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№ 11

June 20, 2024

№ 11. The ear. Ear diseases.

The ear is the sense organ that detects sounds. The vertebrate of the ear shows a common biology from fish to humans, with variations in structure according to order and species. It not only acts as a receiver for sound, but plays a major role in the sense of balance and body position. The ear is part of the auditory system.

The word “ear” may be used correctly to describe the entire organ or just the visible portion. In most animals, the visible ear is a flap of tissue that is also called the pinna. The pinna may be all that shows of the ear, but it serves only the first of many steps in hearing and plays no role in the sense of balance. In people, the pinna is often called the auricle. Vertebrates have a pair of ears, placed symmetrically on opposite sides of the head. This arrangement aids in the ability to localize sound sources.

Introduction to ears and hearing

Audition is the scientific name for the perception of sound. Sound is a form of energy that moves through air, water, and other matter, in waves of pressure. Sound is the means of auditory communication, including frog calls, bird songs and spoken language. Although the ear is the vertebrate sense organ that recognizes sound, it is the brain and central nervous system that “hears”. Sound waves are perceived by the brain through the firing of nerve cells in the auditory portion of the central nervous system. The ear changes sound pressure waves from the outside world into a signal of nerve impulses sent to the brain.

Anatomy of the human ear. (The length of the auditory canal is exaggerated in this image)

The outer part of the ear collects sound. That sound pressure is amplified through the middle portion of the ear and, in land animals, passed from the medium of air into a liquid medium. The change from air to liquid occurs because air surrounds the head and is contained in the ear canal and middle ear, but not in the inner ear. The inner ear is hollow, embedded in the temporal bone, the densest bone of the body. The hollow channels of the inner ear are filled with liquid, and contain a sensory epithelium that is studded with hair cells. The microscopic “hairs” of these cells are structural protein filaments that project out into the fluid. The hair cells are mechanoreceptors that release a chemical neurotransmitter when stimulated. Sound waves moving through fluid push the filaments; if the filaments bend over enough it causes the hair cells to fire. In this way sound waves are transformed into nerve impulses. In vision, the rods and cones of the retina play a similar role with light as the hair cells do with sound. The nerve impulses travel from the left and right ears through the eighth cranial nerve to both sides of the brain stem and up to the portion of the cerebral cortex dedicated to sound. This auditory part of the cerebral cortex is in the temporal lobe.

Humans can generally hear sounds with frequencies between 20 Hz and 20 kHz (the audio range). Although the sensation of hearing requires an intact and functioning auditory portion of the central nervous system as well as a working ear, human deafness (extreme insensitivity to sound) most commonly occurs because of abnormalities of the inner ear, rather than the nerves or tracts of the central auditory system.

Mammalian ear.

The shape of outer ear of mammals varies widely across species. However the inner workings of mammalian ears (including humans’) are very similar.

The main parts of the ear are:

Main anatomical parts of the ear.

Outer ear (pinna, ear canal, surface of ear drum).

The outer ear is the most external portion of the ear. The outer ear includes the pinna (also called auricle), the ear canal, and the very most superficial layer of the ear drum (also called the tympanic membrane). In humans, and almost all vertebrates, the only visible portion of the ear is the outer ear. Although the word “ear” may properly refer to the pinna (the flesh covered cartilage appendage on either side of the head), this portion of the ear is not vital for hearing. The complicated design of the human outer ear does help capture sound (and imposes filtering that helps distinguish the direction of the sound source), but the most important functional aspect of the human outer ear is the ear canal itself. Unless the canal is open, hearing will be dampened. Ear wax (medical name – cerumen) is produced by glands in the skin of the outer portion of the ear canal. This outer ear canal skin is applied to cartilage; the thinner skin of the deep canal lies on the bone of the skull. Only the thicker cerumen-producing ear canal skin has hairs. The outer ear ends at the most superficial layer of the tympanic membrane. The tympanic membrane is commonly called the ear drum.

The outer ear.

The pinna helps direct sound through the ear canal to the tympanic membrane (eardrum). The framework of the auricle consists of a single piece of yellow fibrocartilage with a complicated relief on the anterior, concave side and a fairly smooth configuration on the posterior, convex side. The Darwinian tubercle, which is present in some people, lies in the descending part of the helix and corresponds to the true ear tip of the long-eared mammals. The lobule merely contains subcutaneous tissue. In some animals with mobile pinnae (like the horse), each pinna can be aimed independently to better receive the sound. For these animals, the pinnae help localize the direction of the sound source. Human beings localize sound within the central nervous system, by comparing arrival-time differences and loudness from each ear, in brain circuits that are connected to both ears.

Human outer ear and culture.

Middle ear

The middle ear.

The malleus has a long process (the manubrium, or handle) that is attached to the mobile portion of the eardrum. The incus is the bridge between the malleus and stapes. The stapes is the smallest named bone in the human body. The three bones are arranged so that movement of the tympanic membrane causes movement of the malleus, which causes movement of the incus, which causes movement of the stapes. When the stapes footplate pushes on the oval window, it causes movement of fluid within the cochlea (a portion of the inner ear).

In humans and other land animals, the middle ear (like the ear canal) is normally filled with air. Unlike the open ear canal, however, the air of the middle ear is not in direct contact with the atmosphere outside the body. The Eustachian tube connects from the chamber of the middle ear to the back of the pharynx. The middle ear is very much like a specialized paranasal sinus, called the tympanic cavity; it, like the paranasal sinuses, is a hollow mucosa-lined cavity in the skull that is ventilated through the nose. The mastoid portion of the human temporal bone, which can be felt as a bump in the skull behind the pinna, also contains air, which is ventilated through the middle ear.

Normally, the Eustachian tube is collapsed, but it gapes open both with swallowing and with positive pressure. When taking off in an airplane, the surrounding air pressure goes from higher (on the ground) to lower (in the sky). The air in the middle ear expands as the plane gains altitude, and pushes its way into the back of the nose and mouth. On the way down, the volume of air in the middle ear shrinks, and a slight vacuum is produced. Active opening of the Eustachian tube is required to equalize the pressure between the middle ear and the surrounding atmosphere as the plane descends. The diver also experiences this change in pressure, but with greater rates of pressure change; active opening of the Eustachian tube is required more frequently as the diver goes deeper into higher pressure.

The arrangement of the tympanic membrane and ossicles works to efficiently couple the sound from the opening of the ear canal to the cochlea. There are several simple mechanisms that combine to increase the sound pressure. The first is the “hydraulic principle”. The surface area of the tympanic membrane is many times that of the stapes footplate. Sound energy strikes the tympanic membrane and is concentrated to the smaller footplate. A second mechanism is the “lever principle”. The dimensions of the articulating ear ossicles lead to an increase in the force applied to the stapes footplate compared with that applied to the malleus. A third mechanism channels the sound pressure to one end of the cochlea, and protects the other end from being struck by sound waves. In humans, this is called “round window protection”, and will be more fully discussed in the next section.

Abnormalities such as impacted ear wax (occlusion of the external ear canal), fixed or missing ossicles, or holes in the tympanic membrane generally produce conductive hearing loss. Conductive hearing loss may also result from middle ear inflammation causing fluid build-up in the normally air-filled space. Tympanoplasty is the general name of the operation to repair the middle ear’s tympanic membrane and ossicles. Grafts from muscle fascia are ordinarily used to rebuild an intact ear drum. Sometimes artificial ear bones are placed to substitute for damaged ones, or a disrupted ossicular chain is rebuilt in order to conduct sound effectively.

Inner ear: cochlea, vestibule, and semi-circular canal).

The inner ear includes both the organ of hearing (the cochlea) and a sense organ that is attuned to the effects of both gravity and motion (labyrinth or vestibular apparatus). The balance portion of the inner ear consists of three semi-circular canals and the vestibule. The inner ear is encased in the hardest bone of the body. Within this ivory hard bone, there are fluid-filled hollows. Within the cochlea are three fluid filled spaces: the tympanic canal, the vestibular canal, and the middle canal. The eighth cranial nerve comes from the brain stem to enter the inner ear. When sound strikes the ear drum, the movement is transferred to the footplate of the stapes, which presses into one of the fluid-filled ducts of the cochlea. The fluid inside this duct is moved, flowing against the receptor cells of the Organ of Corti, which fire. These stimulate the spiral ganglion, which sends information through the auditory portion of the eighth cranial nerve to the brain.

Hair cells are also the receptor cells involved in balance, although the hair cells of the auditory and vestibular systems of the ear are not identical. Vestibular hair cells are stimulated by movement of fluid in the semicircular canals and the utricle and saccule. Firing of vestiular hair cells stimulates the Vestibular portion of the eighth cranial nerve.

Ear

The ear is the organ that detects sound. It not only receives sound, but also aids in balance and body position. The ear is part of the auditory system.

Often the entire organ is considered the ear, though it may also be considered just the visible portion. In most mammals, the visible ear is a flap of tissue that is also called the pinna (or auricle in humans) and is the first of many steps in hearing. Vertebrates have a pair of ears placed somewhat symmetrically on opposite sides of the head. This arrangement aids in the ability to localize sound sources.

Introduction to ears and hearing.

Audition is the scientific name for the sense of sound. Sound is a form of energy that moves through air, water, and other matter, in waves of pressure. Sound is the means of auditory communication, including frog calls, bird songs and spoken language. Although the ear is the vertebrate sense organ that recognizes sound, it is the brain and central nervous system that “hears”. Sound waves are perceived by the brain through the firing of nerve cells in the auditory portion of the central nervous system. The ear changes sound pressure waves from the outside world into a signal of nerve impulses sent to the brain.

Anatomy of the human ear. The length of the auditory canal is exaggerated for viewing purposes.

The part of the ear that is dedicated to sensing balance and position also sends impulses through the eighth cranial nerve, the VIIIth nerve’s Vestibular Portion. Those impulses are sent to the vestibular portion of the central nervous system. The human ear can generally hear sounds with frequencies between 20 Hz and 20 kHz (the audio range). Although the sensation of hearing requires an intact and functioning auditory portion of the central nervous system as well as a working ear, human deafness (extreme insensitivity to sound) most commonly occurs because of abnormalities of the inner ear, rather than the nerves or tracts of the central auditory system.

Human outer ear and culture

Stretching of the earlobe and various cartilage piercings.

The auricles also have an effect on facial appearance. In Western societies, protruding ears (present in about 5% of ethnic Europeans) have been considered unattractive, particularly if asymmetric. The first surgery to reduce the projection of prominent ears was published in the medical literature in 1881.

The ears have also been ornamented with jewelry for thousands of years, traditionally by piercing of the earlobe. In some cultures, ornaments are placed to stretch and enlarge the earlobes. Tearing of the earlobe from the weight of heavy earrings, or from traumatic pull of an earring (for example by snagging on a sweater), is fairly common. The repair of such a tear is usually not difficult.

A cosmetic surgical procedure to reduce the size or change the shape of the ear is called an otoplasty. In the rare cases wheo pinna is formed (atresia), or is extremely small (microtia) reconstruction of the auricle is possible. Most often, a cartilage graft from another part of the body (generally, rib cartilage) is used to form the matrix of the ear, and skin grafts or rotation flaps are used to provide the covering skin. Recently ears have been grown on a rat’s back and attached to human heads after. However, when babies are born without an auricle on one or both sides, or when the auricle is very tiny, the human ear canal is ordinarily either small or absent, and the middle ear often has deformities. The initial medical intervention is aimed at assessing the baby’s hearing and the condition of the ear canal, as well as the middle and inner ear. Depending on the results of tests, reconstruction of the outer ear is done in stages, with planning for any possible repairs of the rest of the ear.

Middle ear

The middle ear, an air-filled cavity behind the ear drum (tympanic membrane), includes the three ear bones or ossicles: the malleus (or hammer), incus (or anvil), and stapes (or stirrup). The opening of the Eustachian tube is also within the middle ear. The malleus has a long process (the manubrium, or handle) that is attached to the mobile portion of the eardrum. The incus is the bridge between the malleus and stapes. The stapes is the smallest named bone in the human body. The three bones are arranged so that movement of the tympanic membrane causes movement of the malleus, which causes movement of the incus, which causes movement of the stapes. When the stapes footplate pushes on the oval window, it causes movement of fluid within the cochlea (a portion of the inner ear).The ossicles help in amplification of sound waves by nearly six times.

In humans and other land animals the middle ear (like the ear canal) is normally filled with air. Unlike the open ear canal, however, the air of the middle ear is not in direct contact with the atmosphere outside the body. The Eustachian tube connects from the chamber of the middle ear to the back of the nasopharynx. The middle ear is very much like a specialized paranasal sinus, called the tympanic cavity; it, like the paranasal sinuses, is a hollow mucosa-lined cavity in the skull that is ventilated through the nose. The mastoid portion of the human temporal bone, which can be felt as a bump in the skull behind the pinna, also contains air, which is ventilated through the middle ear.Middle Ear

Components of the middle ear

1. Malleus. The malleus or hammer is a hammer-shaped small bone or ossicle of the middle ear which connects with the incus and is attached to the inner surface of the eardrum. The word is Latin for hammer. It transmits the sound vibrations from the eardrum to the incus. The malleus is unique to mammals, and evolved from a lower jaw bone in basal amniotes called the articular, which still forms part of the jaw joint in reptiles and birds. Embryologically it is derived from the first pharyngeal arch along with the rest of the bones of mastication, such as the maxilla and mandible. Sound waves hit the ear drum and, together with the other bones, it tends to transmit the vibrations from the ear drum to the cochlea, and then to the brain, which enables hearing.

Left malleus. A. From behind. B. From within.

The right membrana tympani with the hammer and the chorda tympani, viewed from within, from behind, and from above. (Malleus visible at center.)

Ossicles

Head and neck of a human embryo eighteen weeks old, with Meckel’s cartilage and hyoid bone exposed.

External and middle ear, opened from the front. Right side.

Chain of ossicles and their ligaments, seen from the front in a vertical, transverse section of the tympanum.

CT image of Malleus.

2. Tensor Tympani. The tensor tympani, the larger of the two muscles of the tympanic cavity (the other being the stapedius), is contained in the bony canal above the osseous portion of the auditory tube. Its role is to dampen sounds, such as those produced from chewing.

The medial wall and part of the posterior and anterior walls of the right tympanic cavity, lateral view. (Label for “Tensor tympani muscle” is at right, second from bottom.)

Origin and insertion

It arises from the cartilaginous portion of the auditory tube and the adjoining part of the great wing of the sphenoid, as well as from the osseous canal in which it is contained.

Passing backward through the canal, it ends in a slender tendon which enters the tympanic cavity, makes a sharp bend around the extremity of the septum, known as the processus cochleariformis, and is inserted into the handle (manubrium) of the malleus, near its root.

Function

When tensed, the action of the muscle is to pull the malleus medially, tensing the tympanic membrane, damping vibration in the ear ossicles and thereby reducing the amplitude of sounds. This muscle is contracted primarily to dampen the noise produced by chewing. (Compare to the more general dampening function of the stapedius muscle.)

In many people with hyperacusis, an increased activity develops in the tensor tympani muscle in the middle ear as part of the startle response to some sounds. This lowered reflex threshold for tensor tympani contraction is activated by the perception/anticipation of loud sound, and is called tonic tensor tympani syndrome (TTTS). In some people with hyperacusis, the tensor tympani muscle can contract just by thinking about a loud sound. Following exposure to intolerable sounds, this contraction of the tensor tympani muscle tightens the ear drum, which can lead to the symptoms of ear pain/a fluttering sensation/a sensation of fullness in the ear (in the absence of any middle or inner ear pathology).

Innervation

Innervation of the tensor tympani is from the tensor tympani nerve, a branch of the mandibular division of the trigeminal nerve (cranial nerve V, specifically V3). As the tensor tympani is innervated by motor fibres of the trigeminal nerve, it does not receive fibres from the trigeminal ganglion, which has sensory fibres only.

Voluntary control

Contracting muscles produce vibration and sound. Slow twitch fibers produce 10 to 30 contractions per second (equivalent to 10 to 30 Hz sound frequency). Fast twitch fibers produce 30 to 70 contractions per second (equivalent to 30 to 70 Hz sound frequency). The vibration can be witnessed and felt by highly tensing one’s muscles, as when making a firm fist. The sound can be heard by pressing a highly tensed muscle against the ear, again a firm fist is a good example. The sound is usually described as a rumbling sound. Some individuals can voluntarily produce this rumbling sound by contracting the tensor tympani muscle of the middle ear. The rumbling sound can also be heard when the neck or jaw muscles are highly tensed as when yawning deeply. This phenomenon is known since (at least) 1884.

Insertion of the tensor tympani muscle onto the malleus. . AA’ ( two fibrous collagenic layers); B йpidermis; C mucous membrane; D head of malleus; E uncus; F stapes; G tensor tympani; H lateral process of malleus; I Manubrium of malleus; J stapes muscle.

Base of skull. Inferior surface.

View of the inner wall of the tympanum (enlarged).

Auditory tube, laid open by a cut in its long axis.

3. Incus. The incus or anvil is the anvil-shaped small bone or ossicle in the middle ear. Incus means “anvil” in Latin. It connects the malleus to the stapes. It was first described by Alessandro Achillini of Bologna. The incus transmits sound vibrations from the malleus to the stapes.

Left incus. A. From within. B. From the front.

4. Stapedius. The stapedius is the smallest skeletal muscle in the human body. At just over one millimeter in length, its purpose is to stabilize the smallest bone in the body, the stapes.

Function

It reflexively dampens the vibrations of the stapes by pulling on the neck of that bone. It prevents excess movement by the stapes, helping to control the amplitude of sound waves from the general external environment to the inner ear. The stapedius muscle dampens the ability of the stapes vibration and protects the inner ear from high noise levels, primarily the volume of your own voice. Compare also the role of the tensor tympani muscle, which primarily dampens those sounds associated with chewing.

Innervation

The stapedius is innervated by the nerve to stapedius, a branch of cranial nerve VII, the facial nerve. This is the first branch of the facial nerve after it exits the facial canal; the second branch is the chorda tympani which carries special sense (taste) and parasympathetic fibres of cranial nerve VII. Chorda tympani provides taste sensation to the anterior 2/3 of the tongue by joining with the lingual nerve – a branch of the Mandibular nerve (V3) – in the infratemporal fossa.

Pathology

Paralysis of the stapedius, such as in injury to the facial nerve (CN VII) distal to the geniculate ganglion prior to its branch to stapedius muscle (which would also cause Bell’s Palsy), allows wider oscillation of the stapes, resulting in heightened reaction of the auditory ossicles to sound vibration. This condition, known as hyperacusis, causes normal sounds to be perceived as very loud.

Evolutionary variation

Like the stapes bone to which it attaches, the stapedius muscle shares evolutionary history with other vertebrate structures.

The mammalian stapedius evolved from a muscle called the depressor mandibulae in other tetrapods, the function of which was to open the jaws (this function was taken over by the digastric muscle in mammals). The depressor mandibulae arose from the levator operculi in bony fish, and is equivalent to the epihyoidean in sharks. Like the stapedius, all of these muscles derive from the hyoid arch and are innervated by cranial nerve VII.

The stapedius emerges from a pinpoint foramen in the apex of the pyramidal eminence (a hollow, cone-shaped prominence in the posterior wall of the tympanic cavity), and inserts into the neck of the stapes.

5. Labyrinth

Ear labyrinth.

6. Stapes. he stapes is the stirrup-shaped small bone or ossicle in the middle ear which is attached through the incudostapedial joint to the incus laterally and to the fenestra ovalis, the “oval window”, medially. Stapes means stirrup in Latin. The oval window is adjacent to the vestibule of the inner ear. The stapes is the smallest and lightest bone in the human body. It was described by the professor Giovanni Filippo Ingrassia in 1546 at the University of Naples.

A. Left stapes. B. Base of stapes, medial surface.

Chain of ossicles and their ligaments, seen from the front in a vertical, transverse section of the tympanum.

Function

The stapes transmits the sound vibrations from the incus to the membrane of the inner ear inside the fenestra ovalis. The stapes is also stabilized by the stapedius muscle, which is innervated by the facial nerve.

Evolutionary variation

In non-mammalian tetrapods, the bone homologous to the stapes is usually called the columella; however, in reptiles, either term may be used. In fish, the homologous bone is called the hyomandibular, and is part of the gill arch supporting either the spiracle or the jaw, depending on species.

Development

As the stapes first develops embryologically from the 6th to 8th week of life, it surrounds the stapedial artery, which supplies the majority of the vasculature of the embryonic head. After that period, the external carotid artery is generated and takes over for the stapedial artery, which subsequently involutes, leaving the stapes with a windowframe-like structure.

7. Auditory Canal. The ear canal (external auditory meatus, external acoustic meatus, EAM) (Latin: meatus acusticus externus), is a tube running from the outer ear to the middle ear. The adult human ear canal extends from the pinna to the eardrum and is about 2.5 centimetres (1 in) in length and 0.7 centimetres (0.3 in) in diameter.

Structure

The human ear canal is divided into two parts. The fibrocartilaginous part forms the outer third of the canal, Its anterior and lower wall are cartilaginous, whereas its superior and back wall are fibrous. The cartilage is the continuation of the cartilage framework of pinna. The bony part forms the inner two thirds. The bony part is much shorter in children and is only a ring (annulus tympanicus) in the newborn.

Size and shape of the canal vary among individuals. The canal is approximately 2.5 centimetres (1 in) long and 0.7 centimetres (0.28 in) in diameter. It has a sigmoid form and runs from behind and above downward and forward. On the cross-section, it is of oval shape. These are important factors to consider when fitting earplugs.

Disorders

Due to its relative exposure to the outside world, the ear canal is susceptible to diseases and other disorders. Some disorders include:

Atresia of the ear canal

Otitis externa (swimmer’s ear), bacteria-caused inflammation of the ear canal

Contact dermatitis of the ear canal

Ear fungus

Ear myiasis, an extremely rare infestation of maggots

Bone exposure, caused by the wearing away of skin in the canal

Granuloma, a scar usually caused by tympanostomy tubes

Stenosis, a gradual closing of the canal

Foreign body in ear

Cholesteatoma

Ear mites in animals.

Earwax

Earwax, also known as cerumen, is a yellowish, waxy substance secreted in the ear canals. It plays an important role in the human ear canal, assisting in cleaning and lubrication, and also provides some protection from bacteria, fungi, and insects. Excess or impacted cerumen can press against the eardrum and/or occlude the external auditory canal and impair hearing.

Left infratemporal fossa.

Lateral head anatomy detail.Facial nerve dissection.

8. Tympanic Membrane/(Ear Drum). The eardrum, or tympanic membrane, is a thin, cone-shaped membrane that separates the external ear from the middle ear in humans and other tetrapods. Its function is to transmit sound from the air to the ossicles inside the middle ear, and then to the oval window in the fluid-filled cochlea. Hence, it ultimately converts and amplifies vibration in air to vibration in fluid. The malleus bone bridges the gap between the eardrum and the other ossicles. There are two general regions of the tympanic membrane: the pars flaccida (upper region, see picture on right) and the pars tensa. The pars flaccida consists of two layers, is relatively fragile, and is associated with eustachian tube dysfunction and cholesteatomas. The larger pars tensa region consists of three layers: skin, fibrous tissue, and mucosa. It is comparatively robust, and is the region most commonly associated with perforations. Rupture or perforation of the eardrum can lead to conductive hearing loss. Collapse or retraction of the eardrum can also cause conductive hearing loss or even cholesteatoma.

Right tympanic membrane as seen through a speculum.

Intentional rupture

The Bajau people of the Pacific intentionally rupture their eardrums at an early age in order to facilitate diving and hunting at sea. Many older Bajau therefore have difficulties hearing During World War II, the German Luftwaffe was known to pierce the ear drums of fighter pilots in order to prevent air pressure issues, and even inserted grommets in the membrane to prevent the hole from healing up. Pilots involved often suffered from chronic hearing loss later in life.

Unintentional rupture

Unintentional rupture of the ear drum has been described in blast injuries during conflict, but also during air travel, usually when the congestion of an upper respiratory infection has prevented equalization of pressure in the middle ear. It is also described in sport and recreation, such as swimming, diving with a poor entry into the water, scuba diving and martial arts. In the published literature, 80% to 95% have recovered completely without intervention in two to four weeks. These injuries, even in a recreational or athletic setting, are blast injuries. Many will experience some short-lived hearing loss and ringing in the ear (tinnitus) but can be reassured that this, in all likelehood, will pass. A very few will experience temporary disequilibrium (vertigo). There may be some bleeding from the ear canal if the eardrum has been ruptured. Naturally, the foregoing reassurances become more guarded as the force of injury increases, as in military or combat situations.

Auditory tube, laid open by a cut in its long axis.

Chain of ossicles and their ligaments, seen from the front in a vertical, transverse section of the tympanum.

Right tympanic membrane as seen through a speculum.

9. Eustachian Tube. The Eustachian tube /juːˌsteɪ.ʃənˈtjuːb/, also auditory tube or pharyngotympanic tube, is a tube that links the nasopharynx to the middle ear. It is a part of the middle ear. In adult humans the Eustachian tube is approximately 35 mm (1.4 in) long. It is named after the sixteenth-century anatomist Bartolomeo Eustachi. Some modern medical books call this the pharyngotympanic tube.

Anatomy

The Eustachian tube extends from the anterior wall of the middle ear to the lateral wall of the nasopharynx, approximately at the level of the inferior nasal concha. A portion of the tube (~1/3) proximal to the middle ear is made of bone; the rest is composed of cartilage and raises a tubal elevation, the torus tubarius, in the nasopharynx where it opens.

In the equids (horses) and some rodent-like species such as the desert hyrax, an evagination of the eustachian tube is known as the guttural pouch and is divided into medial and lateral compartments by the stylohyoid bone of the hyoid apparatus. This is of great importance in equine medicine as the pouches are prone to infections, and, due to their intimate relationship to the cranial nerves (VII, IX, X, XI) and the internal and external carotid artery, various syndromes may arise relating to which is damaged. Epistaxis (nosebleed) is a very common presentation to veterinary surgeons and this may often be fatal unless a balloon catheter can be placed in time to suppress bleeding.

Embryologic development

The Eustachian tube is derived from the first pharyngeal pouch, which during embryogenesis forms the tubotympanic recess. The distal part of the tubotympanic sulcus gives rise to the tympanic cavity, while the proximal tubular structure becomes the Eustachian tube.

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Muscles

There are four muscles associated with the function of the Eustachian tube:

1. Levator veli palatini (innervated by the vagus nerve)

2. Salpingopharyngeus (innervated by the vagus nerve)

3. Tensor tympani (innervated by the mandibular nerve of CN V)

4. Tensor veli palatini (innervated by the mandibular nerve of CN V)

Functions

Pressure equalization

Under normal circumstances, the human Eustachian tube is closed, but it can open to let a small amount of air through to prevent damage by equalizing pressure between the middle ear and the atmosphere. Pressure differences cause temporary conductive hearing loss by decreased motion of the tympanic membrane and ossicles of the ear. Various methods of ear clearing such as yawning, swallowing, or chewing gum, may be used intentionally to open the tube and equalize pressures. When this happens, humans hear a small popping sound, an event familiar to aircraft passengers, scuba divers, or drivers in mountainous regions. Devices assisting in pressure equalization include an ad hoc balloon applied to the nose, creating inflation by positive air pressure. Some people learn to voluntarily ‘click’ their ears, together or separately, which is a noise emitted and its sound heard internally, when deliberating doing a pressure equalizing routine by opening their Eustachian tubes, where pressure changes are experienced (as in ascending/descending in aircraft flight, mountain driving, elevator lift/drops, etc.), whether anticipated or unexpected. Some even are able to deliberately keep their Eustachian tubes open for a brief period, and even increase or decrease air pressure in the middle ear. The ‘clicking your ears’ can actually be heard audibly if one puts one’s ear to another person’s ear for them to hear the clicking sound. Those that are borderline on learning this voluntary control first discover this via yawning or swallowing or other means (above); which later on discover can be done deliberately without force even when there are no pressure issues involved, by ‘clicking one’s ears’ (Can you ‘click your ears’ to equalize air pressure in your inner ear?). When the Eustachian Tubes are deliberately held open voluntarily, one’s voice sounds louder in one’s head than when they are closed.

Mucus drainage

The Eustachian tube also drains mucus from the middle ear. Upper respiratory tract infections or allergies can cause the Eustachian tube, or the membranes surrounding its opening to become swollen, trapping fluid, which serves as a growth medium for bacteria, causing ear infections. This swelling can be reduced through the use of systemic pseudoephedrine or topical oxymetazoline.[citatioeeded] Ear infections are more common in children because the tube is horizontal and shorter, making bacterial entry easier, and it also has a smaller diameter, making the movement of fluid more difficult. In addition, children’s developing immune systems and poor hygiene habits make them more prone to upper respiratory infections.

Disorders

Otitis media, or inflammation of the middle ear, commonly affects the Eustachian tube. Children under 7 are more susceptible to this condition because the Eustachian tube is shorter and at more of a horizontal angle than in the adult ear.

Barotitis, a form of barotrauma, may occur when there is a substantial difference in air or water pressure between the outer inner and the inner ear, for example in a rapid ascent while scuba diving, or a sudden decompression of an aircraft at high altitude.

Some people are born with a dysfunctional Eustachian tube, which is much slimmer than the usual human Eustachian tube. This may be genetic, but it has also been suggested to be a condition in which the patient did not fully recover from the effects of pressure on the middle ear during birth (retained birth compression). This disorder may result in a large amount of mucus accumulating in the middle ear, often impairing hearing to a degree. This condition is known as otitis media with effusion, and may result in the mucus becoming very thick and glue-like, a condition known as glue ear.

A patulous Eustachian tube is a rare condition, in which the Eustachian tube remains intermittently open, causing an echoing sound of the person’s own heartbeat, breathing, and speech. This may be temporarily relieved by moving into a position where the head is upside down.

Smoking can also cause damage to the cilia that protect the Eustachian tube from mucus, which can result in the clogging of the tube and a buildup of bacteria in the ear, leading to a middle ear infection in some cases.

Eustachian tube dysfunction can be caused by recurring and chronic cases of sinus infection. This results from excessive mucus production which causes obstruction to the openings of the Eustachian tubes.

5. Tympanic cavity. The tympanic cavity is a small cavity surrounding the bones of the middle ear. It is formed from the tubotympanic recess, an expansion of the first pharyngeal pouch. On its lateral surface, it abuts the external auditory meatus from which it is separated by the tympanic membrane (eardrum).

Clinical significance

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 small bore needle (tympanocentesis).

Inner ear: cochlea, vestibule, and semicircular canals

1. Posterior Canal

2. Superior Canal

3. Utricle

4. Horizontal

5. Canal

6. Vestibule

7. Cochlea

8. Saccule

The inner ear includes both the organ of hearing (the cochlea) and a sense organ that is attuned to the effects of both gravity and motion (labyrinth or vestibular apparatus). The balance portion of the inner ear consists of three semicircular canals and the vestibule. The inner ear is encased in the hardest bone of the body. Within this ivory hard bone, there are fluid-filled hollows. Within the cochlea are three fluid filled spaces: the scala tympani, the scala vestibuli and the scala media. The eighth cranial nerve comes from the brain stem to enter the inner ear. When sound strikes the ear drum, the movement is transferred to the footplate of the stapes, which presses it into one of its fluid-filled ducts through the oval window of cochlea . The fluid inside this duct is moved, flowing against the receptor cells of the Organ of Corti, which fire. These stimulate the spiral ganglion, which sends information through the auditory portion of the eighth cranial nerve to the brain.The semicircular canals help in both dynamic and static balance. The three semicircular canals and ampulla (with otolith) help in dynamic balance, while utricullus and sacullus help in static balance.

Hair cells are also receptor cells involved in balance, although the hair cells of the auditory and vestibular systems of the ear are not identical. Vestibular hair cells are stimulated by the movement of fluid in the semicircular canals and the utricle and saccule. Firing of vestibular hair cells stimulates the vestibular portion of the eighth cranial nerve.

Damage to the human ear

Outer ear trauma

Auricle

The auricle can be easily damaged. Because it is skin-covered cartilage, with only a thin padding of connective tissue, rough handling of the ear can cause enough swelling to jeopardize the blood-supply to its framework, the auricular cartilage. That entire cartilage framework is fed by a thin covering membrane called the perichondrium (meaning literally: around the cartilage). Any fluid from swelling or blood from injury that collects between the perichondrium and the underlying cartilage puts the cartilage in danger of being separated from its supply of nutrients. If portions of the cartilage starve and die, the ear never heals back into its normal shape. Instead, the cartilage becomes lumpy and distorted, a phenomenon called wrestler’s ear (because wrestling is one of the most common ways such an injury occurs) or Cauliflower ear.

The lobule of the ear (ear lobe) is the one part of the human auricle that normally contains no cartilage. Instead, it is a wedge of adipose tissue (fat) covered by skin. There are many normal variations to the shape of the ear lobe, which may be small or large. Tears of the earlobe can be generally repaired with good results. Since there is no cartilage, there is not the risk of deformity from a blood clot or pressure injury to the ear lobe.

Other injuries to the external ear occur fairly frequently, and can leave a major deformity. Some of the more common ones include, laceration from glass, knives, and bite injuries, avulsion injuries, cancer, frostbite, and burns.

Ear canal

Ear canal injuries can come from firecrackers and other explosives, and mechanical trauma from placement of foreign bodies into the ear. The ear canal is most often self-traumatized from efforts at ear cleaning. The outer part of the ear canal rests on the flesh of the head; the inner part rests in the opening of the bony skull (called the external auditory meatus). The skin is very different on each part. The outer skin is thick, and contains glands as well as hair follicles. The glands make cerumen (also called ear wax). The skin of the outer part moves a bit if the pinna is pulled; it is only loosely applied to the underlying tissues. The skin of the bony canal, on the other hand, is not only among the most delicate skin in the human body, it is tightly applied to the underlying bone. A slender object used to blindly clean cerumen out of the ear often results instead with the wax being pushed in, and contact with the thin skin of the bony canal is likely to lead to laceration and bleeding.

Human ear (from Descent of Man)

It has long been known that humans, and indeed primates such as the orangutan and chimpanzee have ear muscles that are minimally developed and non-functional, yet still large enough to be easily identifiable. These undeveloped muscles are vestigial structures. An ear muscle that cannot move the ear, for whatever reason, cao longer be said to have any biological function. This serves as evidence of homology between related species. In humans there is variability in these muscles, such that some people are able to move their ears in various directions, and it has been said that it may be possible for others to gain such movement by repeated trials. In such primates the inability to move the ear is compensated mainly by the ability to turn the head on a horizontal plane, an ability which is not common to most monkeys—a function once provided by one structure is now replaced by another.

The outer structure of the ear also shows some vestigial features, such as the node or point on the helix of the ear known as Darwin’s tubercle which is found in around 10% of the population, this feature is labelled (a) in the accompanying figure.

VIDEO

The Anatomy of the Human Ear

Diseases of the Human Ear

Damage to the human ear

Outer ear trauma.

called the perichondrium (meaning literally: around the cartilage).

Any fluid from swelling or blood from injury that collects between the perichondrium and the underlying cartilage puts the cartilage in danger of being separated from its supply of nutrients. If portions of the cartilage starve and die, the ear never heals back into its normal shape. Instead, the cartilage becomes lumpy and distorted. Wrestler’s Ear is one term used to describe the result, because wrestling is one of the most common ways such an injury occurs.

Cauliflower ear is another name for the same condition, because the thickened auricle can resemble that vegetable.

Picture of cauliflower ear.

Middle ear trauma

Like outer ear trauma, middle ear trauma most often comes from blast injuries and insertion of foreign objects into the ear. Skull fractures that go through the part of the skull containing the ear structures (the temporal bone) can also cause damage to the middle ear. Small perforations of the tympanic membrane usually heal on their own, but large perforations may require grafting. Displacement of the ossicles will cause a conductive hearing loss that can only be corrected with surgery. Forcible displacement of the stapes into the inner ear can cause a sensory neural hearing loss that cannot be corrected even if the ossicles are put back into proper position. Because human skin has a top waterproof layer of dead skin cells that are constantly shedding, displacement of portions of the tympanic membrane or ear canal into the middle ear or deeper areas by trauma can be particularly traumatic. If the displaced skin lives within a closed area, the shed surface builds up over months and years and forms a cholesteatoma.

Inner ear trauma

There are two principal damage mechanisms to the inner ear in industrialized society, and both injure hair cells. The first is exposure to elevated sound levels (noise trauma), and the second is exposure to drugs and other substances (ototoxicity).

In 1972 the U.S. EPA told Congress that at least 34 million people were exposed to sound levels on a daily basis that are likely to lead to significant hearing loss. The worldwide implication for industrialized countries would place this exposed population in the hundreds of millions.

Ear Diseases

Ear disease causes significant discomfort and hearing loss. It also creates work loss and decreased productivity– this increases as the persons communicative skills decrease when associated hearing loss increases. In children, developmental delays and academic failure may result. Complications such as deafness, meningitis, brain abscesses, and facial nerve paralysis may also occur. Proper management of ear disease is critica.

Otitis Media

The basic underlying problem causing most forms of otitis is Eustachian tube dysfunction. Most otitis occurs in patients whose Eustachian tube, the tube between the nose and the middle ear (the area behind the eardrum), does not work properly. When air cannot adequately get through this tube to the middle ear, the negative pressure created can “suck” fluid out of the lining of the middle ear/mastoid, filling the middle ear and mastoid air cells with fluid. A mild hearing loss usually accompanies the fluid. The hearing loss disappears when the fluid is gone as long as there are no other causes for the hearing loss. Three kinds of otitis can result from Eustachian tube dysfunction. They are serous and secretory otitis, where fluid fills the middle ear and mastoid, acute otitis, where pus fills the middle ear and mastoid but its presence is of short duration, and chronic otitis, where pus fills the middle ear and mastoid and it has been present for months or years. Chronic otitis is associated with infection of the bone itself and thickening and polyp formation of the mucosal lining of the middle ear and mastoid. The highest incidence of otitis media occurs in preschool children and decreases gradually after age 6. The highest incidence occurs poor children, children in day care, and Native Americans. Additional factors that cause or aggravate otitis include the presence of enlarged adenoid tissue, lack of proper muscle in the back of the throat (as in those with a cleft palate), allergy, immune deficiencies, sudden change in atmospheric pressure (like poor pressurization in an airplane dropping from a high altitude), scarring or tumors in the nasopharynx, and abnormal cell function of the mucosa of the ear and nose. Diabetes does not increase the incidence of otitis, but can make it much more difficult to treat.

Serous otitis, where fairly clear fluid fills the middle ear and mastoid, occurs with fairly sudden obstruction of the Eustachian tube. A sudden descent of an airplane with poor pressurization or a bad cold are two of the most common causes of acute serous otitis media. Usually decongestants will clear the fluid or even blood that can be sucked from the mucosa into the middle ear with wither of these processes. If the fluid does not clear within a few weeks, it is considered chronic serous otitis. Older people with poorly functioning Eustachian tubes commonly have recurrent serous otitis and may require intermittent tube placement over many years. Hearing loss is present depending on the amount of fluid in the ear. The hearing loss usually resolves when the fluid is cleared out of the ear, either medically or surgically.

Secretory otitis, where somewhat thicker fluid fills the middle ear and mastoid, is common in small children and is often “outgrown” by the time they reach their teens. It is the most common disease process requiring the placement of PE tubes. This thicker fluid has components that are actually “secreted” by the mucous glands of the middle ear. There are actually tissue breakdown enzymes in this fluid; that, if left untreated, can gradually eat away bone and cause chronic hearing loss/damage. Luckily, it generally takes quite a while for these enzymes to cause damage to the ear, so treating secretory otitis in children with medication for a few weeks or months is safe. Leaving this kind of fluid in an ear for more than several months, however, places the ear tissues (including the tiny ear bones) at risk of damage or destruction by these enzymes. Not treating infections with antibiotics at all places the ear structure at even higher risk of permanent damage/destruction by the fluid.

Acute otitis media occurs when pus fills the middle ear. It is usually sudden in onset and is often associated with sudden obstruction of the eustacian tube at the same time infections bacteria are present to cause the acute otitis. Without antibiotic treatment, a true bacterial acute otitis is often associated with sudden perforation of the eardrum, with profuse drainage from the ear. Often the eardrum will spontaneously heal over after the infection has resolved, but a perforation can be left and damage to the middle ear and/or the inner ear can accompany the infection. The eardrum may be bright red or the creamy color of the fluid can sometimes be seen through the eardrum. It sometimes looks “soggy.” Pain and fever may accompany an ear infection, but usually disappear rapidly if the eardrum perforates. Pain and fever are rarely present if there is a hole (perforation) in the eardrum before the infection starts. The standard treatment of acute otitis media is oral antibiotics. Ear drops are added if the eardrum perforates. IV antibiotics are indicated for severe infections, if the mastoid bone is also infected, or if the facial nerve becomes paralyzed as a “complication” of the acute infections. Hearing loss is present but usually goes away when the infection clears.

Chronic otitis media occurs when chronic infection fills the middle ear space and mastoid cavity. True chronic otitis media is almost always a form of chronic mastoiditis, where the bone of the mastoid cavity (the honeycombed bone behind the ear) is chronically infected along with the tissues of the middle ear space. It is important to realize that antibiotics alone usually cannot remove infection from the bone; surgical removal of the infected bone is usually necessary to accomplish this. Even IV antibiotics do not often eradicate a true bone infection, especially in the mastoid, which has its connection to the bacteria-filled nose through the eustacian tube. A cholesteatoma is a common additional finding along with chronic otitis and mastoiditis. A cholesteatoma is a skin sac that grows back into the middle ear or mastoid from the eardrum, creating a mass of skin and debris that keeps getting larger and larger over time, destroying anything in its path. The ear bones, the inner ear, the facial nerve (the nerve that makes all the muscles of one side of your face work), and the braiext to the ear can all be damaged or destroyed by either spreading infection or cholesteatoma. These diseases must be removed fore the safety of the ear, the head, and the brain. Infection or cholesteatoma involving the inner ear, facial nerve, or the brain requires immediate attention by an ear surgeon and often required immediate surgery.

Hearing loss usually accompanies chronic otitis and cholesteatoma. There is usually a considerable conductive hearing loss and there may be sensorineural hearing loss as well. The longer the ear is infected, the more likely it is that toxins from the infection seep into the inner ear, causing sensorineural hearing loss. Sensorineural hearing loss resulting from infection is generally permanent and can rarely be reversed. Repair of the conductive hearing loss should only be attempted after the infection and/or cholesteatoma is controlled. Sometimes ear surgery has to be done in “stages” because of this fact.

Cholesteatoma

Cholesteatoma is skin cells that grow in the wrong places in the middle ear and mastoid. Less commonly, it can invade the inner ear, brain, or any other structure of the ear area/brain. As the skin mass expands, it can destroy anything in its path. Infection often accompanies a cholesteatoma. The ossicles (ear bones) are often destroyed by even the smallest cholesteatoma. These masses are not cancerous but must be removed to prevent the ear from being severely damaged.

Otosclerosis

Otosclerosis is a kind of ear disease in which the otic capsule, the hard and “different” bone that is present only around the inner ear, is replaced in patches by soft bone at random locations around the inner ear. When this soft bone starts growing at the edge of the stapes footplate, the stapes bone cannot move like it should and sound is not passed properly from the middle ear to the inner ear, creating a conductive hearing loss. This is often repairable. When otosclerotic bone replaces bone in other parts of the otic capsule, a sensorineural hearing loss can result. The nerve hearing loss cannot be repaired surgically.

Meniиre’s Disease

Meniиre’s disease is caused by an imbalance in the fluid in the sacs in the inner ear. When the sacs of the endolymphatic system of the inner balloon within the inner ear, a sudden hearing loss, vertigo, ringing (tinnitus), and/or pressure in the ear occur. This disease is episodic (by definition) and erratic in its progression. If left to its natural course, it may progress to total deafness in the affected ear. At that point, the episodes of vertigo and the tinnitus may spontaneously subside.

Acoustic Neuroma

An acoustic neuroma is a benign tumor of the balance nerve between the inner ear and the brain. It grows very slowly. It can cause vertigo (dizziness), hearing loss, and loss of function of the facial nerve. It causes its damage by local enlargement with destruction of the structures it presses against. It is especially noted for creating a loss in understanding ability (discrimination) of the ear that is significantly worse than the actual hearing loss. When hearing loss is not equal between the two ears (unless there is a known reason for this), an acoustic neuroma should be suspected. An MRI scan enhanced with gadolinium is the test most often used to diagnose an acoustic neuroma. If diagnosed when tiny, it may be observed or removed surgically depending on its size at the time of diagnosis and the age of the patient. Larger tumors should generally be removed surgically. This is generally done by a neurotologist with or without the assistance of a neurosurgeon.

Otitis externa

Otitis externa (also known as “External otitis” and “Swimmer’s ear”) is an inflammation of the outer ear and ear canal. Along with otitis media, external otitis is one of the two human conditions commonly called “earache”. It also occurs in many other species. Inflammation of the skin of the ear canal is the essence of this disorder. The inflammation can be secondary to dermatitis (eczema) only, with no microbial infection, or it can be caused by active bacterial or fungal infection. In either case, but more often with infection, the ear canal skin swells and may become painful or tender to touch.

Classification

In contrast to the chronic otitis externa, acute otitis externa is predominantly a microbial infection, occurs rather suddenly, rapidly worsens, and becomes very painful and alarming. The ear canal has an abundant nerve supply, so the pain is often severe enough to interfere with sleep. Wax in the ear can combine with the swelling of the canal skin and any associated pus to block the canal and dampen hearing to varying degrees, creating a temporary conductive hearing loss. In more severe or untreated cases, the infection can spread to the soft tissues of the face that surround the adjacent parotid gland and the jaw joint, making chewing painful. In its mildest forms, external otitis is so common that some ear nose and throat physicians have suggested that most people will have at least a brief episode at some point in life. While a small percentage of people seem to have an innate tendency toward chronic external otitis, most people can avoid external otitis altogether once they understand the intricate mechanisms of the disease.

The skin of the bony ear canal is unique, in that it is not movable but is closely attached to the bone, and it is almost paper thin. For these reasons it is easily abraded or torn by even minimal physical force. Inflammation of the ear canal skin typically begins with a physical insult, most often from injury caused by attempts at self-cleaning or scratching with cotton swabs, pen caps, finger nails, hair pins, keys, or other small implements. Another causative factor for acute infection is prolonged water exposure in the forms of swimming or exposure to extreme humidity, which can compromise the protective barrier function of the canal skin, allowing bacteria to flourish; hence the name “swimmer’s ear”.

Signs and symptoms

Pain is the predominant complaint and the only symptom directly related to the severity of acute external otitis. Unlike other forms of ear infections, the pain of acute external otitis is worsened when the outer ear is touched or pulled gently. Pushing the tragus, the tablike portion of the auricle that projects out just in front of the ear canal opening, so typically causes pain in this condition as to be diagnostic of external otitis on physical examination. Patients may also experience ear discharge and itchiness. When enough swelling and discharge in the ear canal is present to block the opening, external otitis may cause temporary conductive hearing loss.

Due to the fact that the ear and throat are often interconnected, irritation (whether it be in inflammation or a scratching sensation) is normal. However, excessive throat symptoms may likely point to the throat as the cause of the pain in the ear rather than the other way around.

Because the symptoms of external otitis lead many people to attempt to clean out the ear canal (or scratch it) with slim implements, self-cleaning attempts generally lead to additional trauma of the injured skin, so rapid worsening of the condition often occurs.

Causes

Swimming in polluted water is a common way to contract swimmer’s ear, but it is also possible to contract swimmer’s ear from water trapped in the ear canal after a shower, especially in a humid climate. Constriction of the ear canal from bone growth (Surfer’s ear) can trap debris leading to infection. Saturation divers have reported Otitis externa during occupational exposure. Even without exposure to water, the use of objects such as cotton swabs or other small objects to clear the ear canal is enough to cause breaks in the skin, and allow the condition to develop. Once the skin of the ear canal is inflamed, external otitis can be drastically enhanced by either scratching the ear canal with an object, or by allowing water to remain in the ear canal for any prolonged length of time.

The two factors that are required for external otitis to develop are (1) the presence of germs that can infect the skin and (2) impairments in the integrity of the skin of the ear canal that allow infection to occur. If the skin is healthy and uninjured, only exposure to a high concentration of pathogens, such as submersion in a pond contaminated by sewage, is likely to set off an episode. However, if there are chronic skin conditions that affect the ear canal skin, such as atopic dermatitis, seborrheic dermatitis, psoriasis or abnormalities of keratin production, or if there has been a break in the skin from trauma, even the normal bacteria found in the ear canal may cause infection and full-blown symptoms of external otitis.

Fungal ear canal infections, also known as otomycosis, range from inconsequential to extremely severe. Fungus can be saprophytic, in which there are no symptoms and the fungus simply co-exists in the ear canal in a harmless parasitic relationship with the host, in which case the only physical finding is presence of the fungus. If for any reason the fungus begins active reproduction, the ear canal can fill with dense fungal debris, causing pressure and ever-increasing pain that is unrelenting until the fungus is removed from the canal and anti-fungal medication is used. Most antibacterial ear drops also contain a steroid to hasten resolution of canal edema and pain. Unfortunately such drops make fungal infection worse. Prolonged use of them promotes growth of fungus in the ear canal. Antibacterial ear drops should be used a maximum of one week, but 5 days is usually enough. Otomycosis responds more than 95% of the time to a three day course of the same over-the-counter anti-fungal solutions used for athlete’s foot.

Pathogens

The majority of cases are due to Pseudomonas aeruginosa, followed by a great number of other gram-positive and gram-negative species. Candida albicans and Aspergillus species are the most common fungal pathogens responsible for the condition.

Diagnosis

When the ear is inspected, the canal appears red and swollen in well-developed cases. The ear canal may also appear eczema-like, with scaly shedding of skin. Touching or moving the outer ear increases the pain, and this maneuvre on physical exam is important in establishing the clinical diagnosis. It may be difficult to see the eardrum with an otoscope at the initial examination because of narrowing of the ear canal from inflammation and the presence of drainage and debris. Sometimes the diagnosis of external otitis is presumptive and return visits are required to fully examine the ear. Culture of the drainage may identify the bacteria or fungus causing infection, but is not part of the routine diagnostic evaluation. In severe cases of external otitis, there may be swelling of the lymph node(s) directly beneath the ear.

The diagnosis may be missed in most early cases because the examination of the ear, with the exception of pain with manipulation, is nearly normal. In some early cases, the most striking visual finding is the lack of cerumen. As a moderate or severe case of external otitis resolves, weeks may be required before the ear canal again shows a normal amount of cerumen.

Prevention

The strategies for preventing acute external otitis are similar to those for treatment.

Avoid inserting anything into the ear canal: use of cotton buds or swabs is the most common event leading to acute otitis externa.

Most normal ear canals have a self-cleaning and self-drying mechanism, the latter by simple evaporation.

After prolonged swimming, a person prone to external otitis can dry the ears using a small battery-powered ear dryer, available at many retailers, especially shops catering to watersports enthusiasts. Alternatively, drops containing dilute acetic acid (vinegar diluted 3:1) or Burow’s solution may be used. It is especially important NOT to instrument ears when the skin is saturated with water, as it is very susceptible to injury, which can lead to external otitis.

Avoid swimming in polluted water.

Avoid washing hair or swimming if very mild symptoms of acute external otitis begin

Although the use of earplugs when swimming and shampooing hair may help prevent external otitis, there are important details in the use of plugs. Hard and poorly fitting ear plugs can scratch the ear canal skin and set off an episode. When earplugs are used during an acute episode, either disposable plugs are recommended, or used plugs must be cleaned and dried properly to avoid contaminating the healing ear canal with infected discharge.

Treatment

The goal of treatment is to cure the infection and to return the ear canal skin to a healthy condition. When external otitis is very mild, in its initial stages, simply refraining from swimming or washing hair for a few days, and keeping all implements out of the ear, usually results in resolution. External otitis is often a self-limiting condition. However, if the infection is moderate to severe, or if the climate is humid enough that the skin of the ear remains moist, spontaneous improvement may not occur.

Effective solutions for the ear canal include acidifying and drying agents, used either singly or in combination. When the ear canal skin is inflamed from the acute otitis externa, the use of dilute acetic acid may be painful.

Burow’s solution is a very effective remedy against both bacterial and fungal external otitis. This is a buffered mixture of aluminium sulfate and acetic acid, and is available without prescription in the United States.

Topical solutions or suspensions in the form of ear drops are the mainstays of treatment for external otitis. Some contain antibiotics, either antibacterial or antifungal, and others are simply designed to mildly acidify the ear canal environment to discourage bacterial growth. Some prescription drops also contain anti-inflammatory steroids, which help to resolve swelling and itching. Although there is evidence that steroids are effective at reducing the length of treatment time required, fungal otitis externa (also called otomycosis) may be caused or aggravated by overly prolonged use of steroid-containing drops. In addition to topical antibiotics, oral anti-pseudomonal antibiotics can be used in case of severe soft tissue swelling extending into the face and neck and may hasten recovery.

Removal of debris (wax, shed skin, and pus) from the ear canal promotes direct contact of the prescribed medication with the infected skin and shortens recovery time. When canal swelling has progressed to the point where the ear canal is blocked, topical drops may not penetrate far enough into the ear canal to be effective. The physician may need to carefully insert a wick of cotton or other commercially available, pre-fashioned, absorbent material called an ear wick and then saturate that with the medication. The wick is kept saturated with medication until the canal opens enough that the drops will penetrate the canal without it. Removal of the wick does not require a health professional. Antibiotic ear drops should be dosed in a quantity that allows coating of most of the ear canal and used for no more than 4 to 7 days. The ear should be left open. Do note that it is imperative that there is visualization of an intact tympanic membrane (eardrum). Use of certain medications with a ruptured tympanic membrane can cause tinnitus, vertigo, dizziness and hearing loss in some cases.

Although the acute external otitis generally resolves in a few days with topical washes and antibiotics, complete return of hearing and cerumen gland function may take a few more days. Once healed completely, the ear canal is again self-cleaning. Until it recovers fully, it may be more prone to repeat infection from further physical or chemical insult.

Effective medications include ear drops containing antibiotics to fight infection, and corticosteroids to reduce itching and inflammation. In painful cases a topical solution of antibiotics such as aminoglycoside, polymyxin or fluoroquinolone is usually prescribed. Antifungal solutions are used in the case of fungal infections. External otitis is almost always predominantly bacterial or predominantly fungal, so that only one type of medication is necessary and indicated.

Prognosis

Otitis externa responds well to treatment, but complications may occur if it is not treated. Individuals with underlying diabetes or disorders of the immune system are more likely to develop complications, including malignant otitis externa. In these individuals, rapid examination by an otolaryngologist (ear, nose, and throat physician) is very important.

· Chronic otitis externa

· Spread of infection to other areas of the body

· Necrotizing external otitis

Necrotizing external otitis

Necrotizing external otitis (malignant otitis externa) is an uncommon form of external otitis that occurs mainly in elderly diabetics, being somewhat more likely and more severe when the diabetes is poorly controlled. Even less commonly, it can develop due to a severely compromised immune system. Beginning as infection of the external ear canal, there is extension of infection into the bony ear canal and the soft tissues deep to the bony canal. The hallmark of malignant otitis externa (MOE) is unrelenting pain that interferes with sleep and persists even after swelling of the external ear canal may have resolved with topical antibiotic treatment.

Natural history

MOE follows a much more chronic and indolent course than ordinary acute otitis externa. There may be granulation involving the floor of the external ear canal, most often at the bony-cartilaginous junction. Paradoxically, the physical findings of MOE, at least in its early stages, are often much less dramatic than those of ordinary acute otitis externa. In later stages there can be soft tissue swelling around the ear, even in the absence of significant canal swelling. While fever and leukocytosis might be expected in response to bacterial infection invading the skull region, MOE does not cause fever or elevation of white blood count.

Treatment of MOE

Unlike ordinary otitis externa, MOE requires oral or intravenous antibiotics for cure. Diabetes control is also an essential part of treatment. When MOE goes unrecognized and untreated, the infection continues to smolder and over weeks or months can spread deeper into the head and involve the bones of the skull base, constituting skull base osteomyelitis (SBO). The infecting organism is almost always pseudomonas aeruginosa, but it can instead be fungal (aspergillus or mucor). MOE and SBO are not amenable to surgery, but exploratory surgery may facilitate culture of unusual organism(s) that are not responding to empirically used anti-pseudomonal antibiotics (ciprofloxacin being the drug of choice). The usual surgical finding is diffuse cellulitis without localized abscess formation. SBO can extend into the petrous apex of the temporal bone or more inferiorly into the opposite side of the skull base.

Complications

As the skull base is progressively involved, the adjacent exiting cranial nerves and their branches, especially the facial nerve and the vagus nerve, may be affected, resulting in facial paralysis and hoarseness, respectively. If both of the recurrent laryngeal nerves are paralyzed, shortness of breath may develop and necessitate tracheotomy. Profound deafness can occur, usually later in the disease course due to relative resistance of the inner ear structures. Gallium scans are sometimes used to document the extent of the infection but are not essential to disease management. Skull base osteomyelitis is a chronic disease that can require months of IV antibiotic treatment, tends to recur, and has a significant mortality rate.

Epidemiology

The incidence of otitis externa is high. In the Netherlands, it has been estimated at 12–14 per 1000 population per year, and has been shown to affect more than 1% of a sample of the population in the United Kingdom over a 12 month period.

Otitis interna

Otitis interna (Internal otitis) is an inflammation of the inner ear and is usually considered synonymous with labyrinthitis.

Labyrinthitis is an inflammation of the inner ear that typically results in severe vertigo lasting for one or more days. Its cause is rarely identified, but it is thought most commonly to derive from a viral inflammation of the vestibular labyrinth (the part of the inner ear responsible for balance). Patients usually present with the sudden onset of severe whirling vertigo, nausea, and vomiting. The symptoms can be so severe and disabling that patients frequently go to the emergency room for care and require vestibular suppressants such as diazepam or meclozine in order to tolerate the vertigo. Symptoms typically subside over a few days, but may leave the patient with vague imbalance which slowly improves over weeks to months. Hearing loss rarely accompanies the vertigo in labyrinthitis. Occasionally a bacterial infection of the middle ear can spread to the inner ear and cause this disease. In this situation antibiotic treatment may be helpful.

Labyrinthitis is an ailment of the inner ear and a form of unilateral vestibular dysfunction. It derives its name from the labyrinths that house the vestibular system, which senses changes in head position. Labyrinthitis can cause balance disorders, vertigo, hearing loss and tinnitus.

Labyrinthitis is usually caused by a virus, but it can also arise from bacterial infection, head injury, extreme stress, an allergy or as a reaction to medication. Both bacterial and viral labyrinthitis can cause permanent hearing loss.

Labyrinthitis often follows an upper respiratory tract infection (URI).

Symptoms

A prominent and debilitating symptom of labyrinthitis is severe vertigo. The vestibular system is a set of sensory inputs consisting of three semicircular canals, sensing changes in rotational motion, and the otoliths, sensing changes in linear motion. The brain combines visual cues with sensory input from the vestibular system to determine adjustments required to retain balance. The vestibular system also relays information on head movement to the eye muscle, forming the vestibulo-ocular reflex to retain continuous visual focus during motion. When the vestibular system is affected by labyrinthitis, rapid and undesired eye motion (nystagmus) often results from the improper indication of rotational motion. Nausea, anxiety, and a general ill feeling are common due to the distorted balance signals that the brain receives from the inner ear.

This can also be brought on by pressure changes such as those experienced while flying or scuba diving.

Recovery

Recovery from acute labyrinthine inflammation generally takes from one to six weeks, but it is not uncommon for residual symptoms (dysequilibrium and/or dizziness) to last for many months or even years if permanent damage occurs.

Recovery from a permanently damaged inner ear typically follows three phases:

· An acute period, which may include severe vertigo and vomiting

· approximately two weeks of sub-acute symptoms and rapid recovery

· chronic compensation, which may last for months or years.

A damaged balance system has little ability to repair itself. The body recovers from the injury by having the part of the brain that controls balance re-calibrate itself to compensate for the unmatched signals being sent from the damaged and well ears. This compensation process occurs naturally in most people, but some patients require vestibular rehabilitation therapy (VRT).

Acute (Immediate) Compensation

When a sudden injury occurs to one side of the balance system, the patient may feel very sick for hours to a few days with a spinning feeling, unsteadiness, lightheadedness, and often sweating, nausea, and vomiting. This is because the signals being sent from the two balance organs are no longer equal and opposite, and the brain interprets the difference as constant movement. Researchers theorize that after this initial period the brain recognizes that the signals being received from the ears are incorrect and turns the signals off through a process called the cerebellar clamp. When the clamp is in place, the spinning and much of the ‘sick’ feeling improve. The patient feels unsteady while standing, because the signals normally used to maintain balance have been turned off. The patient may also report dizziness or blurred vision with movements. Vision and proprioception (the sense of pressure at the bottom of the feet) are also used to maintain balance, so the patient can walk but will feel unsteady and may fall in the dark or on soft or bumpy floors such as thick carpet, grass, or gravel.

At this point most patients are well enough to get out of bed and visit a doctor. The doctor sees a person who is not spinning but whose gait is ataxic. If the patient is not given an opportunity to clearly describe what has happened, he or she may be referred to neurology to rule out stroke because of this ataxic gait. If balance testing is performed during the acute (immediate) compensation phase, test results may incorrectly suggest that the patient has damage to both sides of the balance system because the cerebellar clamp reduces the eye movements that are looked for during balance testing. The cerebellar clamp may persist for days to a few weeks after the initial injury.

Chronic (Long-Term) Compensation

During the acute compensation phase, the cerebellum slowly releases the clamp, gradually allowing more signals from the balance organs to pass to the balance areas of the brain. As the brain receives these signals, it fine-tunes their interpretation, in order to account for the difference between the ears. The brain must receive signals from the balance organs to be able to modify its interpretation of these signals.

For most patients, movements made during normal daily activities are enough to achieve chronic (long-term) compensation, usually in two to four weeks after the injury has occurred. Once the chronic compensation process is complete, the patient is essentially symptom-free. If unsteadiness and/or motion provoked dizziness persist after that time, compensation is not complete and the physician may prescribe a program of VRT.

VRT is administered by a specially-trained physical therapist. It is designed to provide small, controlled and repeated ‘doses’ of the movements and activities that provoke dizziness in order to desensitize the balance system to the movements, and enhance the fine-tuning involved in long-term compensation. VRT is most effective when administered by a therapist who has special training and specializes in this unusual form of therapy.

Decompensation

After the symptoms go away the balance system remains injured – the brain has adapted to the injury. For many patients, dizziness will return months or years after compensating for a balance system injury. It is critical for the physician to find out what type of dizziness the patient has. If the patient describes another severe attack of spinning with unsteadiness and nausea lasting hours to days, this suggests decompensation: the brain has ‘forgotten’ the fine-tuning procedure it developed during the chronic compensation phase described above.

Events that can provoke decompensation include a bad cold or the flu, minor surgery, long vacations, or anything that stops normal daily activity for a few days. Recovery after decompensation is exactly like the recovery that occurs during the chronic compensation phase. Movements and activities are the stimuli the braieeds to fine-tune the system. Sufferers are often recommended to keep their exercise program instructions handy so that they can begin the exercises immediately if symptoms return. Usually recovery after decompensation is quicker than the recovery after the initial injury to the balance system.

Failure to Compensate

Two things are required in order to compensate for an injury. First, the brain must receive signals from the balance organs. This means that movements must not be avoided, because movements create the signals the braieeds to compensate for the injury. Secondly, the balance areas of the brain must be capable of change.

During the early stages of dizziness, many physicians counsel their patients to avoid quick movements and reduce their activities. Most patients will be prescribed anti-dizziness medications such as Antivert (meclizine), Valium (diazepam), Xanax, Phenergan, or Compazine. This is fine during the acute stages of a dizziness problem in order to reduce the dizziness symptoms that persist for hours or days even when the patient is not moving. However, once the acute phase is past, inactivity and medications can interfere with the long-term compensation process. Any medication that makes the brain sleepy, including all of the anti-dizziness medications, can slow down or stop the process of compensation, so they are ofteot appropriate for long-term use. Most patients who fail to compensate are found to either be strictly avoiding certain movements, using anti-dizziness medications daily, or both. Treatment includes VRT, gradual reduction, and eventual elimination of these medications.

Labyrinthitis and anxiety

Chronic anxiety is a common side effect of labyrinthitis which can produce tremors, heart palpitations, panic attacks, derealization and depression. Often a panic attack is one of the first symptoms of labyrinthitis. While dizziness can occur from extreme anxiety, labyrinthitis can precipitate a panic disorder. Three models have been proposed to explain the relationship between vestibular dysfunction and panic disorder:

· Psychosomatic model: vestibular dysfunction that occurs as a result of anxiety.

· Somatopsychic model: panic disorder triggered by misinterpreted internal stimuli (e.g., stimuli from vestibular dysfunction), that are interpreted as signifying imminent physical danger. Heightened sensitivity to vestibular sensations leads to increased anxiety and, through conditioning, drives the development of panic disorder.

Network alarm theory: panic that involves noradrenergic, serotonergic, and other connected neuronal systems. According to this theory, panic can be triggered by stimuli that set off a false alarm via afferents to the locus ceruleus, which then triggers the neuronal network. This network is thought to mediate anxiety and includes limbic, midbrain and prefrontal areas. Vestibular dysfunction in the setting of increased locus ceruleus sensitivity may be a potential trigger.

Treatment

VRT is a highly effective way to substantially reduce or eliminate residual dizziness from labyrinthitis. VRT works by causing the brain to use already existing neural mechanisms for adaptation, plasticity, and compensation.

Rehabilitation strategies most commonly used are:

Gaze stability exercises – moving the head from side to side while fixated on a stationary object (aimed to restore the Vestibulo-ocular reflex) An advanced progression of this exercise would be walking in a straight line while looking side to side by turning the head.

Habituation exercises – movements designed to provoke symptoms and subsequently reduce the negative vestibular response upon repetition. Examples of these include Brandt-Daroff exercises.

Functional retraining – including postural control, relaxation, and balance training.

These exercises function by challenging the vestibular system. Progression occurs by increasing the amplitude of the head or focal point movements, increasing the speed of movement, and combining movements such as walking and head turning.

One study found that patients who believed their illness was out of their control showed the slowest progression to full recovery, long after the initial vestibular injury had healed. The study revealed that the patient who compensated well was one who, at the psychological level, was not afraid of the symptoms and had some positive control over them. Notably, a reduction in negative beliefs over time was greater in those patients treated with rehabilitation than in those untreated. “Of utmost importance, baseline beliefs were the only significant predictor of change in handicap at 6 months followup.”

Prochlorperazine is commonly prescribed to help alleviate the symptoms of vertigo and nausea. Cinnarizine can be prescribed instead of Prochlorperazine to help alleviate the symptoms.

Because anxiety interferes with the balance compensation process, it is important to treat an anxiety disorder and/or depression as soon as possible to allow the brain to compensate for any vestibular damage. Acute anxiety can be treated in the short term with benzodiazepines such as diazepam (Valium); however, long-term use is not recommended because of the addictive nature of benzodiazepines and the interference they may cause with vestibular compensation and adaptive plasticity.

Evidence suggests that selective serotonin-reuptake inhibitors may be more effective in treating labyrinthitis. They act by relieving anxiety symptoms and may stimulate new neural growth within the inner ear,[citation needed] allowing more rapid vestibular compensation to occur. Trial have shown that SSRIs do in fact affect the vestibular system in a direct manner and can decrease dizziness.

Some evidence suggests that viral labyrinthitis should be treated in its early stages with corticosteroids such as prednisone, and possibly antiviral medication such as valacyclovir and that this treatment should be undertaken as soon as possible to prevent permanent damage to the inner ear.

Vertigo /ˈvɜː(ɹ)tɨɡoʊ/ (from the Latin vertō “a whirling or spinning movement”) is a subtype of dizziness in which a patient inappropriately experiences the perception of motion (usually a spinning motion) due to dysfunction of the vestibular system. It is often associated with nausea and vomiting as well as a balance disorder, causing difficulties standing or walking. There are three types of vertigo. The first is known as objective and describes when the patient has the sensation that objects in the environment are moving; the second is known as subjective and refers to when the patient feels as if he or she is moving, and the third is known as pseudovertigo, an intensive sensation of rotation inside the patient’s head. While appearing in textbooks, this classification has little to do with the pathophysiology or treatment of vertigo.

Dizziness and vertigo are common medical issues, affecting approximately 20%-30% of the general population. Vertigo may be present in patients of all ages. The prevalence of vertigo rises with age and is about two to three times higher in women than in men. It accounts for about 2-3% of emergency department visits. The main causes of vertigo are: are benign paroxysmal positional vertigo, Mйniиre’s disease, vestibular neuritis, and labyrinthitis, but may also be caused by a concussion or a vestibular migraine. Excessive consumption of ethanol (alcoholic beverages) can also cause symptoms of vertigo. Repetitive spinning, as in familiar childhood games, can induce short-lived vertigo by disrupting the inertia of the fluid in the vestibular system; this is known as physiologic vertigo.

Classification of Vertigo

Vertigo is classified into either peripheral or central depending on the location of the dysfunction of the vestibular pathway, although it can also be caused by psychological factors.

Peripheral

Vertigo caused by problems with the inner ear or vestibular system, which is composed of the semicircular canals, the otolith (utricle and saccule), and the vestibular nerve is called “peripheral”, “otologic” or “vestibular” vertigo. The most common cause is benign paroxysmal positional vertigo (BPPV), which accounts for 32% of all peripheral vertigo. Other causes include Mйniиre’s disease (12%), superior canal dehiscence syndrome, labyrinthitis and visual vertigo. Any cause of inflammation such as common cold, influenza, and bacterial infections may cause transient vertigo if it involves the inner ear, as may chemical insults (e.g., aminoglycosides) or physical trauma (e.g., skull fractures). Motion sickness is sometimes classified as a cause of peripheral vertigo.

Patients with peripheral vertigo typically present with mild to moderate imbalance, nausea, vomiting, hearing loss, tinnitus, fullness, and pain in the ear. In addition, lesions of the internal auditory canal may be associated with ipsilateral facial weakness. Due to a rapid compensation process, acute vertigo as a result of a peripheral lesion tends to improve in a short period of time (days to weeks).

Central

Vertigo that arises from injury to the balance centers of the central nervous system (CNS), often from a lesion in the brainstem or cerebellum and is generally associated with less prominent movement illusion and nausea than vertigo of peripheral origin. Central vertigo has accompanying neurologic deficits (such as slurred speech and double vision), and pathologic nystagmus (which is pure vertical/torsional). Central pathology can cause disequilibrium which is the sensation of being off-balance. The balance disorder associated with central lesions causing vertigo are often so severe that many patients are unable to stand or walk.

A number of conditions that involve the central nervous system may lead to vertigo including: lesions caused by infarctions or hemorrhage, tumors present in the cerebellopontine angle such as a vestibular schwannoma or cerebellar tumors, epilepsy, cervical spine disorders such as cervical spondylosis, degenerative ataxia disorders, migraine headaches, lateral medullary syndrome, Chiari malformation, multiple sclerosis, parkinsonism, as well as cerebral dysfunction. Central vertigo may not improve or may do so more slowly than vertigo caused by disturbance to peripheral structures.

Signs and symptoms

Vertigo is a sensation of spinning while stationary. It is commonly associated with nausea or vomiting, unsteadiness (postural instability), falls, and difficulties walking. Recurrent episodes in those with vertigo are common and they frequently impair the quality of life. Blurred vision, difficulty speaking, a lowered level of consciousness, and hearing loss may also occur. The signs and symptoms of vertigo can present as a persistent (insidious) onset or an episodic (sudden) onset.

The characteristics of persistent onset vertigo is indicated by symptoms lasting for longer than one day and caused by degenerative changes that affect balance as we age. Naturally, the nerve conduction slows with aging and a decreased vibratory sensation is common. Additionally, there is a degeneration of the ampulla and otolith organs with an increase in age. Persistent onset is commonly paired with central vertigo signs and systems.

The characteristics of an episodic onset vertigo is indicated by symptoms lasting for a smaller, more memorable amount of time, typically lasting for only seconds to minutes. Typically, episodic vertigo is correlated with peripheral symptoms and can be the result of but not limited to diabetic neuropathy or autoimmune disease.

Motion sickness

Motion sickness is one of the biggest symptoms of vertigo and it develops most often in persons with inner ear problems. The feeling of dizziness and lightheadedness is often accompanied by nystagmus (an involuntary movement of the eye characterized by a smooth pursuit eye movement followed by a rapid saccade in the opposite direction of the smooth pursuit eye movement). During a single episode of vertigo, this action will occur repeatedly. Symptoms can fade while sitting still with the eyes closed.

Differential diagnosis

A number of specific conditions can cause vertigo. In the elderly, however, the condition is often multifactorial.

Benign paroxysmal positional vertigo

Benign paroxysmal positional vertigo (BPPV) is the most common vestibular disorder and occurs when loose calcium carbonate debris has broken off of the otoconial membrane and enters a semicircular canal thereby creating the sensation of motion. Patients with BPPV may experience brief periods of vertigo, usually under a minute, which occur with change in position. It is the most common process of vertigo. It occurs in 0.6% of the population yearly with 10% having an attack during their lifetime. It is believed to be due to a mechanical malfunction of the inner ear. BPPV may be diagnosed with the Dix-Hallpike test and can be effectively treated with repositioning movements such as the Epley maneuver.

Vestibular migraine

Vestibular migraine is the association of vertigo and migraines and is one of the most common causes of recurrent, spontaneous episodes of vertigo. The etiology of vestibular migraines is currently unclear; however, one hypothesized cause is that the stimulation of the trigeminal nerve leads to nystagmus in individuals suffering from migraines. Other suggested causes of vestibular migraines include: unilateral neuronal instability of the vestibular nerve, idiopathic asymmetric activation of the vestibular nuclei in the brainstem, and vasospasm of the blood vessels supplying the labyrinth or central vestibular pathways resulting in ischemia to these structures. Vestibular migraines are estimated to affect 1-3% of the general population and may affect 10% of migraine patients. Additionally, vestibular migraines tend to occur more often in women than in men and rarely affect individuals after the sixth decade of life.

REFERENCES:

1. Greinwald, John H. Jr MD; Hartnick, Christopher J. MD The Evaluation of Children With Hearing Loss. Archives of Otolaryngology — Head & Neck Surgery. 128(1):84-87, January 2002

2. Stenstrцm, J. Sten: Deformities of the ear; In: Grabb, W., C., Smith, J.S. (Edited): “Plastic Surgery”, Little, Brown and Company, Boston, 1979, ISBN 0-316-32269-5 (C), ISBN 0-316-32268-7 (P)

3. Deborah S. Sarnoff, Robert H. Gotkin, and Joan Swirsky (2002). Instant Beauty: Getting Gorgeous on Your Lunch Break. St. Martin‘s Press. ISBN 0-312-28697-X.

4. Lam SM. Edward Talbot Ely: father of aesthetic otoplasty. [Biography. Historical Article. Journal Article] Archives of Facial Plastic Surgery. 6(1):64, 2004 Jan-Feb.

5. Siegert R. Combined reconstruction of congenital auricular atresia and severe microtia. [Evaluation Studies. Journal Article] Laryngoscope. 113(11):2021-7; discussion 2028-9, 2003 Nov.

6. Trigg DJ. Applebaum EL. Indications for the surgical repair of unilateral aural atresia in children. [Review] [33 refs] [Journal Article. Review], American Journal of Otology. 19(5):679-84; discussion 684-6, 1998 September

7. Stenstrцm, J. Sten: Deformities of the ear; In: Grabb, W., C., Smith, J.S. (Edited): “Plastic Surgery”, Little, Brown and Company, Boston, 1979, ISBN 0-316-32269-5 (C), ISBN 0-316-32268-7 (P)

8. Anson and Donaldson, Surgical Anatomy of the Temporal Bone, 4th Edition, Raven Press, 1992

9. Senate Public Works Committee, Noise Pollution and Abatement Act of 1972, S. Rep. No. 1160, 92nd Cong. 2nd session.

10. Tak SW, Calvert GM, “Hearing Difficulty Attributable to Employment by Industry and Occupation: An Analysis of the National Health Interview Survey – United States, 1997 to 2003,” J. Occup. Env. Med. 2008, 50:46-56