If prolonged ventilation is required, tracheostomy is usually considered. The timing of this procedure is dependent on the clinical situation and an individual's preference. An international multicenter study in 2000 determined that the median time between starting mechanical ventilation and receiving a tracheostomy was 11 days. [ 5 ]  Although the definition varies depending on hospital and provider, early tracheostomy can be considered to be less than 10 days (2 to 14 days) and late tracheostomy to be 10 days or more.


Biphasic cuirass ventilation  is a form of non-invasive mechanical ventilation that can — in a small subset of cases — allow people to avoid a tracheostomy. [ 6 ]


A tracheostomy tube may be single or dual lumen, and also cuffed or uncuffed. A dual lumen tracheostomy tube consists of an outer cannula or main shaft, an inner cannula, and an obturator. The obturator is used when inserting the tracheostomy tube to guide the placement of the outer cannula and is removed once the outer cannula is in place. The outer cannula remains in place but, because of the buildup of secretions, there is an inner cannula that may be removed for cleaning after use or it may be replaced. Single-lumen tracheostomy tubes do not have a removable inner cannula, suitable for narrower airways. Cuffed tracheostomy tubes have inflatable balloons at the end of the tube to secure them in place. A tracheostomy tube may be fenestrated with one or several holes to let air through the  larynx , allowing speech. [ 7 ]


Special tracheostomy tube valves (such as the Passy-Muir valve [ 8 ] ) have been created to assist people in their speech. The patient can inhale through the unidirectional tube. Upon expiration, pressure causes the valve to close, redirecting air around the tube, past the vocal folds, producing sound. [ 9 ]


The typical procedure done is the open surgical tracheotomy (OST) and is usually done in a sterile operating room. The optimal patient position involves a cushion under the shoulders to extend the neck. Commonly a transverse (horizontal) incision is made two fingerbreadths above the  suprasternal notch . Alternatively, a vertical incision can be made in the midline of the neck from the thyroid cartilage to just above the suprasternal notch. Skin, subcutaneous tissue, and strap muscles (a specific group of neck muscles) are retracted aside to expose the thyroid isthmus, which can be cut or retracted upwards. After proper identification of the cricoid cartilage and placement of a tracheal hook to steady the trachea and pull it forward, the trachea is cut open, either through the space between cartilage rings or vertically across multiple rings (cruciate incision). Occasionally a section of a tracheal cartilage ring may be removed to make insertion of the tube easier. Once the incision is made, a properly sized tube is inserted. The tube is connected to a ventilator and adequate ventilation and oxygenation is confirmed. The tracheotomy apparatus is then attached to the neck with tracheotomy ties, skin sutures, or both. [ 10 ] [ 11 ]


The first widely accepted percutaneous tracheotomy technique was described by Pat Ciaglia, a New York surgeon, in 1985. [ 12 ]  The next widely used technique was developed in 1989 by  Bill Griggs , an Australian intensive care specialist. [ 13 ]  In 1995, Fantoni developed a translaryngeal approach of percutaneous tracheostomy. [ 14 ]  The Griggs and Ciaglia Blue Rhino techniques are the two main techniques in current use. A number of comparison studies have been undertaken between these two techniques with no clear differences emerging [ 15 ]  An advantage of PDT over OST is the ability to perform the procedure at the patient's bedside. This significantly decreases costs and time/people-power needed for an operating room (OR) procedure. [ 11 ]  Contraindications for percutaneous tracheostomy include infection at the site of tracheostomy, uncontrolled bleeding disorder, unstable cardiopulmonary status, patient unable to stay still, abnormal anatomy of the tracheolaryngeal structures. [ 2 ]


As with most other surgical procedures, some cases are more difficult than others. Surgery on children is more difficult because of their smaller size. Difficulties such as a short neck and bigger thyroid glands make the trachea hard to open. [ 16 ]  There are other difficulties with patients with irregular necks, the obese, and those with a large  goitre .


The many possible complications include  hemorrhage , loss of airway,  subcutaneous emphysema , wound infections, stoma cellulites, fracture of tracheal rings, poor placement of the tracheostomy tube, and  bronchospasm . [ 17 ]


Early complications include infection, hemorrhage,  pneumomediastinum ,  pneumothorax ,  tracheoesophageal fistula , recurrent laryngeal nerve injury, and tube displacement. Delayed complications include  tracheal-innominate artery fistula ,  tracheal stenosis , delayed tracheoesophageal fistula, and tracheocutaneous fistula. [ 10 ]


A 2013 systematic review (published cases from 1985 to April 2013) studied the complications and risk factors of percutaneous dilatational tracheostomy (PDT), identifying major causes of fatality to be  hemorrhage  (38.0%), airway complications (29.6%), tracheal perforation (15.5%), and  pneumothorax  (5.6%) [ 18 ]  A similar systematic review in 2017 (cases from 1990 to 2015) studying fatality in both open surgical tracheotomy (OST) and PDT identified similar rates of mortality and causes of death between the two techniques. [ 19 ]


Hemorrhage  is rare, but the most likely cause of fatality after a tracheostomy. It usually occurs due to a  tracheoarterial fistula , an abnormal connection between the trachea and nearby blood vessels, and most commonly manifests between 3 days to 6 weeks after the procedure is done. Fistulas can result from incorrectly positioned equipment, high cuff pressures causing pressure sores or mucosal damage, a low surgical trachea site, repetitive neck movement, radiotherapy, or prolonged intubation. [ 20 ]


A potential risk factor identified in a 2013 systematic review of the percutaneous technique was the lack of  bronchoscopic  guidance. Use of the bronchoscope, an instrument inserted through a patient's mouth for internal visualization of the airway, can help with proper placement of instruments and better visualization of anatomical structures. However, this can also be dependent on the skills and familiarity of the surgeon with both the procedure and the patient's anatomy. [ 18 ]


There are a multitude of potential complications related to the airway. The main causes of mortality during PDT include dislodgment of the tube, loss of airway during procedure and misplacement of the tube. [ 18 ]  One of the more urgent complications include displacement or dislodgment of the tracheotomy tube, either spontaneously or during a tube change. Although uncommon (< 1/1000 tracheostomy tube days), the associated fatality is high due to the loss of airway. [ 21 ]  Due to the seriousness of such a situation, individuals with a tracheotomy tube should consult with their healthcare providers to have a specific, written, emergency intubation and tracheostomy recannulation (reinsertion) plan prepared in advance.


Tracheal stenosis , otherwise known as an abnormal narrowing of the airway, is a possible long term complication. The most common symptom of stenosis is gradually-worsening difficulty with breathing ( dyspnea ). However incidence is low, ranging from 0.6 to 2.8% with increased rates if major bleeding or wound infections are present. A 2016 systematic review identified a higher rate of tracheal stenosis in individuals who underwent a surgical tracheostomy, as compared to PDT, however the difference was not statistically significant. [ 22 ]


A 2000 Spanish study of bedside percutaneous tracheostomy reported overall complication rates of 10–15% and a procedural mortality of 0%, [ 23 ]  which is comparable to those of other series reported in the literature from the Netherlands [ 24 ] [ 25 ]  and the United States. [ 26 ] [ 27 ]  A 2013 systematic review calculated procedural mortality to be 0.17% or 1 in 600 cases. [ 18 ]  Multiple systematic reviews identified no significant difference in rates of mortality, major bleeding, or wound infection between the percutaneous or open surgical methods. [ 22 ] [ 19 ]


Specifically a 2017 systematic review calculated the most common causes of death and their frequencies, out of all tracheotomies, to be hemorrhage (OST: 0.26%, PDT: 0.19%), loss of airway (OST: 0.21%, PDT: 0.20%), and misplacement of tube (OST: 0.11%, PDT: 0.20%). [ 19 ]


A 2003 American cadaveric study identified multiple tracheal ring fractures with the Ciaglia Blue Rhino technique as a complication occurring in 100% of their small series of cases. [ 28 ]  The comparative study above also identified ring fractures in 9 of 30 live patients [ 15 ]  while another small series identified ring fractures in 5 of their 20 patients. [ 29 ]  The long term significance of tracheal ring fractures is unknown. [ citation needed ]


Tracheotomy was first potentially depicted on  Egyptian  artifacts in 3600 BC. [ 30 ]   Hippocrates  condemned the practice of tracheotomy as incurring an unacceptable risk of damage to the  carotid artery . Warning against the possibility of death from inadvertent laceration of the carotid artery during tracheotomy, he instead advocated the practice of  tracheal intubation . [ 17 ]


Despite the concerns of Hippocrates, it is believed that an early tracheotomy was performed by  Asclepiades of Bithynia , who lived in Rome around 100 BC. [ 31 ]   Galen  and  Aretaeus , both of whom lived in Rome in the 2nd century AD, credit Asclepiades as being the first physician to perform a non-emergency tracheotomy.  Antyllus , another Roman-era Greek physician of the 2nd century AD, supported tracheotomy when treating oral diseases. He refined the technique to be more similar to that used in modern times, recommending that a  transverse  incision be made between the third and fourth tracheal rings for the treatment of life-threatening airway obstruction. [ 17 ]


The 7th century Byzantine physician  Paul of Aegina , an advocate of the procedure, acknowledged previous Greek authors' works on the subject of tracheotomies and provided descriptions of the procedure in his own works. [ 32 ]  In 1000,  Abu al-Qasim al-Zahrawi  (936–1013), an Arab who lived in  Arabic Spain , published the 30-volume  Kitab al-Tasrif , the first illustrated work on surgery. He never performed a tracheotomy, but he did treat a slave girl who had cut her own throat in a suicide attempt. Al-Zahrawi (known to Europeans as  Albucasis ) sewed up the wound and the girl recovered, thereby proving that an incision in the larynx could heal. Circa AD 1020,  Avicenna  (980–1037) described tracheal intubation in  The Canon of Medicine  in order to facilitate  breathing . [ 33 ]  The first clear description of the tracheotomy operation for treating asphyxiation was given by  Ibn Zuhr  (1091–1161) in the 12th century. According to Mostafa Shehata, Ibn Zuhr (also known as Avenzoar) successfully practiced the tracheotomy procedure on a goat, justifying Galen's approval of the operation. [ 34 ]


The European  Renaissance  brought with it significant advances in all scientific fields, particularly surgery. Increased knowledge of anatomy was a major factor in these developments. Surgeons became increasingly open to experimental surgery on the trachea. During this period, many surgeons attempted to perform tracheotomies, for various reasons and with various methods. Many suggestions were put forward, but little actual progress was made toward making the procedure more successful. The tracheotomy remained a dangerous operation with a very low success rate, [ quantify ]  and many surgeons still considered the tracheotomy to be a useless and dangerous procedure. The high mortality rate [ quantify ]  for this operation, which had not improved, supported their position. From the period 1500 to 1832 there are only 28 known reports of tracheotomy. [ 35 ]


In 1543,  Andreas Vesalius  (1514–1564) wrote that tracheal intubation and subsequent  artificial respiration  could be life-saving.  Antonio Musa Brassavola  (1490–1554) of  Ferrara  treated a patient with  peritonsillar abscess  by tracheotomy after the patient had been refused by  barber surgeons . The patient apparently made a complete recovery, and Brassavola published his account in 1546. This operation has been identified as the first recorded successful tracheostomy, despite many ancient references to the trachea and possibly to its opening. [ 35 ]   Ambroise Paré  (1510–1590) described suture of tracheal lacerations in the mid-16th century. One patient survived despite a concomitant injury to the internal jugular vein. Another sustained wounds to the trachea and esophagus and died.


Towards the end of the 16th century, anatomist and surgeon  Hieronymus Fabricius  (1533–1619) described a useful technique for tracheotomy in his writings, although he had never actually performed the operation himself. He advised using a vertical incision and was the first to introduce the idea of a tracheostomy tube. This was a straight, short  cannula  that incorporated wings to prevent the tube from advancing too far into the trachea. He recommended the operation only as a last resort, to be used in cases of  airway  obstruction by  foreign bodies  or  secretions . Fabricius' description of the tracheotomy procedure is similar to that used today.  Giulio Cesare Casseri  (1552–1616) succeeded Fabricius as professor of anatomy at the University of Padua and published his own writings regarding technique and equipment for tracheotomy. Casseri recommended using a curved silver tube with several holes in it.  Marco Aurelio Severino  (1580–1656), a skillful surgeon and anatomist, performed multiple successful tracheotomies during a  diphtheria   epidemic  in  Naples  in 1610, using the vertical incision technique recommended by Fabricius. He also developed his own version of a trocar. [ 36 ]


In 1620 the French surgeon  Nicholas Habicot  (1550–1624), surgeon of the  Duke of Nemours  and anatomist, published a report of four successful "bronchotomies" which he had performed. [ 37 ]  One of these is the first recorded case of a tracheotomy for the removal of a foreign body, in this instance a blood clot in the larynx of a stabbing victim. He also described the first tracheotomy to be performed on a  pediatric  patient. A 14-year-old boy swallowed a bag containing 9 gold coins in an attempt to prevent its theft by a  highwayman . The object became lodged in his  esophagus , obstructing his trachea. Habicot suggested that the operation might also be effective for patients with inflammation of the larynx. He developed equipment for this surgical procedure which displayed similarities to modern designs (except for his use of a single-tube cannula). [ citation needed ]


Sanctorius  (1561–1636) is believed to be the first to use a trocar in the operation, and he recommended leaving the cannula in place for a few days following the operation. [ 38 ]  Early tracheostomy devices are illustrated in Habicot's  Question Chirurgicale [ 37 ]  and Casseri's posthumous  Tabulae anatomicae  in 1627. [ 39 ]  Thomas Fienus (1567–1631), Professor of Medicine at the  University of Louvain , was the first to use the word "tracheotomy" in 1649, but this term was not commonly used until a century later. [ 40 ]  Georg Detharding (1671–1747), professor of anatomy at the  University of Rostock , treated a drowning victim with tracheostomy in 1714. [ 41 ] [ 42 ] [ 43 ]


In the 1820s, the tracheotomy began to be recognized as a legitimate means of treating severe airway obstruction. In 1832, French physician  Pierre Bretonneau  employed it as a last resort to treat a case of  diphtheria . [ 44 ]  In 1852, Bretonneau's student  Armand Trousseau  reported a series of 169 tracheotomies (158 of which were for  croup , and 11 for "chronic maladies of the larynx") [ 45 ]  In 1858, John Snow was the first to report tracheotomy and cannulation of the trachea for the administration of chloroform anesthesia in an animal model. [ 46 ]  In 1871, the German surgeon  Friedrich Trendelenburg  (1844–1924) published a paper describing the first successful  elective  human tracheotomy to be performed for the purpose of administration of general anesthesia. [ 47 ]  In 1880, the Scottish surgeon  William Macewen  (1848–1924) reported on his use of orotracheal intubation as an alternative to tracheotomy to allow a patient with glottic edema to breathe, as well as in the setting of general anesthesia with  chloroform . [ 48 ] [ 49 ]  At last, in 1880  Morell Mackenzie 's book discussed the symptoms indicating a tracheotomy and when the operation is absolutely necessary. [ 17 ]


In the early 20th century, physicians began to use the tracheotomy in the treatment of patients affected by paralytic  poliomyelitis  who required  mechanical ventilation . However, surgeons continued to debate various aspects of the tracheotomy well into the 20th century. Many techniques were described and employed, along with many different  surgical instruments  and tracheal tubes. Surgeons could not seem to reach a consensus on where or how the tracheal incision should be made, arguing whether the "high tracheotomy" or the "low tracheotomy" was more beneficial. The currently used surgical tracheotomy technique was described in 1909 by  Chevalier Jackson  of  Pittsburgh ,  Pennsylvania . Jackson emphasised the importance of postoperative care, which dramatically reduced the death rate. By 1965, the surgical anatomy was thoroughly and widely understood,  antibiotics  were widely available and useful for treating postoperative infections, and other major complications had also become more manageable.


Notable individuals who have or have had a tracheotomy include  Catherine Zeta-Jones ,  Mika Häkkinen ,  Stephen Hawking ,  Connie Culp ,  Christopher Reeve , [ 50 ]   Roy Horn ,  William Rehnquist ,  Gabby Giffords ,  George Michael ,  Val Kilmer , [ 51 ]  and many others. [ 52 ]


Across movies and TV shows, there are many situations where an emergency procedure is done on an individual's neck to re-establish an airway. An example is in the 2008 horror film,  Saw V , in which a character being drowned from the neck up performs a manual tracheotomy, stabbing his neck with a pen to create an airway to breathe through. The most common procedure is a  cricothyrotomy  (or "crike"), which is an incision through the skin and cricothyroid membrane. This is often confused or misnamed as a tracheotomy (or "trach") and vice versa. However, they are quite different based on location of the opening and length of time the alternate airway is needed.


Another example of an emergency attempt at this procedure is featured in the 2013 comedy film  The Heat , where  Sandra Bullock ’s character, Sarah Ashburn, attempts to perform the operation on a person choking on a pancake in a  Denny's , but fails.  Melissa McCarthy ’s character, Detective Mullens, then presses hard on the man's chest, causing the piece of food to be expelled from his mouth. [ citation needed ]


The  tragus  is a small pointed eminence of the  external ear , situated in front of the  concha , and projecting backward over the  meatus . It also is the name of hair growing at the entrance of the ear. [ 1 ]  Its name comes from the  Ancient Greek   tragos  ( τράγος ), meaning 'goat', and is descriptive of its general covering on its under surface with a tuft of  hair , resembling a  goat 's  beard . [ 2 ]  The nearby  antitragus  projects forwards and upwards. [ 3 ]


Because the tragus faces rearwards, it aids in collecting sounds from behind.  These sounds are delayed more than sounds arriving from the front, assisting the brain to sense front vs. rear sound sources. [ 4 ]


In a positive  fistula  test (for the presence of a fistula from  cholesteatoma  to the  labyrinth ), pressure on the tragus causes  vertigo  or eye deviation by inducing movement of  perilymph . [ 5 ]


The tragus is a key feature in many bat species. As a piece of skin in front of the ear canal, it plays an important role in directing sounds into the ear for prey location and navigation via  echolocation . [ 6 ]  Because the tragus tends to be prominent in bats, it is an important feature in identifying bat species. [ 7 ]
The tragus allows echolocating bat species to vertically discriminate the objects around them, which is key to identifying where prey items and obstacles are in three-dimensional space.
In studies where an individual's tragi are temporarily glued out of their normal positions, the bat's navigational acuity is one-fourth as effective as individuals with unmodified tragi.
Based on this study, the authors concluded that the tragus's function is to create acoustic cues to determine the direction of a target in the vertical plane. [ 8 ]
Not all echolocating bats possess tragi, however.
 Horseshoe bats  are one such family; the way in which the outer bottom edge of the ear folds in on itself is thought to function in a similar way to the tragus in other families. [ 9 ]


This article incorporates text in the  public domain  from  page 1034  of the 20th edition of   Gray's Anatomy   (1918)


Transnasal esophagoscopy  ( TNE ) is a safe and inexpensive way to examine the  esophagus  in patients at risk for  esophageal cancer  and other disorders. [ 1 ] [ 2 ] [ 3 ]  TNE doesn't require sedation, unlike other techniques widely used to look into the esophagus. This is possible because TNE uses a camera that is passed through the  nose , whereas other techniques, such as upper endoscopy, are performed through the  mouth , requiring a patient to be sedated. TNE, as it is used today, was developed by  Jonathan E. Aviv  who published his findings on the first series of TNE that he performed. [ 4 ]   The origins of the idea to pass the camera through the nose date from 1993 as first described by C. A. Prescott, MD, a pediatrician  otolaryngologist  in Cape Town, South Africa  [ 5 ]  and further embellished by Reza Shaker, MD, a  gastroenterologist  in Milwaukee, WI in 1994. [ 6 ]  However, it wasn't until the year 2000 when  Jonathan E. Aviv , MD, published his findings on the first series of TNE he performed, that it began to have a widespread attention by ear, nose, and throat doctors. [ 7 ]  Since that time it has been used by both otolaryngologists and gastroenterologists as a diagnostic tool to detect globus,  dysphagia ,  laryngopharyngeal reflux  (LPR), gastroesophageal reflux disease ( GERD ). TNE may also be useful in detecting  Barrett's , but there is incongruence between TNE findings and biopsy results. [ 8 ]  Experts in the field suggest that TNE may replace radiographic imaging of the esophagus in otolaryngology patients with reflux, globus, and dysphagia. [ 9 ]


Transnasal esophagoscopy  is an office based procedure in which the patient is anesthetized locally in the nose and sometimes the  oropharynx . The scope is advanced into the  ipsilateral   pyriform sinus  and through the esophageal inlet to the stomach, where the esophagus can be examined, with special attention paid to the gastroesophageal (GE) junction. [ 10 ]  An advantage of TNE over other more invasive cancer screening methods that require  conscious sedation  is that it can be performed using topical anesthesia alone with the patient sitting upright in an exam chair unencumbered by cardiac monitoring equipment. [ 11 ]


In  neuroanatomy , the  trigeminal nerve  ( lit.   triplet  nerve), also known as the  fifth cranial nerve ,  cranial nerve V , or simply  CN V , is a  cranial nerve  responsible for  sensation  in the  face  and  motor functions  such as  biting  and  chewing ; it is the most complex of the  cranial nerves . Its name ( trigeminal , from  Latin    tri-  'three' and   -geminus  'twin' [ 1 ] ) derives from each of the two nerves (one on each side of the  pons ) having three major branches: the  ophthalmic nerve  (V 1 ), the  maxillary nerve  (V 2 ), and the  mandibular nerve  (V 3 ). The ophthalmic and maxillary nerves are purely sensory, whereas the mandibular nerve supplies motor as well as sensory (or " cutaneous ") functions. [ 2 ]  Adding to the complexity of this nerve is that  autonomic nerve fibers  as well as special  sensory fibers  ( taste ) are contained within it.


The motor division of the trigeminal nerve derives from the  basal plate  of the  embryonic   pons , and the sensory division originates in the  cranial neural crest . Sensory information from the face and body is processed by parallel pathways in the  central nervous system .


From the trigeminal ganglion, a single, large sensory root  enters the  brainstem  at the level of the  pons . Immediately adjacent to the sensory root, a smaller motor root emerges from the pons [ 3 ]  slightly rostrally and medially to the sensory root. [ 4 ]


Motor fibers pass through the trigeminal ganglion without synapsing on their way to peripheral muscles, their cell bodies being located in the nucleus of the fifth nerve, deep within the pons.


The three major branches of the trigeminal nerve—the  ophthalmic nerve  (V 1 ), the  maxillary nerve  (V 2 ) and the  mandibular nerve  (V 3 )—converge on the  trigeminal ganglion  (also called the semilunar ganglion or gasserian ganglion), located within  Meckel's cave  and containing the cell bodies of incoming sensory-nerve fibers. The trigeminal ganglion is analogous to the  dorsal root  ganglia of the spinal cord, which contain the cell bodies of incoming sensory fibers from the rest of the body.


The ophthalmic, maxillary and mandibular branches leave the skull through three separate  foramina : the  superior orbital fissure , the  foramen rotundum  and the  foramen ovale , respectively. The ophthalmic nerve (V 1 ) carries sensory information from the scalp and forehead, the upper eyelid, the conjunctiva and cornea of the eye, the nose (including the tip of the nose, except alae nasi), the nasal mucosa, the frontal sinuses and parts of the  meninges  (the  dura  and blood vessels). The maxillary nerve (V 2 ) carries sensory information from the lower eyelid and cheek, the  nares  and upper lip, the upper teeth and gums, the nasal mucosa, the palate and roof of the pharynx, the maxillary, ethmoid and sphenoid sinuses and parts of the meninges. The mandibular nerve (V 3 ) carries sensory information from the lower lip, the lower teeth and gums, the chin and jaw (except the angle of the jaw, which is supplied by C2-C3), parts of the external ear and parts of the meninges. The mandibular nerve carries touch-position and pain-temperature sensations from the mouth. Although it does not carry taste sensation (the  chorda tympani  is responsible for taste), one of its branches—the  lingual nerve —carries sensation from the tongue.


The peripheral processes of mesencephalic nucleus of V neurons run in the motor root of the trigeminal nerve and terminate in the muscle spindles in the muscles of mastication. They are proprioceptive fibers, conveying information regarding the location of the masticatory muscles. The central processes of mesencephalic V neurons synapse in the motor nucleus V.


The areas of cutaneous distribution ( dermatomes ) of the three sensory branches of the trigeminal nerve have sharp borders with relatively little overlap (unlike dermatomes in the rest of the body, which have considerable overlap). The injection of a  local anesthetic , such as  lidocaine , results in the complete loss of sensation from well-defined areas of the face and mouth. For example, teeth on one side of the jaw can be numbed by injecting the mandibular nerve. Occasionally, injury or disease processes may affect two (or all three) branches of the trigeminal nerve; in these cases, the involved branches may be termed:


Nerves on the left side of the jaw slightly outnumber the nerves on the right side of the jaw.


The sensory function of the trigeminal nerve is to provide tactile,  proprioceptive , and  nociceptive  afference to the face and mouth. Its motor function activates the  muscles of mastication , the  tensor tympani ,  tensor veli palatini ,  mylohyoid  and the  anterior belly of the digastric .


The trigeminal nerve carries  general somatic afferent fibers  (GSA), which innervate the skin of the face via ophthalmic (V1), maxillary (V2) and mandibular (V3) divisions. The trigeminal nerve also carries  special visceral efferent  (SVE)  axons , which innervate the muscles of mastication via the mandibular (V3) division.


The motor component of the mandibular division (V3) of the trigeminal nerve controls the movement of eight muscles, including the four  muscles of mastication : the  masseter , the  temporal muscle , and the  medial  and  lateral pterygoids . The other four muscles are the  tensor veli palatini , the  mylohyoid , the anterior belly of the  digastric  and the  tensor tympani .


With the exception of the tensor tympani, all these muscles are involved in biting, chewing and swallowing and all have bilateral  cortical  representation.  A unilateral central lesion (for example, a  stroke ), no matter how large, is unlikely to produce an observable deficit. Injury to a peripheral nerve can cause paralysis of muscles on one side of the jaw, with the jaw deviating towards the paralyzed side when it opens. This direction of the mandible is due to the action of the functioning pterygoids on the opposite side.


The two basic types of sensation are touch-position and pain-temperature. Touch-position input comes to attention immediately, but pain-temperature input reaches the level of consciousness after a delay; when a person steps on a pin, the awareness of stepping on something is immediate but the pain associated with it is delayed.


Touch-position information is generally carried by myelinated (fast-conducting) nerve fibers, and pain-temperature information by unmyelinated (slow-conducting) fibers. The primary sensory receptors for touch-position ( Meissner's corpuscles ,  Merkel's receptors ,  Pacinian corpuscles ,  Ruffini's corpuscles ,  hair receptors ,  muscle spindle organs  and  Golgi tendon organs ) are structurally more complex than those for pain-temperature, which are nerve endings.


Sensation in this context refers to the conscious perception of touch-position and pain-temperature information, rather than the  special senses  (smell, sight, taste, hearing and balance) processed by different cranial nerves and sent to the cerebral cortex through different pathways. The perception of magnetic fields, electrical fields, low-frequency vibrations and infrared radiation by some nonhuman vertebrates is processed by their equivalent of the fifth cranial nerve.


Touch in this context refers to the perception of detailed, localized tactile information, such as  two-point discrimination  (the difference between touching one point and two closely spaced points) or the difference between coarse, medium or fine sandpaper. People without touch-position perception can feel the surface of their bodies and perceive touch in a broad sense, but they lack perceptual detail.


Position, in this context, refers to conscious  proprioception . Proprioceptors (muscle spindle and Golgi tendon organs) provide information about joint position and muscle movement. Although much of this information is processed at an unconscious level (primarily by the  cerebellum  and the  vestibular  nuclei), some is available at a conscious level.


Touch-position and pain-temperature sensations are processed by different pathways in the central nervous system. This hard-wired distinction is maintained up to the cerebral cortex. Within the cerebral cortex, sensations are linked with other cortical areas.


Sensory pathways from the periphery to the cortex are separate for touch-position and pain-temperature sensations. All sensory information is sent to specific nuclei in the  thalamus . Thalamic nuclei, in turn, send information to specific areas in the  cerebral cortex . Each pathway consists of three bundles of nerve fibers connected in series:


The secondary neurons in each pathway  decussate  (cross the spinal cord or brainstem), because the spinal cord develops in segments. Decussated fibers later reach and connect these segments with the higher centers. The  optic chiasm  is the primary cause of decussation; nasal fibers of the optic nerve cross (so each cerebral hemisphere receives contralateral—opposite—vision) to keep the  interneuronal  connections responsible for processing information short. All sensory and motor pathways converge and diverge to the contralateral hemisphere. [ 5 ]


Although sensory pathways are often depicted as chains of individual neurons connected in series, this is an oversimplification. Sensory information is processed and modified at each level in the chain by interneurons and input from other areas of the nervous system. For example, cells in the main trigeminal nucleus (Main V in the diagram below) receive input from the  reticular formation  and cerebellar cortex. This information contributes to the final output of the cells in Main V to the thalamus.


Touch-position information from the body is carried to the thalamus by the  medial lemniscus , and from the face by the  trigeminal lemniscus  (both the anterior and posterior trigeminothalamic tracts). Pain-temperature information from the body is carried to the thalamus by the  spinothalamic tract , and from the face by the anterior division of the  trigeminal lemniscus  (also called the  anterior trigeminothalamic tract ).


Pathways for touch-position and pain-temperature sensations from the face and body merge in the brainstem, and touch-position and pain-temperature sensory maps of the entire body are projected onto the thalamus. From the thalamus, touch-position and pain-temperature information is projected onto the cerebral cortex.


The complex processing of pain-temperature information in the thalamus and cerebral cortex (as opposed to the relatively simple, straightforward processing of touch-position information) reflects a  phylogenetically  older, more primitive sensory system. The detailed information received from peripheral touch-position receptors is superimposed on a background of awareness, memory and emotions partially set by peripheral pain-temperature receptors.


Although thresholds for touch-position perception are relatively easy to measure, those for pain-temperature perception are difficult to define and measure. "Touch" is an objective sensation, but "pain" is an individualized sensation which varies among different people and is conditioned by memory and emotion. Anatomical differences between the pathways for touch-position perception and pain-temperature sensation help explain why pain, especially chronic pain, is difficult to manage.


All sensory information from the face, both touch-position and pain-temperature, is sent to the  trigeminal nucleus . In classical anatomy most sensory information from the face is carried by the fifth nerve, but sensation from parts of the mouth, parts of the ear and parts of the  meninges  is carried by  general somatic afferent fibers  in cranial nerves VII (the  facial nerve ), IX (the  glossopharyngeal nerve ) and X (the  vagus nerve ).


All sensory fibers from these nerves terminate in the trigeminal nucleus. On entering the brainstem, sensory fibers from V, VII, IX and X are sorted and sent to the trigeminal nucleus (which contains a sensory map of the face and mouth). The spinal counterparts of the trigeminal nucleus (cells in the  dorsal horn  and  dorsal column  nuclei of the spinal cord) contain a sensory map of the rest of the body.


The trigeminal nucleus extends throughout the brainstem, from the midbrain to the medulla, continuing into the cervical cord (where it merges with the dorsal horn cells of the spinal cord). The nucleus is divided into three parts, visible in microscopic sections of the brainstem. From caudal to rostral (ascending from the medulla to the midbrain), they are the  spinal trigeminal , the  principal sensory  and the  mesencephalic  nuclei. The parts of the trigeminal nucleus receive different types of sensory information; the spinal trigeminal nucleus receives pain-temperature fibers, the principal sensory nucleus receives touch-position fibers and the mesencephalic nucleus receives proprioceptor and mechanoreceptor fibers from the jaws and teeth.


The  spinal trigeminal nucleus  represents pain-temperature sensation from the face. Pain-temperature fibers from peripheral  nociceptors  are carried in cranial nerves V, VII, IX and X. On entering the brainstem, sensory fibers are grouped and sent to the spinal trigeminal nucleus. This bundle of incoming fibers can be identified in cross-sections of the pons and medulla as the spinal tract of the trigeminal nucleus, which parallels the spinal trigeminal nucleus. The spinal tract of V is analogous to, and continuous with,  Lissauer's tract  in the spinal cord.


The spinal trigeminal nucleus contains a pain-temperature sensory map of the face and mouth. From the spinal trigeminal nucleus, secondary fibers cross the midline and ascend in the trigeminothalamic (quintothalamic) tract to the contralateral thalamus. Pain-temperature fibers are sent to multiple thalamic nuclei. The central processing of pain-temperature information differs from the processing of touch-position information.


Exactly how pain-temperature fibers from the face are distributed to the spinal trigeminal nucleus is disputed. The present general understanding is that pain-temperature information from all areas of the human body is represented in the spinal cord and brainstem in an ascending,  caudal-to-rostral  fashion. Information from the lower extremities is represented in the lumbar cord, and that from the upper extremities in the thoracic cord. Information from the neck and the back of the head is represented in the cervical cord, and that from the face and mouth in the spinal trigeminal nucleus.


Within the spinal trigeminal nucleus, information is represented in a layered, or "onion-skin" fashion. The lowest levels of the nucleus (in the upper cervical cord and lower medulla) represent peripheral areas of the face (the scalp, ears and chin). Higher levels (in the upper medulla) represent central areas (nose, cheeks and lips). The highest levels (in the pons) represent the mouth, teeth and pharyngeal cavity.


The onion skin distribution differs from the dermatome distribution of the peripheral branches of the fifth nerve. Lesions which destroy lower areas of the spinal trigeminal nucleus (but spare higher areas) preserve pain-temperature sensation in the nose (V 1 ), upper lip (V 2 ) and mouth (V 3 ) and remove pain-temperature sensation from the forehead (V 1 ), cheeks (V 2 ) and chin (V 3 ). Although analgesia in this distribution is "nonphysiologic" in the traditional sense (because it crosses several dermatomes), this analgesia is found in humans after surgical sectioning of the spinal tract of the trigeminal nucleus.


The spinal trigeminal nucleus sends pain-temperature information to the  thalamus  and sends information to the  mesencephalon  and the  reticular formation  of the brainstem. The latter pathways are analogous to the spinomesencephalic and spinoreticular tracts of the spinal cord, which send pain-temperature information from the rest of the body to the same areas. The mesencephalon modulates painful input before it reaches the level of consciousness. The reticular formation is responsible for the automatic (unconscious) orientation of the body to painful stimuli.  Incidentally,  Sulfur -containing compounds found in plants in the  onion  family stimulate receptors found in trigeminal ganglia, bypassing the  olfactory system . [ 6 ]


The  principal nucleus  represents touch-pressure sensation from the face. It is located in the pons, near the entrance for the fifth nerve. Fibers carrying touch-position information from the face and mouth via cranial nerves V, VII, IX, and X are sent to this nucleus when they enter the brainstem.


The principal nucleus contains a touch-position sensory map of the face and mouth, just as the spinal trigeminal nucleus contains a complete pain-temperature map. This nucleus is analogous to the  dorsal column  nuclei (the  gracile  and  cuneate  nuclei) of the spinal cord, which contain a touch-position map of the rest of the body.


From the principal nucleus, secondary fibers cross the midline and ascend in the  ventral trigeminothalamic tract  to the contralateral  thalamus . The ventral trigeminothalamic tract runs parallel to the  medial lemniscus , which carries touch-position information from the rest of the body to the thalamus.


Some sensory information from the teeth and jaws is sent from the principal nucleus to the  ipsilateral  thalamus via the small  dorsal trigeminal tract . Touch-position information from the teeth and jaws of one side of the face is represented bilaterally in the thalamus and cortex.


The  mesencephalic nucleus  is not a true  nucleus ; it is a sensory  ganglion  (like the  trigeminal ganglion ) embedded in the brainstem [ citation needed ]  and the sole exception to the rule that sensory information passes through peripheral sensory ganglia before entering the central nervous system. It has been found in all  vertebrates  except  lampreys  and  hagfishes . They are the only vertebrates without jaws and have specific cells in their brainstems. These "internal ganglion" cells were discovered in the late 19th century by medical student  Sigmund Freud .


Two types of sensory fibers have cell bodies in the mesencephalic nucleus:  proprioceptor  fibers from the jaw and mechanoreceptor fibers from the teeth. Some of these incoming fibers go to the motor nucleus of the trigeminal nerve (V), bypassing the pathways for conscious perception. The  jaw jerk reflex  is an example; tapping the jaw elicits a reflex closure of the jaw in the same way that tapping the knee elicits a reflex kick of the lower leg. Other incoming fibers from the teeth and jaws go to the main nucleus of V. This information is projected bilaterally to the thalamus and available for conscious perception.


Activities such as biting, chewing and swallowing require symmetrical, simultaneous coordination of both sides of the body. They are automatic activities, requiring little conscious attention and involving a sensory component (feedback about touch-position) processed at the unconscious level in the mesencephalic nucleus.


Sensation has been defined as the conscious perception of touch-position and pain-temperature information. With the exception of smell, all sensory input (touch-position, pain-temperature, sight, taste, hearing and balance) is sent to the thalamus and then the cortex. The thalamus is anatomically subdivided into nuclei.


Touch-position information from the body is sent to the  ventral posterolateral nucleus  (VPL) of the thalamus. Touch-position information from the face is sent to the  ventral posteromedial nucleus  (VPM) of the thalamus. From the VPL and VPM, information is projected to the  primary somatosensory cortex  (SI) in the  parietal lobe .


The representation of sensory information in the postcentral gyrus is organized  somatotopically . Adjacent areas of the body are represented by adjacent areas in the cortex. When body parts are drawn in proportion to the density of their innervation, the result is a "little man": the  cortical homunculus .


Many textbooks have reproduced the outdated  Penfield -Rasmussen diagram [ref?], with the toes and genitals on the  mesial  surface of the cortex when they are actually represented on the convexity. [ 7 ]  The classic diagram implies a single primary sensory map of the body, when there are multiple primary maps. At least four separate, anatomically distinct sensory homunculi have been identified in the postcentral gyrus. They represent combinations of input from surface and deep receptors and rapidly  and slowly adapting peripheral receptors; smooth objects will activate certain cells, and rough objects will activate other cells.


Information from all four maps in SI is sent to the secondary sensory cortex (SII) in the parietal lobe. SII contains two more sensory homunculi. Information from one side of the body is generally represented on the opposite side in SI, but on both sides in SII. Functional MRI imaging of a defined stimulus (for example, stroking the skin with a toothbrush) "lights up" a single focus in SI and two foci in SII.


Pain-temperature information is sent to the VPL (body) and VPM (face) of the thalamus (the same nuclei which receive touch-position information). From the thalamus, pain-temperature and touch-position information is projected onto SI.


Unlike touch-position information, however, pain-temperature information is also sent to other thalamic nuclei and projected onto additional areas of the cerebral cortex. Some pain-temperature fibers are sent to the  medial dorsal thalamic nucleus  (MD), which projects to the anterior  cingulate cortex . Other fibers are sent to the ventromedial (VM) nucleus of the thalamus, which projects to the  insular cortex . Finally, some fibers are sent to the  intralaminar nucleus  (IL) of the thalamus via the  reticular formation . The IL projects diffusely to all parts of the cerebral cortex.


The insular and cingulate cortices are parts of the brain which represent touch-position and pain-temperature in the context of other simultaneous perceptions (sight, smell, taste, hearing and balance) in the context of memory and emotional state. Peripheral pain-temperature information is channeled directly to the brain at a deep level, without prior processing. Touch-position information is handled differently. Diffuse thalamic projections from the IL and other thalamic nuclei are responsible for a given level of consciousness, with the thalamus and reticular formation "activating" the brain; peripheral pain-temperature information also feeds directly into this system.


Lateral medullary syndrome  (Wallenberg syndrome) is a clinical demonstration of the anatomy of the trigeminal nerve, summarizing how it processes sensory information. A stroke usually affects only one side of the body; loss of sensation due to a stroke will be lateralized to the right or the left side of the body. The only exceptions to this rule are certain spinal-cord lesions and the medullary syndromes, of which Wallenberg syndrome is the best-known example. In this syndrome, a stroke causes a loss of pain-temperature sensation from one side of the face and the other side of the body.


This is explained by the anatomy of the brainstem. In the medulla, the ascending  spinothalamic tract  (which carries pain-temperature information from the opposite side of the body) is adjacent to the ascending spinal tract of the trigeminal nerve (which carries pain-temperature information from the same side of the face). A stroke which cuts off the blood supply to this area (for example, a clot in the posterior inferior cerebellar artery) destroys both tracts simultaneously. The result is a loss of pain-temperature (but not touch-position) sensation in a "checkerboard" pattern (ipsilateral face, contralateral body), facilitating diagnosis.


Sensory neuronopathy  (also known as sensory ganglionopathy) is a type of peripheral neuropathy in which sensory nerve cell bodies in the  dorsal root ganglia , commonly including the  trigeminal ganglion  of the trigeminal nerve, are damaged due to a variety of mechanisms leading to sensory symptoms such as  parasthesias ,  dysesthesias , or  hyperalgesia  in the affected nerve distribution including the distribution of the trigeminal nerve. [ 8 ]


Tubomanometry  is a technique for assessing the  eustachian tube  opening function, and sometimes to determine a treatment plan. [ 1 ]  This technique was familiarised by D. Estève  et al  in 2001. [ 2 ] [ 1 ]


The individual is asked to perform a swallowing maneuver. During this time, the  nasal fossae  and the  nasopharynx  are occluded by the velum. A tympanometry earplug is inserted into the external ear of the studied side to avoid fluctuations in ear pressure due to atmospheric conditions. The tubomanometer then creates a dysbarical situation, where the pressure conditions encountered during a rapid drop in altitude is reproduced. This is done by releasing an air bolus into the nasopharynx through airtight nozzles previously placed on both nostrils. At this point, the tubomanometer is able to make several recordings of the pressure variations in the  rhinopharynx  and on the eardrum as the eustachian tube opens. [ 1 ]


Immediate opening of the eustachian tube was observed in healthy subjects at 30-50 mbar pressure. In patients with chronic eustachian tube dysfunction, this opening could be registered in only 42% of the patients at 30 mbar and 58% at 50 mbar. [ 3 ]  The results are usually interpreted as R values. An R-value less than or equal to one indicates regular eustachian tube function and an R-value greater than 1 indicates a delayed opening of eustachian tube, thereby supporting the diagnosis of chronic  eustachian tube dysfunction . [ 3 ]


The  tympanic cavity  is a small cavity surrounding the  bones  of the  middle ear . Within it sit the ossicles, three small bones that transmit vibrations used in the detection of  sound .


On its lateral surface, it abuts the  external auditory meatus  (ear canal) from which it is separated by the  tympanic membrane  (eardrum).


The tympanic cavity is bounded by:


It is formed from the  tubotympanic recess , an expansion of the first  pharyngeal pouch .


If damaged, the  tympanic membrane  can be repaired in a procedure called  tympanoplasty .


Should fluid accumulate within the middle ear as the result of infection or for some other reason, it can be drained by puncturing the tympanic membrane with a large bore needle ( tympanocentesis ).


This article incorporates text in the  public domain  from  page 1037  of the 20th edition of   Gray's Anatomy   (1918)


The  tympanic nerve  ( Jacobson 's nerve ) is a branch of the  glossopharyngeal nerve  passing through the  petrous part of the temporal bone  to reach the  middle ear . It provides sensory innervation for the middle ear, the  Eustachian tube , the  parotid gland , and  mastoid cells . It also carries parasympathetic fibers destined for the  parotid gland .


The tympanic nerve contains sensory axons to the  middle ear  (including the internal surface of the  tympanic membrane ) whose cell bodies are lodged in the  superior ganglion of the glossopharyngeal nerve . [ 1 ] [ verification needed ]


It also contains parasympathetic axons which continue as the  lesser petrosal nerve  to the  otic ganglion , which itself gives off postganglionic parasympathetic neurons. [ 1 ] [ verification needed ]


The tympanic nerve arises from the  inferior ganglion  of the  glossopharyngeal nerve (CN IX) [ 1 ]  in the  jugular fossa . [ 2 ]


It passes through the  petrous part of the temporal bone  within the  tympanic canaliculus  that is situated within the bony ridge separating the  carotid canal  and the  jugular foramen  to reach the  middle ear . [ 2 ]


In the  tympanic cavity  of the  middle ear , it ramifies upon the  promontory of tympanic cavity  to form the  tympanic plexus . [ 2 ] [ 1 ] [ verification needed ]


The tympanic nerve provides sensation to the  middle ear  ( tympanic cavity ). [ 1 ]  This includes the internal surface of the  tympanic membrane . It also supplies the  Eustachian tube , the  parotid gland , and  mastoid air cells . [ 1 ]


The tympanic nerve is also the parasympathetic root of the  otic ganglion . [ 1 ] [ 3 ]  These neurons then provide secretomotor innervation of the  parotid gland  via the  auriculotemporal nerve . [ 1 ]  It is involved in the salivatory reflex to increase  salivation  during  chewing . [ 4 ]


The tympanic nerve usually arises from the  inferior ganglion  of the  glossopharyngeal nerve . Rarely, it may arise from a higher part. [ 1 ] [ verification needed ]  Rarely, it may provide no parasympathetic fibres to the otic ganglion. [ 3 ]


The tympanic nerve is involved in a reflex, where stimulation of the  ear canal  increases  salivation . [ 4 ]


The tympanic nerve may be involved by  paraganglioma , in this location referred to as a glomus tympanicum tumour. [ 5 ]  This causes a soft mass in the  middle ear  ( tympanic cavity ). [ 5 ]  There may also be  pulsatile tinnitus ,  hearing loss  or  hearing problems , and some cardiac abnormalities. [ 5 ]


The tympanic nerve is also known as the nerve of Jacobson, or Jacobson's nerve. [ 1 ]


This article incorporates text in the  public domain  from  page 910  of the 20th edition of   Gray's Anatomy   (1918)


Tympanostomy tube , also known as a  grommet,   myringotomy tube , or  pressure equalizing tube , is a small tube inserted into the  eardrum  via a surgical procedure called  myringotomy  to keep the  middle ear  aerated for a prolonged period of time, typically to prevent accumulation of fluid in the middle ear. [ 1 ]


The tube itself is made in a variety of designs, most often shaped like a  grommet  for short-term use, or with long  flanges  and sometimes resembling a T-shape for long-term use. [ 2 ]  Materials used to manufacture the tubes are often made from  fluoroplastic  or  silicone , which have largely replaced the use of metal tubes made from stainless steel, titanium, or gold. [ 2 ]


Inserting tympanostomy tubes is one of the most common pediatric surgical procedures in the United States, with 9% of children having had tubes placed sometime in their lives. [ 1 ] [ 3 ]  Tympanostomy tubes are typically placed in one or both eardrums to help children suffering from recurrent acute  otitis media  (ear infection) or persistent  otitis media with effusion  (sometimes called "glue ear"). [ 1 ] [ 4 ] [ 5 ]


Tympanostomy tubes work by improving drainage, allowing air to circulate in the middle ear, and offering a direct route for  antibiotics  to enter the middle ear. [ 2 ] [ 6 ]  Tube placement has been shown to increase hearing in children with persistent otitis media with effusion and may lead to fewer ear infections for children with frequent ear infections. [ 1 ] [ 2 ]  Once placed, short-term tubes are designed to stay in the eardrum for 6–15 months, whereas long-term tubes are designed to stay for 15–18 months. [ 2 ] [ 6 ]  Tympanostomy tubes usually fall out on their own as the eardrum heals over time; however, they can sometimes get stuck in the eardrum and require surgical assistance for removal. [ 2 ]


Guidelines state that tubes are an option in:


While tympanostomy tubes are commonly used in children, they are seldom used in adults. Options for use in adults include:


Otorrhea  (ear discharge) is the most common complication of tympanostomy tube placement, affecting between 25–75% of children receiving this procedure. [ 2 ] [ 6 ] [ 9 ] [ 10 ]  Saline washouts and antibiotic drops at the time of surgery are effective measures to reduce rates of otorrhea, which is why antibiotic ear drops are not routinely prescribed. [ 1 ] [ 6 ] [ 9 ]  If children experience persistent ear drainage or have new discharge two weeks following surgery, antibiotic ear drops are an effective treatment and have been shown to work better than oral antibiotics. [ 1 ] [ 9 ] [ 10 ]  Frequent use of ear drops in children may have an  ototoxic  effect, which is why antibiotic ear drop use following surgery should only be recommended by a trained healthcare professional. [ 9 ]


Potential risks of tympanostomy tube placement in children include going under general anesthesia to have the procedure as well as adverse effects following tube placement. [ 1 ]  Estimates of these other adverse effects from tubes being in the eardrum include:


Long term effects include visible changes to the eardrum such as  tympanosclerosis ,  cholesteatoma , focal  atrophy , or  retraction pockets . [ 1 ] [ 11 ]  These changes usually resolve on their own and do not usually require medical treatment or result in hearing problems that are clinically significant. [ 1 ] [ 12 ]


Surgical intervention may be required in cases of persistent perforation or retained tympanostomy tubes. Persistent perforations are corrected via  tympanoplasty  with an 80-90% success rate. [ 1 ]  Most tympanostomy tubes fall out on their own as the eardrum heals; however, when tubes remain after 2–3 years they are often removed to prevent complications. [ 13 ]


Myringotomy  with insertion of tympanostomy tubes is performed by an ENT doctor ( otolaryngologist ) and is one of the most common pediatric surgical procedures, accounting for more than 20% of all  ambulatory  pediatric surgeries in 2006. [ 1 ]  Although myringotomy with tympanostomy tube insertion can be performed in-office under  local anesthesia  for adolescents and adults, children or any patient who may have difficulty lying still during the procedure require  general anesthesia . [ 6 ] [ 14 ]


During the procedure, a small incision is made to the eardrum using either a myringotomy knife or a  CO 2  laser . [ 6 ] [ 15 ]  The middle ear is then usually washed out thoroughly with  saline  before the tympanostomy tubes are placed. Antibiotic drops are commonly used during surgery once tubes are placed but are not routinely prescribed for use following surgery unless recommended by a doctor for individual reasons. [ 1 ] [ 6 ] [ 9 ]


Following surgery, it is suggested that children keep their ears dry for the first two weeks to help prevent complications. After two weeks children do not need to wear earplugs when swimming or to take other measures to prevent water from getting in their ears as there is minimal reduction in adverse effects. [ 1 ] [ 16 ]  It is approximated that a child would need to wear ear plugs for 2.8 years to prevent one additional ear infection. [ 16 ]


Tympanostomy tubes generally remain in the  eardrum  for six months to two years, and about 14% of children will require tympanostomy tubes more than once. [ 1 ]  The eardrum usually closes without a residual hole at the tube site but in a small number of cases a  perforation  can persist. [ 1 ]  For children with otitis media with effusion (glue ear), tympanostomy tubes decrease the prevalence of effusions by 33% and improve hearing by 5-12  decibels , within 1–3 months of the procedure. There is no long-term benefit for hearing by 12–24 months after the procedure. [ 1 ] [ 6 ]


For children with frequent episodes of acute otitis media (ear infection), there is debate about the effectiveness of tympanostomy tubes in reducing rates of infections. There is consensus, however, on the beneficial role of tympanostomy tubes in allowing for drainage of infections and offering direct access to the middle ear with antibiotic drops. [ 1 ]  This aids healthcare providers in identifying the cause of the infection so they can better treat it and decrease the need for systemic antibiotic use. [ 1 ] [ 6 ]


The first myringotomy dates back to 1649 when French anatomist  Jean Riolan  noticed an improvement in his hearing after intentionally perforating his eardrum with a spoon. [ 17 ]  For nearly two hundred years, scientists would study and debate the potential benefits of myringotomy before German scientists Martell Frank and Gustav Lincke had the first documented use of tympanostomy tubes in 1845. These scientists used an approximately 6mm long gold tube in an attempt to prevent the eardrum from closing after myringotomy. [ 18 ]


From 1845 to 1875, seven different types of tympanostomy tubes were manufactured and made of materials including rubber, silver, aluminum, and gold. These tubes were not widely used or accepted due to complications including falling into the middle ear, falling out of the ear, and the tubes getting plugged. [ 18 ]  In 1952, tympanostomy tubes would make a return when American otolaryngologist Beverly Armstrong introduced them as a new treatment for  chronic secretory otitis media . This would lead to numerous types of tympanostomy tubes being developed and studied throughout the 20th century. [ 18 ]


Today,  silicone  and  fluoroplastic  tympanostomy tubes are more commonly used than metal tubes made from stainless steel, titanium, or gold. [ 2 ]  Research on ways to reduce  biofilm  formation on tympanostomy tubes, such as coating the tubes with antibiotics before placement to help prevent tube blockage or infection, has been started, but there is not enough data to determine its effectiveness. [ 2 ]  Dissolvable tubes are also being explored as potential alternatives for current tube materials. [ 2 ]


In the  ethmoid bone , a sickle shaped projection, the  uncinate process , projects posteroinferiorly from the  ethmoid labyrinth .
Between the posterior edge of this process and the anterior surface of the  ethmoid bulla , there is a two-dimensional space, resembling a crescent shape. This space continues laterally as a three-dimensional slit-like space - the  ethmoidal infundibulum . This is bounded by the uncinate process, medially, the  orbital lamina of ethmoid bone  (lamina papyracea), laterally, and the ethmoidal bulla, posterosuperiorly. This concept is easier to understand if one imagine the infundibulum as a prism so that its medial face is the hiatus semilunaris. The "lateral face" of this infundibulum contains the ostium of the maxillary sinus, which, therefore, opens into the infundibulum.


The uncinate process can be attached to either the lateral nasal wall, on the lamina papyracea (50%), the anterior cranial fossa, on the ethmoidal roof (25%), or the middle concha (25%). The superior attachment of the uncinate process determines the drainage pattern of the frontal sinus. In the first case, the infundibulum and the frontal recess are separated from each other, forcing the frontal sinus to drain directly into the middle meatus and not into the ethmoidal infundibulum. With the other configurations, the sinus will drain, firstly, into the infundibulum.


This article incorporates text in the  public domain  from  page 155  of the 20th edition of   Gray's Anatomy   (1918)


G., Arun et alli (2017) - Anatomical variations in superior attachment of uncinate process and localization of frontal sinus outflow tract. International Journal of Otorhinolaryngology and Head and Neck Surgery, 3(2):176-179


P.S., Hechl et alli (1997) - The hiatus semilunaris and infundibulum. Endoscopic Anatomy of the Paranasal Sinuses. Springer, Vienna


Uvulopalatopharyngoplasty  (also known by the  abbreviations   UPPP  and  UP3 ) is a surgical procedure or  sleep surgery  used to remove tissue and/or remodel tissue in the throat. This could be because of sleep issues. Tissues which may typically be removed include:


Tissues which may typically be remodeled include:


UPPP involves removal of the tonsils, the posterior surface of the soft palate, and the uvula. The uvula is then folded toward the soft palate and sutured together as demonstrated in the figures. In the US, UPPP is the most commonly performed procedure for obstructive sleep apnea with approximately 33,000 procedures performed per year. The surgery is more successful in patients who are not obese, and there is a limited role in morbidly obese (>40 kg/m 2 ) individuals.


UPPP is typically administered to patients with obstructive  sleep apnea  in isolation. It is administered as a stand-alone procedure in the hope that the tissue which obstructs the patient's airway is localized in the back of the throat. The rationale is that, by removing the tissue, the patient's airway will be wider and breathing will become easier.


UPPP is also offered to sleep apnea patients who opt for a more comprehensive surgical procedure known as the " Stanford Protocol ", first attempted by Doctors  Nelson Powell  and  Robert Riley  of  Stanford University . The Stanford Protocol consists of two phases.  The first involves surgery of the soft tissue ( tonsillectomy , uvulopalatopharyngoplasty) and the second involves skeletal surgeries ( maxillomandibular advancement ). First, Phase 1 or soft tissue surgery is performed and after re-testing with a new sleep study, if there is residual sleep apnea, then Phase 2 surgery would consist of jaw surgery. The goal is to improve the airway and thereby treat (or possibly cure) sleep apnea. It has been found that obstructive sleep apnea usually involves multiple sites where tissue obstructs the airway; the base of the tongue is often involved. The Protocol successively addresses these multiple sites of obstruction. Note that  genioglossus advancement  can be performed either during Phase 1 or Phase 2 surgeries.


Phase 2 involves maxillomandibular advancement, a surgery which moves the jaw top (maxilla) and bottom (mandible) forward.  The tongue muscle is anchored to the chin, and translation of the mandible forward pulls the tongue forward as well.  If the procedure achieves the desired results, when the patient sleeps and the tongue relaxes, it will no longer be able to block the airway. Success is much better for Phase 2 than for Phase 1 – approximately 90 percent benefit from the second phase, and the success of the Stanford Protocol Operation therefore is due in large part to this second phase.


There is debate among surgeons as to the role of Phase 1 surgery. In 2002, an Atlanta-based surgical team, led by Dr. Jeffrey Prinsell, published  results  which have approximated those of the Stanford team when UPPP was not included in their mix of surgeries.


When UPPP has been administered in isolation, the results are variable. As explained above, sleep apnea is often caused by multiple co-existing obstructions at various locations of the airway such as the  nasal cavity , and particularly the base of the  tongue . The contributing factors in the variability of success include the pre-surgical size of the tonsils, palate, uvula and tongue base. Also, patients who are morbidly obese (body mass index >40 kg/m 2 ) are significantly less likely to have success from this surgery.


Over one thousand people have undergone The Stanford Protocol operation and received follow-up sleep study testing. 60 to 70 percent of patients have been entirely cured. [ 1 ]  In approximately ninety percent of patients, a significant improvement can be expected.


In the recent years, many surgeons have tried to address the multiple levels of obstruction by performing multiple procedures on the same surgical day, called the "multi-level approach".  Typical surgeries in a multi-level approach may include:


Nasal-level surgeries


Soft palate-level surgeries


Hypopharyngeal-level surgeries


UPPP with tonsillectomy improves postoperative results of obstructive sleep apnea depending on tonsil size. The success rate increases with increasing tonsil size. [ 2 ]  This approach improves postoperative results in well-selected patients. [ 3 ]


One of the risks is that by cutting the tissues, excess scar tissue can "tighten" the airway and make it even smaller than it was before UPPP.


After surgery, complications may include these:


In 2008, Labra,  et al. , from Mexico, published a variation of UP3, by adding a uvulopalatal flap, in order to avoid such complications, with a good rate of success. [ 4 ]


The  vestibulocochlear nerve  or  auditory vestibular nerve , also known as the  eighth cranial nerve ,  cranial nerve VIII , or simply  CN VIII , is a  cranial nerve  that transmits  sound  and  equilibrium (balance)  information from the  inner ear  to the  brain . Through  olivocochlear fibers , it also transmits motor and modulatory information from the  superior olivary complex  in the brainstem to the  cochlea . [ 1 ]


The vestibulocochlear nerve consists mostly of  bipolar neurons  and splits into two large divisions: the  cochlear nerve  and the  vestibular nerve .


Cranial nerve 8, the vestibulocochlear nerve, goes to the middle portion of the  brainstem  called the  pons  (which then is largely composed of fibers going to the  cerebellum ).
The 8th cranial nerve runs between the base of the pons and  medulla oblongata  (the lower portion of the brainstem).  This junction between the pons, medulla, and cerebellum that contains the 8th nerve is called the  cerebellopontine angle .
The vestibulocochlear nerve is accompanied by the  labyrinthine artery , which usually branches off from the  anterior inferior cerebellar artery  at the cerebellopontine angle, and then goes with the 7th nerve through the  internal acoustic meatus  to the internal ear.


The cochlear nerve travels away from the  cochlea  of the  inner ear  where it starts as the  spiral ganglia . Processes from the  organ of Corti  conduct afferent transmission to the spiral ganglia. It is the  inner hair cells  of the organ of Corti that are responsible for activation of afferent receptors in response to pressure waves reaching the  basilar membrane  through the transduction of sound. The exact mechanism by which sound is transmitted by the  neurons  of the cochlear nerve is uncertain; the two competing theories are  place theory  and  temporal theory .


The vestibular nerve travels from the  vestibular system  of the inner ear. The  vestibular ganglion  houses the cell bodies of the  bipolar neurons  and extends processes to five sensory organs. Three of these are the  cristae  located in the ampullae of the  semicircular canals . Hair cells of the cristae activate afferent receptors in response to rotational acceleration. The other two sensory organs supplied by the vestibular neurons are the maculae of the  saccule  and  utricle . Hair cells of the maculae in the utricle activate afferent receptors in response to linear acceleration, while hair cells of the maculae in the saccule respond to vertically directed linear force.


The vestibulocochlear nerve is derived from the  embryonic   otic placode .


This is the  nerve  along which the sensory cells (the hair cells) of the inner ear transmit information to the  brain . It consists of the cochlear nerve, carrying details about  hearing , and the vestibular nerve, carrying information about  balance .
It emerges from the  pontomedullary junction  and exits the inner  skull  via the internal acoustic meatus in the  temporal bone .


The vestibulocochlear nerve carries axons of type  special somatic afferent .


Damage to the vestibulocochlear nerve may cause the following symptoms:


Examinations that can be done include the  Rinne  and  Weber tests .


Rinne's test involves Rinne's Right and Left Test, since auditory acuity is equal in both ears. If  bone conduction  (BC) is more than air conduction (AC) (BC>AC) indicates Rinne Test is negative or abnormal. If AC>BC Rinne test is normal or positive. If BC>AC and Weber's test lateralizes to abnormal side then it is Conductive hearing loss. If AC>BC and Weber's test lateralizes to normal side then it concludes Sensorineural hearing loss.


After pure-tone testing, if the AC and BC responses at all frequencies 500–8000 Hz are better than 25 dB HL, meaning 0-24 dB HL, the results are considered normal hearing sensitivity. If the AC and BC are worse than 25 dB HL at any one or more frequency between 500 and 8000 Hz, meaning 25+, and there is a no bigger difference between AC and BC beyond 10 dB at any frequency, there is a sensori-neural hearing loss present. If the BC responses are normal, 0-24 dB HL, and the AC are worse than 25 dB HL, as well as a 10 dB gap between the air and bone responses, a conductive hearing loss is present.
{updated March 2019}


The modified Hughson–Westlake method is used by many audiologists during testing. A battery of (1) otoscopy, to view the ear canal and tympanic membrane, (2) tympanometry, to assess the  immittance  of the tympanic membrane and how well it moves, (3) otoacoustic emissions, to measure the response of the outer hair cells located in the cochlea, (4) audiobooth pure-tone testing, to obtain thresholds to determine the type, severity, and pathology of the hearing loss present, and (5) speech tests, to measure the patients recognition and ability to repeat the speech heard, is all taken into consideration when diagnosing the pathology of the patient.


Some older texts call the nerve the  acoustic  or  auditory nerve , [ 3 ]  but these terms have fallen out of widespread use because they fail to recognize the nerve's role in the vestibular system.  Vestibulocochlear nerve  is therefore preferred by most.


Vocal cord dysfunction  ( VCD ) is a condition affecting the  vocal cords . [ 1 ]  It is characterized by abnormal closure of the vocal folds, which can result in significant difficulties and distress during  breathing , particularly during  inhalation . [ 1 ]


Due to the similarity in symptoms, VCD attacks are often mistaken for  asthma  attacks or  laryngospasms . Symptoms of VCD are not always present. [ 2 ]  Rather, they often occur as episodic "attacks," where the patient will be symptomatic for a short period. [ 1 ]  Although several contributing factors have been identified, the exact cause of VCD is unknown. [ 3 ]


Diagnosis of VCD may include a series of evaluations, including  pulmonary function tests ,  medical imaging , and the evaluation or visualization of the vocal folds during an episode through the use of  videolaryngoscopy . [ 3 ]  Such evaluations can also help to rule out other conditions that can affect the upper and lower airways. [ 3 ]  Treatment of VCD often combines behavioral, medical, and psychological approaches, most often including an  otolaryngologist , a psychologist, and a  speech-language pathologist . [ 1 ]  Although information on the incidence and prevalence of VCD is limited, it is known to occur most frequently in young women. [ 4 ]


Many of the symptoms are not limited to the disorder, as they may resemble a number of conditions that affect the upper and lower airways. Such conditions include  asthma ,  angioedema , vocal cord tumors, and  vocal cord paralysis . [ 5 ] [ 6 ] [ 7 ] [ 8 ]


People with vocal cord dysfunction often complain of "difficulty in breathing in" or "fighting for breath", [ 6 ]  which can lead to subjective respiratory distress, [ 5 ]  and in severe cases, loss of consciousness. [ 4 ]  They may report tightness in the throat or chest, choking, stridor on inhalation and wheezing, which can resemble the symptoms of asthma. [ 5 ] [ 6 ] [ 7 ]  These episodes of  dyspnea  can be recurrent and symptoms can range from mild to severe and prolonged in some cases. [ 5 ]  Agitation and a sense of panic are not uncommon and can result in hospitalization. [ 6 ]


Different subtypes of vocal cord dysfunction are characterized by additional symptoms. For instance, momentary  aphonia  can be caused by laryngospasm, an involuntary spasm of the vocal cords [ 5 ]  and a strained or hoarse voice may be perceived when the vocal cord dysfunction occurs during speech. [ 5 ]


Many of the symptoms are not specific to vocal cord dysfunction and can resemble a number of conditions that affect the upper and lower airways.


VCD can mimic asthma,  anaphylaxis ,  collapsed lungs ,  pulmonary embolism , or  fat embolism , which can lead to an inaccurate diagnosis and inappropriate, potentially harmful, treatment. [ 9 ]  Some cases of VCD are misdiagnosed as asthma, but are unresponsive to asthma therapy, including bronchodilators and steroids. [ citation needed ]  Among adult patients, women tend to be diagnosed more often. [ 10 ]  Among children and teenage patients, VCD has been linked with high participation in competitive sports and family orientation towards high achievement. [ citation needed ]


Vocal cord dysfunction co-occurs with asthma approximately 40% of the time. [ 11 ]  This frequently results in a misdiagnosis of asthma alone. Even young children can tell the difference between an asthma attack (primarily difficulty exhaling) and a VCD attack (primarily difficulty inhaling). [ citation needed ]  Knowing the difference between the two will help those who have both know when to use the rescue inhaler prescribed or when to use the breathing recovery exercises trained by a speech-language pathologist. [ citation needed ]


Episodes can be triggered suddenly or develop gradually and triggers are numerous. Primary causes are believed to be  gastroesophageal reflux disease  (GERD),  extra-esophageal reflux  (EERD), exposure to inhaled allergens,  post-nasal drip , exercise, or neurological conditions that can cause difficulty inhaling only during waking. [ 11 ]  Published studies emphasize anxiety or stress as a primary cause while more recent literature indicates a likely physical etiology. [ citation needed ]  This disorder has been observed from infancy through old age, with the observation of its occurrence in infants leading some to believe that a physiological cause such as reflux or allergy is likely. Certain medications, such as antihistamines for allergies, cause drying of the mucous membranes, which can cause further irritation or hypersensitivity of the vocal cords. [ citation needed ]


VCD has long been strongly associated with a variety of psychological or psychogenic factors, including  conversion disorder ,  major depression ,  obsessive-compulsive disorder ,  anxiety  (especially in adolescents), stress (particularly stress relating to competitive sports), physical and sexual abuse,  post-traumatic stress disorder ,  panic attacks ,  factitious disorder  and  adjustment disorder . [ 10 ] [ 5 ] [ 6 ] [ 4 ]


Anxiety and depression may occur in certain patients as a result of having VCD, rather than being the cause of it. [ 10 ] [ 5 ]  Psychological factors are important precipitating factors for many patients with VCD; although exercise is also a major trigger for episodes of VCD, some patients experience VCD co-occurring with anxiety regardless of whether or not they are physically active at the time of the VCD/anxiety episode. [ 4 ]  Experiencing or witnessing a traumatic event related to breathing (such as a near-drowning or life-threatening asthma attack, for example), has also been identified as a risk factor for VCD. [ 10 ]


VCD has also been associated with certain  neurologic  diseases including  Arnold-Chiari malformation , cerebral aqueduct  stenosis , cortical or  upper motor neuron  injury (such as that resulting from  stroke ),  amyotrophic lateral sclerosis  (ALS),  parkinsonism  syndromes and other movement disorders. [ 10 ] [ 4 ]  However, this association occurs only rarely. [ 4 ]  In addition, it has been associated with  Ehlers-Danlos Syndromes , a group of  connective tissue  disorders. [ 12 ]


The exact cause of VCD is not known, and it is unlikely that a single underlying cause exists. [ 5 ] [ 6 ]  Several contributing factors have been identified, which vary widely among VCD patients with different medical histories. [ 10 ]  Physical exercise (including, but not limited to, competitive athletics) is one of the major triggers for VCD episodes, leading to its frequent misdiagnosis as exercise-induced asthma. [ 10 ] [ 5 ] [ 6 ]  Other triggers include airborne pollutants and irritants such as smoke, dust, gases, soldering fumes, cleaning chemicals such as ammonia, perfumes, and other odors. [ 5 ] [ 4 ]   Gastroesophageal reflux disease  (GERD) and  rhinosinusitis  (inflammation of the  paranasal sinuses  and  nasal cavity ) may also play a role in inflaming the  airway  and leading to symptoms of VCD as discussed below. [ 5 ] [ 4 ]


Laryngeal hyperresponsiveness is considered the most likely physiologic cause of VCD, brought on by a range of different triggers that cause inflammation and/or irritation of the  larynx  (voice box). [ 10 ] [ 6 ]  The glottic closure  reflex  (or laryngeal adductor reflex) serves to protect the airway, and it is possible that this reflex becomes hyperactive in some individuals, resulting in the paradoxical vocal fold closure seen in VCD. [ 10 ] [ 4 ]  Two major causes of laryngeal inflammation and hyperresponsiveness are gastroesophageal reflux disease (GERD) and  postnasal drip  (associated with  rhinosinusitis , allergic or nonallergic  rhinitis , or a viral  upper respiratory tract infection  (URI)). [ 10 ] [ 5 ] [ 6 ] [ 4 ]  Rhinosinusitis is very common among patients with VCD and for many patients, VCD symptoms are ameliorated when the rhinosinusitis is treated. [ 5 ]  GERD is also common among VCD patients, but only some experience an improvement in VCD symptoms when GERD is treated. [ 5 ] [ 6 ]  Other causes of laryngeal hyperresponsiveness include inhalation of toxins and irritants, cold and dry air, episodic  croup  and  laryngopharyngeal reflux  (LPR). [ 6 ]


The following increases an individual's chances for acquiring VCD: [ 13 ]


The most effective diagnostic strategy is to perform  laryngoscopy  during an episode, at which time abnormal movement of the cords, if present, can be observed. If the  endoscopy  is not performed during an episode, it is likely that the vocal folds will be moving normally, a ' false negative ' finding. [ citation needed ]


Spirometry  may also be useful to establish the diagnosis of VCD when performed during a crisis or after a  nasal provocation test . [ 14 ]  With spirometry, just as the expiratory loop may show flattening or concavity when expiration is affected in asthma, so may the inspiratory loop show truncation or flattening in VCD. Of course, testing may well be negative when symptoms are absent. [ 15 ]


The symptoms of VCD are often inaccurately attributed to asthma, [ 5 ]  which in turn results in the unnecessary and futile intake of  corticosteroids ,  bronchodilators  and  leukotriene modifiers , [ 7 ]  although there are instances of comorbidity of asthma and VCD. [ 16 ]


The  differential diagnosis  for vocal cord dysfunction includes vocal fold swelling from allergy, asthma, or some obstruction of the vocal folds or throat. Anyone suspected of this condition should be evaluated and the vocal folds (voice box) visualized.  In individuals who experience a persistent difficulty with inhaling, consideration should be given to a neurological cause such as brain stem compression, cerebral palsy, etc. [ 17 ]


The main difference between VCD and asthma is the audible stridor or wheezing that occurs at different stages of the breath cycle: VCD usually causes stridor on the inhalation, while asthma results in wheezing during exhalation. [ 5 ] [ 6 ] [ 7 ]  Patients with asthma usually respond to the usual medication and see their symptoms resolve. [ 6 ] [ 7 ]  Clinical measures that can be done to differentiate VCD from asthma include: [ 6 ]


Once a diagnosis of VCD has been confirmed by a medical professional, a specific treatment plan can be implemented. If vocal cord dysfunction is secondary to an underlying condition, such as asthma, gastroesophageal reflux disease (GERD), or  postnasal drip , it is important to treat the primary condition as this will help control VCD symptoms. [ 4 ]
Conventional treatments for VCD are often multidisciplinary and include speech-language pathology,  psychotherapy ,  behavioral therapy , use of anti-anxiety and anti-depressant medications, medical interventions, and hypnotherapy. [ 4 ] [ 18 ] [ 19 ]  There is no uniform approach. [ 19 ]
The information from randomized, blinded studies is limited. [ 18 ]


Speech-language pathologists provide behavioral treatment for VCD. Speech therapy usually involves educating the client on the nature of the problem, what happens when symptoms are present, and then comparing this to what happens during normal breathing and  phonation . [ 1 ]  Intervention goals target teaching a client breathing and relaxation exercises so that they can control their throat muscles and keep the airway open, allowing air to flow in and out. [ 4 ]


Breathing techniques can be taught to reduce tension in the throat, neck, and upper body and bring attention to the flow of air during respiration. [ 20 ]  Diaphragm support during breathing decreases muscle tension in the larynx. [ 20 ]  These techniques are meant to move awareness away from the act of breathing in and focus on the  auditory feedback  provided by the air moving in and out. [ 4 ]


Other techniques can involve breathing through a straw and panting, which widens the opening of the throat by activating the  Posterior cricoarytenoid  (PCA) muscle. [ 4 ] [ 19 ]  Endoscopic feedback can also be used to show a patient what is happening when they are doing simple tasks such as taking a deep breath or speaking on an inspiration. [ 1 ]  This provides the client with visual information so that they can actually see what behaviors help to open the throat and what behaviors constrict the throat. [ 1 ]  Respiratory muscle strength training, a form of increased resistance training using a hand-held breathing device has also been reported to alleviate symptoms. [ 1 ]


Speech therapy has been found to eliminate up to 90% of ER visits in patients with VCD. [ 19 ]


Medical often works in conjunction with behavioral approaches. A pulmonary or ENT ( otolaryngologist ) specialist will screen for and address any potential underlying pathology that may be associated with VCD. Managing GERD has also been found to relieve laryngospasm, a spasm of the vocal cords that makes breathing and speaking difficult. [ 21 ]


Non-invasive positive pressure ventilation can be used if a patient's vocal cords adduct (close) during exhalation. [ 4 ]  Mild sedatives have also been employed to reduce anxiety as well as reduce acute symptoms of VCD. [ 4 ] [ 19 ]  Benzodiazepines are an example of one such treatment, though they have been linked to a risk of suppression of the respiratory drive. [ 19 ]  While Ketamine, a dissociative anesthetic, does not suppress respiratory drive, it has been thought to be associated with laryngospasms. [ 19 ]


For more severe VCD cases, physicians may inject  botulinum toxin  into the vocal ( thyroarytenoid ) muscles to weaken or decrease muscle tension. [ 4 ] [ 1 ]  Nebulized Lignocaine can also been used in acute cases and helium-oxygen inhalation given by a face mask has been used in cases of respiratory distress. [ 4 ] [ 21 ] [ 22 ]


Psychological interventions including psychotherapy,  cognitive behavioral therapy  (CBT), Biofeedback, and teaching self-hypnosis are also suggested to treat VCD. [ 18 ]  Intervention is generally targeted at making the client aware of stressors that may trigger VCD symptoms, to implement strategies to reduce stress and anxiety, and to teach techniques for coping with their symptoms. [ 18 ] [ 1 ]


CBT can focus on bringing awareness to negative thought patterns and help reframe them by focusing on problem solving strategies. [ 18 ]  Psychologists may also use relaxation to reduce distress when a patient is experiencing symptoms. [ 4 ] [ 1 ]   Biofeedback  can be a helpful addition to psychotherapy. The aim of Biofeedback is to educate the client on what happens to the vocal cords during breathing and to help them learn to control their symptoms. [ 4 ]


Choosing an intervention strategy needs to be assessed by a multidisciplinary team and individualized therapy planned carefully, keeping the characteristics of each patient in mind. [ 18 ]


The natural prognosis of VCD in both children and adults are not well described in the literature. [ 7 ]  Additionally, there is currently no research that has studied whether the underlying cause of VCD makes a difference in the resolution of symptoms or in the long-term prognosis of the impairment. [ 23 ]


Information on the prognosis of VCD after acute therapies is also limited. Minimal response has been documented with the continued treatment of asthma in people with VCD using  inhaled bronchodilators ,  corticosteroids  and other asthma medications. [ 23 ]  While using  Botox  in VCD has limited reports, those that are available report successful resolution of exercise-induced VCD symptoms for up to 2 months. [ 23 ]


Outcomes of chronic VCD treatment are similarly limited. When pediatric patients undergoing hypnosis therapy were studied, more than half saw either a reduction or resolution of VCD. [ 23 ]  Even though it is widely used, no long-term studies have been done to study the prognosis of VCD after psychotherapy. [ 23 ]


Speech therapy  is the main course of treatment for long-term management of VCD and includes a variety of techniques such as relaxed-throat breathing, respiratory retraining therapy, and vocal hygiene counseling. [ 5 ]  Most studies agree that symptoms of VCD improve in patients and few continue to require asthma medications six months post speech therapy intervention. [ 7 ] [ 23 ]  Significant improvements were reported for respiratory retraining therapy, including fewer episodes of  dyspnea  per month and decreased respiratory stress severity. [ 24 ]


For those adolescent patients who recovered from VCD, the average time before the symptoms were resolved was 4–5 months. [ 7 ]  However, some adolescents had VCD symptoms even 5 years post VCD onset, regardless of intervention. [ 7 ]  It has been noted that some patients do not respond to standard VCD therapies and continue to express recurrent symptoms. [ 23 ]


There is currently a limited amount of information available on the incidence and  prevalence  of VCD, and the various rates reported in the literature are most likely an underestimate. [ 4 ] [ 25 ]  Although VCD is thought to be rare overall, its prevalence among the population at large is not known. [ 6 ]


However, numerous studies have been conducted on its incidence and prevalence among patients presenting with asthma and  exertional dyspnea . A VCD incidence rate of 2% has been reported among patients whose primary complaint was either asthma or dyspnea; the same incidence rate has also been reported among patients with acute asthma exacerbation. [ 6 ] [ 25 ]  Meanwhile, much higher VCD incidence rates have also been reported in asthmatic populations, ranging from 14% in children with refractory asthma to 40% in adults with the same complaint. [ 25 ]  It has also been reported that the VCD incidence rate is as high as 27% in non-asthmatic teenagers and young adults. [ 25 ]


Data on the prevalence of VCD is also limited. An overall prevalence of 2.5% has been reported in patients presenting with asthma. [ 19 ]  Among adults with asthma considered "difficult to control", 10% were found to have VCD while 30% were found to have both VCD and asthma. [ 6 ]  Among children with severe asthma, a VCD prevalence rate of 14% has been reported. [ 6 ]  However, higher rates have also been reported; among one group of schoolchildren thought to have exercise-induced asthma, it was found that 26.9% actually had VCD and not asthma. [ 4 ]  Among intercollegiate athletes with exercise-induced asthma, the VCD rate has been estimated at 3%. [ 4 ]


In patients presenting with symptoms of dyspnea, prevalence rates ranging from 2.8% to 22% have been reported in various studies. [ 6 ] [ 4 ] [ 19 ]  It has been reported that two to three times more females than males have VCD. [ 6 ] [ 4 ] [ 25 ]  VCD is especially common in females who have psychological conditions. [ 4 ]  There is an increased risk associated with being young and female. [ 4 ]  Among patients with VCD, 71% are over the age of 18. [ 6 ]  In addition, 73% of those with VCD have a previous psychiatric diagnosis. [ 6 ]  VCD has also been reported in newborns with gastroesophageal reflux disorder (GERD). [ 4 ]


In humans, the  vocal cords , also known as  vocal folds , are folds of throat tissues that are key in creating sounds through  vocalization . The length of the vocal cords affects the pitch of voice, similar to a violin string. Open when breathing and vibrating for  speech  or  singing , the folds are controlled via the  recurrent laryngeal branch  of the  vagus nerve . They are composed of twin infoldings of  mucous membrane  stretched horizontally, from back to front, across the  larynx . They  vibrate , modulating the flow of air being expelled from the lungs during  phonation . [ 1 ]


The 'true vocal cords' are distinguished from the 'false vocal folds', known as  vestibular folds  or  ventricular folds , which sit slightly superior to the more delicate true folds. These have a minimal role in normal  phonation , but can produce deep sonorous tones, screams and growls.


The length of the vocal fold at birth is approximately six to eight millimeters and grows to its adult length of eight to sixteen millimeters by adolescence.  DHT , an  androgen  metabolite of  testosterone  which is secreted by the gonads, causes changes in the cartilages and musculature of the larynx when present in high enough concentrations, such as during an adolescent boy's  puberty : The thyroid prominence appears, the vocal folds lengthen and become rounded, and the epithelium thickens with the formation of three distinct layers in the  lamina propria . [ citation needed ] . These changes are only partially reversible via  reconstructive surgery  such as  chondrolaryngoplasty ,  feminization laryngoplasty , and laser tuning of the vocal cords.


The vocal folds are located within the larynx at the top of the  trachea . They are attached at the back to the  arytenoid cartilages , and at the front to the  thyroid cartilage  via Broyles ligament. They are part of the  glottis . Their outer edges are attached to muscle in the larynx while their inner edges form an opening called the  rima glottidis . They are constructed from  epithelium , but they have a few muscle-fibres in them, namely the  vocalis muscle  which tightens the front part of the  ligament  near to the thyroid cartilage. They are flat triangular bands and are pearly white in color. Above both sides of the  glottis  are the two  vestibular folds  or false vocal folds which have a small sac between them.


The vocal folds are sometimes called 'true vocal folds' to distinguish them from the 'false vocal folds' known as  vestibular folds  or  ventricular folds . These are a pair of thick folds of mucous membrane that protect and sit slightly higher to the more delicate true folds.  They have a minimal role in normal  phonation , but are often used to produce deep sonorous tones in  Tibetan chant  and  Tuvan throat singing , [ 2 ]  as well as in musical  screaming  and the  death growl  vocal style. [ citation needed ]


The vocal cords are composed of twin infoldings of 3 distinct tissues: an outer layer of flat cells that do not produce  keratin  ( squamous epithelium ). Below this is the superficial layer of the  lamina propria , a gel-like layer, which allows the vocal fold to vibrate and produce sound. The  vocalis  and  thyroarytenoid muscles  make up the deepest portion. These vocal folds are covered with a  mucous membrane  and are stretched horizontally, from back to front, across the  larynx .


Males and females have different vocal fold sizes. Adult male  voices  are usually lower-pitched due to longer and thicker folds. The male's vocal folds are between 1.75 cm and 2.5 cm (approx 0.75" to 1.0") in length, [ 3 ]  while females' vocal folds are between 1.25 cm and 1.75 cm (approx 0.5" to 0.75") in length. The vocal folds of children are much shorter than those of adult males and females. The difference in vocal fold length and thickness between males and females causes a difference in vocal pitch. Additionally, genetic factors cause variations between members of the same sex, with males' and females' voices being categorized into  voice types .


Newborns have a uniform single layered lamina propria, which appears loose with no vocal ligament. [ 4 ]  The monolayered lamina propria is composed of ground substances such as  hyaluronic acid  and  fibronectin ,  fibroblasts , elastic fibers, and collagenous fibers. While the fibrous components are sparse, making the lamina propria structure loose, the hyaluronic acid (HA) content is high.


HA is a bulky, negatively charged glycosaminoglycan, whose strong affinity with water procures hyaluronic acid its viscoelastic and shock absorbing properties essential to vocal biomechanics. [ 5 ]  Viscosity and elasticity are critical to voice production. Chan, Gray and Titze, quantified the effect of hyaluronic acid on both the viscosity and the elasticity of vocal folds by comparing the properties of tissues with and without HA. [ 6 ]  The results showed that removal of hyaluronic acid decreased the stiffness of the vocal cords by an average of 35%, but increased their dynamic viscosity by an average of 70% at frequencies higher than 1 Hz. Newborns have been shown to cry an average of 6.7 hours per day during the first 3 months, with a sustained pitch of 400–600 Hz, and a mean duration per day of 2 hours. [ 7 ]  Similar treatment on adult vocal cords would quickly result in edema, and subsequently aphonia. Schweinfurth and al. presented the hypothesis that high  hyaluronic acid  content and distribution in newborn vocal cords is directly associated with newborn crying endurance. [ 7 ]  These differences in newborn vocal fold composition would also be responsible for newborns inability to articulate sounds, besides the fact that their lamina propria is a uniform structure with no vocal ligament. The layered structure necessary for phonation will start to develop during the infancy and until the adolescence. [ 4 ]


The  fibroblasts  in the newborn  Reinke's space  are immature, showing an oval shape, and a large nucleus-cytoplasm ratio. [ 4 ]  The rough endoplasmic reticulum and Golgi apparatus, as shown by electron micrographs, are not well developed, indicating that the cells are in a resting phase. The collagenous and reticular fibers in the newborn the vocal cords are fewer than in the adult one, adding to the immaturity of the vocal fold tissue.


In the infant, many fibrous components were seen to extend from the macula flava towards the Reinke's space. Fibronectin is very abundant in the Reinke's space of newborn and infant. Fibronectin is a glycoprotein that is believed to act as a template for the oriented deposition of the collagen fibers, stabilizing the collagen fibrils. Fibronectin also acts as a skeleton for the elastic tissue formation. [ 4 ]  Reticular and collagenous fibers were seen to run along the edges of the vocal cords throughout the entire lamina propria. [ 4 ]  Fibronectin in the Reinke's space appeared to guide those fibers and orient the fibril deposition. The elastic fibers remained sparse and immature during infancy, mostly made of microfibrils. The fibroblasts in the infant Reinke's space were still sparse but spindle-shaped. Their rough endoplasmic reticulum and Golgi apparatus were still not well developed, indicating that despite the change in shape, the fibroblasts still remained mostly in a resting phase. Few newly released materials were seen adjacent to the fibroblasts. The ground substance content in the infant  Reinke's space  seemed to decrease over time, as the fibrous component content increased, thus slowly changing the vocal fold structure.