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Stirnhöhle – frontal; Sehr gross ausgebildete Stirnhöhle im Röntgenbild des menschlichen Schädels, im Bild eingefärbt.Von Hellerhoff - Eigenes Werk, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=9057711

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Ausmass und Form der Stirnhöhle sind grossen Schwankungen unterworfen. Es sind für den Menschen vier Grundformen beschrieben: Bohnen-, Blatt-, Mitral- und Pyramidenform. Die Grösse der menschlichen Stirnhöhle schwankt zwischen 0,05 und 7,8 cm³, nicht selten ist die Stirnhöhle gar nicht (Aplasie) oder nur gering (Hypoplasie) ausgebildet. Auch das knöcherne Dach der Augenhöhle kann in variablem Ausmass durch die Stirnhöhle pneumatisiert sein...

Quelle:

https://de.wikipedia.org/wiki/Stirnh%C3%B6hle#/media/Datei:Stirnhoehle_frontal.jpg

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Nasennebenhöhlen (Sinus paranasales):

1. Stirnhöhle (Sinus frontalis) (grün)

2. Siebbeinzellen (Cellulae ethmoidales) (lila)

3. Keilbeinhöhle (Sinus sphenoidalis) (rot)

4. Kieferhöhle (Sinus maxillaris) (blau)

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You rely on the inner ear, an intricate sensory organ, to hear and to maintain balance. The inner ear is a complex system of communicating chambers and tubes called a labyrinth. Each ear has two parts to the labyrinth-the bony (osseus) labyrinth and the membranous labyrinth (Figure 1). The bony labyrinth is a cavity within the temporal bone. The membranous labyrinth is a tube of similar shape that lies within the bony labyrinth. Between the bony and membranous labyrinths is a fluid called perilymph, which is secreted by cells in the wall of the bony labyrinth. The membranous labyrinth contains another fluid, called endolymph.

The parts of the labyrinths include three membranous semicircular ducts within three bony semicircular canals, and a cochlea. The semicircular canals and associated structures provide a sense of equilibrium (balance). The cochlea functions in hearing.

The cochlea has a bony core and a thin, bony shelf that extends out from the core and coils around it. The shelf divides the bony labyrinth of the cochlea into upper and lower compartments. The upper compartment, called the scala vestibuli, leads from the oval window to the tip of the cochlea. The lower compartment, the scala tympani, extends from the tip of the cochlea to a membrane-covered opening in the wall of the middle ear called the round window.

The part of the membranous labyrinth within the cochlea is called the cochlear duct. It lies between the two bony compartments and ends as a closed sac near the tip of the cochlea. The cochlear duct is separated from the scala vestibuli by a vestibular membrane (Reissner's membrane) and from the scala tympani by a basilar membrane. The basilar membrane has many thousands of elastic fibers, allowing it to move in response to sound vibrations. Sound vibrations entering the perilymph at the oval window travel along the scala vestibuli and pass through the vestibular membrane and into the endolymph of the cochlear duct, where they move the basilar membrane.

After passing through the basilar membrane, the vibrations enter the perilymph of the scala tympani. Their forces are dissipated into the air in the tympanic cavity by movement of the membrane covering the round window.

The spiral organ (organ of Corti) contains the hearing receptors. It is located on the upper surface of the basilar membrane and stretches from the apex to the base of the cochlea. The receptor cells, called hair cells, are organized in rows and have many hairlike processes that project into the endolymph of the cochlear duct. Above these hair cells is a tectorial membrane attached to the bony shelf of the cochlea, passing over the receptor cells and contacting the tips of their hairs.

As sound vibrations move the basilar membrane, the hairs move back and forth against the tectorial membrane and the resulting mechanical deformation of the hairs stimulates the hair cells (Figure 4. The Cochlea). Hair cells at different locations along the length of the cochlear duct respond to different frequencies (pitch) of sound vibrations. This enables us to hear sounds of different pitch simultaneously.

Hair cells are epithelial but function somewhat like neurons. For example, when a hair cell is at rest, its membrane is polarized. When it is stimulated, selective ion channels open, depolarizing the membrane and making it more permeable to calcium ions. The hair cell has no axon or dendrites, but it has neurotransmitter-containing vesicles near its base. As calcium ions diffuse into the cell, some of these vesicles fuse with the cell membrane and release a neurotransmitter by exocytosis. The neurotransmitter stimulates the dendrites of nearby sensory neurons. In response these neurons send action potentials along the cochlear branch of the vestibulocochlear nerve to the auditory cortex of the temporal lobe of the brain.

The ear of a young person with normal hearing can detect sound waves with frequencies ranging from 20 to more than 20,000 vibrations per second. The range of greatest sensitivity is 2,000 to 3,000 vibrations per second. More-intense stimulation of the hair cells causes more action potentials per second to reach the auditory cortex, and we sense a louder sound.

Units called decibels (dB) measure sound intensity on a logarithmic scale. The decibel scale begins at 0 dB, which is the intensity of the sound that is least perceptible by a normal human ear. A sound of 10 dB is 10 times as intense as the least perceptible sound; a sound of 20 dB is 100 times as intense; and a sound of 30 dB is 1,000 times as intense. A whisper has an intensity of about 40 dB, normal conversation measures 60 to 70 dB, and heavy traffic produces about 80 dB. A sound of 120 dB, common at a rock concert, produces discomfort, and a sound of 140 dB, such as that emitted by a jet plane at takeoff, causes pain.

Frequent or prolonged exposure to sounds with intensities above 85 dB can damage hearing receptors and cause permanent hearing loss.

Auditory Pathways

The nerve fibers associated with hearing enter the auditory pathways, which pass into the auditory cortices of the temporal lobes of the cerebrum. Here they are interpreted. On the way, some of these fibers cross over, so that impulses arising from each ear are interpreted on both sides of the brain. Consequently, damage to a temporal lobe on one side of the brain does not necessarily cause complete hearing loss in the ear on that side.

Several factors cause partial or complete hearing loss. Interference with the transmission of vibrations to the inner ear is called conductive hearing loss. Conductive hearing loss may be due to plugging of the external acoustic meatus or to changes in the eardrum or auditory ossicles. For example, the eardrum may harden as a result of disease and become less responsive to sound waves, or disease or injury may tear or perforate the eardrum.

Damage to the cochlea, auditory nerve, or auditory pathways can cause sensorineural hearing loss. Loud sounds, tumors in the central nervous system, brain damage from vascular accidents, or use of certain drugs can also cause sensorineural hearing loss.

Steps in the Generation of Sensory Impulses from the Ear

1. Sound waves enter external acoustic meatus.

2. Sound waves cause eardrum to reproduce vibrations coming from sound source.

3. Auditory ossicles amplify and transfer vibrations to end of stapes.

4. Movement of stapes at oval window transfers vibrations to perilymph in scala vestibuli.

5. Vibrations pass through vestibular membrane and enter endolymph of cochlear duct, where they move the basilar membrane.

6. Different frequencies of vibration of basilar membrane stimulate different sets of receptor cells.

7. As a receptor cell depolarizes, its membrane becomes more permeable to calcium ions.

8. Inward diffusion of calcium ions causes vesicles at base of the receptor cell to release neurotransmitter.

9. Neurotransmitter stimulates dendrites of nearby sensory neurons.

10. Sensory impulses are triggered on fibers of the cochlear branch of vestibulocochlear nerve.

11. Auditory cortices of temporal lobes interpret sensory impulses.

Figure 1. Inner ear anatomy Figure 2. Parts of the inner ear
Footnotes: The inner ear (internal ear) is the innermost part of your ear consisting of the cochlea (the snail-shaped portion on the right), and the semicircular canals on the left represent the vestibular system. The inner ear is mainly responsible for sound detection and balance. The inner ear consists of the bony labyrinth, a hollow cavity in the temporal bone of the skull with a system of passages comprising two main functional parts: (1) The cochlea, dedicated to hearing; converting sound pressure patterns from the outer ear into electrochemical impulses which are passed on to the brain via the auditory nerve. (2) The vestibular system, dedicated to balance. The inner ear is innervated by cranial nerve eight (CN VIII) also known as vestibulocochlear nerve that consists of the vestibular and cochlear nerves . The vestibular nerve is primarily responsible for maintaining body balance and eye movements, while the cochlear nerve is responsible for hearing . Damage to the vestibular nerve results in vertigo, a balance disorder, and nystagmus . The endolymph (blue and purple fluid) is the fluid contained in the membranous labyrinth of the inner ear and has a higher level of potassium than sodium.
Figure 3. Inner ear bones
Note: A closer look at the inner ear. Perilymph separates the bony (osseous) labyrinth of the inner ear from the membranous labyrinth, which contains endolymph. Note that areas of bony labyrinth have been removed to reveal underlying structures.
Figure 4. The Cochlea (cross section view)
Note: a) Cross section of the cochlea. (b) The spiral organ and the tectorial membrane.

Vestibulo-ocular reflex

The Vestibulo-Ocular Reflex is an essential function of your vestibular system that helps you maintain a stable perception of the world around you by maintaining your postural balance and spatial orientation in response to changes in your environment such as while you engage in normal movements throughout your day like walking , . The vestibulo-ocular reflex keeps you steady and balanced even though your eyes and head are continuously moving when you perform most actions. When you make a head movement, your eye muscles are triggered instantly to create an eye movement opposite to that of your head movement at the exact same speed to readjust your visual world, which, in turn, stabilizes your retinal image (line of sight in space) by keeping your eyes still in space and focused on an object, despite you head moving .

The Vestibulo-Ocular Reflex (VOR) involves three parts , , :

1. Peripheral sensory apparatus which consists of a set of motion sensors: the semicircular canals (anterior, posterior, horizontal) and the otolith organs (saccule and utricle) (Figures 1 to 5).

The semicircular canals are tubes coiled within your inner ear filled with liquid called the endolymph and lined with hair cells. Instead of sound waves, these tiny hairs react to sense rotational and angular movements of your head. The semicircular canals are mostly responsible for rotary motion or motion not in a straight line.

Humans have a total of 6 semicircular canals arranged in three main planes (anterior, posterior, horizontal) on both sides; each plane has a pair of canals. The 3 in the right ear are functionally paired with the 3 in the left ear. The semicircular canals are referred to according to their orientation: lateral (horizontal), anterior (superior), and posterior. These structures are positioned at roughly right angles in relation to one another. The horizontal (lateral) semicircular canal, the shortest of the three, is set at an angle of about 30 degrees to the horizontal plane. The anterior (superior) and posterior loops are in diagonal vertical planes that intersect at a 90-degree angle. The 3 semicircular canals (anterior, posterior, horizontal) are positioned at 90-degree angles to one another and thus can sense rotation in all directions:

The right horizontal with the left horizontal

The right anterior with the left posterior

The right posterior with the left anterior.

A semicircular canal will get stimulated by head motion towards that semicircular canal . When a semicircular canal on one side is activated, there is inhibition of the other one during angular head movements. For example, when turning your head to look over your right shoulder, the right horizontal semicircular canal is excited and the left horizontal is inhibited. When there are head movements and rotation, the velocity of the movements dictates the difference in firing rate between the two semicircular canals . Hair cells are embedded in a fluid and gelatinous structure called the ampulla in each semicircular canal. When you rotate your head, the canal will move relative to the fluid inside of it, which will create a force against the ampulla, causing hair cells to bend. When your head is at rest, vestibular afferents have tonic discharge; this results in a balance between the semicircular canal pairs. Cases of nystagmus and ocular misalignment may be interpreted by understanding the organization and structure of the semicircular canals and otolith organs within the head . Information regarding linear head acceleration, angular velocity, and orientation of the head relative to gravity are all collected by these peripheral motion sensors. These sensors relay this information to the central nervous system (brain and spinal cord). Here, information from somatosensors (carrying other sensory information) is combined with motion sensory information to calculate head orientation.

The semicircular canals (anterior, posterior, horizontal) sense angular head acceleration are responsible for detecting head rotation and the otolith organs (saccule and utricle) sense linear head acceleration and therefore detect the position of your head relative to gravity and head translation, providing your internal cues for orientation of position in space, movement, gaze stabilization, and postural control. Body movements cause the fluid in the semicircular canals to move and stimulate cilia on sensory hair cells. This triggers transmission of neural signals to the brain to initiate appropriate reflex responses for the eyes, head, and postural adjustments. These reflexive movements allow you to see things clearly when your head and body are in motion and keep you from falling.

Each semicircular canal has an ampulla, an expanded bulb-shaped structure that contains the hair cells (crista ampullaris), as well as a fan-like structure known as the cupula, which separates the semicircular canal from the vestibule (see Figures 1 and 3). The ampulla contains a fluid known as endolymph, which is also present in the cochlea, and the crista, a cone-shaped structure lined with hair cells and supporting cells. The hair cells form stereocilia, protrusions that extend into the crista. The longest of the stereocilia are the kinocilia, which point in a single direction and are sensitive to movement. The kinocilia extend from the crista into the cupula, a jellylike mass that surrounds the hair cells completely, separating them from the endolymph. The crista is flexible. When your head moves, endolymph pushes the cupula one way or the other, which in turn displaces the hairs and alters the electrical potential of the hair cells.

The cupula has the same density as the endolymph and therefore semicircular canal does not respond to changes in the orientation of the head with respect to gravity. With angular head movements, however, the inertia of the endolymph results in a pressure on the cupula, which stimulates the hair cells through facilitation (increased firing rate) or inhibition (decreased firing rate). If the fluid is moving toward the ampulla, the horizontal canal is facilitated, while the semicircular canals in the vertical plane on the same side are inhibited. Hence, neural activities of the semicircular canal pairs are opposite, which results in a push-pull mechanism of facilitation on one side and inhibition on the other . The resting firing rate in the absence of motion would therefore be equal for the right and left labyrinths.

The otolith organs (saccule and utricle) contain dense crystals called otoconia resting on top of the sensory organs, are gravity-sensitive and provide sensory neural input related to linear head acceleration.

The utricle senses linear movements of the head in the horizontal plane.

The saccule senses linear movements of the head in the vertical plane.

Additionally, the utricle and saccule convey information about spinal and leg muscles for balance strategies (ankle, hip, and stepping) via the Vestibulo-Spinal Reflex (VSR), which is primarily to maintain upright posture during movement. The otoliths (otoconia) further convey information regarding the direction of gravity through head tilt, which is incorporated into locomotion. The function of the otolith organs is accomplished by otoconia (otoliths) - calcium carbonate crystals that are denser than the surrounding endolymph - remaining partially stable while the head moves around them (Figure 4). It is important to note that the utricle and saccule also have connections with eyes muscles as noted with the semicircular canal. However, the direct pathways of rotational compensatory eye movements are much greater than those of linear translation, resulting in minimal contributions from the otoliths to the Vestibulo-Ocular Reflex (VOR) as compared to the semicircular canal. With linear head movements (e.g., leaning to your side), the otoconia move, signaling reflexive responses similar to those of the semicircular canals to maintain eye, head, and body equilibrium.

If otoconia (otoliths) become displaced from the utricle into the semicircular canals, then brief spells of vertigo are experienced related to position changes, a condition called benign paroxysmal positional vertigo (BPPV). Traumatic brain injury is a common cause of benign paroxysmal positional vertigo (BPPV) in the adult population, although it rarely occurs in adolescents , , .

The first-order information processing from the inner ear involves a number of associated reflexes: the Vestibulo-Collic Reflex (VCR), the Cervico-Ocular Reflex (COR), the Cervico-Spinal Reflex (CSR), and the Cervico-Collic Reflex (CCR) . The Vestibulo-Collic Reflex (VCR) acts on the neck muscles to stabilize the head in space during body movements and is considered a righting reflex . The Vestibulo-Collic Reflex (VCR) lessens head oscillations that occur in more rapid, dynamic movements . Although the neural pathways and actions are not fully understood, it is suspected that Vestibulo-Collic Reflex (VCR) is mediated through the otolith organs and medial Vestibulo-Spinal Reflex (VSR) . The Cervico-Ocular Reflex (COR) acts on eye movements similar to the Vestibulo-Ocular Reflex (VOR), receiving input from the neck proprioceptors, and is of particular importance as a compensatory strategy if bilateral vestibular nerve loss occurs. The Cervico-Ocular Reflex (COR) is not thought to make any notable contributions to gaze stability in normal subjects because the gain is notably less than the Vestibulo-Ocular Reflex (VOR) . The Cervico-Spinal Reflex (CSR) acts on the extremities and is synonymous with the tonic neck reflex. The Cervico-Spinal Reflex (CSR) interacts with the Vestibulo-Spinal Reflex (VSR) . Finally, the Cervico-Collic Reflex (CCR) acts on deep neck muscles to assist in head stabilization during head and body movements. Body rotation with the head stabilized elicits the Cervico-Collic Reflex (CCR), whereas head rotation with the body stabilized elicits the Vestibulo-Ocular Reflex (VOR) .

2. A central processing mechanism

Vestibular information is primarily processed in the brainstem via the cranial nerve eight (CN VIII) also known as vestibulocochlear nerve that consists of the vestibular and cochlear nerves , . The signals enter the vestibular nuclear complex, located in the medulla and pons . Four main nuclei comprise the vestibular nuclear complex (superior, inferior, medial, and lateral) , , . Most of the semicircular canal inputs synapse with the superior and medial vestibular nuclei via first-order sensory neurons of cranial nerve eight (CN VIII), while second-order sensory neurons send signals ipsilaterally and contralaterally via the medial longitudinal fasciculus to the oculomotor cranial nerves, oculomotor nerve (the third cranial nerve; CN III), trochlear nerve (fourth cranial nerve; CN IV), and abducens nerve (sixth cranial nerve; (CN VI). Lastly, a third motor neuron excites the extraocular muscles, causing conjugate eye movements that are equal to and opposite of head movements , . This results in gaze stabilization during head movements.

The vestibular system is unique in that it also sends information via the inferior cerebellar peduncle to the cerebellum to modulate or fine-tunine the Vestibulo-Ocular Reflex (VOR). The flocculonodular lobe and fastigial nuclei are responsible for this fine-tuning. Vestibular data is also processed by the cerebellum, which then aids in the regulation of vestibular reflexes, maintaining posture, and coordination , . Other connections to the cerebral cortex, thalamus, and reticular formation assist in coordinating efforts between other central networks and the vestibular system, allowing for enhanced spatial awareness .

There are additional vestibular connections to the thalamus, cerebral (vestibular) cortex, and reticular formation. These extensive connections result in a coordinated effort between the vestibular system and other central networks to contribute to arousal and conscious awareness of the head and body in space .

3. A motor output which are the eye muscles.
The central nervous system (brain and spinal cord) is the central processing mechanism, which sends its outputs to the spinal cord and eye muscles to generate the Vestibulo-Ocular Reflex. Each semicircular canal has excitatory projections to a pair of extraocular muscles in each eye and inhibitory projections to an antagonistic pair of muscles . In addition to the Vestibulo-Ocular Reflex (VOR), you also have a Vestibulo-Spinal Reflex (VSR), which prevents falls by maintaining head and postural stability. It does this by creating compensatory body movements . To attain an even better orientation, this information also goes to cortical structures (posterior insular vestibular cortex) for further integration with tactile, auditory, and proprioceptive inputs. Actions of the Vestibulo-Ocular Reflex (VOR) and Vestibulo-Spinal Reflex (VSR) become controlled and continuously adjusted as needed by the central nervous system (brain and spinal cord) .

Ewald's three laws for vestibular diagnostic testing

1. Stimulation of a semicircular canal generates eye movements in the plane of that canal.

2. In the horizontal semicircular canals, movement of the endolymph toward the ampulla (ampullopetal) causes deflection of the cupula toward the utricle (utriculopetal) and results in excitation (greater neural activity) compared to movement away from the utricle (utriculofugal).

3. In the vertical semicircular canals (anterior and posterior), movement of the endolymph away from the ampulla (ampullofugal) causes greater deflection of the cupula away from the utricle (utriculofugal) and results in a greater excitation compared to utriculopetal movement, which is opposite to that in the horizontal canals.

Figure 5. Semicircular canals and the otolith organs
Footnote: The 3 semicircular canals (anterior, posterior, horizontal) sense angular head accelerations and the otolith organs (saccule, uticle) sense linear head accelerations, providing internal cues for orientation of position in space, movement, gaze stabilization, and postural control.

[Source ]
Figure 6. Semicircular canal anatomy
Footnote: The semicircular canals are part of the vestibular system of the inner ear. The semicircular canals are curved, looped structures that are referred to according to their orientation: lateral (horizontal), anterior (superior), and posterior. These structures are positioned at roughly right angles in relation to one another. The lateral semicircular canal, the shortest of the three, is set at an angle of about 30 degrees to the horizontal plane. The anterior and posterior loops are in diagonal vertical planes that intersect at a 90-degree angle.
Figure 7. Vestibulo-ocular reflex (VOR)
Footnote: The vestibulo-ocular reflex (VOR). A rotation of the head is detected, which triggers an inhibitory signal to the extraocular muscles on one side and an excitatory signal to the muscles on the other side. The result is a compensatory movement of the eyes.

[Source ]

Sense of Equilibrium

The sense of equilibrium (balance) is really two senses:

1. Static equilibrium and

2. Dynamic equilibrium-that come from different sensory organs.

The organs of static equilibrium sense the position of the head, maintaining balance, stability and posture when the head and body are still. When the head and body suddenly move or rotate, the organs of dynamic equilibrium detect such motion and aid in maintaining balance.

Static Equilibrium

The organs of static equilibrium are in the vestibule, a bony chamber between the semicircular canals and the cochlea. The membranous labyrinth inside the vestibule consists of two expanded chambers-a utricle and a saccule (see Figures 2 and 3).

The saccule and utricle each have a tiny structure called a macula. Maculae have many hair cells, which serve as sensory receptors. The hairs of the hair cells project into a mass of gelatinous material, which has grains of calcium carbonate (otoliths) embedded in it. These particles add weight to the gelatinous structure.

Bending the head forward, backward, or to either side tilts the gelatinous masses of the maculae, and as they sag in response to gravity, the hairs projecting into them bend. This action causes the hair cells to signal the sensory neurons associated with them in a manner similar to that of hair cells associated with hearing. The resulting action potentials are conducted into the central nervous system on the vestibular branch of the vestibulocochlear nerve, informing the brain of the head's new position. The brain responds by adjusting the pattern of motor impulses to skeletal muscles, which contract or relax to maintain balance.
Figure 8. Inner ear maculae respond to changes in head position
Footn ote:The hair cells within the utricle are surrounded by a gelatinous substance and hold the microscopic otoliths (otoconia). (a) Orientation of hair cells within the macula of the utricle with the head in an upright position. (b) Macula of the utricle with the head bent forward, which results in a deflection of the hair cells due to a gravitational pull.

Dynamic Equilibrium

The organs of dynamic equilibrium are the three semicircular canals in the labyrinth. They detect motion of the head and aid in balancing the head and body during sudden movement. These canals lie at right angles to each other (see Figure 2).

Suspended in the perilymph of the bony portion of each semicircular canal is a membranous semicircular duct that ends in a swelling called an ampulla, which
houses the sensory organs of the semicircular canals. Each of these sensory organs, called a crista ampullaris, contains a number of sensory hair cells and supporting cells. Like the hairs of the maculae, the hair cells of the crista ampullaris extend upward into a dome-shaped, gelatinous mass called the cupula (Figure 6). When the head is stationary, the cupula of the crista ampullaris remains upright. When the head is moving rapidly, the cupula bends opposite the motion of the head, stimulating sensory receptors.

Rapid movement of the head or body stimulates the hair cells of the crista ampullaris (Figure 9). At such times, the semicircular canals move with the head or body, but the fluid inside the membranous ducts remains stationary. Imagine turning rapidly while holding a full glass of water. This action bends the cupula in one or more of the canals in a direction opposite that of the head or body movement, and the hairs embedded in it also bend. The stimulated hair cells signal their associated neurons, which conduct impulses to the brain. The brain interprets these impulses as a movement in a particular direction.

Parts of the cerebellum are particularly important in interpreting impulses from the semicircular canals. Analysis of such information allows the brain to predict the consequences of rapid body movements. By modifying signals to appropriate skeletal muscles, the cerebellum can maintain balance.

Other sensory structures aid in maintaining equilibrium. For example, certain mechanoreceptors (proprioceptors), particularly those associated with the joints of the neck, inform the brain about the position of body parts. In addition, the eyes detect changes in position that result from body movements. Such visual information is so important that even if the organs of equilibrium are damaged, a person may be able to maintain normal balance by keeping the eyes open and moving slowly.

The nausea, vomiting, dizziness, and headache of motion sickness arise from sensations that don't make sense. The eyes of a person reading in a moving car, for example, signal the brain that the person is stationary, because the print doesn't move. However, receptors in the skin detect bouncing, swaying, starting, and stopping as the inner ear detects movement. The contradiction triggers the symptoms. Similarly, in a passenger of an airplane flying through heavy turbulence, receptors in the skin and inner ear register the chaos outside, but the eyes focus on the immobile seats and surroundings.

To prevent or lessen the misery of motion sickness, focus on the horizon or an object in the distance ahead. Medications are available by pill (diphenhydramine and dimenhydrinate) and, for longer excursions, in a skin patch (scopolamine).
Figure 9. Dynamic inner ear balance organs (crista ampullaris) within the Semicricular ducts
Inner ear vertigo

The relative frequencies of various syndromes presenting with dizziness and vertigo are listed in table 1.
Table 1. The relative frequencies of different dizziness and vertigo syndromes
[Source ]

The important criteria for distinguishing among them are as follows :

The type of dizziness/vertigo: rotatory vertigo resembles the sensation of being on a merry-go-round (in vestibular neuritis and other disorders), while postural vertigo resembles the sensation of riding in a boat (e.g., in bilateral vestibulopathy). Many patients use the term "dizziness" for lightheadedness without any sensation of movement (e.g., in drug intoxication).

The duration of dizziness/vertigo: attacks may last for seconds or minutes (as in vestibular paroxysm) or hours (as in Menière's disease or vestibular migraine). Persistent vertigo lasting days or weeks is seen in vestibular neuritis, among other conditions. Attacks of postural vertigo lasting minutes to hours can be produced, for example, by brainstem transient ischemic attacks.
Nystagmus in Acute Severe Dizziness
Precipitating and exacerbating factors of dizziness and vertigo: the symptoms arise at rest in some conditions (e.g., vestibular neuritis); they can also arise when the patient walks (as in bilateral vestibulopathy) or be induced by turning the head to the right or left (as in vestibular paroxysm). Other possible precipitating factors include turning in bed (as in benign paroxysmal positioning vertigo [BPPV]), coughing, pressing, and loud tones of a particular frequency (Tullio's phenomenon, seen in perilymph fistula), as well as certain social or environmental conditions (e.g., phobic postural vertigo).

The accompanying symptoms, if present, may arise from the inner ear - e.g., attacks of intense tinnitus, hearing impairment, and a pressure sensation in the ear, which are typical of Menière's disease. Diplopia, sensory disturbances, dysphagia, dysarthria, and paralysis of arms and legs are symptoms of central origin that usually arise in the brainstem. Headache or a history of migraine may point to the diagnosis of vestibular migraine but can also be caused by brainstem ischemia or posterior fossa hemorrhage.

Acute Severe Dizziness

Nystagmus is a term used to describe alternating slow and fast movements of the eyes. These alternating movements give the appearance that the eyes are beating toward one or more directions. Patients with vestibular neuritis have a peripheral vestibular pattern of nystagmus. In this setting, the peripheral vestibular pattern is a unidirectional, principally horizontal pattern of nystagmus. This description means that the nystagmus beats is in only one direction (i.e., a left-beating nystagmus never converts to right-beating, or a right-beating nystagmus never converts to left-beating). Patients with a peripheral disorder demonstrate nystagmus to the contralateral side which suppresses with visual fixation. Nystagmus improves with gaze towards the lesion and worsens with gaze opposite the lesion . Conversely, bi-directional gaze-evoked nystagmus (i.e., right beating nystagmus present with gaze toward the right, and left-beating nystagmus present with gaze toward the left side) is a central nervous system pattern of nystagmus. Other central nervous system patterns are pure torsional nystagmus or spontaneous vertical (typically downbeat) nystagmus. With an acute peripheral vestibular lesion, the only pattern of nystagmus that can result is unidirectional nystagmus. In acute severe dizziness presentations, any other pattern should be considered a central nervous system sign. Patients often prefer to keep their eyes closed early on, but the eyes should be opened and the pattern of nystagmus defined.

Nystagmus in vestibular neuritis is spontaneous (i.e., present in primary gaze) for at least the first several hours of symptoms. Following this initial time period, the nystagmus may only be identified during gaze testing (i.e., having the patient look to each side) or if visual fixation is blocked. Patients can suppress peripheral vestibular nystagmus by visual fixation on a target, so removing the patient's ability to fixate can bring out the spontaneous nystagmus. The simplest way to block fixation is to place a blank sheet of paper a few inches in front of the patient and then observe for spontaneous nystagmus from the side.

The reason for the characteristic pattern of nystagmus in vestibular neuritis is an imbalance in the peripheral vestibular signals to the brain. Normally, the peripheral vestibular system on each side has a baseline firing rate of action potentials that functions to drive the eyes toward the other side. When the peripheral vestibular system on each side is intact, the input from each side is balance so the eyes remain stationary. When an acute lesion occurs on one side, the input from the opposite side is unopposed. As a result, the eyes will be "pushed" toward the lesioned side. This movement of the eyes is the slow phase of nystagmus. When the eyes reach a critical point off center, the brain responds by generating a corrective eye movement to move the eyes back. This is the fast phase of nystagmus. Since the direction of the fast phase gives the appearance that the eyes are beating in that direction, an acute left peripheral vestibular lesion leads to spontaneous right beating nystagmus. Over time, the asymmetry resolves or the brain compensates for the asymmetry.

Vascular Causes of Acute Severe Dizziness

Although vestibular neuritis is the most common cause of the acute dizziness presentation, no laboratory or imaging test exists to confirm a viral etiology. A peripheral vestibular lesion can be caused by a vascular occlusion of the blood supply to the peripheral vestibular components, though presumably this cause is much less common.

Stroke should be a serious consideration in the patient who presents with the acute dizziness presentation. Dizziness is a symptom of stroke in 50% of stroke presentations . Most stroke patients that report dizziness as a symptom have other prominent central nervous system features, but a small stroke of the cerebellum or brain stem can present with isolated dizziness (i.e., dizziness without other accompanying central nervous system signs or symptoms). In a population-based study, about 3% of patients with dizziness had a stroke etiology, but less than 1% of patients with isolated dizziness had stroke as the etiology . However, a prospective study of 24 patients with acute severe dizziness reported 6 patients (25%) with stroke etiology . Patients with stroke presenting as isolated dizziness may report imbalance, true vertigo, a more vague dizziness sensation, or a combination of these. Nausea and vomiting are also common, as they are with vestibular neuritis. Unfortunately, computerized tomography (CT) scans are an extremely insensitive test for acute stroke presentations in general , and particularly so for infarction within the posterior fossa . A stroke within the posterior fossa may not appear on a CT scan for days or weeks because of artifacts or poor resolution. Because of this, CT should never be considered as a means of excluding stroke. Magnetic resonance imaging (MRI) is a much more sensitive test, but is not a practical test to screen for stroke in emergency department dizziness presentations. Like CT, the sensitivity of the test is the lowest for stroke of the posterior fossa .

The key features discriminating stroke from vestibular neuritis are the pattern of nystagmus and the results of the head thrust test. Down-beating nystagmus or bidirectional gaze-evoked nystagmus are both immediate indications that the localization must be in the central nervous system. These patterns are not caused by lesions of the peripheral vestibular system. This is the reason that an examination of ocular movements is required before a diagnosis is even considered. Another highly suspicious pattern of nystagmus is a pure torsional pattern. There are now case reports of patients who have unidirectional horizontal nystagmus and a stroke etiology so the pattern of nystagmus should not be the sole criterion.3-5 A patient with unidirectional nystagmus, a positive head thrust in the direction opposite the fast phase of nystagmus, and no other neurological features can be diagnosed with vestibular neuritis with a high level of certainty. It would take a well placed and small stroke to cause the peripheral vestibular pattern of nystagmus and a corresponding positive head thrust test without any other central nervous system features. Though all patients with vestibular neuritis are unsteady walking, the inability to walk is another red flag.5 Finally, a person's risk for stroke based on stroke risk factors should be considered. Though no validated scale exists to grade stroke risk based on stroke risk factors in this population, a stroke work-up is reasonable in patients with a high risk for stroke. One should not be over reliant on stroke risk factors as discriminators, however, since other stroke mechanisms - such as arterial dissection - occur in the absence of stroke risk factors.

Management of Acute Severe Dizziness

Treatment for vertigo

The treatment of dizziness and vertigo may include medication, physical therapy, and psychotherapy; a few limited cases may require surgical treatment. Before the treatment is begun, the patient should be told that the prognosis is generally good: many of these conditions have a favorable spontaneous course, both because peripheral vestibular dysfunction tends to improve and because there is central vestibular compensation for asymmetrical peripheral vestibular tone. Moreover, most of these conditions can be treated successfully.

Labyrinthitis

1. Chronic, bilateral dysfunction of the vestibular nerve or the peripheral vestibular organs;

2. Acute, unilateral vestibular dysfunction;

3. Paroxysmal pathological excitation or inhibition of the vestibular nerve or vestibular organs.

Table 2. The presenting manifestations and causes of peripheral vestibular types of vertigo
Treatment is aimed primarily at eradication of the underlying infection and supportive care . Middle ear effusions and mastoiditis should be drained and treated with antibiotics. Meningitis should be treated with culture-directed antibiotics with central nervous system penetration and appropriate consultation. Anti-emetics and anti-nausea medications are helpful during the acute phase.

Peripheral vestibular vertigo

A functional classification of peripheral vestibular disorders divides them into three main types, which can be distinguished on the basis of their typical symptoms and signs (table 2):

Chronic, bilateral peripheral vestibular dysfunction

Oscillopsia on head movement (loss of the vestibulo-ocular reflex)

Unsteadiness of stance and gait, worsening in darkness and on uneven ground (because of the partial or total removal of visual or somatosensory cues)

Impairment of spatial memory

Bilateral vestibulopathy due to (e.g.):

ototoxic substances (aminoglycosides)

bilateral Menière's disease

meningitis

bilateral acoustic neuromas
(= neurofibromatosis type 2)

Acute/subacute unilateral vestibular dysfunction (labyrinth and/or vestibular nerve) with asymmetrical vestibular tone

Rotatory vertigo (lasting a few days to weeks),

Oscillopsia due to spontaneous nystagmus,

Tendency to fall to a particular side

Nausea

due to reactivation of a latent herpes simplex virus type 1 infection

Inappropriate unilateral paroxysmal excitation or loss of function of the peripheral vestibular system

Attacks of rotational or swaying vertigo that (depending on their cause) may or may not be externally precipitated, are of varying duration, and are accompanied by various other symptoms

Benign peripheral paroxysmal positioning vertigo due to canalolilthiasis;

Menière's disease due to rupture of the endolymphatic membrane; Vestibular paroxysm due to neurovascular contact

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Benign paroxysmal positioning vertigo (BPPV)
Epley Maneuver to treat BPPV Vertigo Deep Head Hanging Maneuver to treat BPPV Vertigo Lempert (BBQ) Maneuver to treat BPPV Vertigo Half Somersault Maneuver to treat BPPV Vertigo Figure 10. The treatment of benign paroxysmal positioning vertigo with the Semont maneuver
This is the most common type of vertigo; it mainly affects older patients (Table 1) and has a lifetime prevalence of 2.4% . It is characterized by brief attacks of rotational vertigo, accompanied by vertical positioning nystagmus that rotates toward the lower of the two ears and beats toward the forehead. Nystagmus is a term used to describe alternating slow and fast movements of the eyes . These alternating movements give the appearance that the eyes are beating toward one or more directions. The attacks are precipitated by reclination of the head, or by lateral positioning of the head or body, with the affected ear downward . After a change in position of one of these types, rotational vertigo and nystagmus arise after a latency of a few seconds and then take a characteristic crescendo-decrescendo course, lasting a total of 30 to 60 seconds . The nystagmus corresponds to a so-called ampullofugal excitation of the affected posterior vertical semicircular canal of the affected (lower) ear.

The canalolithiasis hypothesis explains all of the manifestations of positioning vertigo and nystagmus . According to this hypothesis, the condition is due to the presence of agglomerates of many otoconia (small crystals of calcium carbonate in the saccule and utricle of the inner ear) that nearly fill the lumen of the semicircular canal and are freely mobile within it, instead of the small pieces of particulate matter that adhere firmly to the cupula (so-called cupulolithiasis).

Benign paroxysmal positioning vertigo is treated with positioning maneuvers: rapid repositioning of the head can move the otoconial agglomerate out of the semicircular canal so that it can no longer cause positioning vertigo . The treatments of choice are the Semont and Epley maneuvers. For the Semont maneuver, see Figure 7; the Epley maneuver involves rotation of the patient in the recumbent position with the head hanging down. Most patients can perform these maneuvers themselves after brief training. The two are equally effective, and the cure rate is more than 95% within a few days, as shown by multiple controlled studies and meta-analyses . The rate of recurrence of benign paroxysmal positioning vertigo is about 15% to 30% per year. The symptoms eventually recur at some time after effective treatment in about 50% of patients but can then be treated effectively a second time in the same manner.

Footnote: The illustration shows the treatment of benign paroxysmal positioning vertigo (BPPV) due to canalolithiasis of the right posterior semicircular canal.

a) In the initial, sitting position, the head is turned 45° to the side of the unaffected ("healthy") ear.

b) The patient is laid on the right side, i.e., on the side of the affected ear, while the head is kept in 45° of rotation to the other side. This induces movement of the particulate matter in the posterior semicircular canal by gravity, leading to rotatory nystagmus toward the lower ear that extinguishes after a brief interval. The patient should maintain this position for about one minute.

c) While the head is still kept in 45° of rotation toward the side of the healthy ear, the patient is rapidly swung over to the side of the unaffected ear, so that the nose now points downward. The particulate matter in the semicircular canal now moves toward the exit from the canal. This position, too, should be maintained for at least one minute.

d) The patient returns slowly to the initial, sitting position. The particulate matter settles in the utricular space, where it can no longer induce rotatory vertigo. This sequence (a-d) should be performed three times in a row three times per day, in the morning, at noon, and at night. Most patients are free of symptoms after doing this for three days.

Persistent rotational vertigo with a pathological inclination of the visual vertical axis toward the side of the affected labyrinth

Spontaneous, horizontally rotating nystagmus toward the unaffected side, producing apparent movement of the environment ("oscillopsia")

Gait deviation and falling tendency toward the affected side

Nausea and vomiting

Unilateral dysfunction of the horizontal semicircular canal, as revealed by the Halmagyi-Curthoys head impulse test for the function of the vestibulo-ocular reflex, as well as by caloric testing.

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Symptomatic treatment: antivertiginous medications, such as 100 to 300 mg of dimenhydrinate, should be given only in the first three days and only if necessary to treat severe nausea and vomiting, because they delay the development of central compensation mechanisms.

"Causal" treatment: a four-armed, placebo-controlled trial was performed, based on the assumption that vestibular neuritis is caused by the reactivation of a latent herpes simplex virus type 1 infection. The trial revealed that monotherapy with a glucocorticoid-methylprednisolone at an initial dose of 100 mg daily, reduced in 20-mg steps every four days, significantly improved the recovery of peripheral vestibular function. The administration of valacyclovir alone had no effect, nor did its administration in combination with the glucocorticoid have any additional effect .

Physical therapy: a further principle of treatment is the promotion of central compensation by physical therapy. Equilibrium training significantly lessens the time required for vestibulospinal compensation and postural regulation to develop . Voluntary eye movements and fixation are exercised in order to improve impaired visual fixation; furthermore, active head movements are exercised to realign the vestibular reflex, as well as balance tasks and goal-directed movements.

Vestibular neuritis

The clinical syndrome of vestibular neuritis is characterized by the following:

A viral and/or autoimmune as cause for vestibular neuritis is probable but has not yet been proven. Autopsy studies have revealed inflammatory degeneration of the vestibular nerve, the presence of viral DNA from herpes simplex virus type I, and the so-called "latency-associated transcript" (LAT) in vestibular ganglion cells . The treatment is symptomatic, causal, and physiotherapeutic:

Menière's disease

Its treatment is based on two principles:

Treatment of individual attacks: vertigo and nausea can be improved with antivertiginous medications just as in the treatment of other types of acute labyrinthine dysfunction. For example, 100 mg dimenhydrate suppositories can be used.

Attack prophylaxis: this type of treatment is aimed at improving the underlying endolymphatic hydrops. Despite the high prevalence of Menière's disease and the large number of clinical studies that have been performed, there is still no treatment of this type that has been conclusively shown to be effective. The spectrum of recommendations ranges from a sodium-free diet to diuretics, transtympanic gentamicin instillation (20 to 40 mg given repeatedly, at intervals of several weeks, until symptoms improve), betahistine, and surgical procedures . A beneficial effect on the frequency of attacks has been reported for transtympanic gentamicin and for the prolonged high-dose administration of betahistine hydrochloride (48 mg tid for 12 months). The latter dose of betahistine hydrochloride is currently recommended on the basis of a recently reported observational treatment study in 112 patients who were treated for at least 12 months at doses of 16, 24, or 48 mg tid . The highest dose led to a statistically significantly greater reduction of attack frequency and was well tolerated.

Vestibular Schwannoma

Patients may present with episodic or positional vertigo, disequilibrium, tinnitus, and usually asymmetric hearing loss. Early in the disease, when the tumor is small, patients complain of dizziness, hearing loss, and tinnitus, due to compression of the vestibulocochlear nerve. The slow growth often allows for central compensation, alleviating vertigo. With continued growth, the tumor can press against the facial or trigeminal nerve causing facial weakness and numbness, respectively. Eventually, the tumor grows to a size where it compresses the brainstem and cerebellum causing truncal ataxia, dysmetria, disequilibrium, and possibly death.

Diagnosis begins with a thorough history and physical examination. An audiogram is important in documenting hearing loss and any asymmetries which may exist. If you suspect vestibular schwannoma, then imaging is necessary. Computed tomography of the head with contrast is helpful, but magnetic resonance imaging with and without enhancement is the preferred imaging modality.

Once vestibular schwannoma is confirmed radiographically, a decision should be made on how to proceed with treatment. Treatment options include surgical excision, radiation therapy, and observation with serial magnetic resonance imaging. In making this decision, one should consider the size of the lesion, age and health of the patient, and what symptoms are present. These patients should be referred to a neuro-otologist for management of their care.

Central vestibular syndromes

Motion sickness

Motion sickness is attributed to an incongruence in the sensory input from the vestibular, visual, and somato-sensory systems . Motion sickness occurs while riding in a car, boat, or airplane if the vestibular and somato-sensory systems sense movement, but the visual system does not.

On the first sensation of motion sickness, efforts should be made to bring vestibular, visual, and somato-sensory input back in congruence. For example, a person on a boat who starts to feel seasick should immediately watch the horizon. Seasickness can be prevented by applying a scopolamine patch (Transderm-Scop) behind one ear at least four hours before boating .

Vertebrobasilar Ischemic Stroke

The blood supply to the brainstem, cerebellum, and inner ear is derived from the vertebrobasilar system . Occlusion of any of the major branches of this system may result in vertigo. Symptoms of vertebrobasilar ischemic stroke are highly variable and depend on which of the three major circumferential branches are occluded; the posterior inferior cerebellar artery, anterior inferior cerebellar artery, or superior cerebellar artery. Numerous processes may occlude the vertebrobasilar system. The most common are atherosclerosis, emboli, and vertebral artery dissection. Vertebral artery dissection can result from trauma or neck manipulation, or can occur spontaneously. Less common causes include subclavian steal syndrome, hypercoagulation disorders, and inflammatory conditions.

As mentioned earlier, the symptoms associated with ischemic stroke in this area are highly variable and greatly dependent upon which branch of the system is occluded. Occlusion of the posterior inferior cerebellar artery will cause a lateral medullary infarction and result in lateral medullary syndrome, also known as Wallenberg's syndrome. Expected manifestations include vertigo, nystagmus, gait disturbance, ipsilateral limb ataxia and facial pain or numbness, contralateral body hemianesthesia, Horner's syndrome, dysphagia, hoarseness, and rarely, facial nerve paralysis.

Lateral pontomedullary infarction secondary to occlusion of the anterior inferior cerebellar artery will result in lateral inferior pontine syndrome. This syndrome is characterized by symptoms similar to Wallenberg's syndrome with notable differences. Involvement of cranial nerves VII and VIII results in ipsilateral facial paralysis and tinnitus and hearing loss, respectively. Dysphagia and hoarseness, however, are not apparent as cranial nerves IX and X nuclei are uninvolved with occlusion of the anterior inferior cerebellar artery.

Lateral superior pontine syndrome occurs when the superior cerebellar artery is occluded. With this syndrome, one can expect vertigo, nystagmus, gait disturbance, ipsilateral limb ataxia and facial pain or numbness, contralateral body hemianesthesia, and Horner's syndrome. Distinguishing this syndrome is the finding of contralateral impairment of vibration and temperature due to medial lemniscus involvement.

A high index of suspicion must be kept with any patient presenting with spontaneous vertigo to avoid missing the diagnosis of ischemic stroke. It is essential to consider stroke in any acutely vertiginous patient with concomitant neurological signs and symptoms. Once vertebrobasilar ischemic stroke is suspected, an expeditious work-up is necessary. This should include a thorough physical examination, imaging, and neurology consultation for both evaluation and treatment.

Vertebrobasilar Insufficiency

Vertebrobasilar insufficiency is a common cause of vertigo in the elderly. Symptoms may last from minutes to hours, but typically average 8 minutes in duration. In as many as one third of patients, vertigo is the only manifestation of their disease. Although this disease should always be in the differential, several months of recurrent vertigo unaccompanied by other neurological signs suggests another disorder. The likelihood of immediate stroke is less in patients presenting with only episodic vertigo. Patients who also present with paresis, blindness, or altered consciousness, however, should be evaluated urgently for fear of impending stroke. Evaluation is similar to that of an ischemic stroke. Treatment includes antiplatelets, anticoagulation, possible thrombolysis and percutaneous transluminal angioplasty, and neurological consultation.

The sudden onset of vertigo in a patient with additional neurologic symptoms (e.g., diplopia, dysarthria, dysphagia, ataxia, weakness) suggests the presence of vascular ischemia.

Treatment of transient ischemic attack and stroke includes preventing future events through blood pressure control, cholesterol-level lowering, smoking cessation, inhibition of platelet function (e.g., aspirin, clopidogrel [Plavix], aspirin-dipyridamole [Aggrenox]) and, possibly, anticoagulation (warfarin [Coumadin]).

Downbeat and upbeat nystagmus

Episodic ataxia type 2
Clinical features

The patient has postural vertigo with unsteadiness of stance and gait; the neurological examination and ancillary tests are generally unremarkable

Fluctuating unsteadiness of stance and gait with attacks of fear of falling, but without an actual fall

Anxiety and autonomic disturbances sometimes occur during or just after the attacks

The attacks are precipitated or exacerbated by typical situations, e.g., crowds, empty spaces, driving

The symptoms often improve during sporting activity or after the consumption of a small amount of alcohol

Increasingly severe avoidance behavior is common

The familial episodic ataxias are rare genetic diseases of autosomal dominant transmission. There are at least two well-defined varieties. Type 2 (EA 2) is characterized by recurrent attacks of dizziness and ataxia that are precipitated by physical activity, stress, or alcohol and usually last for hours. In between attacks, more than 90% of patients have marked central ocular motor disturbances, often downbeat nystagmus. EA 2 is caused by mutations in the CACNA1A gene (PQ calcium channel gene). Most patients can be treated successfully with acetazolamide. If this treatment is ineffective, or if adverse effects such as kidney stones develop, patients with EA 2 can also be treated with 4-aminopyridine (5 mg tid) .
Treatment

A thorough diagnostic assessment to allay the patient's fear of having a serious organic disease

Psycho-educative therapy to inform the patient about the pathological mechanism and the precipitating factors and situations

Desensitization by self-exposure, i.e., the deliberate seeking out of situations that precipitate vertigo. Light sporting activities are also helpful.

If the symptoms persist, pharmacotherapy, e.g., with selective serotonin reuptake inhibitors, and/or cognitive behavioral therapy are indicated

Aminopyridines are thus an effective treatment for downbeat nystagmus, upbeat nystagmus, and episodic ataxias type 2 which is well tolerated at the low dose that is generally used. These studies have also led to the development of a new principle of treatment; activation of cerebellar Purkinje cells through potassium-channel blockade enhances the cerebellar inhibitory influence on the vestibular and cerebellar nuclei.

Vestibular migraine or migraine with vestibular aura

Phobic postural vertigo

Phobic postural vertigo is the second most common diagnosis in a specialized neurological ambulatory clinic for dizziness and vertigo. This disorder is not found in the diagnostic repertoire of most neurologists and ENT specialists. Patients with phobic postural vertigo usually complain of swaying vertigo, lightheadedness, and gait unsteadiness that are continually present but fluctuate in severity. These symptoms are often accompanied by anxiety and are situationally dependent. The precipitating factor may be the presence of a large crowd, or waiting in the check-out line at a store; often, avoidance behavior results . The symptoms typically improve when the patient participates in sports or has had a small amount of alcohol to drink. The affected patients often have an obsessive-compulsive personality, in the sense of "accentuated" personality traits, with a marked tendency toward introspection and a need to "have everything under control." The central problem in phobic postural vertigo is the patient's attempt to establish conscious control over body equilibrium, which leads to a "spiral of self-observation." When this happens, the body's own movements may be perceived as movements of the outside world. The main features of this disorder and its treatment are summarized in the box. The clinical neurological examination and ancillary tests reveal no relevant pathological findings.

The patient's personality is usually of an obsessive-compulsive or reactive-depressive type. At the onset of the disorder, there is often a vestibular disturbance (25%) or a situation giving rise to particular stress (70%).

Treatment markedly improves symptoms in about 70% of patients .

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Inner Ear Problems - Causes & Treatment of inner ear Dizziness & Vertigo

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Inner ear anatomy - function of inner ear bones, fluid & crystals. What causes inner ear dizziness & balance problems. How to treat inner ear vertigo & dizziness.

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Weitere:

https://healthjade.com/inner-ear-problems/

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The ear is divided into three anatomical regions: the external ear, the middle ear, and the internal ear (Figure 2). The external ear is the visible portion of the ear, and it collects and directs sound waves to the eardrum. The middle ear is a chamber located within the petrous portion of the temporal bone. Structures within the middle ear amplify sound waves and transmit them to an appropriate portion of the internal ear. The internal ear contains the sensory organs for equilibrium (balance) and hearing.
Figure 1. Ear structure Figure 2. Ear anatomy
Parts of the ear

External (Outer) Ear

The external (outer) ear consists of the auricle, external auditory canal, and eardrum (Figure 1 and 2). The auricle or pinna is a flap of elastic cartilage shaped like the flared end of a trumpet and covered by skin. The rim of the auricle is the helix; the inferior portion is the lobule. Ligaments and muscles attach the auricle to the head. The external auditory canal is a curved tube about 2.5 cm (1 in.) long that lies in the temporal bone and leads to the eardrum.

The tympanic membrane or ear drum is a thin, semitransparent partition between the external auditory canal and middle ear. The tympanic membrane is covered by epidermis and lined by simple cuboidal epithelium. Between the epithelial layers is connective tissue composed of collagen, elastic fibers, and fibroblasts. Tearing of the tympanic membrane is called a perforated eardrum. It may be due to pressure from a cotton swab, trauma, or a middle ear infection, and usually heals within a month. The tympanic membrane may be examined directly by an otoscope, a viewing instrument that illuminates and magnifies the external auditory canal and tympanic membrane.

Near the exterior opening, the external auditory canal contains a few hairs and specialized sweat glands called ceruminous glands that secrete earwax or cerumen. The combination of hairs and cerumen helps prevent dust and foreign objects from entering the ear. Cerumen also prevents damage to the delicate skin of the external ear canal by water and insects. Cerumen usually dries up and falls out of the ear canal. However, some people produce a large amount of cerumen, which can become impacted and can muffle incoming sounds. The treatment for impacted cerumen is usually periodic ear irrigation or removal of wax with a blunt instrument by trained medical personnel.

The middle ear is a small, air-filled cavity in the petrous portion of the temporal bone that is lined by epithelium. It is separated from the external ear by the tympanic membrane and from the internal ear by a thin bony partition that contains two small openings: the oval window and the round window.

Extending across the middle ear and attached to it by ligaments are the three smallest bones in the body, the auditory ossicles, which are connected by synovial joints. The bones, named for their shapes, are the malleus, incus, and stapes-commonly called the hammer, anvil, and stirrup, respectively. The "handle" of the malleus attaches to the internal surface of the tympanic membrane. The head of the malleus articulates with the body of the incus. The incus, the middle bone in the series, articulates with the head of the stapes. The base or footplate of the stapes fits into the oval window. Directly below the oval window is another opening, the round window, which is enclosed by a membrane called the secondary tympanic membrane. Besides the ligaments, two tiny skeletal muscles also attach to the ossicles (Figure 3).
Figure 3. Middle ear and auditory ossicles
The tensor tympani muscle, which is supplied by the mandibular branch of the trigeminal (V) nerve, limits movement and increases tension on the eardrum to prevent damage to the inner ear from loud noises. The stapedius muscle, which is supplied by the facial (VII) nerve, is the smallest skeletal muscle in the human body. By dampening large vibrations of the stapes due to loud noises, it protects the oval window, but it also decreases the sensitivity of hearing. For this reason, paralysis of the stapedius muscle is associated with hyperacusia, which is abnormally sensitive hearing. Because it takes a fraction of a second for the tensor tympani and stapedius muscles to contract, they can protect the inner ear from prolonged loud noises but not from brief ones such as a gunshot.

The anterior wall of the middle ear contains an opening that leads directly into the auditory tube or pharyngotympanic tube, commonly known as the eustachian tube. The auditory tube, which consists of both bone and elastic cartilage, connects the middle ear with the nasopharynx (superior portion of the throat). It is normally closed at its medial (pharyngeal) end. During swallowing and yawning, it opens, allowing air to enter or leave the middle ear until the pressure in the middle ear equals the atmospheric pressure. Most of us have experienced our ears popping as the pressures equalize. When the pressures are balanced, the tympanic membrane vibrates freely as sound waves strike it. If the pressure is not equalized, intense pain, hearing impairment, ringing in the ears, and vertigo could develop. The auditory tube also is a route for pathogens to travel from the nose and throat to the middle ear, causing the most common type of ear infection.

Internal (Inner)

Ear The internal (inner) ear is also called the labyrinth because of its complicated series of canals (Figure 4, 5 and 6). Structurally, it consists of two main divisions: an outer bony labyrinth that encloses an inner membranous labyrinth. It is like long balloons put inside a rigid tube. The bony labyrinth is a series of cavities in the petrous portion of the temporal bone divided into three areas: (1) the semicircular canals, (2) the vestibule, and (3) the cochlea.
Figure 4. Parts of the inner ear
The bony labyrinth is lined with periosteum and contains perilymph. This fluid, which is chemically similar to cerebrospinal fluid, surrounds the membranous labyrinth, a series of epithelial sacs and tubes inside the bony labyrinth that have the same general form as the bony labyrinth and house the receptors for hearing and equilibrium. The epithelial membranous labyrinth contains endolymph. The level of potassium ions (K+) in endolymph is unusually high for an extracellular fluid, and potassium ions play a role in the generation of auditory signals.

The vestibule is the oval central portion of the bony labyrinth. The membranous labyrinth in the vestibule consists of two sacs called the utricle (little bag) and the saccule (little sac), which are connected by a small duct. Projecting superiorly and posteriorly from the vestibule are the three bony semicircular canals, each of which lies at approximately right angles to the other two. Based on their positions, they are named the anterior, posterior, and lateral semicircular canals. The anterior and posterior semicircular canals are vertically oriented; the lateral one is horizontally oriented. At one end of each canal is a swollen enlargement called the ampulla. The portions of the membranous labyrinth that lie inside the bony semicircular canals are called the semicircular ducts. These structures connect with the utricle of the vestibule.

The vestibular branch of the vestibulocochlear (cranial nerve VIII) nerve consists of ampullary, utricular, and saccular nerves. These nerves contain both first-order sensory neurons and efferent neurons that synapse with receptors for equilibrium. The first-order sensory neurons carry sensory information from the receptors, and the efferent neurons carry feedback signals to the receptors, apparently to modify their sensitivity. Cell bodies of the sensory neurons are located in the vestibular ganglia.
Figure 5. Inner ear bones
Note: A closer look at the inner ear. Perilymph separates the bony (osseous) labyrinth of the inner ear from the membranous labyrinth, which contains endolymph. Note that areas of bony labyrinth have been removed to reveal underlying structures.
Figure 6. The Cochlea (cross section view)
Note: a) Cross section of the cochlea. (b) The spiral organ and the tectorial membrane.

Anterior to the vestibule is the cochlea, a bony spiral canal that resembles a snail's shell and makes almost three turns around a central bony core called the modiolus. Sections through the cochlea reveal that it is divided into three channels: cochlear duct, scala vestibuli, and scala tympani. The cochlear duct or scala media is a continuation of the membranous labyrinth into the cochlea; it is filled with endolymph. The channel above the cochlear duct is the scala vestibuli, which ends at the oval window. The channel below is the scala tympani, which ends at the round window. Both the scala vestibuli and scala tympani are part of the bony labyrinth of the cochlea; therefore, these chambers are filled with perilymph. The scala vestibuli and scala tympani are completely separated by the cochlear duct, except for an opening at the apex of the cochlea, the helicotrema.

The cochlea adjoins the wall of the vestibule, into which the scala vestibuli opens. The perilymph in the vestibule is continuous with that of the scala vestibuli. The vestibular membrane separates the cochlear duct from the scala vestibuli, and the basilar membrane separates the cochlear duct from the scala tympani. Resting on the basilar membrane is the spiral organ or organ of Corti. The spiral organ is a coiled sheet of epithelial cells, including supporting cells and about 16,000 hair cells, which are the receptors for hearing.

There are two groups of hair cells: The inner hair cells are arranged in a single row, whereas the outer hair cells are arranged in three rows. At the apical tip of each hair cell are stereocilia that extend into the endolymph of the cochlear duct. Despite their name, stereocilia are actually long, hairlike microvilli arranged in several rows of graded height.

At their basal ends, inner and outer hair cells synapse both with first-order sensory neurons and with motor neurons from the cochlear branch of the vestibulocochlear (VIII) nerve. Cell bodies of the sensory neurons are located in the spiral ganglion. Although outer hair cells outnumber them by 3 to 1, the inner hair cells synapse with 90-95% of the first-order sensory neurons in the cochlear nerve that relay auditory information to the brain. By contrast, 90% of the motor neurons in the cochlear nerve synapse with outer hair cells. The tectorial membrane, a flexible gelatinous membrane, covers the hair cells of the spiral organ. In fact, the ends of the stereocilia of the hair cells are embedded in the tectorial membrane while the bodies of the hair cells rest on the basilar membrane. Inner and outer hair cells have diff erent functional roles. Inner hair cells are the receptors for hearing: They convert the mechanical vibrations of sound into electrical signals. Outer hair cells do not serve as hearing receptors; instead, they increase the sensitivity of the inner hair cells.

Mechanism for Hearing

First, sound vibrations travel from the eardrum through the ossicles, causing the stapes to oscillate back and forth against the oval window. This oscillation sets up pressure waves in the perilymph of the scala vestibuli, which are transferred to the endolymph of the cochlear duct. These waves cause the basilar membrane to vibrate up and down. The hair cells in the spiral organ move along with the basilar membrane, but the overlying tectorial membrane (in which the hairs are anchored) does not move. Therefore, the movements of the hair cells cause their hairs to bend. Each time such bending occurs in a specific direction, the hair cells release neurotransmitters that excite the cochlear nerve fibers, which carry the vibratory (sound) information to the brain. The vibrations of the basilar membrane set the perilymph vibrating in the underlying scala tympani. These vibrations then travel to the round window, where they push on the membrane that covers that window, thereby dissipating their remaining energy into the air of the middle ear cavity. Without this release mechanism, echoes would reverberate within the rigid cochlear box, disrupting sound reception.

The inner and outer hair cells in the spiral organ have different functions. The inner hair cells are the true receptors that transmit the vibrations of the basilar membrane to the cochlear nerve. The outer hair cells are involved with actively tuning the cochlea and amplifying the signal. The outer hair cells receive efferent fibers from the brain that cause these cells to stretch and contract, enhancing the responsiveness of the inner hair cell receptors. Overall, this active mechanism amplifies sounds some 100 times, so that we can hear the faintest sounds.The mobility of the outer hair cells is also responsible for producing ear sounds (otoacoustic emissions). Detection of spontaneous otoacoustic emissions is used to test hearing in newborns.

Ear problems

Swimmer's ear

Swimmer's ear is an infection in the outer ear canal, which runs from your eardrum to the outside of your head . It's often brought on by water that remains in your ear after swimming, creating a moist environment that aids bacterial growth.

Putting fingers, cotton swabs or other objects in your ears also can lead to swimmer's ear by damaging the thin layer of skin lining your ear canal .

Swimmer's ear is also known as otitis externa. The most common cause of this infection is bacteria invading the skin inside your ear canal. Usually you can treat swimmer's ear with eardrops. Prompt treatment can help prevent complications and more-serious infections.

Causes of Swimmer's ear

Swimmer's ear is an infection that's usually caused by bacteria commonly found in water and soil. Infections caused by a fungus or a virus are less common. Swimmer's ear is more common among children in their teens and young adults. It may occur with a middle ear infection or a respiratory infection such as a cold.

Swimming in unclean water can lead to swimmer's ear. Bacteria commonly often found in water can cause ear infections. Rarely, the infection may be caused by a fungus.
Other causes of swimmer's ear include:

Scratching the ear or inside the ear

Getting something stuck in the ear

Trying to clean (wax from the ear canal) with cotton swabs or small objects can damage the skin.
Long-term (chronic) swimmer's ear may be due to:

Allergic reaction to something placed in the ear

Chronic skin conditions, such as eczema or psoriasis

Your ear's natural defenses
Your outer ear canals have natural defenses that help keep them clean and prevent infection. Protective features include:

Glands that secrete a waxy substance (cerumen). These secretions form a thin, water-repellent film on the skin inside your ear. Cerumen is also slightly acidic, which helps further discourage bacterial growth. In addition, cerumen collects dirt, dead skin cells and other debris and helps move these particles out of your ear. The waxy clump that results is the familiar earwax you find at the opening of your ear canal.

Downward slope of your ear canal. Your ear canal slopes down slightly from your middle ear to your outer ear, helping water drain out.

How the swimmer's ear occurs

If you have swimmer's ear, your natural defenses have been overwhelmed. Conditions that can weaken your ear's defenses and promote bacterial growth include:

Risk factors for swimmer's ear

Swimming

Swimming in water with elevated bacteria levels, such as a lake rather than a well-maintained pool

A narrow ear canal - for example, in a child - that can more easily trap water

Aggressive cleaning of the ear canal with cotton swabs or other objects

Use of certain devices, such as headphones or a hearing aid

Skin allergies or irritation from jewelry, hair spray or hair dyes

Factors that may increase your risk of swimmer's ear include:

Symptoms of Swimmer's ear
Mild signs and symptoms Moderate progression

More intense itching

Increasing pain

More extensive redness in your ear

Excessive fluid drainage

Discharge of pus

Feeling of fullness inside your ear and partial blockage of your ear canal by swelling, fluid and debris

Decreased or muffled hearing

Advanced progression
Swimmer's ear symptoms are usually mild at first, but they may get worse if your infection isn't treated or spreads. Doctors often classify swimmer's ear according to mild, moderate and advanced stages of progression.

When to see a doctor

See your doctor if you're experiencing any signs or symptoms of swimmer's ear, even if they're mild.

Call your doctor immediately or visit the emergency room if you have:

Complications of Swimmer's ear

Swimmer's ear usually isn't serious if treated promptly, but complications can occur.

Prevention of Swimmer's ear

Keep your ears dry. Dry your ears thoroughly after exposure to moisture from swimming or bathing. Dry only your outer ear, wiping it slowly and gently with a soft towel or cloth. Tip your head to the side to help water drain from your ear canal. You can dry your ears with a blow dryer if you put it on the lowest setting and hold it at least a foot (about 0.3 meters) away from the ear.

At-home preventive treatment. If you know you don't have a punctured eardrum, you can use homemade preventive eardrops before and after swimming. A mixture of 1 part white vinegar to 1 part rubbing alcohol may help promote drying and prevent the growth of bacteria and fungi that can cause swimmer's ear. Pour 1 teaspoon (about 5 milliliters) of the solution into each ear and let it drain back out. Similar over-the-counter solutions may be available at your drugstore.

Swim wisely. Watch for signs alerting swimmers to high bacterial counts and don't swim on those days.

DO NOT scratch the ears or insert cotton swabs or other objects in the ears.

Avoid putting foreign objects in your ear. Never attempt to scratch an itch or dig out earwax with items such as a cotton swab, paper clip or hairpin. Using these items can pack material deeper into your ear canal, irritate the thin skin inside your ear or break the skin.

Protect your ears from irritants. Put cotton balls in your ears while applying products such as hair sprays and hair dyes.

Use caution after an ear infection or surgery. If you've recently had an ear infection or ear surgery, talk to your doctor before you go swimming.

Follow these tips to avoid swimmer's ear:

Diagnosis of swimmer's ear

Doctors can usually diagnose swimmer's ear during an office visit. If your infection is at an advanced stage or persists, you may need further evaluation.
Initial testing

Examination of your ear canal with a lighted instrument (otoscope). Your ear canal may appear red, swollen and scaly. Flakes of skin and other debris may be present in the ear canal.

Visualization of your eardrum (tympanic membrane) to be sure it isn't torn or damaged. If the view of your eardrum is blocked, your doctor will clear your ear canal with a small suction device or an instrument with a tiny loop or scoop on the end (ear curette).

Further testing
Your doctor will likely diagnose swimmer's ear based on symptoms you report, questions he or she asks, and an office examination. You probably won't need a lab test at your first visit. Your doctor's initial evaluation will usually include:

If your eardrum is damaged or torn, your doctor will likely refer you to an ear, nose and throat specialist (ENT). The specialist will examine the condition of your middle ear to determine if that's the primary site of infection. This examination is important because some treatments intended for an infection in the outer ear canal aren't appropriate for treating the middle ear.

If your infection doesn't respond to treatment, your doctor may take a sample of discharge or debris from your ear at a later appointment and send it to a lab to identify the exact microorganism causing your infection.

Depending on the initial assessment, symptom severity or the stage of your swimmer's ear, your doctor may recommend additional evaluation.
Cleaning
Treatment for swimmer's ear
Medications for infection
The goal of treatment is to stop the infection and allow your ear canal to heal.

Cleaning your outer ear canal is necessary to help eardrops flow to all infected areas. Your doctor will use a suction device or ear curette to clean away any discharge, clumps of earwax, flaky skin and other debris.

For most cases of swimmer's ear, your doctor will prescribe eardrops that have some combination of the following ingredients, depending on the type and seriousness of your infection:

Ask your doctor about the best method for taking your eardrops. Some ideas that may help you use eardrops include the following:
Medications for pain
If your ear canal is completely blocked by swelling, inflammation or excess discharge, your doctor may insert a wick made of cotton or gauze to promote drainage and help draw medication into your ear canal.

If your infection is more advanced or doesn't respond to treatment with eardrops, your doctor may prescribe oral antibiotics.
Helping your treatment work
Your doctor may recommend easing the discomfort of swimmer's ear with over-the-counter pain relievers, such as ibuprofen (Advil, Motrin IB, others), naproxen sodium (Aleve, others) or acetaminophen (Tylenol, others).

If your pain is severe or your swimmer's ear is at a more advanced stage, your doctor may prescribe a stronger medication for pain relief.

During treatment, the following steps will help keep your ears dry and avoid further irritation:

Ruptured eardrum (perforated eardrum)

A ruptured eardrum - or tympanic membrane perforation as it's medically known - is a hole or tear in the thin tissue that separates your ear canal from your middle ear (eardrum) .

A ruptured eardrum can result in hearing loss. A ruptured eardrum can also make your middle ear vulnerable to infections or injury.

A ruptured eardrum usually heals within a few weeks without treatment. Sometimes, however, a ruptured eardrum requires a procedure or surgical repair to heal.

If you think that you have a ruptured eardrum, be careful to keep your ears dry to prevent infection. Don't go swimming. To keep water out of your ear when showering or bathing, use a moldable, waterproof silicone earplug or put a cotton ball coated with petroleum jelly in your outer ear.

Don't put medication drops in your ear unless your doctor prescribes them specifically for infection related to your perforated eardrum.

Causes of a ruptured or perforated eardrum

Causes of a ruptured, or perforated, eardrum may include:

Hearing. When sound waves strike it, your eardrum vibrates - the first step by which structures of your middle and inner ears translate sound waves into nerve impulses.

Protection. Your eardrum also acts as a barrier, protecting your middle ear from water, bacteria and other foreign substances.

Complications of of a ruptured or perforated eardrum

Your eardrum (tympanic membrane) has two primary roles:

If your eardrum ruptures, complications can occur while your eardrum is healing or if it fails to heal. Possible complications include:

Prevention of a ruptured or perforated eardrum

Follow these tips to avoid a ruptured or perforated eardrum:

Ear pain that may subside quickly

Clear, pus-filled or bloody drainage from your ear

Hearing loss

Ringing in your ear (tinnitus)

Spinning sensation (vertigo)

Nausea or vomiting that can result from vertigo

Symptoms of a ruptured or perforated eardrum

Signs and symptoms of a ruptured eardrum may include:

When to see a doctor

Call your doctor if you experience any of the signs or symptoms of a ruptured eardrum or pain or discomfort in your ears. Your middle and inner ears are composed of delicate mechanisms that are sensitive to injury or disease. Prompt and appropriate treatment is important to preserve your hearing.

Diagnosis of a ruptured or perforated eardrum

Your family doctor or ENT specialist can often determine if you have a perforated eardrum with a visual inspection using a lighted instrument (otoscope).

He or she may conduct or order additional tests to determine the cause of the rupture or degree of damage. These tests include:

Eardrum patch. If the tear or hole in your eardrum doesn't close on its own, an ENT specialist may seal it with a patch. With this office procedure, your ENT doctor may apply a chemical to the edges of the tear to stimulate growth and then apply a patch over the hole. The procedure may need to be repeated more than once before the hole closes.

Surgery. If a patch doesn't result in proper healing or your ENT doctor determines that the tear isn't likely to heal with a patch, he or she may recommend surgery. The most common surgical procedure is called tympanoplasty. Your surgeon grafts a tiny patch of your own tissue to close the hole in the eardrum. This procedure is done on an outpatient basis, meaning you can usually go home the same day unless medical anesthesia conditions require a longer hospital stay.

Treatment of a ruptured or perforated eardrum

Most perforated eardrums heal without treatment within a few weeks. Your doctor may prescribe antibiotic drops if there's evidence of infection. If the tear or hole in your eardrum doesn't heal by itself, treatment will involve procedures to close the perforation. These may include:

Home remedies for a ruptured or perforated eardrum

A ruptured eardrum usually heals on its own within weeks. In some cases, healing takes months. Until your doctor tells you that your ear is healed, protect it by doing the following:

Middle Ear Infection

An middle ear infection (acute otitis media) is most often a bacterial or viral infection that affects the middle ear, the air-filled space behind the eardrum that contains the tiny vibrating bones of the ear . Children are more likely than adults to get ear infections.

Ear infections frequently are painful because of inflammation and buildup of fluids in the middle ear.

Because ear infections often clear up on their own, treatment may begin with managing pain and monitoring the problem. Ear infection in infants and severe cases in general often require antibiotic medications. Long-term problems related to ear infections - persistent fluids in the middle ear, persistent infections or frequent infections - can cause hearing problems and other serious complications.
Children
Symptoms of middle ear infection

Ear pain, especially when lying down

Tugging or pulling at an ear

Difficulty sleeping

Crying more than usual

Acting more irritable than usual

Difficulty hearing or responding to sounds

Loss of balance

Fever of 100 F (38 C) or higher

Drainage of fluid from the ear

Headache

Loss of appetite

Adults
The onset of signs and symptoms of ear infection is usually rapid.

Signs and symptoms common in children include:

Common signs and symptoms in adults include:

When to see a doctor

Signs and symptoms of an ear infection can indicate a number of conditions. It's important to get an accurate diagnosis and prompt treatment. Call your child's doctor if:

An adult with ear pain or discharge should see a doctor as soon as possible.
Role of eustachian tubes
Causes of middle ear infection

An ear infection is caused by a bacterium or virus in the middle ear. This infection often results from another illness - cold, flu or allergy - that causes congestion and swelling of the nasal passages, throat and eustachian tubes.

The eustachian tubes are a pair of narrow tubes that run from each middle ear to high in the back of the throat, behind the nasal passages. The throat end of the tubes open and close to:
Role of adenoids
Swelling, inflammation and mucus in the eustachian tubes from an upper respiratory infection or allergy can block them, causing the accumulation of fluids in the middle ear. A bacterial or viral infection of this fluid is usually what produces the symptoms of an ear infection.

Ear infections are more common in children, in part, because their eustachian tubes are narrower and more horizontal - factors that make them more difficult to drain and more likely to get clogged.
Related conditions
Adenoids are two small pads of tissues high in the back of the nose believed to play a role in immune system activity. This function may make them particularly vulnerable to infection, inflammation and swelling.

Because adenoids are near the opening of the eustachian tubes, inflammation or enlargement of the adenoids may block the tubes, thereby contributing to middle ear infection. Inflammation of adenoids is more likely to play a role in ear infections in children because children have relatively larger adenoids.

Conditions of the middle ear that may be related to an ear infection or result in similar middle ear problems include the following:

Risk factors for middle ear infection

Risk factors for ear infections include:

Complications of middle ear infection

Most ear infections don't cause long-term complications. Frequent or persistent infections and persistent fluid buildup can result in some serious complications:

Prevention of middle ear infection

The following tips may reduce the risk of developing ear infections:
Pneumatic otoscope
Diagnosis of middle ear infection
Additional tests
Your doctor can usually diagnose an ear infection or another condition based on the symptoms you describe and an exam. The doctor will likely use a lighted instrument (an otoscope) to look at the ears, throat and nasal passage. He or she will also likely listen to your child breathe with a stethoscope.

Tympanometry. This test measures the movement of the eardrum. The device, which seals off the ear canal, adjusts air pressure in the canal, thereby causing the eardrum to move. The device quantifies how well the eardrum moves and provides an indirect measure of pressure within the middle ear.

Acoustic reflectometry. This test measures how much sound emitted from a device is reflected back from the eardrum - an indirect measure of fluids in the middle ear. Normally, the eardrum absorbs most of the sound. However, the more pressure there is from fluid in the middle ear, the more sound the eardrum will reflect.

Tympanocentesis. Rarely, a doctor may use a tiny tube that pierces the eardrum to drain fluid from the middle ear - a procedure called tympanocentesis. Tests to determine the infectious agent in the fluid may be beneficial if an infection hasn't responded well to previous treatments.
Other tests. If your child has had persistent ear infections or persistent fluid buildup in the middle ear, your doctor may refer you to a hearing specialist (audiologist), speech therapist or developmental therapist for tests of hearing, speech skills, language comprehension or developmental abilities.

An instrument called a pneumatic otoscope is often the only specialized tool a doctor needs to make a diagnosis of an ear infection. This instrument enables the doctor to look in the ear and judge whether there is fluid behind the eardrum. With the pneumatic otoscope, the doctor gently puffs air against the eardrum. Normally, this puff of air would cause the eardrum to move. If the middle ear is filled with fluid, your doctor will observe little to no movement of the eardrum.

Your doctor may perform other diagnostic tests if there is any doubt about a diagnosis, if the condition hasn't responded to previous treatments, or if there are other persistent or serious problems.

What a diagnosis means
A wait-and-see approach
Treatment for middle ear infection

Children 6 to 23 months with mild inner ear pain in one ear for less than 48 hours and a temperature less than 102.2 F (39 C)

Children 24 months and older with mild inner ear pain in one or both ears for less than 48 hours and a temperature less than 102.2 F (39 C)

Some ear infections resolve without treatment with antibiotics. What's best for your child depends on many factors, including your child's age and the severity of symptoms.
Managing pain
Symptoms of ear infections usually improve within the first couple of days, and most infections clear up on their own within one to two weeks without any treatment. The American Academy of Pediatrics and the American Academy of Family Physicians recommend a wait-and-see approach as one option for:

A warm compress. Placing a warm, moist washcloth over the affected ear may lessen pain.

Pain medication. Your doctor may advise the use of over-the-counter acetaminophen (Tylenol, others) or ibuprofen (Advil, Motrin IB, others) to relieve pain. Use the drugs as directed on the label. Use caution when giving aspirin to children or teenagers. Children and teenagers recovering from chickenpox or flu-like symptoms should never take aspirin because aspirin has been linked with Reye's syndrome. Talk to your doctor if you have concerns.

Antibiotic therapy
Some evidence suggests that treatment with antibiotics might be beneficial for certain children with ear infections. Talk to your doctor about the benefits of antibiotics weighed against the potential side effects and concern about overuse of antibiotics creating strains of resistant disease.

Your doctor will advise you on treatments to lessen pain from an ear infection. These may include the following:

After an initial observation period, your doctor may recommend antibiotic treatment for an ear infection in the following situations:
Ear tubes
Children younger than 6 months of age with confirmed acute otitis media are more likely to be treated with antibiotics without the initial observational waiting time.

Even after symptoms have improved, be sure to use all of the antibiotic as directed. Failing to do so can result in recurring infection and resistance of bacteria to antibiotic medications. Talk to your doctor or pharmacist about what to do if you accidentally skip a dose.

If your child has recurrent otitis media or otitis media with effusion, your doctor may recommend a procedure to drain fluid from the middle ear. Otitis media is defined as three episodes of infection in six months or four episodes of infection in a year with at least one occurring in the past six months. Otitis media with effusion is persistent fluid buildup in the ear after an infection has cleared up or in the absence of any infection.

During an outpatient surgical procedure called a myringotomy, a surgeon creates a tiny hole in the eardrum that enables him or her to suction fluids out of the middle ear. A tiny tube (tympanostomy tube) is placed in the opening to help ventilate the middle ear and prevent the accumulation of more fluids. Some tubes are intended to stay in place for six months to a year and then fall out on their own. Other tubes are designed to stay in longer and may need to be surgically removed.

The eardrum usually closes up again after the tube falls out or is removed.

Treatment for chronic suppurative otitis media

Chronic infection that results in perforation of the eardrum - chronic suppurative otitis media - is difficult to treat. It's often treated with antibiotics administered as drops. You'll receive instructions on how to suction fluids out through the ear canal before administering drops.

Monitoring

Children with frequent or persistent infections or with persistent fluid in the middle ear will need to be monitored closely. Talk to your doctor about how often you should schedule follow-up appointments. Your doctor may recommend regular hearing and language tests.

What is Tinnitus

Tinnitus is the perception of noise or ringing in the ears . A common problem, tinnitus affects about 1 in 5 people. Tinnitus isn't a condition itself - it's a symptom of an underlying condition, such as age-related hearing loss, ear injury or a circulatory system disorder.

Although bothersome, tinnitus usually isn't a sign of something serious. Although it can worsen with age, for many people, tinnitus can improve with treatment. Treating an identified underlying cause sometimes helps. Other treatments reduce or mask the noise, making tinnitus less noticeable.

Symptoms of Tinnitus
There are two kinds of tinnitus.

Subjective tinnitus is tinnitus only you can hear. This is the most common type of tinnitus. It can be caused by ear problems in your outer, middle or inner ear. It also can be caused by problems with the hearing (auditory) nerves or the part of your brain that interprets nerve signals as sound (auditory pathways).

Objective tinnitus is tinnitus your doctor can hear when he or she does an examination. This rare type of tinnitus may be caused by a blood vessel problem, a middle ear bone condition or muscle contractions.

Tinnitus involves the annoying sensation of hearing sound when no external sound is present. Tinnitus symptoms include these types of phantom noises in your ears:

The phantom noise may vary in pitch from a low roar to a high squeal, and you may hear it in one or both ears. In some cases, the sound can be so loud it can interfere with your ability to concentrate or hear actual sound. Tinnitus may be present all the time, or it may come and go.

When to see a doctor

You develop tinnitus after an upper respiratory infection, such as a cold, and your tinnitus doesn't improve within a week.

If you have tinnitus that bothers you, see your doctor.

You have tinnitus that occurs suddenly or without an apparent cause.

You have hearing loss or dizziness with the tinnitus.

Make an appointment to see your doctor if:

See your doctor as soon as possible if:

Causes of Tinnitus

A number of health conditions can cause or worsen tinnitus. In many cases, an exact cause is never found.
Common causes of tinnitus
A common cause of tinnitus is inner ear cell damage. Tiny, delicate hairs in your inner ear move in relation to the pressure of sound waves. This triggers ear cells to release an electrical signal through a nerve from your ear (auditory nerve) to your brain. Your brain interprets these signals as sound. If the hairs inside your inner ear are bent or broken, they can "leak" random electrical impulses to your brain, causing tinnitus.

Age-related hearing loss. For many people, hearing worsens with age, usually starting around age 60. Hearing loss can cause tinnitus. The medical term for this type of hearing loss is presbycusis.

Exposure to loud noise. Loud noises, such as those from heavy equipment, chain saws and firearms, are common sources of noise-related hearing loss.

Portable music devices, such as MP3 players or iPods, also can cause noise-related hearing loss if played loudly for long periods. Tinnitus caused by short-term exposure, such as attending a loud concert, usually goes away; long-term exposure to loud sound can cause permanent damage.

Earwax blockage. Earwax protects your ear canal by trapping dirt and slowing the growth of bacteria. When too much earwax accumulates, it becomes too hard to wash away naturally, causing hearing loss or irritation of the eardrum, which can lead to tinnitus.

Ear bone changes. Stiffening of the bones in your middle ear (otosclerosis) may affect your hearing and cause tinnitus. This condition, caused by abnormal bone growth, tends to run in families.

Other causes of tinnitus
Other causes of tinnitus include other ear problems, chronic health conditions, and injuries or conditions that affect the nerves in your ear or the hearing center in your brain.
Blood vessel disorders linked to tinnitus
In many people, tinnitus is caused by one of these conditions:

Atherosclerosis. With age and buildup of cholesterol and other deposits, major blood vessels close to your middle and inner ear lose some of their elasticity - the ability to flex or expand slightly with each heartbeat. That causes blood flow to become more forceful, making it easier for your ear to detect the beats. You can generally hear this type of tinnitus in both ears.

Head and neck tumors. A tumor that presses on blood vessels in your head or neck (vascular neoplasm) can cause tinnitus and other symptoms.

High blood pressure. Hypertension and factors that increase blood pressure, such as stress, alcohol and caffeine, can make tinnitus more noticeable.

Turbulent blood flow. Narrowing or kinking in a neck artery (carotid artery) or vein in your neck (jugular vein) can cause turbulent, irregular blood flow, leading to tinnitus.

Malformation of capillaries. A condition called arteriovenous malformation (AVM), abnormal connections between arteries and veins, can result in tinnitus. This type of tinnitus generally occurs in only one ear.

Medications that can cause tinnitus
Some causes of tinnitus are less common, including:

Antibiotics, including polymyxin B, erythromycin, vancomycin and neomycin

Cancer medications, including mechlorethamine and vincristine

Water pills (diuretics), such as bumetanide, ethacrynic acid or furosemide

Quinine medications used for malaria or other health conditions

Certain antidepressants may worsen tinnitus

Aspirin taken in uncommonly high doses (usually 12 or more a day)

In rare cases, tinnitus is caused by a blood vessel disorder. This type of tinnitus is called pulsatile tinnitus. Causes include:

A number of medications may cause or worsen tinnitus. Generally, the higher the dose of these medications, the worse tinnitus becomes. Often the unwanted noise disappears when you stop using these drugs. Medications known to cause or worsen tinnitus include:

Loud noise exposure. Prolonged exposure to loud noise can damage the tiny sensory hair cells in your ear that transmit sound to your brain. People who work in noisy environments - such as factory and construction workers, musicians, and soldiers - are particularly at risk.

Age. As you age, the number of functioning nerve fibers in your ears declines, possibly causing hearing problems often associated with tinnitus.

Gender. Men are more likely to experience tinnitus.

Smoking. Smokers have a higher risk of developing tinnitus.

Cardiovascular problems. Conditions that affect your blood flow, such as high blood pressure or narrowed arteries (atherosclerosis), can increase your risk of tinnitus.

Risk factors for Tinnitus

Anyone can experience tinnitus, but these factors may increase your risk:

Fatigue

Stress

Sleep problems

Trouble concentrating

Memory problems

Depression

Anxiety and irritability

Complications of Tinnitus

Tinnitus can significantly affect quality of life. Although it affects people differently, if you have tinnitus, you also may experience:

Treating these linked conditions may not affect tinnitus directly, but it can help you feel better.

Prevention of Tinnitus

In many cases, tinnitus is the result of something that can't be prevented. However, some precautions can help prevent certain kinds of tinnitus.

Diagnosis of Tinnitus

Your doctor will examine your ears, head and neck to look for possible causes of tinnitus. Tests include:

The sounds you hear can help your doctor identify a possible underlying cause.
Treating an underlying health condition
In many cases, the cause of tinnitus is never found. Your doctor can discuss with you steps you can take to reduce the severity of your tinnitus or to help you cope better with the noise.
Noise suppression
Treatment of Tinnitus
Medications
To treat your tinnitus, your doctor will first try to identify any underlying, treatable condition that may be associated with your symptoms. If tinnitus is due to a health condition, your doctor may be able to take steps that could reduce the noise. Examples include:

Tricyclic antidepressants, such as amitriptyline and nortriptyline, have been used with some success. However, these medications are generally used for only severe tinnitus, as they can cause troublesome side effects, including dry mouth, blurred vision, constipation and heart problems.

Alprazolam (Niravam, Xanax) may help reduce tinnitus symptoms, but side effects can include drowsiness and nausea. It can also become habit-forming.

In some cases white noise may help suppress the sound so that it's less bothersome. Your doctor may suggest using an electronic device to suppress the noise. Devices include:

Drugs can't cure tinnitus, but in some cases they may help reduce the severity of symptoms or complications. Possible medications include:
Alternative medicine
Home remedies for Tinnitus

Often, tinnitus can't be treated. Some people, however, get used to it and notice it less than they did at first. For many people, certain adjustments make the symptoms less bothersome. These tips may help:

There's little evidence that alternative medicine treatments work for tinnitus. However, some alternative therapies that have been tried for tinnitus include:

Neuromodulation using transcranial magnetic stimulation (TMS) is a painless, noninvasive therapy that has been successful in reducing tinnitus symptoms for some people. Currently, TMS is utilized more commonly in Europe and in some trials in the U.S. It is still to be determined which patients might benefit from such treatments.

Coping and support for Tinnitus

Tinnitus doesn't always improve or completely go away with treatment. Here are some suggestions to help you cope:

Balance problems

Balance problems are conditions that make you feel unsteady or dizzy. If you are standing, sitting or lying down, you might feel as if you are moving, spinning or floating. If you are walking, you might suddenly feel as if you are tipping over or generally unsteady.

Many body systems - including your muscles, bones, joints, vision, the balance organ in the inner ear, nerves, heart and blood vessels - must work normally for you to have normal balance. When these systems aren't functioning well, you can experience balance problems.

Many medical conditions can cause balance problems. However, most balance problems result from issues in your balance end-organ in the inner ear (vestibular system).

Symptoms of balance problem

Signs and symptoms of balance problems include:

Causes of balance problem

Benign paroxysmal positional vertigo (BPPV). BPPV occurs when calcium crystals in your inner ear - which help control your balance - are dislodged from their normal position and move elsewhere in the inner ear. BPPV is the most common cause of vertigo. You might experience a spinning sensation when turning in bed or tilting your head back to look up.

Meniere's disease. In addition to sudden and severe vertigo, Meniere's disease can cause fluctuating hearing loss and buzzing, ringing or a feeling of fullness in your ear. The cause of Meniere's disease isn't fully known. Meniere's disease is rare and typically develops in people who are between the ages of 20 and 60.

Migraine. Dizziness and sensitivity to motion (vestibular migraine) can occur due to migraine headache. Migraine is a common cause of dizziness.

Acoustic neuroma. This noncancerous (benign), slow-growing tumor develops on a nerve that affects your hearing and balance. You might experience dizziness or loss of balance, but the most common symptoms are hearing loss and ringing in your ear. Acoustic neuroma is a rare condition.

Vestibular neuritis. This inflammatory disorder, probably caused by a virus, can affect the nerves in the balance portion of your inner ear. Symptoms are often severe and persistent, and include nausea and difficulty walking. Symptoms can last several days and gradually improve on their own.

Ramsay Hunt syndrome. Also known as herpes zoster otitis, this condition occurs when a shingles infection affects the facial nerve near one of your ears. You might experience vertigo, ear pain and hearing loss.

Head injury. You might experience vertigo due to a concussion or other head injury.

Motion sickness. You might experience dizziness in boats, cars and airplanes, or on amusement park rides.

Persistent postural-perceptual dizziness. This disorder occurs frequently with other types of vertigo. Symptoms include unsteadiness or a sensation of motion in your head. Symptoms often worsen when you watch objects move, when you read, or when you are in a visually complex environment such as a shopping mall.

Feeling of faintness (presyncope)
Balance problems can be caused by several different conditions. The cause of balance problems is usually related to the specific sign or symptom.
Sense of motion or spinning (vertigo)

Orthostatic hypotension (postural hypotension). Standing or sitting up too quickly can cause some people to experience a significant drop in their blood pressure, resulting in presyncope.

Cardiovascular disease. Abnormal heart rhythms (heart arrhythmia), narrowed or blocked blood vessels, a thickened heart muscle (hypertrophic cardiomyopathy), or a decrease in blood volume can reduce blood flow and cause presyncope.

Loss of balance (disequilibrium)
Vertigo can be associated with many conditions, including:
Dizziness
Presyncope can be associated with:

Losing your balance while walking, or feeling imbalanced, can result from:

A sense of dizziness or lightheadedness can result from:

Diagnosis of balance problem

Hearing tests. Difficulties with hearing are frequently associated with balance problems.

Posturography test. Wearing a safety harness, you try to remain standing on a moving platform. A posturography test indicates which parts of your balance system you rely on most.

Electronystagmography and video nystagmography. Both tests record your eye movements, which play a role in vestibular function and balance. Electronystagmography uses electrodes and video nystagmography uses small cameras to record eye movements.

Rotary chair test. Your eye movements are analyzed while you sit in a computer-controlled chair that moves slowly in one place in a circle.

Dix-Hallpike maneuver. Your doctor carefully turns your head in different positions while watching your eye movements to determine if you have a false sense of motion or spinning.

Vestibular evoked myogenic potentials test. Sensor pads attached to your neck and forehead and under your eyes measure tiny changes in muscle contractions in reaction to sounds.

Imaging tests. MRI and CT scans can determine if underlying medical conditions might be causing your balance problem.

Blood pressure and heart rate tests. Your blood pressure might be checked when sitting and then after standing for 2 to 3 minutes to determine if you have significant drops in blood pressure. Your heart rate might be checked when standing to help determine if a heart condition is causing your symptoms.

Your doctor will start by reviewing your medical history and conducting a physical and neurological examination.

To determine if your symptoms are caused by problems in the balance function in your inner ear, your doctor is likely to recommend tests. They might include:

Treatment of balance problem

Treatment depends on the cause of your balance problems. Your treatment may include:

What is hearing loss ?

The ear can be divided into three parts:

Sound waves enter the ear canal and cause a vibration of the tympanic membrane (ear drum) which is then passed through three tiny bones behind the ear drum in the middle ear space: the malleus (hammer), incus (anvil) and stapes (stirrup). The sound vibrations in the ossicles are then transmitted to the nerves and fluids in the cochlea (inner ear), which generates a nerve impulse that passes along the auditory nerve to the brain.

1. Conductive Hearing Loss, which is essentially a mechanical problem with the conduction of sound vibrations, and

2. Sensorineural Hearing Loss, a problem with the generation and/or transmission of nerve impulses from the inner ear to the brain.

3. Mixed hearing loss refers to a combination of these two types.

What are the types of hearing loss ?

Hearing loss can be divided into two types:

The preliminary classification of hearing loss as conductive or sensorineural can be determined by a physician using a tuning fork in the office. A formal audiogram, or hearing test, is the best way to determine the type and degree of hearing loss. The distinction between these two types of hearing loss is important because many cases of conductive hearing loss can be improved with medical or surgical intervention. An otolaryngologist, also called an Ear Nose and Throat or ENT doctor, can determine the specific diagnosis and treatments for either type of hearing loss and perform surgical treatments, if necessary.
Problems with the External Ear

Cerumen (ear wax) obstruction: Ear wax can be identified by a medical examination and can usually be removed quickly. This condition may actually be aggravated by cotton tipped applicators (Q-tips) that many patients use in an attempt to clean their ears.

Otitis Externa: Often referred to as "swimmer's ear", an infection of the ear canal may be related to water exposure. Although the most common symptoms of otitis externa are pain and tenderness of the ear, conductive hearing loss can also occur if there is severe swelling of the ear canal.

Foreign body in Ear Canal: This is also readily identified on examination and can usually be cleared in the office. Occasionally, a brief anesthesia is required for this procedure in children. Common foreign bodies include beads and beans in children and cotton or the tips of cotton-tipped applicators in adults. Uncommonly, the foreign object is a live bug such as a cockroach which can cause itching, pain and noise.

Bony lesions of Ear Canal: These are benign growths of bone along the walls of the ear canal resulting in a narrowing of the ear canal which may then lead to frequent obstruction from a small amount of wax or water. These bony lesions can generally be managed with vigilant cleaning of ear wax to prevent obstruction. In rare cases these lesions require surgical removal.

Atresia of the Ear Canal: Complete malformation of the external ear canal is called atresia. It may be seen along with complete or partial malformation of the pinna (outer ear) and is noted at birth. It is rarely associated with other congenital abnormalities and is most often only on one side (unilateral). Management of congenital aural atresia is complex. Surgical treatment may be beneficial to either reconstruct the ear canal in select cases or to implant a device that vibrates the bone of the ear directly.

Problems with the Middle Ear structures
What can cause Conductive Hearing Loss ?

Conductive hearing loss may result from diseases that affect the external ear or middle ear structures. Some of the causes of conductive hearing loss include:

Many types of hearing loss can also be ameliorated with the use of conventional hearing aids. In addition, many implantable hearing devices are available for various types of hearing loss. An otolaryngologist can determine the specific cause of the hearing loss, advise patients of their treatment and rehabilitative options, and help patients achieve the best possible hearing outcome and hearing related quality of life.

When should a hearing test be performed related to frequent infections or fluid ?

A hearing test should be performed for children who have frequent ear infections, hearing loss that lasts more than six weeks, or fluid in the middle ear for more than three months. There are a wide range of medical devices now available to test a child's hearing, Eustachian tube function, and flexibility of the ear drum. They include the otoscopy, tympanometer, and audiometer.

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Human Ear Anatomy - Parts of Ear Structure, Diagram and Ear Problems

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Learn about human ear including its anatomy, parts of the ear, ear diagram, ear structure & human ear problems, infection, vertigo, hearing loss & tinnitus

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Complete Ear and Inner Ear Diagram: Detailed Anatomy

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An ear and inner ear diagram is a crucial visual aid for understanding the complex anatomy of the auditory system. It depicts the three main sections of the ear the outer, middle, and inner ear illustrating their interconnectedness and the pathway of sound. These diagrams are invaluable tools for medical professionals, students, and anyone seeking to learn more about hearing and balance. Clear visualizations aid comprehension and improve retention of complex information regarding the intricate structures within the ear. Furthermore, a detailed diagram allows for precise identification of potential problem areas within the auditory system. Understanding the components showcased in an ear and inner ear diagram is essential for diagnosing and treating hearing impairments.

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Bionik, Ohr mit Cochlea-Implantat im Innenohr – Medical Pictures

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Professionelle HNO-Expert*innen ✓ Fachwissen in Cochlea-Implantaten ➤ Was ist ein Cochlea-Implantat?

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Weitere:

www.neurologen-und-psychiater-im-netz.org/neurologie/erkrankungen/migraene

https://hirnstiftung.org/erkrankung/migraene/#downloads

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Migräne | Neurochirurgie Inselspital Bern

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https://ihs-headache.org/en/resources/

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This site promotes the Society and its activities, and is home to the Society's international journal Cephalalgia. We welcome Society members and all who work or seek information in the field of headache.

As a charity, the purpose of IHS is to advance headache science, education, and management, and promote headache awareness worldwide.

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Leading headache science, education and management globally. The world's leading membership organisation for those with a professional commitment to helping people affected by headache.

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Augenmigräne

(Weitergeleitet von Ophthalmische Migräne): https://flexikon.doccheck.com/de/Ophthalmische_Migr%C3%A4ne

Migräne mit Aura: https://flexikon.doccheck.com/de/Migr%C3%A4ne_mit_Aura

Migränöser Hirninfarkt: https://flexikon.doccheck.com/de/Migr%C3%A4n%C3%B6ser_Hirninfarkt

Migräne ohne Aura:

Status migraenosus:

https://flexikon.doccheck.com/de/Status_migraenosus

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The ear is divided into three anatomical regions: the external ear, the middle ear, and the internal ear (Figure 2). The external ear is the visible portion of the ear, and it collects and directs sound waves to the eardrum. The middle ear is a chamber located within the petrous portion of the temporal bone. Structures within the middle ear amplify sound waves and transmit them to an appropriate portion of the internal ear. The internal ear contains the sensory organs for equilibrium (balance) and hearing.
Figure 1. Ear structure Figure 2. Ear anatomy
Parts of the ear

External (Outer) Ear

The external (outer) ear consists of the auricle, external auditory canal, and eardrum (Figure 1 and 2). The auricle or pinna is a flap of elastic cartilage shaped like the flared end of a trumpet and covered by skin. The rim of the auricle is the helix; the inferior portion is the lobule. Ligaments and muscles attach the auricle to the head. The external auditory canal is a curved tube about 2.5 cm (1 in.) long that lies in the temporal bone and leads to the eardrum.

The tympanic membrane or ear drum is a thin, semitransparent partition between the external auditory canal and middle ear. The tympanic membrane is covered by epidermis and lined by simple cuboidal epithelium. Between the epithelial layers is connective tissue composed of collagen, elastic fibers, and fibroblasts. Tearing of the tympanic membrane is called a perforated eardrum. It may be due to pressure from a cotton swab, trauma, or a middle ear infection, and usually heals within a month. The tympanic membrane may be examined directly by an otoscope, a viewing instrument that illuminates and magnifies the external auditory canal and tympanic membrane.

Near the exterior opening, the external auditory canal contains a few hairs and specialized sweat glands called ceruminous glands that secrete earwax or cerumen. The combination of hairs and cerumen helps prevent dust and foreign objects from entering the ear. Cerumen also prevents damage to the delicate skin of the external ear canal by water and insects. Cerumen usually dries up and falls out of the ear canal. However, some people produce a large amount of cerumen, which can become impacted and can muffle incoming sounds. The treatment for impacted cerumen is usually periodic ear irrigation or removal of wax with a blunt instrument by trained medical personnel.

The middle ear is a small, air-filled cavity in the petrous portion of the temporal bone that is lined by epithelium. It is separated from the external ear by the tympanic membrane and from the internal ear by a thin bony partition that contains two small openings: the oval window and the round window.

Extending across the middle ear and attached to it by ligaments are the three smallest bones in the body, the auditory ossicles, which are connected by synovial joints. The bones, named for their shapes, are the malleus, incus, and stapes-commonly called the hammer, anvil, and stirrup, respectively. The "handle" of the malleus attaches to the internal surface of the tympanic membrane. The head of the malleus articulates with the body of the incus. The incus, the middle bone in the series, articulates with the head of the stapes. The base or footplate of the stapes fits into the oval window. Directly below the oval window is another opening, the round window, which is enclosed by a membrane called the secondary tympanic membrane. Besides the ligaments, two tiny skeletal muscles also attach to the ossicles (Figure 3).
Figure 3. Middle ear and auditory ossicles
The tensor tympani muscle, which is supplied by the mandibular branch of the trigeminal (V) nerve, limits movement and increases tension on the eardrum to prevent damage to the inner ear from loud noises. The stapedius muscle, which is supplied by the facial (VII) nerve, is the smallest skeletal muscle in the human body. By dampening large vibrations of the stapes due to loud noises, it protects the oval window, but it also decreases the sensitivity of hearing. For this reason, paralysis of the stapedius muscle is associated with hyperacusia, which is abnormally sensitive hearing. Because it takes a fraction of a second for the tensor tympani and stapedius muscles to contract, they can protect the inner ear from prolonged loud noises but not from brief ones such as a gunshot.

The anterior wall of the middle ear contains an opening that leads directly into the auditory tube or pharyngotympanic tube, commonly known as the eustachian tube. The auditory tube, which consists of both bone and elastic cartilage, connects the middle ear with the nasopharynx (superior portion of the throat). It is normally closed at its medial (pharyngeal) end. During swallowing and yawning, it opens, allowing air to enter or leave the middle ear until the pressure in the middle ear equals the atmospheric pressure. Most of us have experienced our ears popping as the pressures equalize. When the pressures are balanced, the tympanic membrane vibrates freely as sound waves strike it. If the pressure is not equalized, intense pain, hearing impairment, ringing in the ears, and vertigo could develop. The auditory tube also is a route for pathogens to travel from the nose and throat to the middle ear, causing the most common type of ear infection.

Internal (Inner)

Ear The internal (inner) ear is also called the labyrinth because of its complicated series of canals (Figure 4, 5 and 6). Structurally, it consists of two main divisions: an outer bony labyrinth that encloses an inner membranous labyrinth. It is like long balloons put inside a rigid tube. The bony labyrinth is a series of cavities in the petrous portion of the temporal bone divided into three areas: (1) the semicircular canals, (2) the vestibule, and (3) the cochlea.
Figure 4. Parts of the inner ear
The bony labyrinth is lined with periosteum and contains perilymph. This fluid, which is chemically similar to cerebrospinal fluid, surrounds the membranous labyrinth, a series of epithelial sacs and tubes inside the bony labyrinth that have the same general form as the bony labyrinth and house the receptors for hearing and equilibrium. The epithelial membranous labyrinth contains endolymph. The level of potassium ions (K+) in endolymph is unusually high for an extracellular fluid, and potassium ions play a role in the generation of auditory signals.

The vestibule is the oval central portion of the bony labyrinth. The membranous labyrinth in the vestibule consists of two sacs called the utricle (little bag) and the saccule (little sac), which are connected by a small duct. Projecting superiorly and posteriorly from the vestibule are the three bony semicircular canals, each of which lies at approximately right angles to the other two. Based on their positions, they are named the anterior, posterior, and lateral semicircular canals. The anterior and posterior semicircular canals are vertically oriented; the lateral one is horizontally oriented. At one end of each canal is a swollen enlargement called the ampulla. The portions of the membranous labyrinth that lie inside the bony semicircular canals are called the semicircular ducts. These structures connect with the utricle of the vestibule.

The vestibular branch of the vestibulocochlear (cranial nerve VIII) nerve consists of ampullary, utricular, and saccular nerves. These nerves contain both first-order sensory neurons and efferent neurons that synapse with receptors for equilibrium. The first-order sensory neurons carry sensory information from the receptors, and the efferent neurons carry feedback signals to the receptors, apparently to modify their sensitivity. Cell bodies of the sensory neurons are located in the vestibular ganglia.
Figure 5. Inner ear bones
Note: A closer look at the inner ear. Perilymph separates the bony (osseous) labyrinth of the inner ear from the membranous labyrinth, which contains endolymph. Note that areas of bony labyrinth have been removed to reveal underlying structures.
Figure 6. The Cochlea (cross section view)
Note: a) Cross section of the cochlea. (b) The spiral organ and the tectorial membrane.

Anterior to the vestibule is the cochlea, a bony spiral canal that resembles a snail's shell and makes almost three turns around a central bony core called the modiolus. Sections through the cochlea reveal that it is divided into three channels: cochlear duct, scala vestibuli, and scala tympani. The cochlear duct or scala media is a continuation of the membranous labyrinth into the cochlea; it is filled with endolymph. The channel above the cochlear duct is the scala vestibuli, which ends at the oval window. The channel below is the scala tympani, which ends at the round window. Both the scala vestibuli and scala tympani are part of the bony labyrinth of the cochlea; therefore, these chambers are filled with perilymph. The scala vestibuli and scala tympani are completely separated by the cochlear duct, except for an opening at the apex of the cochlea, the helicotrema.

The cochlea adjoins the wall of the vestibule, into which the scala vestibuli opens. The perilymph in the vestibule is continuous with that of the scala vestibuli. The vestibular membrane separates the cochlear duct from the scala vestibuli, and the basilar membrane separates the cochlear duct from the scala tympani. Resting on the basilar membrane is the spiral organ or organ of Corti. The spiral organ is a coiled sheet of epithelial cells, including supporting cells and about 16,000 hair cells, which are the receptors for hearing.

There are two groups of hair cells: The inner hair cells are arranged in a single row, whereas the outer hair cells are arranged in three rows. At the apical tip of each hair cell are stereocilia that extend into the endolymph of the cochlear duct. Despite their name, stereocilia are actually long, hairlike microvilli arranged in several rows of graded height.

At their basal ends, inner and outer hair cells synapse both with first-order sensory neurons and with motor neurons from the cochlear branch of the vestibulocochlear (VIII) nerve. Cell bodies of the sensory neurons are located in the spiral ganglion. Although outer hair cells outnumber them by 3 to 1, the inner hair cells synapse with 90-95% of the first-order sensory neurons in the cochlear nerve that relay auditory information to the brain. By contrast, 90% of the motor neurons in the cochlear nerve synapse with outer hair cells. The tectorial membrane, a flexible gelatinous membrane, covers the hair cells of the spiral organ. In fact, the ends of the stereocilia of the hair cells are embedded in the tectorial membrane while the bodies of the hair cells rest on the basilar membrane. Inner and outer hair cells have diff erent functional roles. Inner hair cells are the receptors for hearing: They convert the mechanical vibrations of sound into electrical signals. Outer hair cells do not serve as hearing receptors; instead, they increase the sensitivity of the inner hair cells.

Mechanism for Hearing

First, sound vibrations travel from the eardrum through the ossicles, causing the stapes to oscillate back and forth against the oval window. This oscillation sets up pressure waves in the perilymph of the scala vestibuli, which are transferred to the endolymph of the cochlear duct. These waves cause the basilar membrane to vibrate up and down. The hair cells in the spiral organ move along with the basilar membrane, but the overlying tectorial membrane (in which the hairs are anchored) does not move. Therefore, the movements of the hair cells cause their hairs to bend. Each time such bending occurs in a specific direction, the hair cells release neurotransmitters that excite the cochlear nerve fibers, which carry the vibratory (sound) information to the brain. The vibrations of the basilar membrane set the perilymph vibrating in the underlying scala tympani. These vibrations then travel to the round window, where they push on the membrane that covers that window, thereby dissipating their remaining energy into the air of the middle ear cavity. Without this release mechanism, echoes would reverberate within the rigid cochlear box, disrupting sound reception.

The inner and outer hair cells in the spiral organ have different functions. The inner hair cells are the true receptors that transmit the vibrations of the basilar membrane to the cochlear nerve. The outer hair cells are involved with actively tuning the cochlea and amplifying the signal. The outer hair cells receive efferent fibers from the brain that cause these cells to stretch and contract, enhancing the responsiveness of the inner hair cell receptors. Overall, this active mechanism amplifies sounds some 100 times, so that we can hear the faintest sounds.The mobility of the outer hair cells is also responsible for producing ear sounds (otoacoustic emissions). Detection of spontaneous otoacoustic emissions is used to test hearing in newborns.

Ear problems

Swimmer's ear

Swimmer's ear is an infection in the outer ear canal, which runs from your eardrum to the outside of your head . It's often brought on by water that remains in your ear after swimming, creating a moist environment that aids bacterial growth.

Putting fingers, cotton swabs or other objects in your ears also can lead to swimmer's ear by damaging the thin layer of skin lining your ear canal .

Swimmer's ear is also known as otitis externa. The most common cause of this infection is bacteria invading the skin inside your ear canal. Usually you can treat swimmer's ear with eardrops. Prompt treatment can help prevent complications and more-serious infections.

Causes of Swimmer's ear

Swimmer's ear is an infection that's usually caused by bacteria commonly found in water and soil. Infections caused by a fungus or a virus are less common. Swimmer's ear is more common among children in their teens and young adults. It may occur with a middle ear infection or a respiratory infection such as a cold.

Swimming in unclean water can lead to swimmer's ear. Bacteria commonly often found in water can cause ear infections. Rarely, the infection may be caused by a fungus.
Other causes of swimmer's ear include:

Scratching the ear or inside the ear

Getting something stuck in the ear

Trying to clean (wax from the ear canal) with cotton swabs or small objects can damage the skin.
Long-term (chronic) swimmer's ear may be due to:

Allergic reaction to something placed in the ear

Chronic skin conditions, such as eczema or psoriasis

Your ear's natural defenses
Your outer ear canals have natural defenses that help keep them clean and prevent infection. Protective features include:

Glands that secrete a waxy substance (cerumen). These secretions form a thin, water-repellent film on the skin inside your ear. Cerumen is also slightly acidic, which helps further discourage bacterial growth. In addition, cerumen collects dirt, dead skin cells and other debris and helps move these particles out of your ear. The waxy clump that results is the familiar earwax you find at the opening of your ear canal.

Downward slope of your ear canal. Your ear canal slopes down slightly from your middle ear to your outer ear, helping water drain out.

How the swimmer's ear occurs

If you have swimmer's ear, your natural defenses have been overwhelmed. Conditions that can weaken your ear's defenses and promote bacterial growth include:

Risk factors for swimmer's ear

Swimming

Swimming in water with elevated bacteria levels, such as a lake rather than a well-maintained pool

A narrow ear canal - for example, in a child - that can more easily trap water

Aggressive cleaning of the ear canal with cotton swabs or other objects

Use of certain devices, such as headphones or a hearing aid

Skin allergies or irritation from jewelry, hair spray or hair dyes

Factors that may increase your risk of swimmer's ear include:

Symptoms of Swimmer's ear
Mild signs and symptoms Moderate progression

More intense itching

Increasing pain

More extensive redness in your ear

Excessive fluid drainage

Discharge of pus

Feeling of fullness inside your ear and partial blockage of your ear canal by swelling, fluid and debris

Decreased or muffled hearing

Advanced progression
Swimmer's ear symptoms are usually mild at first, but they may get worse if your infection isn't treated or spreads. Doctors often classify swimmer's ear according to mild, moderate and advanced stages of progression.

When to see a doctor

See your doctor if you're experiencing any signs or symptoms of swimmer's ear, even if they're mild.

Call your doctor immediately or visit the emergency room if you have:

Complications of Swimmer's ear

Swimmer's ear usually isn't serious if treated promptly, but complications can occur.

Prevention of Swimmer's ear

Keep your ears dry. Dry your ears thoroughly after exposure to moisture from swimming or bathing. Dry only your outer ear, wiping it slowly and gently with a soft towel or cloth. Tip your head to the side to help water drain from your ear canal. You can dry your ears with a blow dryer if you put it on the lowest setting and hold it at least a foot (about 0.3 meters) away from the ear.

At-home preventive treatment. If you know you don't have a punctured eardrum, you can use homemade preventive eardrops before and after swimming. A mixture of 1 part white vinegar to 1 part rubbing alcohol may help promote drying and prevent the growth of bacteria and fungi that can cause swimmer's ear. Pour 1 teaspoon (about 5 milliliters) of the solution into each ear and let it drain back out. Similar over-the-counter solutions may be available at your drugstore.

Swim wisely. Watch for signs alerting swimmers to high bacterial counts and don't swim on those days.

DO NOT scratch the ears or insert cotton swabs or other objects in the ears.

Avoid putting foreign objects in your ear. Never attempt to scratch an itch or dig out earwax with items such as a cotton swab, paper clip or hairpin. Using these items can pack material deeper into your ear canal, irritate the thin skin inside your ear or break the skin.

Protect your ears from irritants. Put cotton balls in your ears while applying products such as hair sprays and hair dyes.

Use caution after an ear infection or surgery. If you've recently had an ear infection or ear surgery, talk to your doctor before you go swimming.

Follow these tips to avoid swimmer's ear:

Diagnosis of swimmer's ear

Doctors can usually diagnose swimmer's ear during an office visit. If your infection is at an advanced stage or persists, you may need further evaluation.
Initial testing

Examination of your ear canal with a lighted instrument (otoscope). Your ear canal may appear red, swollen and scaly. Flakes of skin and other debris may be present in the ear canal.

Visualization of your eardrum (tympanic membrane) to be sure it isn't torn or damaged. If the view of your eardrum is blocked, your doctor will clear your ear canal with a small suction device or an instrument with a tiny loop or scoop on the end (ear curette).

Further testing
Your doctor will likely diagnose swimmer's ear based on symptoms you report, questions he or she asks, and an office examination. You probably won't need a lab test at your first visit. Your doctor's initial evaluation will usually include:

If your eardrum is damaged or torn, your doctor will likely refer you to an ear, nose and throat specialist (ENT). The specialist will examine the condition of your middle ear to determine if that's the primary site of infection. This examination is important because some treatments intended for an infection in the outer ear canal aren't appropriate for treating the middle ear.

If your infection doesn't respond to treatment, your doctor may take a sample of discharge or debris from your ear at a later appointment and send it to a lab to identify the exact microorganism causing your infection.

Depending on the initial assessment, symptom severity or the stage of your swimmer's ear, your doctor may recommend additional evaluation.
Cleaning
Treatment for swimmer's ear
Medications for infection
The goal of treatment is to stop the infection and allow your ear canal to heal.

Cleaning your outer ear canal is necessary to help eardrops flow to all infected areas. Your doctor will use a suction device or ear curette to clean away any discharge, clumps of earwax, flaky skin and other debris.

For most cases of swimmer's ear, your doctor will prescribe eardrops that have some combination of the following ingredients, depending on the type and seriousness of your infection:

Ask your doctor about the best method for taking your eardrops. Some ideas that may help you use eardrops include the following:
Medications for pain
If your ear canal is completely blocked by swelling, inflammation or excess discharge, your doctor may insert a wick made of cotton or gauze to promote drainage and help draw medication into your ear canal.

If your infection is more advanced or doesn't respond to treatment with eardrops, your doctor may prescribe oral antibiotics.
Helping your treatment work
Your doctor may recommend easing the discomfort of swimmer's ear with over-the-counter pain relievers, such as ibuprofen (Advil, Motrin IB, others), naproxen sodium (Aleve, others) or acetaminophen (Tylenol, others).

If your pain is severe or your swimmer's ear is at a more advanced stage, your doctor may prescribe a stronger medication for pain relief.

During treatment, the following steps will help keep your ears dry and avoid further irritation:

Ruptured eardrum (perforated eardrum)

A ruptured eardrum - or tympanic membrane perforation as it's medically known - is a hole or tear in the thin tissue that separates your ear canal from your middle ear (eardrum) .

A ruptured eardrum can result in hearing loss. A ruptured eardrum can also make your middle ear vulnerable to infections or injury.

A ruptured eardrum usually heals within a few weeks without treatment. Sometimes, however, a ruptured eardrum requires a procedure or surgical repair to heal.

If you think that you have a ruptured eardrum, be careful to keep your ears dry to prevent infection. Don't go swimming. To keep water out of your ear when showering or bathing, use a moldable, waterproof silicone earplug or put a cotton ball coated with petroleum jelly in your outer ear.

Don't put medication drops in your ear unless your doctor prescribes them specifically for infection related to your perforated eardrum.

Causes of a ruptured or perforated eardrum

Causes of a ruptured, or perforated, eardrum may include:

Hearing. When sound waves strike it, your eardrum vibrates - the first step by which structures of your middle and inner ears translate sound waves into nerve impulses.

Protection. Your eardrum also acts as a barrier, protecting your middle ear from water, bacteria and other foreign substances.

Complications of of a ruptured or perforated eardrum

Your eardrum (tympanic membrane) has two primary roles:

If your eardrum ruptures, complications can occur while your eardrum is healing or if it fails to heal. Possible complications include:

Prevention of a ruptured or perforated eardrum

Follow these tips to avoid a ruptured or perforated eardrum:

Ear pain that may subside quickly

Clear, pus-filled or bloody drainage from your ear

Hearing loss

Ringing in your ear (tinnitus)

Spinning sensation (vertigo)

Nausea or vomiting that can result from vertigo

Symptoms of a ruptured or perforated eardrum

Signs and symptoms of a ruptured eardrum may include:

When to see a doctor

Call your doctor if you experience any of the signs or symptoms of a ruptured eardrum or pain or discomfort in your ears. Your middle and inner ears are composed of delicate mechanisms that are sensitive to injury or disease. Prompt and appropriate treatment is important to preserve your hearing.

Diagnosis of a ruptured or perforated eardrum

Your family doctor or ENT specialist can often determine if you have a perforated eardrum with a visual inspection using a lighted instrument (otoscope).

He or she may conduct or order additional tests to determine the cause of the rupture or degree of damage. These tests include:

Eardrum patch. If the tear or hole in your eardrum doesn't close on its own, an ENT specialist may seal it with a patch. With this office procedure, your ENT doctor may apply a chemical to the edges of the tear to stimulate growth and then apply a patch over the hole. The procedure may need to be repeated more than once before the hole closes.

Surgery. If a patch doesn't result in proper healing or your ENT doctor determines that the tear isn't likely to heal with a patch, he or she may recommend surgery. The most common surgical procedure is called tympanoplasty. Your surgeon grafts a tiny patch of your own tissue to close the hole in the eardrum. This procedure is done on an outpatient basis, meaning you can usually go home the same day unless medical anesthesia conditions require a longer hospital stay.

Treatment of a ruptured or perforated eardrum

Most perforated eardrums heal without treatment within a few weeks. Your doctor may prescribe antibiotic drops if there's evidence of infection. If the tear or hole in your eardrum doesn't heal by itself, treatment will involve procedures to close the perforation. These may include:

Home remedies for a ruptured or perforated eardrum

A ruptured eardrum usually heals on its own within weeks. In some cases, healing takes months. Until your doctor tells you that your ear is healed, protect it by doing the following:

Middle Ear Infection

An middle ear infection (acute otitis media) is most often a bacterial or viral infection that affects the middle ear, the air-filled space behind the eardrum that contains the tiny vibrating bones of the ear . Children are more likely than adults to get ear infections.

Ear infections frequently are painful because of inflammation and buildup of fluids in the middle ear.

Because ear infections often clear up on their own, treatment may begin with managing pain and monitoring the problem. Ear infection in infants and severe cases in general often require antibiotic medications. Long-term problems related to ear infections - persistent fluids in the middle ear, persistent infections or frequent infections - can cause hearing problems and other serious complications.
Children
Symptoms of middle ear infection

Ear pain, especially when lying down

Tugging or pulling at an ear

Difficulty sleeping

Crying more than usual

Acting more irritable than usual

Difficulty hearing or responding to sounds

Loss of balance

Fever of 100 F (38 C) or higher

Drainage of fluid from the ear

Headache

Loss of appetite

Adults
The onset of signs and symptoms of ear infection is usually rapid.

Signs and symptoms common in children include:

Common signs and symptoms in adults include:

When to see a doctor

Signs and symptoms of an ear infection can indicate a number of conditions. It's important to get an accurate diagnosis and prompt treatment. Call your child's doctor if:

An adult with ear pain or discharge should see a doctor as soon as possible.
Role of eustachian tubes
Causes of middle ear infection

An ear infection is caused by a bacterium or virus in the middle ear. This infection often results from another illness - cold, flu or allergy - that causes congestion and swelling of the nasal passages, throat and eustachian tubes.

The eustachian tubes are a pair of narrow tubes that run from each middle ear to high in the back of the throat, behind the nasal passages. The throat end of the tubes open and close to:
Role of adenoids
Swelling, inflammation and mucus in the eustachian tubes from an upper respiratory infection or allergy can block them, causing the accumulation of fluids in the middle ear. A bacterial or viral infection of this fluid is usually what produces the symptoms of an ear infection.

Ear infections are more common in children, in part, because their eustachian tubes are narrower and more horizontal - factors that make them more difficult to drain and more likely to get clogged.
Related conditions
Adenoids are two small pads of tissues high in the back of the nose believed to play a role in immune system activity. This function may make them particularly vulnerable to infection, inflammation and swelling.

Because adenoids are near the opening of the eustachian tubes, inflammation or enlargement of the adenoids may block the tubes, thereby contributing to middle ear infection. Inflammation of adenoids is more likely to play a role in ear infections in children because children have relatively larger adenoids.

Conditions of the middle ear that may be related to an ear infection or result in similar middle ear problems include the following:

Risk factors for middle ear infection

Risk factors for ear infections include:

Complications of middle ear infection

Most ear infections don't cause long-term complications. Frequent or persistent infections and persistent fluid buildup can result in some serious complications:

Prevention of middle ear infection

The following tips may reduce the risk of developing ear infections:
Pneumatic otoscope
Diagnosis of middle ear infection
Additional tests
Your doctor can usually diagnose an ear infection or another condition based on the symptoms you describe and an exam. The doctor will likely use a lighted instrument (an otoscope) to look at the ears, throat and nasal passage. He or she will also likely listen to your child breathe with a stethoscope.

Tympanometry. This test measures the movement of the eardrum. The device, which seals off the ear canal, adjusts air pressure in the canal, thereby causing the eardrum to move. The device quantifies how well the eardrum moves and provides an indirect measure of pressure within the middle ear.

Acoustic reflectometry. This test measures how much sound emitted from a device is reflected back from the eardrum - an indirect measure of fluids in the middle ear. Normally, the eardrum absorbs most of the sound. However, the more pressure there is from fluid in the middle ear, the more sound the eardrum will reflect.

Tympanocentesis. Rarely, a doctor may use a tiny tube that pierces the eardrum to drain fluid from the middle ear - a procedure called tympanocentesis. Tests to determine the infectious agent in the fluid may be beneficial if an infection hasn't responded well to previous treatments.
Other tests. If your child has had persistent ear infections or persistent fluid buildup in the middle ear, your doctor may refer you to a hearing specialist (audiologist), speech therapist or developmental therapist for tests of hearing, speech skills, language comprehension or developmental abilities.

An instrument called a pneumatic otoscope is often the only specialized tool a doctor needs to make a diagnosis of an ear infection. This instrument enables the doctor to look in the ear and judge whether there is fluid behind the eardrum. With the pneumatic otoscope, the doctor gently puffs air against the eardrum. Normally, this puff of air would cause the eardrum to move. If the middle ear is filled with fluid, your doctor will observe little to no movement of the eardrum.

Your doctor may perform other diagnostic tests if there is any doubt about a diagnosis, if the condition hasn't responded to previous treatments, or if there are other persistent or serious problems.

What a diagnosis means
A wait-and-see approach
Treatment for middle ear infection

Children 6 to 23 months with mild inner ear pain in one ear for less than 48 hours and a temperature less than 102.2 F (39 C)

Children 24 months and older with mild inner ear pain in one or both ears for less than 48 hours and a temperature less than 102.2 F (39 C)

Some ear infections resolve without treatment with antibiotics. What's best for your child depends on many factors, including your child's age and the severity of symptoms.
Managing pain
Symptoms of ear infections usually improve within the first couple of days, and most infections clear up on their own within one to two weeks without any treatment. The American Academy of Pediatrics and the American Academy of Family Physicians recommend a wait-and-see approach as one option for:

A warm compress. Placing a warm, moist washcloth over the affected ear may lessen pain.

Pain medication. Your doctor may advise the use of over-the-counter acetaminophen (Tylenol, others) or ibuprofen (Advil, Motrin IB, others) to relieve pain. Use the drugs as directed on the label. Use caution when giving aspirin to children or teenagers. Children and teenagers recovering from chickenpox or flu-like symptoms should never take aspirin because aspirin has been linked with Reye's syndrome. Talk to your doctor if you have concerns.

Antibiotic therapy
Some evidence suggests that treatment with antibiotics might be beneficial for certain children with ear infections. Talk to your doctor about the benefits of antibiotics weighed against the potential side effects and concern about overuse of antibiotics creating strains of resistant disease.

Your doctor will advise you on treatments to lessen pain from an ear infection. These may include the following:

After an initial observation period, your doctor may recommend antibiotic treatment for an ear infection in the following situations:
Ear tubes
Children younger than 6 months of age with confirmed acute otitis media are more likely to be treated with antibiotics without the initial observational waiting time.

Even after symptoms have improved, be sure to use all of the antibiotic as directed. Failing to do so can result in recurring infection and resistance of bacteria to antibiotic medications. Talk to your doctor or pharmacist about what to do if you accidentally skip a dose.

If your child has recurrent otitis media or otitis media with effusion, your doctor may recommend a procedure to drain fluid from the middle ear. Otitis media is defined as three episodes of infection in six months or four episodes of infection in a year with at least one occurring in the past six months. Otitis media with effusion is persistent fluid buildup in the ear after an infection has cleared up or in the absence of any infection.

During an outpatient surgical procedure called a myringotomy, a surgeon creates a tiny hole in the eardrum that enables him or her to suction fluids out of the middle ear. A tiny tube (tympanostomy tube) is placed in the opening to help ventilate the middle ear and prevent the accumulation of more fluids. Some tubes are intended to stay in place for six months to a year and then fall out on their own. Other tubes are designed to stay in longer and may need to be surgically removed.

The eardrum usually closes up again after the tube falls out or is removed.

Treatment for chronic suppurative otitis media

Chronic infection that results in perforation of the eardrum - chronic suppurative otitis media - is difficult to treat. It's often treated with antibiotics administered as drops. You'll receive instructions on how to suction fluids out through the ear canal before administering drops.

Monitoring

Children with frequent or persistent infections or with persistent fluid in the middle ear will need to be monitored closely. Talk to your doctor about how often you should schedule follow-up appointments. Your doctor may recommend regular hearing and language tests.

What is Tinnitus

Tinnitus is the perception of noise or ringing in the ears . A common problem, tinnitus affects about 1 in 5 people. Tinnitus isn't a condition itself - it's a symptom of an underlying condition, such as age-related hearing loss, ear injury or a circulatory system disorder.

Although bothersome, tinnitus usually isn't a sign of something serious. Although it can worsen with age, for many people, tinnitus can improve with treatment. Treating an identified underlying cause sometimes helps. Other treatments reduce or mask the noise, making tinnitus less noticeable.

Symptoms of Tinnitus
There are two kinds of tinnitus.

Subjective tinnitus is tinnitus only you can hear. This is the most common type of tinnitus. It can be caused by ear problems in your outer, middle or inner ear. It also can be caused by problems with the hearing (auditory) nerves or the part of your brain that interprets nerve signals as sound (auditory pathways).

Objective tinnitus is tinnitus your doctor can hear when he or she does an examination. This rare type of tinnitus may be caused by a blood vessel problem, a middle ear bone condition or muscle contractions.

Tinnitus involves the annoying sensation of hearing sound when no external sound is present. Tinnitus symptoms include these types of phantom noises in your ears:

The phantom noise may vary in pitch from a low roar to a high squeal, and you may hear it in one or both ears. In some cases, the sound can be so loud it can interfere with your ability to concentrate or hear actual sound. Tinnitus may be present all the time, or it may come and go.

When to see a doctor

You develop tinnitus after an upper respiratory infection, such as a cold, and your tinnitus doesn't improve within a week.

If you have tinnitus that bothers you, see your doctor.

You have tinnitus that occurs suddenly or without an apparent cause.

You have hearing loss or dizziness with the tinnitus.

Make an appointment to see your doctor if:

See your doctor as soon as possible if:

Causes of Tinnitus

A number of health conditions can cause or worsen tinnitus. In many cases, an exact cause is never found.
Common causes of tinnitus
A common cause of tinnitus is inner ear cell damage. Tiny, delicate hairs in your inner ear move in relation to the pressure of sound waves. This triggers ear cells to release an electrical signal through a nerve from your ear (auditory nerve) to your brain. Your brain interprets these signals as sound. If the hairs inside your inner ear are bent or broken, they can "leak" random electrical impulses to your brain, causing tinnitus.

Age-related hearing loss. For many people, hearing worsens with age, usually starting around age 60. Hearing loss can cause tinnitus. The medical term for this type of hearing loss is presbycusis.

Exposure to loud noise. Loud noises, such as those from heavy equipment, chain saws and firearms, are common sources of noise-related hearing loss.

Portable music devices, such as MP3 players or iPods, also can cause noise-related hearing loss if played loudly for long periods. Tinnitus caused by short-term exposure, such as attending a loud concert, usually goes away; long-term exposure to loud sound can cause permanent damage.

Earwax blockage. Earwax protects your ear canal by trapping dirt and slowing the growth of bacteria. When too much earwax accumulates, it becomes too hard to wash away naturally, causing hearing loss or irritation of the eardrum, which can lead to tinnitus.

Ear bone changes. Stiffening of the bones in your middle ear (otosclerosis) may affect your hearing and cause tinnitus. This condition, caused by abnormal bone growth, tends to run in families.

Other causes of tinnitus
Other causes of tinnitus include other ear problems, chronic health conditions, and injuries or conditions that affect the nerves in your ear or the hearing center in your brain.
Blood vessel disorders linked to tinnitus
In many people, tinnitus is caused by one of these conditions:

Atherosclerosis. With age and buildup of cholesterol and other deposits, major blood vessels close to your middle and inner ear lose some of their elasticity - the ability to flex or expand slightly with each heartbeat. That causes blood flow to become more forceful, making it easier for your ear to detect the beats. You can generally hear this type of tinnitus in both ears.

Head and neck tumors. A tumor that presses on blood vessels in your head or neck (vascular neoplasm) can cause tinnitus and other symptoms.

High blood pressure. Hypertension and factors that increase blood pressure, such as stress, alcohol and caffeine, can make tinnitus more noticeable.

Turbulent blood flow. Narrowing or kinking in a neck artery (carotid artery) or vein in your neck (jugular vein) can cause turbulent, irregular blood flow, leading to tinnitus.

Malformation of capillaries. A condition called arteriovenous malformation (AVM), abnormal connections between arteries and veins, can result in tinnitus. This type of tinnitus generally occurs in only one ear.

Medications that can cause tinnitus
Some causes of tinnitus are less common, including:

Antibiotics, including polymyxin B, erythromycin, vancomycin and neomycin

Cancer medications, including mechlorethamine and vincristine

Water pills (diuretics), such as bumetanide, ethacrynic acid or furosemide

Quinine medications used for malaria or other health conditions

Certain antidepressants may worsen tinnitus

Aspirin taken in uncommonly high doses (usually 12 or more a day)

In rare cases, tinnitus is caused by a blood vessel disorder. This type of tinnitus is called pulsatile tinnitus. Causes include:

A number of medications may cause or worsen tinnitus. Generally, the higher the dose of these medications, the worse tinnitus becomes. Often the unwanted noise disappears when you stop using these drugs. Medications known to cause or worsen tinnitus include:

Loud noise exposure. Prolonged exposure to loud noise can damage the tiny sensory hair cells in your ear that transmit sound to your brain. People who work in noisy environments - such as factory and construction workers, musicians, and soldiers - are particularly at risk.

Age. As you age, the number of functioning nerve fibers in your ears declines, possibly causing hearing problems often associated with tinnitus.

Gender. Men are more likely to experience tinnitus.

Smoking. Smokers have a higher risk of developing tinnitus.

Cardiovascular problems. Conditions that affect your blood flow, such as high blood pressure or narrowed arteries (atherosclerosis), can increase your risk of tinnitus.

Risk factors for Tinnitus

Anyone can experience tinnitus, but these factors may increase your risk:

Fatigue

Stress

Sleep problems

Trouble concentrating

Memory problems

Depression

Anxiety and irritability

Complications of Tinnitus

Tinnitus can significantly affect quality of life. Although it affects people differently, if you have tinnitus, you also may experience:

Treating these linked conditions may not affect tinnitus directly, but it can help you feel better.

Prevention of Tinnitus

In many cases, tinnitus is the result of something that can't be prevented. However, some precautions can help prevent certain kinds of tinnitus.

Diagnosis of Tinnitus

Your doctor will examine your ears, head and neck to look for possible causes of tinnitus. Tests include:

The sounds you hear can help your doctor identify a possible underlying cause.
Treating an underlying health condition
In many cases, the cause of tinnitus is never found. Your doctor can discuss with you steps you can take to reduce the severity of your tinnitus or to help you cope better with the noise.
Noise suppression
Treatment of Tinnitus
Medications
To treat your tinnitus, your doctor will first try to identify any underlying, treatable condition that may be associated with your symptoms. If tinnitus is due to a health condition, your doctor may be able to take steps that could reduce the noise. Examples include:

Tricyclic antidepressants, such as amitriptyline and nortriptyline, have been used with some success. However, these medications are generally used for only severe tinnitus, as they can cause troublesome side effects, including dry mouth, blurred vision, constipation and heart problems.

Alprazolam (Niravam, Xanax) may help reduce tinnitus symptoms, but side effects can include drowsiness and nausea. It can also become habit-forming.

In some cases white noise may help suppress the sound so that it's less bothersome. Your doctor may suggest using an electronic device to suppress the noise. Devices include:

Drugs can't cure tinnitus, but in some cases they may help reduce the severity of symptoms or complications. Possible medications include:
Alternative medicine
Home remedies for Tinnitus

Often, tinnitus can't be treated. Some people, however, get used to it and notice it less than they did at first. For many people, certain adjustments make the symptoms less bothersome. These tips may help:

There's little evidence that alternative medicine treatments work for tinnitus. However, some alternative therapies that have been tried for tinnitus include:

Neuromodulation using transcranial magnetic stimulation (TMS) is a painless, noninvasive therapy that has been successful in reducing tinnitus symptoms for some people. Currently, TMS is utilized more commonly in Europe and in some trials in the U.S. It is still to be determined which patients might benefit from such treatments.

Coping and support for Tinnitus

Tinnitus doesn't always improve or completely go away with treatment. Here are some suggestions to help you cope:

Balance problems

Balance problems are conditions that make you feel unsteady or dizzy. If you are standing, sitting or lying down, you might feel as if you are moving, spinning or floating. If you are walking, you might suddenly feel as if you are tipping over or generally unsteady.

Many body systems - including your muscles, bones, joints, vision, the balance organ in the inner ear, nerves, heart and blood vessels - must work normally for you to have normal balance. When these systems aren't functioning well, you can experience balance problems.

Many medical conditions can cause balance problems. However, most balance problems result from issues in your balance end-organ in the inner ear (vestibular system).

Symptoms of balance problem

Signs and symptoms of balance problems include:

Causes of balance problem

Benign paroxysmal positional vertigo (BPPV). BPPV occurs when calcium crystals in your inner ear - which help control your balance - are dislodged from their normal position and move elsewhere in the inner ear. BPPV is the most common cause of vertigo. You might experience a spinning sensation when turning in bed or tilting your head back to look up.

Meniere's disease. In addition to sudden and severe vertigo, Meniere's disease can cause fluctuating hearing loss and buzzing, ringing or a feeling of fullness in your ear. The cause of Meniere's disease isn't fully known. Meniere's disease is rare and typically develops in people who are between the ages of 20 and 60.

Migraine. Dizziness and sensitivity to motion (vestibular migraine) can occur due to migraine headache. Migraine is a common cause of dizziness.

Acoustic neuroma. This noncancerous (benign), slow-growing tumor develops on a nerve that affects your hearing and balance. You might experience dizziness or loss of balance, but the most common symptoms are hearing loss and ringing in your ear. Acoustic neuroma is a rare condition.

Vestibular neuritis. This inflammatory disorder, probably caused by a virus, can affect the nerves in the balance portion of your inner ear. Symptoms are often severe and persistent, and include nausea and difficulty walking. Symptoms can last several days and gradually improve on their own.

Ramsay Hunt syndrome. Also known as herpes zoster otitis, this condition occurs when a shingles infection affects the facial nerve near one of your ears. You might experience vertigo, ear pain and hearing loss.

Head injury. You might experience vertigo due to a concussion or other head injury.

Motion sickness. You might experience dizziness in boats, cars and airplanes, or on amusement park rides.

Persistent postural-perceptual dizziness. This disorder occurs frequently with other types of vertigo. Symptoms include unsteadiness or a sensation of motion in your head. Symptoms often worsen when you watch objects move, when you read, or when you are in a visually complex environment such as a shopping mall.

Feeling of faintness (presyncope)
Balance problems can be caused by several different conditions. The cause of balance problems is usually related to the specific sign or symptom.
Sense of motion or spinning (vertigo)

Orthostatic hypotension (postural hypotension). Standing or sitting up too quickly can cause some people to experience a significant drop in their blood pressure, resulting in presyncope.

Cardiovascular disease. Abnormal heart rhythms (heart arrhythmia), narrowed or blocked blood vessels, a thickened heart muscle (hypertrophic cardiomyopathy), or a decrease in blood volume can reduce blood flow and cause presyncope.

Loss of balance (disequilibrium)
Vertigo can be associated with many conditions, including:
Dizziness
Presyncope can be associated with:

Losing your balance while walking, or feeling imbalanced, can result from:

A sense of dizziness or lightheadedness can result from:

Diagnosis of balance problem

Hearing tests. Difficulties with hearing are frequently associated with balance problems.

Posturography test. Wearing a safety harness, you try to remain standing on a moving platform. A posturography test indicates which parts of your balance system you rely on most.

Electronystagmography and video nystagmography. Both tests record your eye movements, which play a role in vestibular function and balance. Electronystagmography uses electrodes and video nystagmography uses small cameras to record eye movements.

Rotary chair test. Your eye movements are analyzed while you sit in a computer-controlled chair that moves slowly in one place in a circle.

Dix-Hallpike maneuver. Your doctor carefully turns your head in different positions while watching your eye movements to determine if you have a false sense of motion or spinning.

Vestibular evoked myogenic potentials test. Sensor pads attached to your neck and forehead and under your eyes measure tiny changes in muscle contractions in reaction to sounds.

Imaging tests. MRI and CT scans can determine if underlying medical conditions might be causing your balance problem.

Blood pressure and heart rate tests. Your blood pressure might be checked when sitting and then after standing for 2 to 3 minutes to determine if you have significant drops in blood pressure. Your heart rate might be checked when standing to help determine if a heart condition is causing your symptoms.

Your doctor will start by reviewing your medical history and conducting a physical and neurological examination.

To determine if your symptoms are caused by problems in the balance function in your inner ear, your doctor is likely to recommend tests. They might include:

Treatment of balance problem

Treatment depends on the cause of your balance problems. Your treatment may include:

What is hearing loss ?

The ear can be divided into three parts:

Sound waves enter the ear canal and cause a vibration of the tympanic membrane (ear drum) which is then passed through three tiny bones behind the ear drum in the middle ear space: the malleus (hammer), incus (anvil) and stapes (stirrup). The sound vibrations in the ossicles are then transmitted to the nerves and fluids in the cochlea (inner ear), which generates a nerve impulse that passes along the auditory nerve to the brain.

1. Conductive Hearing Loss, which is essentially a mechanical problem with the conduction of sound vibrations, and

2. Sensorineural Hearing Loss, a problem with the generation and/or transmission of nerve impulses from the inner ear to the brain.

3. Mixed hearing loss refers to a combination of these two types.

What are the types of hearing loss ?

Hearing loss can be divided into two types:

The preliminary classification of hearing loss as conductive or sensorineural can be determined by a physician using a tuning fork in the office. A formal audiogram, or hearing test, is the best way to determine the type and degree of hearing loss. The distinction between these two types of hearing loss is important because many cases of conductive hearing loss can be improved with medical or surgical intervention. An otolaryngologist, also called an Ear Nose and Throat or ENT doctor, can determine the specific diagnosis and treatments for either type of hearing loss and perform surgical treatments, if necessary.
Problems with the External Ear

Cerumen (ear wax) obstruction: Ear wax can be identified by a medical examination and can usually be removed quickly. This condition may actually be aggravated by cotton tipped applicators (Q-tips) that many patients use in an attempt to clean their ears.

Otitis Externa: Often referred to as "swimmer's ear", an infection of the ear canal may be related to water exposure. Although the most common symptoms of otitis externa are pain and tenderness of the ear, conductive hearing loss can also occur if there is severe swelling of the ear canal.

Foreign body in Ear Canal: This is also readily identified on examination and can usually be cleared in the office. Occasionally, a brief anesthesia is required for this procedure in children. Common foreign bodies include beads and beans in children and cotton or the tips of cotton-tipped applicators in adults. Uncommonly, the foreign object is a live bug such as a cockroach which can cause itching, pain and noise.

Bony lesions of Ear Canal: These are benign growths of bone along the walls of the ear canal resulting in a narrowing of the ear canal which may then lead to frequent obstruction from a small amount of wax or water. These bony lesions can generally be managed with vigilant cleaning of ear wax to prevent obstruction. In rare cases these lesions require surgical removal.

Atresia of the Ear Canal: Complete malformation of the external ear canal is called atresia. It may be seen along with complete or partial malformation of the pinna (outer ear) and is noted at birth. It is rarely associated with other congenital abnormalities and is most often only on one side (unilateral). Management of congenital aural atresia is complex. Surgical treatment may be beneficial to either reconstruct the ear canal in select cases or to implant a device that vibrates the bone of the ear directly.

Problems with the Middle Ear structures
What can cause Conductive Hearing Loss ?

Conductive hearing loss may result from diseases that affect the external ear or middle ear structures. Some of the causes of conductive hearing loss include:

Many types of hearing loss can also be ameliorated with the use of conventional hearing aids. In addition, many implantable hearing devices are available for various types of hearing loss. An otolaryngologist can determine the specific cause of the hearing loss, advise patients of their treatment and rehabilitative options, and help patients achieve the best possible hearing outcome and hearing related quality of life.

When should a hearing test be performed related to frequent infections or fluid ?

A hearing test should be performed for children who have frequent ear infections, hearing loss that lasts more than six weeks, or fluid in the middle ear for more than three months. There are a wide range of medical devices now available to test a child's hearing, Eustachian tube function, and flexibility of the ear drum. They include the otoscopy, tympanometer, and audiometer.

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Human Ear Anatomy - Parts of Ear Structure, Diagram and Ear Problems

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Learn about human ear including its anatomy, parts of the ear, ear diagram, ear structure & human ear problems, infection, vertigo, hearing loss & tinnitus

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What Is ATP and Why Is It So Important for the Brain?

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What Is ATP and Why Is It So Important for the Brain?

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Adenosine triphosphate (ATP) is the primary energy currency for all cellular activities. ATP provides the power for countless processes, from muscle contraction to nerve impulses. This energy is stored in the high-energy bonds linking its three phosphate groups; when one of these bonds is broken, energy is released for the cell to use. While all cells depend on ATP, this reliance is pronounced in the brain, the body's most energy-demanding organ.

The Brain's Constant Energy Demand

The brain has a high metabolic rate, consuming about 20% of the body's oxygen and calories despite being only 2% of its weight. This energy consumption is continuous, supporting a massive amount of baseline activity that occurs even during rest. This "housekeeping" energy is used to maintain the readiness of neurons to fire, a state governed by the resting membrane potential. Most of this energy is spent establishing the electrochemical gradients necessary for neuronal excitability.

This resting state is maintained by millions of sodium-potassium pumps embedded in the membrane of every neuron. These pumps use a constant supply of ATP to move sodium ions out of the cell and potassium ions into it. This process creates an ion gradient across the neuronal membrane, which is a store of potential energy. This energy is ready to be used when the neuron needs to send a signal.

To meet this demand, the brain requires a constant supply of glucose and oxygen delivered via the bloodstream. These substances are transported into the mitochondria, the powerhouses within brain cells. Here, they are used in a process called cellular respiration to generate the needed ATP, ensuring the neural network is always prepared for action.

Powering Active Neural Processes

Beyond the baseline energy required to keep neurons ready, ATP is consumed during active neural processes like thinking, learning, and communication. This additional energy expenditure is dedicated to neurotransmission, which is how neurons talk to one another across junctions called synapses. Every step of this communication chain is energetically expensive and fueled by ATP.

The process begins with the synthesis of neurotransmitters, the chemical messengers of the brain. Once synthesized, these molecules are packaged into small sacs called vesicles, another step that requires ATP. When a neuron fires, these vesicles release their contents into the synapse to signal the next neuron. This sequence is a major consumer of cellular energy.

After neurotransmitters have delivered their message, they must be cleared from the synapse to terminate the signal. This is accomplished through reuptake, where the neurotransmitters are transported back into the original neuron, or by enzymatic degradation. Both clearance mechanisms are active processes that rely on ATP. This cycle of neurotransmitter release and recycling happens billions of times a second throughout the brain.

ATP also provides the energy for synaptic plasticity, the cellular mechanism underlying learning and memory. The brain's ability to strengthen or weaken connections between neurons in response to new information is what allows us to learn. These structural and functional changes at the synapse, such as building new receptors or modifying existing ones, are all powered by the constant supply of ATP.

ATP as a Direct Brain Messenger

Separate from its role as an energy source, ATP also functions as a direct signaling molecule in the brain. In this capacity, ATP is released from neurons and glial cells to transmit messages to neighboring cells. This form of communication is called purinergic signaling and represents a distinct way that brain cells interact.

When released into the space outside of cells, ATP can bind to purinergic receptors on the surface of adjacent neurons and glia. This binding action triggers a response within the receiving cell, influencing its activity. For instance, this signaling can modulate the excitability of neurons, either increasing or decreasing their likelihood of firing.

Purinergic signaling is also a mechanism through which glial cells, such as astrocytes and microglia, communicate with each other and with neurons. This interaction is important for functions like regulating local blood flow to match the energy demands of active neurons. When neurons are highly active, the associated release of ATP can signal nearby blood vessels to dilate, ensuring a greater supply of oxygen and glucose to that brain region.

This signaling system also plays a part in the brain's response to injury and inflammation. When brain cells are damaged, they release large amounts of ATP, which acts as a danger signal to alert nearby immune cells like microglia. This initiates a response aimed at containing the damage and clearing away cellular debris.

Consequences of Brain Energy Failure

The brain's heavy reliance on a continuous supply of ATP means that any disruption to this energy pipeline can have severe consequences. An energy failure occurs when the amount of ATP available is not sufficient to meet the metabolic demands of the brain's cells. This leads to impaired function and, in severe cases, cell death.

An example of acute energy failure is a stroke, where a blood clot or hemorrhage cuts off the supply of oxygen and glucose to a part of the brain. Without these fuels, mitochondrial ATP production halts almost immediately. The first cellular systems to fail are the energy-intensive sodium-potassium pumps, which can no longer maintain proper ion gradients, leading to a cascade of destructive events and the death of the neuron.

Subtler, long-term deficits in brain energy metabolism are implicated in the progression of chronic neurodegenerative diseases. Conditions like Alzheimer's and Parkinson's disease are associated with mitochondrial dysfunction, where the cellular powerhouses become less efficient at producing ATP over time. This chronic energy shortage may not cause rapid cell death but can lead to a slow decline in neuronal function and resilience.

This persistent energy deficit can impair a neuron's ability to handle stress, repair damage, and conduct normal synaptic communication. Over years, this cumulative damage contributes to the gradual loss of neurons and the cognitive and motor impairments characteristic of these diseases. Research suggests that even mild energy failure can render neurons more vulnerable to the toxic proteins and inflammatory processes associated with neurodegeneration.

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What Is ATP and Why Is It So Important for the Brain?

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Beyond being simple fuel, discover how ATP governs the brain's baseline operations, active thought, and is fundamental to long-term neurological health.

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ATP in the Brain: Fueling Cognitive Function and Neuronal Activity

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Explore ATP’s crucial role in brain function, from energy production to cognitive processes, and learn how to optimize ATP levels for better brain health.

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Overview of the Innervation of Ankle Joint

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Overview of the Innervation of Ankle Joint

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Overview of the Innervation of Ankle Joint - PubMed

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In this article, the literature describing the origin, course, and termination of the nerves innervating the ankle joint is reviewed and discussed. The anterior aspect of the joint capsule receives innervation from articular branches from the saphenous, superficial, and deep fibular nerves; laterall …

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In 1858, Drs. Henry Gray and Henry Vandyke Carter created a book for their surgical colleagues that established an enduring standard among anatomical texts. After more than 150 years of continuous publication, Gray’s Anatomy remains the definitive, comprehensive reference on the subject, offering ready access to the information you need to ensure safe, effective practice. This 41st edition has been meticulously revised and updated throughout, reflecting the very latest understanding of clinical anatomy from field leaders around the world. The book’s traditional lavish art programme and clear text have been further honed and enhanced, while major advances in imaging techniques and the new insights they bring are fully captured in new state-of-the-art X-ray, CT, MR, and ultrasonic images. - Presents the most detailed and dependable coverage of anatomy available anywhere. - Regional organization collects all relevant material on each body area together in one place, making access to core information easier for clinical readers. - Anatomical information is matched with key clinical information where relevant. - Numerous clinical discussions emphasize considerations that may affect medical care. - Each chapter has been edited by experts in their field, ensuring access to the very latest evidence-based information on that topic. - More than 1,000 completely new photographs, including an extensive electronic collection of the latest X-ray, CT, MR, and histological images. - The downloadable Expert Consult eBook version included with your purchase allows you to search all of the text, figures, references and videos from the book on a variety of devices. - Carefully selected electronic enhancements include additional text, tables, illustrations, labelled imaging and videos – as well as 24 specially invited ‘Commentaries’ on new and emerging topics related to anatomy.

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The lumbar plexus is a web of nerves (a nervous plexus) in the lumbar region of the body which forms part of the larger lumbosacral plexus. It is formed by the divisions of the first four lumbar nerves (L1-L4) and from contributions of the subcostal nerve (T12), which is the last thoracic nerve. Additionally, the ventral rami of the fourth lumbar nerve pass communicating branches, the lumbosacral trunk, to the sacral plexus. The nerves of the lumbar plexus pass in front of the hip joint and mainly support the anterior part of the thigh.

The plexus is formed lateral to the intervertebral foramina and passes through psoas major. Its smaller motor branches are distributed directly to psoas major, while the larger branches leave the muscle at various sites to run obliquely down through the pelvis to leave under the inguinal ligament with the exception of the obturator nerve which exits the pelvis through the obturator foramen.

The iliohypogastric nerve runs posterior to the psoas major on its proximal lateral border to run laterally and obliquely on the anterior side of quadratus lumborum. Lateral to this muscle, it pierces the transversus abdominis to run above the iliac crest between that muscle and abdominal internal oblique. It gives off several motor branches to these muscles and a sensory branch to the skin of the lateral hip. Its terminal branch then runs parallel to the inguinal ligament to exit the aponeurosis of the abdominal external oblique above the external inguinal ring where it supplies the skin above the inguinal ligament (i.e. the hypogastric region) with the anterior cutaneous branch.

The ilioinguinal nerve closely follows the iliohypogastric nerve on the quadratus lumborum, but then passes below it to run at the level of the iliac crest. It pierces the lateral abdominal wall and runs medially at the level of the inguinal ligament where it supplies motor branches to both transversus abdominis and sensory branches through the external inguinal ring to the skin over the pubic symphysis and the lateral aspect of the labia majora or scrotum.

The genitofemoral nerve pierces psoas major anteriorly below the former two nerves to immediately split into two branches that run downward on the anterior side of the muscle. The lateral femoral branch is purely sensory. It pierces the vascular lacuna near the saphenous hiatus and supplies the skin below the inguinal ligament (i.e. proximal, lateral aspect of femoral triangle). The genital branch differs in males and females. In males it runs in the spermatic cord and in females in the inguinal canal together with the teres uteri ligament. It then sends sensory branches to the scrotal skin in males and the labia majora in females. In males it supplies motor innervation to the cremaster.

The lateral cutaneous femoral nerve pierces psoas major on its lateral side and runs obliquely downward below the iliac fascia. Medial to the anterior superior iliac spine it leaves the pelvic area through the lateral muscular lacuna it enters the thigh by passing behind the lateral end of the inguinal ligament . In the thigh it briefly passes under the fascia lata before it breaches the fascia and supplies the skin of the anterior thigh.

The obturator nerve leaves the lumbar plexus and descends behind psoas major on it medial side, then follows the linea terminalis into the lesser pelvis, and finally leaves the pelvic area through the obturator canal. In the thigh, it sends motor branches to obturator externus before dividing into an anterior and a posterior branch, both of which continues distally. These branches are separated by adductor brevis and supply all thigh adductors with motor innervation: pectineus, adductor longus, adductor brevis, adductor magnus, adductor minimus, and gracilis. The anterior branch contributes a terminal, sensory branch which passes along the anterior border of gracilis and supplies the skin on the medial, distal part of the thigh.

The femoral nerve is the largest and longest of the plexus' nerves. It gives motor innervation to iliopsoas, pectineus, sartorius, and quadriceps femoris; and sensory innervation to the anterior thigh, posterior lower leg, and hindfoot. In the pelvic area, it runs in a groove between psoas major and iliacus giving off branches to both muscles, and exits the pelvis through the medial aspect of muscular lacuna. In the thigh it divides into numerous sensory and muscular branches and the saphenous nerve, its long sensory terminal branch which continues down to the foot.

Lumbar plexus after dissection

Schematic diagram of the lumbar plexus

Thieme Atlas of Anatomy: General Anatomy and Musculoskeletal System. Thieme. 2006. ISBN 1-58890-419-9.

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The lumbar plexus is a web of nerves (a nervous plexus) in the lumbar region of the body which forms part of the larger lumbosacral plexus. It is formed by the divisions of the first four lumbar nerves (L1-L4) and from contributions of the subcostal nerve (T12), which is the last thoracic nerve.

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Gun Shot Wounds : Wheeless' Textbook of Orthopaedics

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Discussion: - firearms tutorial - missile characteristics: - NRA website - Weapons Effects and Parachute Injuries - Shooting Soldiers: Civil War Medical Images, Memory, and Identity in America - General Management: - most important issue is to get the correct diagnosis (no viceral injury, no compartment syndrome, no ...

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Gunshot Wound Management Review - EMTprep

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Managing gunshot wounds requires a working knowledge of several mechanisms. Understanding the anatomy and physiology of the body is imperative; the severity of the damage and impacted body structures must be quickly assessed. This assessment also requires knowledge of bullet mechanics as it travels through the human body. Gunshot wounds present different problems for prehospital providers depending on how many bullets made an impact, what part of the body the bullet traveled through, and what type of bullet the firearm ejected.

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Concept

Treat the wound, not the gun velocity

Management based on gun velocity old fashioned because

1. Only 1/3 guns are known

2. High velocity guns can produce low energytransfer wounds

Wound Ballistics

Kinetic Energy = 1/2mv²

- important factor is tissue interaction

- energy transfer

Two mechanisms of tissue injury

1. Permanent cavity

- tissue actually hit by the bullet

- increases with distance travelled through tissue

2. Temporary cavity

- tissue stretched by the bullet passage

- as vacuum created, microbes can be sucked in at exit or entry

- increased with distance travelled through tissue

Microbes

Bullets are not sterile

- suck microbes in as well

- clothing fabric gets pulled in too

- wadding also gets into wound

Pathology

Amount of tissue damage depends on

1. Bullet type

- partially jacketed fall apart

- Dum Dum - soft nosed bullets deform and start to spin earlier

2. Target tissue

- inelastic brain worse than elastic muscle

- bone fragments can produce their own injury

3. Tissue width

- bullets really cause damage after they spin 180°

- occurs when hit tissue

- has to be > 12cm tissue thickness for this to start

- hence calf may have low energy transfer wound

- thigh / abdomen have high energy transfer

- energy transfer can increase as travel along wound

4. High velocity bullets

- have more kinetic energy to transfer

- much worse if start to spin / > 12 cm tissue

- better outcome if already exited prior to spin or fragmentation

Management

Initial

ATLS

- secondary survey

- entry wound / exit wound

- NV injury

- history gun type & range

- cover wound

- ADT & antibiotics

- splint

Abdomen

- all GSW that pass through the abdomen become infected without 2/52 antibiotic treatment

Lumbar spine

- all bullets retained in the lumbar spine should be removed acutely

- the cauda equina involves multiple levels & LMN have a better chance of recovery

- better if < 48/24 or > 2/52 to avoid oedema

Operative Management

First OT

- scrub

- large incisions to explore wound

- excise all devitalised tissue

- washout +++

- skeletal stabilisation

- always leave wound open

Remove bullet if

- easy to do so

- danger of later migration causing injury

- likely to cause later pain (i.e. hand / foot)

Second OT

- 48 hours

- DPC if wound clean

- SSG / muscle flaps as needed

Non-Operative Management

In USA good success with non-op management of low energy transfer wounds

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Treat the wound, not the gun velocity Management based on gun velocity old fashioned because 1. Only 1/3 guns are known 2. High velocity guns can produce low energytransfer wounds Kinetic Energy = 1/2mv2 - important factor is tissue interaction - energy transfer Two mechanisms of tissue injury 1.

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Schrägansicht des Sprunggelenks mit Darstellung der Retinacula und verschiedener Muskelsehnen

Bild vonBioDigital, bearbeitet von Lecturio

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Laterale Projektion des Sprunggelenks mit dem Retinaculum musculorum flexorum des Sprunggelenks

Bild vonBioDigital, bearbeitet von Lecturio

Quelle: www.lecturio.de/artikel/medizin/sprunggelenk/

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Seitenansicht des Sprunggelenks mit den Stützbändern des OSG und des Articulatio subtalaris

Bild vonBioDigital, bearbeitet von Lecturio

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Mediale Ansicht des Sprunggelenks mit Hervorhebung der verschiedenen Bänder des medialen Bandapparats

Bild vonBioDigital, bearbeitet von Lecturio

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Quelle: www.lecturio.de/artikel/medizin/sprunggelenk/

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Ansicht von oben auf das Sprunggelenk bei entferntem Talus mit den Gelenkflächen und Stützbändern des unteren Sprunggelenks

Bild vonBioDigital, bearbeitet von Lecturio

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Sprunggelenk: Anatomie, Knochen, Bänder | Lecturio

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Das Sprunggelenk ist die gelenkige Verbindung zwischen Unterschenkel und Fuß und besteht aus zwei Gelenkteilen.

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Pro verstrichener Minute sinkt die Überlebenschance um 10%
In der Schweiz sterben pro Stunde 1 - 2 Menschen an akutem Kreislaufversagen
Daher ist es notwendig, dass alle die Reanimation beherrschen
Der einzige Fehler den man machen kann ist: nicht reanimieren

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Super Poster NHK 20./21.05.2022

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Das Herz schlägt ab dem 20./21. Tag der Schwangerschaft
Es erbringt täglich grandiose Höchstleistungen

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Verschluss eines Blutgefässes im Hirn bei 85% der Betroffenen
Blutung im Gehirn bei 15% der Betroffenen
Die Zeit rennt - daher Stroke Heroes Act Fast

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- rot: sauerstoffreich, Arterien
- blau: sauerstoffarm, Venen

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Es gibt:
Obere Atemwege
Untere Atemwege

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A 25-year-old man, frozen within a snow drift, has been "brought back to life" by doctors after they initially thought he was dead. Justin Smith was ice-cold to the touch, and paramedics assumed he had succumbed to severe hypothermia. However, as reported by The Washington Post, after a last-ditch effort to restart his heart, he was saved against all odds in a first for medical science.

Last February, Smith was found almost entirely covered by snow on the side of an empty road. The coroner, arriving at the scene, thought that he had been lying there, in temperatures of -20°C (-4°F), for 12 hours. He checked for a pulse and found nothing. The man's body temperature was not even registering using a digital thermometer.

Smith was flown by helicopter to Lehigh Valley Hospital. The team of doctors and nurses there tried to warm him up and restart his heart using cardiopulmonary resuscitation (CPR), but to no avail. Gerald Coleman, the emergency department physician on duty at the hospital, decided to give Smith a potassium test.

Potassium is vital for the communication between nerves and muscles, including within the heart. A high concentration within the bloodstream indicates that the heart muscle activity is significantly reduced; in Smith's case, this would mean his heart was very unlikely to restart. When the results came back normal, however, the hospital thought he had a chance.

Using a technique called extracorporeal membrane oxygenation (ECMO), warm, oxygenated blood was passed into Smith's heart and through to the rest of his body; it was effectively an artificially beating heart. Improbably, his heart began to quiver, or "fibrillate." Doctors then managed to shock his heart into restarting.

Ventilators were used to breathe for him, and the ECMO procedure was continued for some time. Medical staff thought he might have been brain-dead, but scans designed to pick up on the electrical signals given off by neurological activity came back entirely normal. He awoke from his coma, and a year on, apart from losing his toes and little fingers to frostbite, Smith, as reported by BBC News, is a completely healthy individual.

"No human being should be able to survive the cold and a body temperature of 18°C (64°F) and a lack of pulse for 12 hours - but Justin Smith did," John E. Castaldo, chief of the division of neurology within the Lehigh Valley Health Network, said in a network-produced video.

The secret to his survival lies in the body's ability to slow down its metabolism - the process that converts oxygen and nutrients into energy. For every degree celsius that the body temperature drops, metabolism drops as much as 7 percent. This means that, at colder temperatures, cells in the body require less oxygen, and the heart rate begins to slow, conserving the body's energy.

Even though Smith's internal body temperature meant that his heart had apparently stopped beating, his body had cooled at just the right rate to allow his metabolism to adapt, operating at minimal levels. The medical staff recognized this, and brought him back to life from his state of suspended animation.

He is the coldest person known to medical science to have survived such extreme hypothermia, and scientists are still not entirely sure how his brain was left completely undamaged.

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Man Frozen Under Snow For Hours Is Brought Back To Life

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A 25-year-old man, frozen within a snow drift, has been "brought back to life" by doctors after they initially thought he was dead. Justin Smith was ice-cold to the touch, and paramedics assumed he had succumbed to severe hypothermia.

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Der Lungenkreislauf ist der kleine Kreislauf
Dabei findet der Gasaustausch statt

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zum B E F A S T

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Schütz Deinen Kopf.de

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Found Frozen: Man Found After Record Cold Survives Hypothermia - Lehigh Valley Health Network

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Rauchen
Stress
Übergewicht
Fehlernährung
Bewegungsmangel
Bluthochdruck
Folgeschäden der Diabetes
Schlafapnoe
Vererbung

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BE-FAST-Schema ist ein Untersuchungsschema für neurologische Auffälligkeiten (insbesondere apoplektischer d.h. plötzlich auftretender Natur)

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Von Kalumet - selbst erstellt = Eigenes Werk, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=438152

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Abstract

Hypothermic cardiac arrest has high mortality and few known prognostic factors. We studied retrospectively 34 victims of accidental hypothermia with cardiac arrest admitted to The University Hospital of North Norway during 1985-2013 who were resuscitated and rewarmed by extracorporeal circulation. No patient survived prior to 1999, while nine out of 24 (37.5%) survived hypothermic cardiac arrest from 1999 to 2013. The lowest measured core temperature among survivors was 13.7 °C; the longest time from cardiac arrest to return of spontaneous circulation was 6 h and 52 min. The only predictor of survival identified was lower blood potassium concentration in the nine survivors compared with the non-survivors. Submersion was not associated with reduced survival. Non-survivors consumed modest hospital resources. Most survivors had a favourable neurological outcome.

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"Nobody is dead until warm and dead": Prolonged resuscitation is warranted in arrested hypothermic victims also in remote areas - A retrospective study from northern Norway

# data[].attributes.attachment_link.description
Hypothermic cardiac arrest has high mortality and few known prognostic factors. We studied retrospectively 34 victims of accidental hypothermia with cardiac arrest admitted to The University Hospital of North Norway during 1985-2013 who were resuscitated and rewarmed by extracorporeal circulation. No patient survived prior to 1999, while nine out of 24 (37.5%) survived hypothermic cardiac arrest from 1999 to 2013.

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Quelle: LECTURIO

https://www.lecturio.de/artikel/medizin/sprunggelenk/

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Die Bewegungsebenen des Sprunggelenks

Bild vonBioDigital, bearbeitet von Lecturio

Quelle: www.lecturio.de/artikel/medizin/sprunggelenk/

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Die verschiedenen Ebenen und Bewegungen des Sprunggelenks

Bild von Lecturio

Quelle: www.lecturio.de/artikel/medizin/sprunggelenk/

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CSE Kraus und Straubinger, Klausenstr. 29, 84489 Burghausen, www.cse-online.de

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Differentialdiagnose Ohr || Medizin kompakt

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Differentialdiagnosen und Leitbilder im Bereich des Ohrs werden hier ausführlich und kompakt beschrieben