment, the facial nerve runs through the  tympanic cavity , medial to the  incus .


The  pyramidal eminence  is the second bend in the facial nerve, where the nerve runs downward as the mastoid segment, the longest segment of the facial nerve.  In the temporal part of the facial canal, the nerve gives branch to the  stapedius muscle  and  chorda tympani . The chorda tympani supplies taste fibers to the anterior two thirds of the tongue, and also synapses with the  submandibular ganglion . Postsynaptic fibers from the submandibular ganglion supply the  sublingual  and  submandibular glands .


Upon emerging from the  stylomastoid foramen , the facial nerve gives rise to the  posterior auricular branch .  It then gives rise to the branch to the posterior belly of the digastric, and then the branch to the stylohyoid.  The facial nerve then passes through the  parotid gland , which it does not innervate, to form the  parotid plexus . The nerve then bifurcates at the  pes anserinus  to become the upper and lower divisions of the facial nerve. [ 4 ]  It then splits into five branches (temporal, zygomatic, buccal, marginal mandibular and cervical), innervating the  muscles of facial expression . [ 5 ] [ 6 ]


The  greater petrosal nerve  arises at the  superior salivatory nucleus  of the pons and provides parasympathetic innervation to several glands, including the  nasal glands , the  palatine glands , the  lacrimal gland , and the  pharyngeal gland . It also provides parasympathetic innervation to the  sphenoid sinus ,  frontal sinus ,  maxillary sinus ,  ethmoid sinus , and  nasal cavity . This nerve also includes taste fibers for the  palate  via the  lesser palatine nerve  and  greater palatine nerve .


The communicating branch to the  otic ganglion  arises at the  geniculate ganglion  and joins the  lesser petrosal nerve  to reach the otic ganglion. [ 7 ]


The  nerve to stapedius  provides motor innervation for the  stapedius muscle  in middle ear


The  chorda tympani  provides parasympathetic innervation to the sublingual and submandibular glands, as well as special sensory taste fibers for the anterior two thirds of the tongue. [ 1 ]


Distal to  stylomastoid foramen , the following nerves branch off the facial nerve:


Intra operatively the facial nerve is recognized at 3 constant landmarks: [ citation needed ]


The  cell bodies  for the facial nerve are grouped in anatomical areas called  nuclei  or  ganglia . The cell bodies for the afferent nerves are found in the  geniculate ganglion  for taste sensation.  The cell bodies for muscular efferent nerves are found in the  facial motor nucleus  whereas the cell bodies for the parasympathetic efferent nerves are found in the  superior salivatory nucleus .


The facial nerve is developmentally derived from the second  pharyngeal arch , or branchial arch.  The second arch is called the hyoid arch because it contributes to the formation of the lesser horn and upper body of the  hyoid bone  (the rest of the hyoid is formed by the third arch).  The facial nerve supplies motor and sensory innervation to the muscles formed by the second pharyngeal arch, including the muscles of facial expression, the posterior belly of the digastric, stylohyoid, and stapedius.  The motor division of the facial nerve is derived from the  basal plate  of the embryonic pons, while the sensory division originates from the  cranial neural crest . [ 9 ]


Although the anterior two thirds of the tongue are derived from the first pharyngeal arch, which gives rise to the trigeminal nerve, not all innervation of the tongue is supplied by it.  The lingual branch of the  mandibular division  (V3) of the  trigeminal nerve  supplies non-taste sensation (pressure, heat, texture) to the anterior part of the tongue via  general somatic afferent fibers .  Nerve fibers for taste are supplied by the chorda tympani branch of the facial nerve via  special visceral afferent  fibers. [ 10 ]


The main function of the facial nerve is motor control of all the  muscles of facial expression . It also innervates the posterior belly of the  digastric muscle , the  stylohyoid muscle , and the  stapedius muscle  of the  middle ear . These  skeletal muscles  are developed from the  second pharyngeal arch .


In addition, the facial nerve receives  taste  sensations from the anterior two-thirds of the  tongue  via the  chorda tympani . Taste sensation is sent to the gustatory portion (superior part) of the  solitary nucleus . General sensation from the anterior two-thirds of tongue are supplied by afferent fibers of the third division of the fifth cranial nerve ( CN V -3). These sensory ( CN V3 ) and taste (VII) fibers travel together as the lingual nerve briefly before the chorda tympani leaves the lingual nerve to enter the tympanic cavity (middle ear) via the petrotympanic fissure. It joins the rest of the facial nerve via the canaliculus for chorda tympani. The facial nerve then forms the  geniculate ganglion , which contains the cell bodies of the taste fibers of chorda tympani and other taste and sensory pathways. From the geniculate ganglion, the taste fibers continue as the intermediate nerve which goes to the upper anterior quadrant of the fundus of the  internal acoustic meatus  along with the motor root of the facial nerve. The intermediate nerve reaches the posterior cranial fossa via the internal acoustic meatus before synapsing in the  solitary nucleus .


The facial nerve also supplies a small amount of afferent innervation to the  oropharynx  below the  palatine tonsil . There is also a small amount of cutaneous sensation carried by the  nervus intermedius  from the skin in and around the  auricle  (outer ear).


The facial nerve also supplies  parasympathetic  fibers to the  submandibular gland  and  sublingual glands  via  chorda tympani . Parasympathetic innervation serves to increase the flow of saliva from these glands. It also supplies parasympathetic innervation to the nasal mucosa and the  lacrimal gland  via the  pterygopalatine ganglion . The parasympathetic fibers that travel in the facial nerve originate in the  superior salivatory nucleus .


The facial nerve also functions as the efferent limb of the  corneal reflex .


The facial nerve carries axons of type GSA,  general somatic afferent , to skin of the posterior ear.


The facial nerve also carries axons of type GVE,  general visceral efferent , which innervate the sublingual, submandibular, and lacrimal glands, also mucosa of nasal cavity.


Axons of type SVE,  special visceral efferent , innervate muscles of facial expression, stapedius, the posterior belly of digastric, and the stylohyoid.


The axons of type SVA,  special visceral afferent , provide taste to the anterior two-thirds of tongue via  chorda tympani .


People may suffer from  acute facial nerve paralysis , which is usually manifested by facial paralysis. [ 11 ]   Bell's palsy  is one type of  idiopathic  acute facial nerve paralysis, which is more accurately described as a multiple cranial nerve ganglionitis that involves the facial nerve, and most likely results from viral infection and also sometimes as a result of  Lyme disease . Iatrogenic Bell's palsy may also be as a result of an incorrectly placed dental local-anesthetic ( inferior alveolar nerve block ). Although giving the appearance of a hemiplegic stroke, effects dissipate with the drug. When the facial nerve is permanently damaged due to a birth defect, trauma, or other disorder, surgery including a cross facial nerve graft or masseteric facial nerve transfer may be performed to help regain facial movement. [ citation needed ]   Facial nerve decompression  surgery is also sometimes carried out in certain cases of facial nerve compression.


Voluntary facial movements, such as wrinkling the brow, showing teeth, frowning, closing the eyes tightly (inability to do so is called  lagophthalmos ), [ 12 ]  pursing the lips and puffing out the cheeks, all test the facial nerve. There should be no noticeable asymmetry.


In an  upper motor neuron  lesion, called  central seven , only the lower part of the face on the contralateral side will be affected, due to the bilateral control to the upper facial muscles ( frontalis  and  orbicularis oculi ).


Lower motor neuron  lesions can result in a CN VII palsy (Bell's palsy is the idiopathic form of facial nerve palsy), manifested as both upper and lower facial weakness on the same side of the lesion.


Taste can be tested on the anterior two-thirds of the tongue. This can be tested with a swab dipped in a flavored solution, or with electronic stimulation (similar to putting your tongue on a battery).


Corneal reflex . The afferent arc is mediated by the general sensory afferents of the trigeminal nerve.  The efferent arc occurs via the facial nerve. The reflex involves consensual blinking of both eyes in response to stimulation of one eye. This is due to the facial nerves' innervation of the muscles of facial expression, namely orbicularis oculi, responsible for blinking. Thus, the corneal reflex effectively tests the proper functioning of both cranial nerves V and VII.


This article incorporates text in the  public domain  from  page 901  of the 20th edition of   Gray's Anatomy   (1918)


Facial nerve paralysis  is a common problem that involves the  paralysis  of any structures innervated by the  facial nerve . The pathway of the facial nerve is long and relatively convoluted, so there are a number of causes that may result in facial nerve paralysis. [ 2 ]  The most common is  Bell's palsy , [ 3 ] [ 4 ]  a disease of unknown cause that may only be diagnosed by exclusion of identifiable serious causes.


Facial nerve paralysis is characterised by facial weakness, usually only in one side of the face, with other symptoms possibly including  loss of taste ,  hyperacusis  and  decreased salivation  and tear secretion [ ambiguous ] . Other signs may be linked to the cause of the paralysis, such as  vesicles  in the ear, which may occur if the facial palsy is due to  shingles . Symptoms may develop over several hours. [ 5 ]   : 1228   Acute facial pain radiating from the ear may precede the onset of other symptoms. [ 6 ]   : 2585


Bell's palsy is the most common cause of acute facial nerve paralysis. [ 3 ] [ 4 ]  There is no known cause of Bell's palsy, [ 5 ] [ 6 ]  although it has been associated with  herpes simplex  infection. Bell's palsy may develop over several days, and may last several months, in the majority of cases recovering spontaneously. It is typically diagnosed clinically, in patients with no risk factors for other causes, without vesicles in the ear, and with no other  neurological signs . Recovery may be delayed in the elderly, or those with a complete paralysis. Bell's palsy is often treated with  corticosteroids . [ 5 ] [ 6 ]


Lyme disease , an infection caused by  Borrelia burgdorferi  bacteria and spread by  ticks , can account for about 25% of cases of facial palsy in areas where Lyme disease is common. [ 7 ]  In the U.S., Lyme is most common in the  New England  and  Mid-Atlantic  states and parts of  Wisconsin  and  Minnesota , but it is expanding into other areas. [ 8 ]  The first sign of about 80% of Lyme infections, typically one or two weeks after a tick bite, is usually an  expanding rash  that may be accompanied by headaches, body aches, fatigue, or fever. [ 9 ]  In up to 10-15% of Lyme infections, facial palsy appears several weeks later, and may be the first sign of infection that is noticed, as the Lyme rash typically does not itch and is not painful. Lyme disease is treated with antibiotics. [ 10 ] [ 11 ]


Reactivation of  varicella zoster virus , as well as being associated with Bell's palsy, may also be a direct cause of facial nerve palsy. Reactivation of latent virus within the  geniculate ganglion  is associated with vesicles affecting the ear canal, and termed  Ramsay Hunt syndrome type 2 . [ 6 ]  In addition to facial paralysis, symptoms may include ear pain and vesicles,  sensorineural hearing loss , and  vertigo . Management includes  antiviral drugs  and oral  steroids .


Otitis media  is an infection in the middle ear, which can spread to the facial nerve and inflame it, causing compression of the nerve in its canal.  Antibiotics  are used to control the otitis media, and other options include a wide  myringotomy  (an incision in the  tympanic membrane ) or decompression if the patient does not improve.
Chronic otitis media usually presents in an ear with chronic discharge ( otorrhea ), or hearing loss, with or without ear pain ( otalgia ). Once suspected, there should be immediate surgical exploration to determine if a  cholesteatoma  has formed as this must be removed if present.  Inflammation from the middle ear can spread to the canalis facialis of the temporal bone - through this canal travels the facial nerve together with the statoacoustisus nerve. In the case of inflammation the nerve is exposed to edema and subsequent high pressure, resulting in a periferic type palsy.


In  blunt trauma , the facial nerve is the most commonly injured  cranial nerve . [ 12 ]   Physical trauma , especially  fractures  of the  temporal bone , may also cause acute facial nerve paralysis. Understandably, the likelihood of facial paralysis after trauma depends on the location of the trauma. Most commonly, facial paralysis follows temporal bone fractures, though the likelihood depends on the type of fracture.


Transverse fractures  in the horizontal plane present the highest likelihood of facial paralysis (40-50%). Patients may also present with blood behind the tympanic membrane, sensory deafness, and  vertigo ; the latter two symptoms due to damage to  vestibulocochlear nerve  and the inner ear.  Longitudinal fracture  in the vertical plane present a lower likelihood of paralysis (20%). Patients may present with blood coming out of the  external auditory meatus ),  tympanic membrane  tear, fracture of  external auditory canal , and  conductive hearing loss . In patients with mild injuries, management is the same as with Bell's palsy – protect the  eyes  and wait. In patients with severe injury, progress is followed with nerve conduction studies. If nerve conduction studies show a large (>90%) change in nerve conduction, the nerve should be decompressed. The facial paralysis can follow immediately the trauma due to direct damage to the facial nerve, in such cases a surgical treatment may be attempted. In other cases the facial paralysis can occur a long time after the trauma due to oedema and inflammation. In those cases steroids can be a good help.


A  tumor  compressing the facial nerve anywhere along its complex pathway can result in facial paralysis. Common culprits are  facial neuromas , congenital  cholesteatomas ,  hemangiomas ,  acoustic neuromas ,  parotid gland   neoplasms , or  metastases  of other tumours. [ 13 ] [ 14 ]


Often, since facial neoplasms have such an intimate relationship with the facial nerve, removing tumors in this region becomes perplexing as the physician is unsure how to manage the tumor without causing even more palsy. Typically, benign tumors should be removed in a fashion that preserves the facial nerve, while malignant tumors should always be resected along with large areas of tissue around them, including the facial nerve.  While this will inevitably lead to facial paralysis, safe removal of a malignant neoplasm is vital for patient survival. After tumor removal, the facial nerve can be reinnervated with techniques such as cross-facial nerve grafting, nerve transfers and end-to-end nerve repair. [ 15 ]  Alternative treatment methods include muscle transfer techniques, such as the gracilis free muscle transfer [ 16 ]  or static procedures.


Patients with facial nerve paralysis resulting from tumours usually present with a progressive, twitching paralysis, other neurological signs, or a recurrent Bell's palsy-type presentation.
The latter should always be suspicious, as Bell's palsy should not recur. A chronically discharging ear must be treated as a cholesteatoma until proven otherwise; hence, there must be immediate  surgical  exploration. Computed tomography (CT) or magnetic resonance (MR) imaging should be used to identify the location of the tumour, and it should be managed accordingly.


Other neoplastic causes include  leptomeningeal carcinomatosis .


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 . Unlike peripheral facial palsy, central facial palsy does not affect the forehead, because the forehead is served by nerves coming from both motor cortexes. [ 7 ]


Other causes may include:


A  medical history  and  physical examination , including a  neurological examination , are needed for diagnosis. The first step is to observe what parts of the face do not move normally when the person tries to smile, blink, or raise the eyebrows. If the forehead wrinkles normally, a diagnosis of  central facial palsy  is made, and the person should be evaluated for  stroke . [ 7 ]  Otherwise, the diagnosis is peripheral facial palsy, and its cause needs to be identified, if possible. Ramsey Hunt's syndrome causes pain and small blisters in the ear on the same side as the palsy. Otitis media, trauma, or post-surgical complications may alternatively become apparent from history and physical examination. If there is a history of trauma, or a tumour is suspected, a  CT scan  or  MRI  may be used to clarify its impact. Blood tests or  x-rays  may be ordered depending on suspected causes. [ 6 ]  The likelihood that the facial palsy is caused by  Lyme disease  should be estimated, based on recent history of outdoor activities in likely tick habitats during warmer months, recent history of rash or symptoms such as headache and fever, and whether the palsy affects both sides of the face (much more common in Lyme than in Bell's palsy). If that likelihood is more than negligible, a serological test for Lyme disease should be performed. If the test is positive, the diagnosis is Lyme disease. If no cause is found, the diagnosis is Bell's Palsy.


Facial nerve paralysis may be divided into supranuclear and infranuclear lesions. In a clinical setting, other commonly used classifications include: intra-cranial and extra-cranial; acute, subacute and chronic duration. [ 17 ]


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 refer to the majority of causes of facial palsy.


If an underlying cause has been found for the facial palsy, it should be treated. If it is estimated that the likelihood that the facial palsy is caused by  Lyme disease  exceeds 10%,  empiric therapy  with antibiotics should be initiated, without  corticosteroids , and reevaluated upon completion of laboratory tests for Lyme disease. [ 7 ]  All other patients should be treated with corticosteroids and, if the palsy is severe,  antivirals . Facial palsy is considered severe if the person is unable to close the affected eye completely or the face is asymmetric even at rest. Corticosteroids initiated within three days of Bell's palsy onset have been found to increase chances of recovery, reduce time to recovery, and reduce residual symptoms in case of incomplete recovery. [ 7 ]  However, for facial palsy caused by Lyme disease, corticosteroids have been found in some studies to harm outcomes. [ 7 ]  Other studies have found antivirals to possibly improve outcomes relative to corticosteroids alone for severe Bell's palsy. [ 7 ]  In those whose blinking is disrupted by the facial palsy, frequent use of artificial tears while awake is recommended, along with ointment and a patch or taping the eye closed when sleeping. [ 7 ] [ 18 ]  Several surgical treatment options exist to restore symmetry to the paralyzed face in patients where function does not return (see section Tumors above).


A study followed thirty individuals with facial paralysis following a stroke. Six months after the onset of paralysis, two-thirds of the patients had fully recovered or only had mild facial paralysis. [ 19 ]


In the case of Bell's palsy, 71% of individuals fully recover without any  sequelae . Additionally, the majority of individuals begin to recover within seven days after the onset of paralysis. [ 20 ]


Facial rejuvenation  is a cosmetic treatment (or series of cosmetic treatments), which aims to restore a youthful appearance to the human  face . Facial rejuvenation can be achieved through either  surgical  and/or non-surgical options. Procedures can vary in  invasiveness  and depth of treatment. Surgical procedures can restore  facial symmetry  through targeted procedures and facial restructuring and skin alterations. Non-surgical procedures can target specific depths of facial structures and treat localized facial concerns such as  wrinkles , skin laxity,  hyperpigmentation  and  scars .


Surgical (invasive) facial rejuvenation procedures can include a  brow lift  (forehead lift), eye lift ( blepharoplasty ),  facelift  (rhytidectomy), chin lift and  neck lift . Non-surgical (non-invasive) facial rejuvenation treatments can include  chemical peels , neuromodulator (such as  botox ),  dermal fillers ,  laser resurfacing ,  photorejuvenation ,  radiofrequency  and  Ultrasound .


Human  visual perception  is notable for its sensitivity and accuracy in estimating our perceived age by instant  pattern recognition  of facial features. Often, human faces with no measurable difference in  facial geometry  and appearance are perceived as having different ages. This mechanism is not yet entirely understood, but there may be a relation to the subtle changes in facial bone structure related below. [ 1 ]


Facial symmetry  has a direct relationship to perceived beauty. A guiding approach to facial rejuvenation and balancing facial symmetry is through an application of the  golden ratio . [ 2 ]  Artists and architects have been using this ratio to create works that are pleasing to the eye for centuries. [ 3 ]   Aesthetic medicine  and facial rejuvenation techniques has adopted this mathematical approach to facial restoration and enhancement. [ 4 ]


More recent research has pointed out the influence of changes in the facial  skeleton  with age on the appearance of aging, especially in the mid-face area and the lower part of the  orbits  around the  nose . Quantitative study with  CAT scans  of the faces of men and women in several age brackets has revealed that there is an appreciable amount of   bone  tissue loss in these regions with age, leading to changes in angles, lengths and volumes, and also decreasing the distance between the  eyes . [ 4 ]  It has been hypothesized that skin sagging and wrinkles may occur not only because of loss of soft tissue and fat, but also because bone retraction creates an excess of skin which is no longer flexible. Many of the facial manifestations of aging reflect the combined effects of gravity, progressive  bone resorption , decreased tissue elasticity, and redistribution of subcutaneous fullness. [ 5 ]  Future facial rejuvenation techniques may take into account these findings and restore bone lost by aging processes. [ 6 ]


According to the  American Society of Plastic Surgeons , more than 133,000 facelifts and nearly 216,000 eyelid surgeries were performed in the US in 2013, a six per cent increase from 2012. Facial rejuvenation procedures experienced the most growth, as 2013 marked the highest number of botulinum toxin type A injections to date, with 6.3 million injections. [ 7 ]  A significant upward trend on the number of facial rejuvenation procedures is predicted, [ 5 ]  and could be due to the following factors:


However, while surgical procedures are still preferred to achieve a more dramatic improvement, the current trend is towards less invasive procedures, such as injectables (Botox, fillers) and laser skin treatments. While these treatments achieve temporary results, they tend to be preferred because of their reduced cost and less intensive recovery period. [ 6 ]


Facial rejuvenation procedures can include (but are not limited to):


A  forehead lift , also known as a browlift or browplasty, is a  cosmetic surgery  procedure used to elevate a drooping eyebrow that may obstruct vision and/or to remove the deep "worry" lines that run across the  forehead .


The first documented medical discussion about a forehead lift was written in 1910 by the famous German surgeon  Erich Lexer . [ 1 ]


Since the advent of the hugely popular wrinkle remover,  Botox  (Dysport in the United Kingdom and Europe) many consumers have eschewed the invasive surgery altogether, opting for Botox injections every four to six months to get the same results. Botox is also used after some forehead lift procedures to increase the effects of the surgeries. [ 2 ]


Endoscopic  surgery is often employed in forehead lifts. [ 3 ]  An endoscope is a surgical system with thin, pencil-sized arms that are inserted through three to five incisions about 3/8 of an inch long. One of the instrument's arms is a lighted camera that displays what it sees under the patient's skin on a television monitor. [ 4 ]  Other arms on the Endoscope carry actual surgical tools that perform cutting, or grasping functions. The surgeon watches the television monitor to guide his movements.


Another type of surgical technique is the coronal brow lift, in which a bicoronal incision is made. This technique was popularized in the 1980s and 1990s, but has fallen out of favor compared to the endoscopic technique. [ 5 ]  Other techniques include the direct brow lift, [ 6 ]  mid-forehead brow lift, [ 7 ]  pretrichial brow lift, [ 8 ]  temporal brow lift, and internal (transblepharoplasty) brow lift.


When surgeons have problems with an endoscopic forehead lift, – in about one percent of cases – they finish the procedure by switching to the open forehead lift method.


Complications are said to be rare and minor when a forehead lift is performed by a surgeon trained in the technique. However, it is possible for the surgical process to damage the nerves that control eyebrow and forehead movements. Hair loss can also occur along the scar edges in the scalp when an incision is made through the hairline.  Moreover, infection and bleeding are possible with any surgical procedure. [ 9 ]  Compared to endoscopic techniques, coronal brow lift techniques have a higher risk of elevating the frontal hairline and decreasing scalp sensation.


Patients who have Endotine implants in their foreheads risk moving their newly adjusted tissues with relatively small movements just after the operation and before complete healing takes place. While the implant absorbs into the body, the Endotine generally does not support the very thick forehead flesh and heavy brows often seen in some overweight males. [ 10 ]


Foreign body aspiration  occurs when a foreign body enters the  airway  which can cause difficulty breathing or  choking . [ 1 ]  Objects may reach the respiratory tract and the digestive tract from the mouth and nose, but when an object enters the respiratory tract it is termed aspiration. The foreign body can then become lodged in the trachea or further down the respiratory tract such as in a bronchus. [ 2 ]  Regardless of the type of object, any aspiration can be a life-threatening situation and requires timely recognition and action to minimize risk of complications. [ 3 ]  While advances have been made in management of this condition leading to significantly improved clinical outcomes, there were still 2,700 deaths resulting from foreign body aspiration in 2018. [ 4 ]   Approximately one child dies every five days due to choking on food in the United States, highlighting the need for improvements in education and prevention. [ 5 ]


Signs and symptoms of foreign body aspiration vary based on the site of obstruction, the size of the foreign body, and the severity of obstruction. [ 2 ]  20% of foreign bodies become lodged in the upper airway, while 80% become lodged in a  bronchus . [ 6 ]  Signs of foreign body aspiration are usually abrupt in onset and can involve coughing, choking, and/or  wheezing ; however, symptoms can be slower in onset if the foreign body does not cause a large degree of obstruction of the airway. [ 2 ]  With this said, aspiration can also be asymptomatic on rare occasions. [ 1 ]


Classically, patients present with acute onset of choking. [ 2 ]  In these cases, the obstruction is classified as a partial or complete obstruction. [ 2 ]  Signs of partial obstruction include choking with drooling,  stridor , and the patient maintains the ability to speak. [ 2 ]  Signs of complete obstruction include choking with inability to speak or absence of bilateral breath sounds among other signs of respiratory distress such as  cyanosis . [ 2 ]  A fever may be present. When this is the case, it is possible the object may be chemically irritating or contaminated. [ 7 ]


Foreign bodies above the  larynx  often present with stridor, while objects below the larynx present with wheezing. [ 6 ]  Foreign bodies above the vocal cords often present with difficulty and pain with swallowing and excessive drooling. [ 8 ]  Foreign bodies below the vocal cords often present with pain and difficulty with speaking and breathing. [ 8 ]  Increased respiratory rate may be the only sign of foreign body aspiration in a child who cannot verbalize or report if they have swallowed a foreign body. [ 6 ]


If the foreign body does not cause a large degree of obstruction, patients may present with chronic cough, asymmetrical breath sounds on exam, or recurrent  pneumonia  of a specific lung lobe. [ 2 ]  If the aspiration occurred weeks or even months ago, the object may lead to an obstructive pneumonia or even a lung abscess. Therefore, it is important to consider chronic foreign body aspiration in patients whose histories include unexplained recurrent pneumonia or lung abscess with or without fever. [ 7 ]


In adults, the right lower lobe of the lung is the most common site of recurrent pneumonia in foreign body aspiration. [ 2 ]  This is due to the fact that the anatomy of the right main bronchus is wider and steeper than that of the left main bronchus, allowing objects to enter more easily than the left side. [ 2 ]  Unlike adults, there is only a slight propensity towards objects lodging in the right bronchus in children. [ 7 ]  This is likely due to the bilateral bronchial angles being symmetric until about 15 years of age when the  aortic knob  fully develops and displaces the  left main bronchus . [ 7 ]


Signs and symptoms of foreign body aspiration in adults may also mimic other lung disorders such as  asthma ,  COPD , and  lung cancer . [ 9 ]
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Most cases of foreign body aspiration are in children ages 6 months to 3 years due to the tendency for children to place small objects in the mouth and nose. Children of this age usually lack molars and cannot grind up food into small pieces for proper swallowing. [ 8 ]  Small, round objects including nuts, hard candy, popcorn kernels, beans, and berries are common causes of foreign body aspiration. [ 2 ]  Latex balloons are also a serious choking hazard in children that can result in death. A latex balloon will conform to the shape of the  trachea , blocking the airway and making it difficult to expel with the  Heimlich maneuver . [ 10 ]  In addition, if the foreign body is able to absorb water, such as a bean, seed, or corn, among other things, it may swell over time leading to a more severe obstruction. [ 4 ]


In adults, foreign body aspiration is most prevalent in populations with impaired swallowing mechanisms such as the following: neurological disorders, alcohol use, advanced age leading to senility (most common in the 6th decade of life), and loss of consciousness. [ 11 ]  This inadequate airway protection may also be attributed to poor dentition, seizure, general anesthesia, or  sedative  drug use. [ 4 ]


The most important aspect of the assessment for a clinician is an accurate history provided by an event witness. [ 7 ]  Unfortunately, this is not always available.


A physical examination by a clinician should include, at a minimum, a general assessment in addition to cardiac and pulmonary exams. Auscultation of breath sounds may give additional information regarding object location and the degree of airway obstruction. [ 7 ]  The presence of drooling and dysphagia (drooling) should always be noted alongside the classic signs of airway obstruction as these can indicate involvement of the esophagus and impact management. [ 12 ]


Radiography is the most common form of imaging used in the initial assessment of a foreign body presentation. Most patients receive a  chest x-ray  to determine the location of the foreign body. [ 2 ]  Lateral neck, chest, and bilateral decubitus end-expiratory chest x-rays should be obtained in patients suspected of having aspirated a foreign body. [ 6 ]  However, the presence of normal findings on chest radiography should not rule out foreign body aspiration as not all objects can be visualized. [ 2 ]  In fact, up to 50% of cases can have normal findings on radiography. [ 7 ]  This is because visibility of an object depends on many factors, such as the object's material, size, anatomic location and surrounding structures, as well as the patient's body habitus. [ 13 ]  X-ray beams only show an object if that object's composition blocks the rays from traveling through, making it  radiopaque  and appearing lighter or white on the image. This also requires it to not be stuck behind something that blocks the beams first. [ 13 ]  Objects that are radiopaque include items made of most metals except aluminum, bones except most fish bones, and glass. If the material does not block the x-ray beams it is considered  radiolucent  and will appear dark which prevents visualization. [ 13 ]  This includes material such as most plastics, most fish bones, wood, and most aluminum objects. [ 13 ]


Other diagnostic imaging modalities, such as  magnetic resonance imaging ,  computed tomography , and  ventilation perfusion scans  play a limited role in the diagnosis of foreign body aspiration. [ 7 ]


Signs on x-ray that are more commonly seen than the object itself and can be indicative of foreign body aspiration include visualization of the foreign body or hyperinflation of the affected lung. [ 13 ]  Other x-ray findings that can be seen with foreign body aspiration include obstructive  emphysema ,  atelectasis , and consolidation. [ 8 ]


While, x-ray can be used to visualize the location and identity of a foreign body,  rigid bronchoscopy  under general anesthesia is the gold-standard for diagnosis since the foreign body can be visualized and removed with this intervention. [ 2 ]  Rigid bronchoscopy is indicated when two of the three following criteria are met: report of foreign body aspiration by the patient or a witness, abnormal lung exam findings, or abnormal chest x-ray findings. [ 2 ]


See also:   Choking § Treatment ,  Basic Life Support ,  Advanced Cardiovascular Life Support


Treatment of foreign body aspiration is determined by the age of the patient and the severity of obstruction of the airway involved. [ 2 ]


An airway obstruction can be partial or complete. In partial obstruction, the patient can usually clear the foreign body with coughing. [ 2 ]  In complete obstruction, acute intervention is required to remove the foreign body. [ 2 ]


If foreign body aspiration is suspected, finger sweeping in the mouth is not recommended due to the increased risk of displacing the foreign object further into the airway. [ 2 ]


For choking children less than 1 year of age, the child should be placed face down over the rescuer's arm. [ 2 ]  Back blows should be delivered with the heel of the hand, then the patient should be turned face-up and chest thrusts should be administered. [ 2 ]  The rescuer should alternate five back blows followed by five chest thrusts until the object is cleared. [ 2 ]  The  Heimlich maneuver  should be used in choking patients older than 1 year of age to dislodge a foreign body. [ 2 ]  If the patient becomes unresponsive during physical intervention,  cardiopulmonary resuscitation  (CPR) should be started. [ 2 ]


In the event that the basic measures do not remove the foreign body, and adequate ventilation cannot be restored, need for treatment by trained personnel becomes necessary. [ 2 ]   Laryngoscopy  should be performed in unresponsive patients if non-invasive airway clearance techniques are unsuccessful. [ 6 ]  Laryngoscopy involves placing a device in the mouth to visualize the back of the airway. [ 6 ]  If the foreign body can be seen, it can be removed with  forceps . [ 6 ]  An  endotracheal tube  should then be placed in order to prevent airway compromise from resulting inflammation after the procedure. [ 6 ]  If the foreign body cannot be visualized, intubation,  tracheotomy , or needle  cricothyrotomy  can be done to restore an airway for patients who have become unresponsive due to airway compromise. [ 2 ]


If non-invasive measures do not dislodge the foreign body, and the patient can maintain adequate ventilation,  rigid bronchoscopy  under general anesthesia should be performed. [ 2 ]  Supplemental oxygen,  cardiac monitoring , and a  pulse oximeter  should be applied to the patient. [ 6 ]  Efforts should be made to keep the patient calm and avoid agitating the patient to prevent further airway compromise. [ 6 ]  Flexible rather than rigid bronchoscopy might be used when the diagnosis or object location are unclear. When  flexible bronchoscope  is used, rigid bronchoscope is typically on standby and readily available as this is the preferred approach for removal. [ 14 ]  Rigid bronchoscopy allows good airway control, ready bleeding management, better visualization, and ability to manipulate the aspirated object with a variety of forceps. [ 14 ]  Flexible bronchoscopy may be used for extraction when distal access is needed and the operator is experienced in this technique. [ 14 ]  Potential advantages include avoidance of  general anesthesia  as well as the ability to reach subsegmental bronchi which are smaller in diameter and further down the respiratory tract than the main bronchi. [ 14 ]  The main disadvantage of using a flexible scope is the risk of further dislodging the object and causing airway compromise. [ 14 ]  Bronchoscopy is successful in removing the foreign body in approximately 95% of cases with a complication rate of only 1%. [ 14 ]


After the foreign body is removed, patients should receive nebulized beta-adrenergic medication and  chest physiotherapy  to further protect the airway. [ 2 ]   Steroidal anti-inflammatories  and antibiotics are not routinely administered except in certain scenarios. [ 2 ]  These include situations such as when the foreign body is difficult or impossible to extract, when there is a documented respiratory tract infection, and when swelling within the airway occurs after removal of the object. [ 14 ]   Glucocorticoids  may be administered when the foreign body is surrounded by inflamed tissue and extraction is difficult or impossible. [ 14 ]  In such cases, extraction may be delayed for a short course of glucocorticoids so that the inflammation may be reduced before subsequent attempts. [ 14 ]  These patients should remain under observation in the hospital until successful extraction as this practice can result in dislodgement of the foreign body. [ 14 ]  Antibiotics are appropriate when an infection has developed but should not delay extraction. [ 14 ]  In fact, removal of the object may improve infection control by removing the infectious source as well as using cultures taken during the bronchoscopy to guide antibiotic choice. [ 14 ]  When airway  edema  or swelling occur, the patient may have  stridor . In these cases, glucocorticoids, aerosolized  epinephrine , or helium oxygen therapy may be considered as part of the management plan. [ 14 ]


Patients who are clinically stable with no need for supplemental oxygen after extraction may be discharged from the hospital the same day as the procedure. [ 4 ]  Routine imaging such as a follow-up chest x-ray are not needed unless symptoms persist or worsen, or if the patient had imaging abnormalities previously to verify return to normal. [ 4 ]  Most children are discharged within 24 hours of the procedure. [ 7 ]


Many complications can develop if a foreign body remains in the airway. There are also complications that may occur after removal of the object depending on the timeline of events. [ 2 ]   Cardiac arrest and death are possible complications if a sudden complete obstruction occurs and immediate medical care is not performed. [ 7 ]  The most common complication from a foreign body aspiration is a pulmonary infection, such as  pneumonia  or a lung  abscess . [ 7 ]  This can be more difficult to overcome in the elderly population and lead to even further complications. Patients may develop inflammation of the airway walls from a foreign body remaining in the airway. [ 2 ]  Airway secretions can be retained behind the obstruction which creates an ideal environment for subsequent bacterial overgrowth. [ 7 ]  Hyperinflation of the airway distal to the obstruction can also occur if the foreign body is not removed. [ 9 ]  Episodes of recurrent pneumonia in the same lung field should prompt evaluation for a possible foreign body in the airway. [ 9 ]


Whether or not the foreign body is removed, complications such as chemical  bronchitis , mucosal reactions, and the development of granulation tissue are possible. [ 11 ]


Complications can also arise from interventions used to remove a foreign body from the airway. [ 15 ]  Rigid bronchoscopy is the gold standard for removal of a foreign body, however this intervention does have potential risks. [ 15 ]  The most common complication from rigid bronchoscopy is damage to the patient's teeth. [ 15 ]  Other less common complications include cuts to the mouth or esophagus, perforation of the bronchial tree, damage to the vocal cords, pneumothorax, atelectasis, stricture, and perforation. [ 7 ]


There are many factors to consider when determining how to decrease the likelihood of aspiration, especially in the extremely young and elderly populations. [ 5 ]


The major considerations in children are their developmental level in terms of swallowing and protecting their airway via mechanisms such as coughing and the gag reflex. [ 5 ]  Also, certain object characteristics such as size, shape, and material can increase their potential to cause choking among children. [ 5 ]  When there are multiple children in a shared environment, toys and foods that are acceptable for older children often pose a choking risk to the younger children. [ 5 ]  Education for parents and caretakers should continue to be prioritized when possible. This can be through positions such as pediatricians, dentists, and school teachers as well as media advertisements and printed materials. This education should include educating caretakers on how to recognize choking and perform first aid and cardiopulmonary resuscitation, check for warning labels and toy recalls, and avoid high risk objects and foods. [ 4 ]


Thanks to numerous public advancements, such as the  Child Safety Protection Act  and the  Federal Hazardous Substance Act  (FHSA), warning labels for choking hazards are required on packaging for small balls, marbles, balloons, and toys with small parts when these are intended for use by children in at-risk age groups. [ 5 ]  Also, the  Consumer Product Safety Improvement Act  of 2008 amended the FHSA to also require advertisements on websites, catalogues, and other printed materials to include the choking hazard warnings. [ 5 ]


The  frontal sinuses  are one of the four pairs of  paranasal sinuses  that are situated behind the  brow ridges .  Sinuses  are  mucosa -lined airspaces within the bones of the face and skull. Each opens into the anterior part of the corresponding  middle nasal meatus  of the nose through the  frontonasal duct  which traverses the anterior part of the labyrinth of the  ethmoid . These structures then open into the  semilunar hiatus  in the  middle meatus .


Each frontal sinus is situated between the external and internal plates of the frontal bone. [ 1 ] [ 2 ]  Their average measurements are as follows: height 28 mm, breadth 24 mm, depth 20 mm, creating a space of 6-7 ml. [ 3 ]


Each frontal sinus extends into the  squamous part of the frontal bone  superiorly, and into the  orbital part of frontal bone  posteriorly to come to occupy the medial part of the roof of the orbit. [ 2 ]


Each sinus drains through an opening in its inferomedial part into the  frontonasal duct . [ 2 ]


The mucous membrane of [ citation needed ]  the frontal sinus receives arterial supply from the  supraorbital artery , and  anterior ethmoidal artery . [ 2 ]


Venous drainage is provided by the  superior ophthalmic vein . [ 2 ]


Lymph is drained into the  submandibular lymph nodes . [ 2 ]


The mucous membrane of [ citation needed ]  the sinus is innervated by the  supraorbital nerve , [ 2 ]  which contains the  postganglionic   parasympathetic  nerve fibers for  mucous   secretion  from the  ophthalmic nerve . [ citation needed ]


Frontal sinuses are rarely symmetrical as the  septum  between them frequently deviates to either side of the midline. [ 3 ] [ 1 ]  The two sinuses also vary in extent compared to one another. [ 2 ]


Their size of the frontal sinuses is highly variable. [ 2 ]  Rarely, one or both sinuses is hypoplastic [ 1 ]  or even absent. [ 1 ] [ 2 ]


Prominence of frontal sinuses is  sexual dimorphic ; they are more prominent in males, whereas less so in children and in females, resulting in an oblique forehead in males that is a male  sexual characteristic . [ 1 ]


The frontal sinuses are the only sinuses that are [ 2 ]  absent at birth. [ 2 ] [ 4 ]  They begin to appear during the second year of life as excavations in the  diploë . [ 2 ]  The development of these sinuses accounts for the suddenly increased mucus production at this age. [ citation needed ]  They are generally well developed, and functional between the sixth and eighth years, though they continue to grow slower until reaching their maximum size after  puberty . [ 4 ]


Through its copious mucus production, the sinus is an essential part of the immune defense/air filtration carried out by the nose. Nasal and sinal mucosae are  ciliated  and move mucus to the  choanae  and finally to the stomach.  The thick upper layers of nasal mucus trap bacteria and small particles in tissue abundantly provided with  immune cells ,  antibodies , and antibacterial proteins.  The layers beneath are thinner and provide a substrate in which the cilia are able to beat and move the upper layer with its debris through the  ostia  toward the  choanae .


Infection of the frontal sinus causing sinusitis can give rise to serious complications, as it is in close proximity to the orbit and cranial cavity ( orbital cellulitis ,  epidural  and  subdural abscess ,  meningitis ). [ 4 ]
Endonasal approach into the frontal sinus in children with acute and chronic frontal sinusitis without the usage of surgical optics is not successful, because in this case the operation is performed almost blindly and technically difficult even in adults. [ 5 ]


Frontal sinus fractures occur from trauma to the part of the frontal bone that overlies the sinus, often from motor vehicle accidents and falls. The hallmarks of a frontal sinus fracture is a frontal depression in the anterior table of the bone. Additionally, clear fluid leaking from the nose may indicate that fractures to the posterior table have torn into the  dura mater , creating a  cerebrospinal fluid  leak. [ 6 ]


Goals in management are to protect the intracranial structure, control any existing CSF leakage, prevent late complications, and aesthetically correct the deformity caused, if any. In anterior table fractures, if the table is minimally displaced, there will be no treatment necessary, only observation. If largely displaced, the correction is open reduction and internal fixation. If inhibiting the nasofrontal outflow tract, procedure is to undergo open reduction and internal fixation of the anterior table and osteoplastic flap with obliteration. [ citation needed ]


In posterior table fractures, a nondiplaced fracture with no CSF leak will only be observed. Those with a CSF leak will undergo sinus exploration if the CSF leak is not internally resolved within 4 to 7 days. With more dramatic displacements, sinus exploration will be required to determine the required level of cranialization, obliteration, and reparation to the dura. [ citation needed ]


In the case of  facial feminization surgery , modifications to the frontal sinus can be made to make the face more feminine, alongside softening the orbital rims. The forehead operations for feminization were first described by Dr.  Douglas Ousterhout  in the 1980s. Those operations consisted of four different techniques based on the anatomy of the patient. They were named arbitrarily by number (Type 1, Type 2, Type 3 and Type 4), with no particular relevance to their level of difficulty or frequency.


The Type I forehead describes a forehead with an absent frontal sinus or alternatively with sufficiently thick bone overlaying the frontal sinus so that burring alone is enough to correct the forehead. This type of forehead tends to occur in approximately 3% to 5% of the population. In these situations, the operation consists of using rotary instruments to shape and contour the bone to the desired level, while observing the thickness of the bone to avoid penetrating the intracranial space. The main risks associated with this operation tend to be bleeding. There are often venous lakes present throughout the frontal bone.


The Type II forehead describes another uncommon situation. This describes a patient with brow bossing; however, the bossing is at the correction position in terms of prominence. Therefore, the problem lies primarily above the bossing. We see this forehead type at about the same frequency as we see the Type I forehead. The Type II forehead is corrected by using a filling material such as methyl methacrylate.7 Other materials may be more ideal at this point; however, none are superior in terms of cost to methyl methacrylate. Although many surgeons do not consider the cost of the materials they are using, hydroxyapatite and calcium phos-phate bone cements cost approximately 1000 times that of methyl methacrylate. The advantage of bone cement is its adherence to the underlying bone, and the more analogous nature to native bone substrate. The material is applied to fill in the area above the bossing, and then gently contoured to blend with the transverse forehead bossing thereby-creating a uniformly round forehead


The Type III forehead is the most common situation and occurs in more than 90% of patients. The forehead, in this situation, has a prominent bossing across the top of the brows, and that bossing is overly projected. A frontal sinus is present. The thinness of the sinus precludes using exclusively rotary instruments to thin the bone. An osteotomy and reconstruction are the only operations to provide the proper round shape to the forehead with the decreased prominence that is necessary for a soft forehead, which involves a setback of the anterior table of the frontal sinus. This procedure is described as Type 3 Forehead Cranioplasty.


This operation can be described as an extended Type II operation. In this situation, the entire forehead is diminutive, including the area underlying the brows, and the entire forehead requires augmentation. Regardless of the material type, care should be taken to avoid having the implant sit directly underneath the incision as this leads to a higher rate of infection and removal.


Treatment of the orbital rim is almost always necessary in all these various forehead operations, regardless of what is done with the frontal bossing. [ 7 ]


This article incorporates text in the  public domain  from  page 998  of the 20th edition of   Gray's Anatomy   (1918)


Functional endoscopic sinus surgery  ( FESS ) is a procedure that is used to treat  sinusitis  and other conditions that affect the  sinuses . Sinusitis is an  inflammation  of the sinuses that can cause symptoms such as congestion, headaches, and difficulty breathing through the nose.


FESS is a minimally invasive procedure that is performed using an  endoscope , a thin, rigid tube with a camera on the end. The endoscope is inserted through the nostrils, allowing the surgeon to visualize the inside of the  nasal passages  and sinuses. The surgeon can then remove any tissue or obstruction that is blocking the sinuses, such as swollen or infected tissue.


FESS is generally considered to be a safe and effective treatment for sinusitis and other conditions that affect the sinuses. It can help to alleviate symptoms and improve the overall functioning of the sinuses. However, as with any medical procedure, there are potential risks and complications that should be discussed with a healthcare provider.


The first recorded instance of endoscopy being used to visualize the nasal passage took place in  Berlin  in 1901. [ 1 ]  Alfred Hirschmann, a designer and maker of medical instruments, modified a  cystoscope  for use in the nasal cavity. In October 1903, Hirschmann published "Endoscopy of the nose and its accessory sinuses." [ 2 ]  In 1910, M. Reichart performed the first endoscopic sinus surgery using a 7 mm endoscope.


In 1925,  Maxwell Maltz  created the term "sinuscopy," referring to the endoscopic method of visualizing the sinuses. Maltz also encouraged the use of endoscopes as a diagnostic tool for nasal and sinus abnormalities. [ 1 ]


In the 1960s,  Harold Hopkins , then a PhD at the  University of Reading , used his background in physics to develop an endoscope that provided more light and had drastically better resolution than previous endoscopes. Hopkins' rod optic system is widely credited with being a turning point for nasal endoscopy. [ 1 ]  Utilizing Hopkins' rod optic system, Walter Messenklinger visualized, recorded, and mapped the anatomy of the paranasal sinuses and the lateral nasal walls - specifically, the mucociliary routes - in cadavers. [ 3 ]  In 1978, Messerklinger published the book titled "Endoscopy of the Nose" on his findings, and his proposed methods to utilize nasal endoscopy for diagnosis. [ 4 ]


Heinz Stammberger, [ 5 ]  a  head and neck surgeon  who worked at the University of Graz with Messerklinger was captivated by the technique and the implications for pathophysiology and treatment of sinus disease. He adopted the technique and became identified with it. He traveled the world advocating and popularizing the technique and he carried out multiple courses both at University of Graz and around the world. He later met David Kennedy, a physician at  Johns Hopkins University , and together, they worked with the surgical instrument maker  Karl Storz  to develop instruments for use in endoscopic sinus surgery, and coined the term  Functional Endoscopic Sinus Surgery . [ 3 ]  Stammberger and Kennedy published multiple papers on FESS use and technique, and in 1985 the first North American course on FESS was taught at  Johns Hopkins Hospital  in  Baltimore . [ 1 ]  Stammberger, the chair of  otolaryngology  at University of Graz, and Kennedy, refined the techniques and provided hands-on courses on the techniques throughout the world. Stammberger retired from his position as the chair of the department in Graz and moved to  Dubai , where he worked with  Muaaz Tarabichi , also known as "the father of  endoscopic ear surgery ", to establish the Tarabichi Stammberger Ear and Sinus Institute (TSESI), a center dedicated to the advancement of endoscopic ear and sinus surgery. [ 6 ]  Stammberger died in 2018. [ 5 ]  There was a rise in the overall number of endoscopic sinus surgery procedures performed between 2010 - 2019 in the UK which coincided with a reduction in the number of open procedures performed over the same period. [ 7 ]


Functional endoscopic sinus surgery is most commonly used to treat chronic rhinosinusitis (CRS), [ 8 ]  only after all non-surgical treatment options such as antibiotics,  topical   nasal   corticosteroids , and  nasal lavage  with  saline solutions [ 9 ]  have been exhausted. CRS is an inflammatory condition in which the nose and at least one sinus become swollen and interfere with mucus drainage. [ 9 ]  It can be caused by anatomical factors such as a deviated septum or nasal polyps (growths), as well as infection. Symptoms include difficulty breathing through the nose, swelling and pain around the nose and eyes, postnasal drainage down the throat, and difficulty sleeping. [ 10 ]  CRS is a common condition in children and young adults. [ 11 ]


The purpose of FESS in treatment of CRS is to remove any anatomical obstructions that prevent proper mucosal drainage. A standard FESS includes removal of the uncinate process, and opening of the ethmoid air cells and Haller cells [ 12 ]  as well as the  maxillary ostium , if necessary. If any nasal polyps obstructing ventilation or drainage are present, they are also removed. [ 8 ]  In the case of paranasal sinus/nasal cavity tumors (benign or cancerous), an otolaryngologist can perform FESS to remove the growths, sometimes with the help of a  neurosurgeon , depending on the extent of the tumor. In some cases, a graft of bone or skin is placed by FESS to repair damages by the tumor. [ 13 ]


In the thyroid disorder known as  Graves' ophthalmopathy , inflammation and fat accumulation in the orbitonasal region cause severe  proptosis . [ 14 ]  In cases that have not responded to corticosteroid treatment, FESS can be used to decompress the orbital region by removing the ethmoid air cells and lamina papyracea. Bones of the orbital cavity or portions of the orbital floor may also be removed. [ 1 ] [ citation needed ]


The endoscopic approach to FESS is a less invasive method than open sinus surgery, which allows patients to be more comfortable during and after the procedure. Entering the surgical field via the nose, rather than through an incision in the mouth as in the previous Caldwell-Luc method, decreases risk of damaging nerves which innervate the teeth. [ 8 ]  Because of its less-invasive nature, FESS is a common option for children with CRS or other sinonasal complications.


It has been suggested that one of the main objectives in FESS surgery is to allow for the introduction of local therapeutic agents (such as steroids) to the sinuses. Research has shown that a special modification of the nozzle of the nasal spray in patients who had FESS allows for better delivery of local therapeutic agents into the ethmoid sinuses. [ 15 ]


Functional Endoscopic Sinus Surgery is considered a success if most of the symptoms, including nasal obstruction, sleep quality, olfaction and facial pain, are resolved after a 1–2 month postoperative healing period. [ 8 ] [ 16 ] [ 17 ]  Reviews of FESS as a method for treating chronic rhinosinusitis have shown that a majority of patients report increased quality of life after undergoing surgery. [ 18 ] [ 16 ]  The success rate of FESS in treating adults with CRS has been reported as 80-90%, [ 19 ]  and the success rate in treating children with CRS has been reported as 86–97%. [ 11 ]


The most common complication of FESS is  cerebrospinal fluid leak  (CSFL), which has been observed in about 0.2% of patients. Generally, CSFL arises during surgery and can be repaired with no additional related complications postoperatively. Other risks of surgery include  infection , bleeding, double vision usually lasting a few hours, numbness of the front teeth,  orbital hematoma , decreased sense of smell, and blindness. [ 20 ] [ 21 ]  The  medial rectus muscle  may be damaged. [ 22 ]  Blindness is the single most serious complication of FESS, and results from damage to the optic nerve during surgery. Serious complications such as blindness occur in only 0.44% of cases, as determined by a study performed in the United Kingdom. [ 8 ]


A  Cochrane review  in 2006 based on three  randomized control trials  concluded that FESS has not been shown to provide significantly better results than medical treatment for chronic rhinosinusitis. [ 23 ]  Another Cochrane review looked at postoperative care of patients after FESS using debridement (removal of blood clots, crusts, and secretions from the nasal and sinus cavities under local anaesthetic), but the evidence from the available clinical trials was uncertain. The debridement procedure after FESS may make little or no difference to health‐related quality of life or disease severity. There may be a lower risk of adhesions but whether this has any impact on long‐term outcomes is unknown. [ 24 ]


Functional sinus surgery had been grossly overutilized as a way of treating headache based on an assumption of a sinus etiology of the different types of primary headache. Many patients, primary care providers, and even specialists confuse any frontal migraine for sinus disease. Multiple attempts at further definition of primary headache and or sinus headache has been suggested by the International Headache Society and the American Academy of Otolaryngology–Head and Neck Surgery. [ 25 ]  It has been suggested early on that such a confusion might be  a cause of failure of functional endoscopic sinus surgery. [ 26 ]


The  geniculate ganglion  (from  Latin   genu , for "knee" [ 1 ] ) is a bilaterally paired special sense ganglion [ 2 ]  of the  intermediate nerve  component of the  facial nerve (CN VII) . [ 3 ]  It is situated within  facial canal  of the  head . [ citation needed ]


It contains cell bodies of first-order  unipolar   sensory neurons  which convey  gustatory (taste)  afferents from  taste receptors  of the anterior two-thirds of the tongue by way of the  chorda tympani , and of the  palate  by way of the  greater petrosal nerve , From the ganglion, the proximal fibres proceed to the gustatory (i.e. superior/rostral [ 3 ] ) part of the  solitary nucleus  where they synapse with second-order neurons. [ 2 ]


The geniculate ganglion is conical in shape. The  greater petrosal nerve  diverges from CNVII and the  lesser petrosal nerve  diverges from CN IX at the geniculate ganglion. [ 3 ]


It is located close to the  internal auditory meatus . [ 4 ]  It is covered superiorly by the  petrous part of the temporal bone  (which is sometimes absent over the ganglion). [ 5 ]


The geniculate ganglion is an important  surgical landmark  near the  internal auditory meatus . [ 4 ]


The geniculate ganglion may become  inflamed  due  herpes zoster virus  virus infection. Swelling of the ganglion may result in facial palsy ( Ramsay Hunt syndrome ). The syndrome presents with intense pain in one ear that is followed by a vesicular rash around the  ear canal . [ 2 ]


The  glossopharyngeal nerve  ( / ˌ ɡ l ɒ s oʊ f ə ˈ r ɪ n ( d ) ʒ i ə l ,   - ˌ f ær ən ˈ dʒ iː ə l / [ 1 ] ), also known as the  ninth cranial nerve ,  cranial nerve IX , or simply  CN IX , [ 2 ]  is a  cranial nerve  that exits the  brainstem  from the sides of the upper  medulla , just anterior (closer to the  nose ) to the  vagus nerve . Being a mixed nerve (sensorimotor), it carries afferent sensory and efferent motor information. The motor division of the glossopharyngeal nerve is derived from the  basal plate  of the  embryonic   medulla oblongata , whereas the sensory division originates from the  cranial neural crest .


From the anterior portion of the  medulla oblongata , the glossopharyngeal nerve passes laterally across or below the  flocculus , and leaves the skull through the central part of the  jugular foramen . From the superior and inferior ganglia in jugular foramen, it has its own sheath of  dura mater . The inferior ganglion on the inferior surface of petrous part of temporal is related with a triangular depression into which the aqueduct of cochlea opens. On the inferior side, the glossopharyngeal nerve is lateral and anterior to the  vagus nerve  and  accessory nerve .


In its passage through the foramen (with X and XI), the glossopharyngeal nerve passes between the  internal jugular vein  and  internal carotid artery . [ 3 ]  It descends in front of the latter vessel and beneath the  styloid process  and the muscles connected with it, to the posterior lower border of the  stylopharyngeus muscle . [ 4 ]  It then curves forward, forming an arch on the side of the neck and lying upon the  stylopharyngeus  and  middle pharyngeal constrictor  muscle. From there, it passes under cover of the  hyoglossus  muscle and is finally distributed to the  palatine tonsil , the  mucous membrane  of the  fauces  and base of the  tongue , and the serous glands of the  mouth .


Note: The glossopharyngeal nerve contributes in the formation of the  pharyngeal plexus  along with the vagus nerve.


The glossopharyngeal nerve has five distinct general functions:


The glossopharyngeal nerve as noted above is a mixed nerve consisting of both sensory and motor nerve fibers. The sensory fibers' origin include the pharynx, middle ear, posterior one-third of the tongue (including taste buds); and the carotid body and sinus. These fibers terminate at the  medulla oblongata . The motor fibers' origin is the medulla oblongata, and they terminate at the parotid salivary gland, the glands of the posterior tongue, and the  stylopharyngeus  muscle (which dilates the pharynx during swallowing).


The  branchial motor  component of CN IX provides voluntary control of the stylopharyngeus muscle, which elevates the pharynx during swallowing and speech.


Origin and central course


The branchial motor component originates from the  nucleus ambiguus  in the reticular formation of the rostral  medulla . Fibers leaving the nucleus ambiguus travel anteriorly and laterally to exit the medulla, along with the other components of CN IX, between the olive and the  inferior cerebellar peduncle .


Intracranial course


Upon emerging from the lateral aspect of the medulla the branchial motor component joins the other components of CN IX to exit the skull via the jugular foramen. The glossopharyngeal fibers travel just anterior to the cranial nerves X and XI, which also exit the skull via the  jugular foramen .


Extra-cranial course and final innervation


Upon exiting the skull the branchial motor fibers descend deep to the  temporal styloid process  and wrap around the posterior border of the  stylopharyngeus muscle  before innervating it.


Voluntary control of the stylopharyngeus muscle


Signals for the voluntary movement of  stylopharyngeus muscle  originate in the pre-motor and motor cortex (in association with other cortical areas) and pass via the  corticobulbar  tract in the genu of the internal capsule to synapse bilaterally on the ambiguus nuclei in the medulla.


Parasympathetic component of the glossopharyngeal nerve that innervates the ipsilateral parotid gland.


The  preganglionic  nerve fibers originate in the  inferior salivatory nucleus  of the rostral medulla and travel anteriorly and laterally to exit the brainstem between the  medullary olive  and the  inferior cerebellar peduncle  with the other components of CN IX.  Note: These neurons do not form a distinct nucleus visible on cross-section of the brainstem. The position indicated on the diagram is representative of the location of the cell bodies of these fibers.


Upon emerging from the lateral aspect of the medulla, the  visceral motor  fibers join the other components of CN IX to enter the  jugular foramen . Within the jugular foramen, there are two glossopharyngeal ganglia that contain nerve cell bodies that mediate general, visceral, and special sensation. The visceral motor fibers pass through both ganglia without synapsing and exit the inferior ganglion with CN IX general sensory fibers as the  tympanic nerve . Before exiting the jugular foramen, the tympanic nerve enters the  petrous portion of the temporal bone  and ascends via the  inferior tympanic canaliculus  to the  tympanic cavity . Within the tympanic cavity the tympanic nerve forms a  plexus  on the surface of the  promontory of the middle ear  to provide general sensation. The visceral motor fibers pass through this plexus and merge to become the  lesser petrosal nerve . The lesser petrosal nerve re-enters and travels through the temporal bone to emerge in the  middle cranial fossa  just lateral to the  greater petrosal nerve . It then proceeds anteriorly to exit the skull via the  foramen ovale  along with the  mandibular nerve  component of CN V (V3).


Extra-cranial course and final innervations


Upon exiting the skull, the lesser petrosal nerve synapses in the  otic ganglion , which is suspended from the  mandibular nerve  immediately below the  foramen ovale . Postganglionic fibers from the otic ganglion travel with the  auriculotemporal branch  of CN V3 to enter the substance of the  parotid gland .


Hypothalamic Influence


Fibers from the  hypothalamus  and  olfactory system  project via the  dorsal longitudinal fasciculus  to influence the output of the  inferior salivatory nucleus . Examples include: 1) dry mouth in response to fear (mediated by the hypothalamus); 2) salivation in response to smelling food (mediated by the olfactory system)


This component of CN IX innervates the baroreceptors of the  carotid sinus  and chemoreceptors of the  carotid body .


Clinical correlation
The visceral sensory fibers of CN IX mediate the afferent limb of the pharyngeal reflex in which touching the back of the pharynx stimulates the patient to gag (i.e., the gag reflex). The efferent signal to the musculature of the pharynx is carried by the branchial motor fibers of the vagus nerve.  [ 5 ]


This component of CN IX carries general sensory information (pain, temperature, and touch) from the skin of the external ear, internal surface of the tympanic membrane, the walls of the upper pharynx, and the posterior one-third of the tongue, anterior surface of the epiglottis, vallecula.


The special sensory component of CN IX provides taste sensation from the posterior one-third of the tongue.


Damage to the glossopharyngeal nerve can result in loss of taste sensation to the posterior one third of the tongue, and impaired  swallowing .


The clinical tests used to determine if the glossopharyngeal nerve has been damaged include testing the  gag reflex  of the mouth, asking the patient to  swallow  or  cough , and evaluating for speech impediments. The clinician may also test the posterior one-third of the tongue with bitter and sour substances to evaluate for impairment of taste.


The integrity of the glossopharyngeal nerve may be evaluated by testing the patient's general sensation and that of taste on the posterior third of the tongue. The gag reflex can also be used to evaluate the glossopharyngeal nerve.


Saladin, Anatomy and Physiology: The Unity of Form and Function, 6th edition


The  greater palatine artery  is a branch of the descending palatine artery (a terminal branch of the  maxillary artery ) and contributes to the blood supply of the  hard palate  and  nasal septum .


The  descending palatine artery  branches off of the maxillary artery in the  pterygopalatine fossa  and descends through the  greater palatine canal  along with the  greater palatine nerve  (from the  pterygopalatine ganglion ).  Once emerging from the  greater palatine foramen , it changes names to the greater palatine artery and begins to supply the  hard palate . [ 1 ]  As it terminates it travels through the  incisive canal  to  anastomose  with the  sphenopalatine artery  to supply the  nasal septum . [ 1 ]


The  greater palatine nerve  is a branch of the  pterygopalatine ganglion . This nerve is also referred to as the  anterior palatine nerve , due to its location anterior to the   lesser palatine nerve . It carries both general sensory fibres from the  maxillary nerve , and parasympathetic fibers from the  nerve of the pterygoid canal . It may be anaesthetised for  procedures  of the  mouth  and maxillary (upper)  teeth .


The greater palatine nerve is a branch of the  pterygopalatine ganglion . It descends through the  greater palatine canal , moving anteriorly and inferiorly. [ 1 ] [ 2 ]  Here, it is accompanied by the  descending palatine artery . [ 1 ]  It emerges upon the  hard palate  through the  greater palatine foramen . It then passes forward in a groove in the hard palate, nearly as far as the  incisor  teeth.


While in the  pterygopalatine canal , it gives off  lateral posterior inferior nasal branches , which enter the nasal cavity through openings in the  palatine bone , and ramify over the  inferior nasal concha  and middle and inferior meatuses. At its exit from the canal, a palatine branch is distributed to both surfaces of the  soft palate .


The greater palatine nerve carries both general sensory fibres from the  maxillary nerve , and parasympathetic fibers from the  nerve of the pterygoid canal . It supplies the gums, the  mucous membrane  and glands of the hard palate, and communicates in front with the terminal filaments of the  nasopalatine nerve .


The greater palatine nerve may be  anaesthetised  to perform  dental procedures  on the maxillary (upper)  teeth , and sometimes for  cleft lip and cleft palate   surgery . [ 1 ]


This article incorporates text in the  public domain  from  page 893  of the 20th edition of   Gray's Anatomy   (1918)


The  greater petrosal nerve  (or  greater superficial petrosal nerve ) is a  nerve  of the head mainly containing pre-ganglionic parasympathetic fibres [ 1 ] : 370   which ultimately synapse in the  pterygopalatine ganglion .


It branches from the  facial nerve (CN VII)  and is derived from the parasympathetic part of the  nervus intermedius  component of CN VII, with its cell bodies located in the  superior salivary nucleus . [ 2 ]  In the connective tissue substance of the  foramen lacerum , [ citation needed ]  the greater petrosal nerve unites with the ( sympathetic )  deep petrosal nerve  to form the  nerve of the pterygoid canal  (vidian nerve) which proceeds to the pterygopalatine ganglion. [ 2 ]


It forms part of a chain of nerves that provide secretomotor innervation to the  lacrimal gland  and mucosal glands of nasal cavity and palate. [ citation needed ]


Preganglionic  parasympathetic  fibres arise in the  superior salivary nucleus  of the  pontine tegmentum . They join with general somatic sensory and special sensory fibres to form the  nervus intermedius . The nervus intermedius exits the cranial cavity at the  internal auditory meatus , and joins with the motor root of the facial nerve at the  geniculate ganglion . While preganglionic parasympathetic fibres pass through the geniculate ganglion, they neither synapse, nor have their cell bodies located there. [ citation needed ]


Preganglionic parasympathetic fibres exit the geniculate ganglion as the greater petrosal nerve. [ citation needed ]


The greater petrosal nerve also conveys some special sensory nerve fibres which carry gustatory (taste) sensory information from the  palate [ 1 ] : 22   that are relayed to the pterygopalatine ganglion by the  lesser palatine nerves  and are in turn conveyed to the geniculate ganglion by the greater petrosal nerve to synapse in the ganglion. [ 1 ] : 370


The greater petrosal nerve enters the  petrous part of the temporal bone  and travels anteromedially through it at a 45° angle. It emerges into the  middle cranial fossa  upon the anterosuperior surface of the bone [ 1 ] : 498   through the  hiatus for greater petrosal nerve  alongside the  petrosal branch  of the  middle meningeal artery . [ 3 ] : 842


In the middle cranial fossa, the nerve is situated between the two layers of the dura mater [ 1 ] : 450, 498   and passes obliquely anterior-ward [ 1 ] : 450   along a groove upon the floor of the fossa [ 1 ] : 509   - the  groove for the greater petrosal nerve  - that is situated upon the anterosuperior aspect of the  petrous part of the temporal bone [ 3 ] : 842   and anteromedial to the  arcuate eminence , and adjacent and parallel to the  lesser petrosal nerve  and its own groove. [ 1 ] : 509   The nerve passes deep to the  trigeminal ganglion  to reach the  foramen lacerum . [ 1 ] : 498, 509


At the foramen lacerum, it unites with the (sympathetic)  deep petrosal nerve , forming the  nerve of the pterygoid canal  (which continues anterior-ward through the  pterygoid canal  to reach the  pterygopalatine fossa  and form the  pterygopalatine ganglion ). [ 1 ] : 498


During surgery of the middle cranial fossa, manipulation of the dura mater may damage the greater petrosal nerve, [ 1 ] : 450, 498   causing bleeding [ 1 ] : 498   or swelling at the geniculate ganglion; this can compress the facial nerve and cause facial paralysis. [ 1 ] : 450, 498


Head and neck cancer  is a general term encompassing multiple  cancers  that can develop in the head and neck region. These include cancers of the mouth, tongue, gums and lips ( oral cancer ), voice box ( laryngeal ), throat ( nasopharyngeal ,  oropharyngeal , [ 1 ]   hypopharyngeal ),  salivary glands ,  nose and sinuses . [ 5 ]


Head and neck cancer can present a wide range of symptoms depending on where the cancer developed. These can include an  ulcer in the mouth  that does not heal,  changes in the voice ,  difficulty swallowing ,  red or white patches in the mouth , and a  neck lump . [ 6 ] [ 7 ]


The majority of head and neck cancer is caused by the use of  alcohol  or  tobacco  (including  smokeless tobacco ). An increasing number of cases are caused by the  human papillomavirus  (HPV). [ 8 ] [ 2 ]  Other risk factors include the  Epstein–Barr virus , chewing  betel quid  (paan),  radiation exposure , poor nutrition and workplace exposure to certain toxic substances. [ 8 ]  About 90% are pathologically classified as  squamous cell cancers . [ 9 ] [ 2 ]  The diagnosis is confirmed by a  tissue biopsy . [ 8 ]  The degree of surrounding tissue invasion and distant spread may be determined by  medical imaging  and  blood tests . [ 8 ]


Not using tobacco or alcohol can reduce the risk of head and neck cancer. [ 2 ]  Regular dental examinations may help to identify signs before the cancer develops. [ 1 ]  The  HPV vaccine  helps to prevent  HPV-related oropharyngeal cancer . [ 10 ]  Treatment may include a combination of surgery,  radiation therapy ,  chemotherapy , and  targeted therapy . [ 8 ]  In the early stage head and neck cancers are often curable but 50% of people see their doctor when they already have an advanced disease. [ 11 ]


Globally, head and neck cancer accounts for 650,000 new cases of cancer and 330,000 deaths annually on average. In 2018, it was the seventh most common cancer worldwide, with 890,000 new cases documented and 450,000 people dying from the disease. [ 12 ]  The usual age at diagnosis is between 55 and 65 years old. [ 13 ]  The average  5-year survival  following diagnosis in the  developed world  is 42–64%. [ 13 ] [ 14 ]


Head and neck cancers can cause a broad range of symptoms, many of which occur together. These can be categorised local (head and neck cancer-specific), general and  gastrointestinal  symptoms. Local symptoms include changes in taste and voice, inflammation of the mouth or throat ( mucositis ), dry mouth ( xerostomia ), and difficulty swallowing ( dysphagia ). General symptoms include difficulty sleeping, tiredness, depression, nerve damage ( peripheral neuropathy ). Gastrointestinal symptoms are typically nausea and vomiting. [ 6 ]


Symptoms predominantly include a sore on the face or oral cavity that does not heal, trouble swallowing, or a change in voice. In those with advanced disease, there may be unusual bleeding, facial pain, numbness or swelling, and visible lumps on the outside of the neck or oral cavity. [ 15 ]  Head and neck cancer often begins with benign signs and symptoms of the disease, like an enlarged  lymph node  on the outside of the neck, a  hoarse-sounding voice , or a progressive worsening cough or sore throat. In the case of head and neck cancer, these symptoms will be notably persistent and become chronic. There may be a lump or a sore in the throat or neck that does not heal or go away. There may be difficulty or pain in swallowing. Speaking may become difficult. There may also be a persistent  earache . [ 16 ]


Other symptoms can include: a lump in the lip, mouth, or gums; ulcers or mouth sores that do not heal; bleeding from the mouth or numbness; bad breath; discolored patches that persist in the mouth; a sore tongue; and slurring of speech if the cancer is affecting the tongue. There may also be congested sinuses, weight loss, and some numbness or paralysis of  facial muscles . [ citation needed ]


Oral cancer affects the areas of the mouth, including the inner lip,  tongue ,  floor of the mouth ,  gums , and  hard palate . Cancers of the mouth are strongly associated with  tobacco  use, especially the use of  chewing tobacco  or  dipping tobacco , as well as heavy  alcohol  use. Cancers of this region, particularly the tongue, are more frequently treated with  surgery  than other head and neck cancers. Lip and oral cavity cancers are the most commonly encountered types of head and neck cancer. [ 5 ]


Surgeries for oral cancers include: [ citation needed ]


The defect is typically covered or improved by using another part of the body and/or skin grafts and/or wearing a  prosthesis . [ citation needed ]


Paranasal sinus and nasal cavity cancer  affects the  nasal cavity  and the  paranasal sinuses . Most of these cancers are  squamous cell carcinomas . [ 17 ]


Nasopharyngeal cancer arises in the  nasopharynx , the region in which the  nasal cavities  and the  Eustachian tubes  connect with the upper part of the throat. While some nasopharyngeal cancers are biologically similar to the common head and neck cancers, "poorly differentiated" nasopharyngeal carcinoma is  lymphoepithelioma , which is distinct in its  epidemiology , biology, clinical behavior, and treatment and is treated as a separate disease by many experts. [ citation needed ]


Most  oropharyngeal cancers  begin in the  oropharynx  (throat), the middle part of the throat that includes the  soft palate , the base of the  tongue , and the  tonsils . [ 1 ]  Cancers of the tonsils are more strongly associated with  human papillomavirus  infection than are cancers of other regions of the head and neck.  HPV-positive oropharyngeal cancer  generally has a better outcome than HPV-negative disease, with a 54% better survival rate, [ 18 ]  but this advantage for HPV-associated cancer applies only to oropharyngeal cancers. [ 19 ]


People with oropharyngeal carcinomas are at high risk of developing a second primary head and neck cancer. [ 20 ]


The  hypopharynx  includes the pyriform sinuses, the posterior pharyngeal wall, and the postcricoid area. Tumors of the hypopharynx frequently have an advanced stage at diagnosis and have the most adverse prognoses of pharyngeal tumors. They tend to  metastasize  early due to the extensive lymphatic network around the  larynx . [ citation needed ]


Laryngeal cancer begins in the  larynx , or "voice box", and is the second most common type of head and neck cancer encountered. [ 5 ]  Cancer may occur on the  vocal folds  themselves ("glottic" cancer) or on tissues above and below the true cords ("supraglottic" and "subglottic" cancers, respectively). Laryngeal cancer is strongly associated with  tobacco smoking . [ citation needed ]


Surgery can include laser excision of small vocal cord lesions, partial laryngectomy (removal of part of the larynx), or total laryngectomy (removal of the whole larynx). If the whole larynx has been removed, the person is left with a permanent tracheostomy. Voice rehabilitation in such patients can be achieved in three important ways: esophageal speech, tracheoesophageal puncture, or electrolarynx. One would likely require intensive teaching, speech therapy, and/or an electronic device. [ citation needed ]


Cancer of the trachea  is a rare cancer usually classified as a  lung cancer . [ 21 ]


Most  tumors of the salivary glands  differ from the common head and neck cancers in cause,  histopathology , clinical presentation, and therapy. Other uncommon tumors arising in the head and neck include  teratomas ,  adenocarcinomas ,  adenoid cystic carcinomas , and  mucoepidermoid carcinomas . [ 22 ]  Rarer still are  melanomas  and  lymphomas  of the upper aerodigestive tract. [ citation needed ]


Alcohol  and  tobacco  use are major risk factors for head and neck cancer.  72% of head and neck cancer cases are caused by using both alcohol and tobacco. [ 23 ]  This rises to 89% when looking specifically at laryngeal cancer. [ 24 ]


There is thought to be a dose-dependent relationship between alcohol use and development of head and neck cancer where higher rates of alcohol consumption contribute to an increased risk of developing head and neck cancer. [ 25 ] [ 26 ]  Alcohol use following a diagnosis of head and neck cancer also contributes to other negative outcomes. These include physical effects such as an increased risk of developing a second primary cancer or other malignancies, [ 27 ] [ 28 ]  cancer recurrence, [ 29 ]  and worse prognosis [ 30 ]  in addition to an increased chance of having a future  feeding tube  placed and  osteoradionecrosis  of the jaw. Negative social factors are also increased with sustained alcohol use after diagnosis including unemployment and work disability. [ 31 ] [ 32 ]


The way in which alcohol contributes to cancer development is not fully understood. It is thought to be related to permanent damage of DNA strands by a metabolite of alcohol called  acetaldehyde . Other suggested mechanisms include nutritional deficiencies and genetic variations. [ 31 ]


Tobacco smoking  is one of the main risk factors for head and neck cancer. Cigarette smokers have a lifetime increased risk for head and neck cancer that is 5 to 25 times higher than the general population. [ 33 ]  The ex-smoker's risk of developing head and neck cancer begins to approach the risk in the general population 15 years after  smoking cessation . [ 34 ]  In addition, people who smoke have a worse prognosis than those who have never smoked. [ 35 ]  Furthermore, people who continue to smoke after diagnosis of head and neck cancer have the highest probability of dying compared to those who have never smoked. [ 36 ] [ 37 ]  This effect is seen in patients with HPV-positive head and neck cancer as well. [ 38 ] [ 39 ] [ 40 ]  It has also been demonstrated that  passive smoking , both at work and at home, increases the risk of head and neck cancer. [ 23 ]


A major carcinogenic compound in  tobacco smoke  is  acrylonitrile . [ 41 ]  Acrylonitrile appears to indirectly cause  DNA damage  by increasing  oxidative stress , leading to increased levels of  8-oxo-2'-deoxyguanosine  (8-oxo-dG) and  formamidopyrimidine  in DNA. [ 42 ]  (see image). Both 8-oxo-dG and formamidopyrimidine are  mutagenic . [ 43 ] [ 44 ]   DNA glycosylase   NEIL1  prevents  mutagenesis  by 8-oxo-dG [ 45 ]  and removes formamidopyrimidines from DNA. [ 46 ]


Smokeless tobacco  (including products where tobacco is  chewed ) is a cause of  oral cancer . Increased risk of oral cancer caused by smokeless tobacco is present in countries such as the United States but particularly prevalent in  Southeast Asian countries  where the use of smokeless tobacco is common. [ 5 ] [ 47 ] [ 48 ]  Smokeless tobacco is associated with a higher risk of developing head and neck cancer  due to the presence of the tobacco-specific carcinogen  N'-nitrosonornicotine . [ 48 ]


Cigar  and  pipe smoking  are also important risk factors for oral cancer. [ 49 ]  They have a dose dependent relationship with more consumption leading to higher chances of developing cancer. [ 23 ]  The use of  electronic cigarettes  may also lead to the development of head and neck cancers due to the substances like  propylene glycol ,  glycerol ,  nitrosamines , and metals contained therein, which can cause damage to the airways. [ 50 ] [ 5 ]  Exposure to e-vapour has been shown to reduce cell viability and increase the rate of  cell death  via  apoptosis  or  necrosis  with or without nicotine. [ 51 ]  This area of study requires more research, however. [ 50 ] [ 5 ]  Similarly, additional research is needed to understand how  marijuana  possibly promotes head and neck cancers. [ 52 ]  A 2019 meta-analysis did not conclude that marijuana was associated with head and neck cancer risk. [ 53 ]  Yet individuals with cannabis use disorder were more likely to be diagnosed with such cancers in a large study published 2024. [ 52 ]


Many dietary nutrients are associated with cancer protection and its development. Generally, foods with a protective effect with respect to oral cancer demonstrate  antioxidant  and  anti-inflammatory effects  such as fruits, vegetables,  curcumin  and  green tea . Conversely, pro-inflammatory food substances such as  red meat ,  processed meat  and fried food can increase the risk of developing head and neck cancer. [ 23 ] [ 54 ]  An increased adherence to the  Mediterranean diet  is also related to a lower risk of cancer mortality and a reduced risk of developing multiple cancers including head and neck cancer. [ 55 ]  Elevated levels of  nitrites  in preserved meats and  salted fish  have been shown to increase the risk of nasopharyngeal cancer. [ 56 ] [ 57 ]  Overall, a poor nutritional intake (often associated with alcoholism) with subsequent  vitamin deficiencies  is a risk factor for head and neck cancer. [ 56 ] [ 22 ]


In terms of nutritional supplements, antioxidants such as  vitamin E  and  beta-carotene  might reduce the toxic effect of radiotherapy in people with head and neck cancer but they can also increase recurrence rates, especially in smokers. [ 58 ]


Betel nut chewing  is associated with an increased risk of head and neck cancer. [ 1 ] [ 59 ]  When chewed with additional tobacco in its preparation (like in  gutka ), there is an even higher risk, especially for oral and oropharyngeal cancers. [ 23 ]


People who develop head and neck cancer may have a  genetic predisposition  for the condition.  There are seven known genetic variations ( loci ) which specifically increase the chances of developing oral and pharyngeal cancer. [ 60 ] [ 61 ]  Family history, that is having a first-degree relative with head and neck cancer, is also a risk factor. In addition, genetic variations in pathways involved in  alcohol metabolism  (for example  alcohol dehydrogenase ) have been associated with an increased head and neck cancer risk. [ 23 ]