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Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
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With patulous Eustachian tube, variations in upper airway pressure associated with respiration are transmitted to the middle ear through the Eustachian tube. This causes an unpleasant fullness feeling in the middle ear and alters the auditory perception. Complaints seem to include muffled hearing and autophony. In addition, patulous Eustachian tube generally feels dry with no clogged feeling or sinus pressure.
Some patients with this condition are disturbed by the perceived volume of their voice, causing them to speak very quietly. Their own voice may also sound lower to other people, because the trachea has more volume when the Eustachian tube is open. The patient may also sound as if they have congestion when speaking. Some sufferers may have difficulty in normal activities. They may also experience increased breathing rate, such as that brought on by physical activity. The increased activity not only increases the rate and force of pressure changes in the airway, which is therefore transmitted more forcefully into the middle ear, but also drives increased blood flow to peripheral muscles, compounding the problem by further depleting the Eustachian tube of extracellular fluid and increasing patency. The combination can lead to severe exacerbation of the symptoms. The urge to clear the ear is often mentioned.
Patulous Eustachian tube, also known as patent Eustachian tube or PET, is the name of a physical disorder where the Eustachian tube, which is normally closed, instead stays intermittently open. When this occurs, the patient experiences autophony, the hearing of self-generated sounds. These sounds, such as one's own breathing, voice, and heartbeat, vibrate directly onto the ear drum and can create a "bucket on the head" effect.
This might have occurred due to barotrauma of descent, and/or the effects of nasal decongestants. It is due to unequal increase in middle ear pressures on ascent, is usually mild, and most often cleared by further ascent. When the pressures in both ears reach ambient levels, the stimulus for the dizziness stops. Although most often mild, the vertigo can persist until the diver reaches the surface continuing the unequal pressures, which can damage the inner ear or ear drum.
Alternobaric vertigo is most pronounced when the diver is in the vertical position; the spinning is towards the ear with the higher pressure and tends to develop when the pressures differ by 60 cm of water or more. Ear clearing may be a remedy. A similar vertigo can also occur as a result of unequal heating stimulation of one inner ear labyrinth over the other due to diving in a prone position in cold water - the undermost ear being stimulated.
The majority of tympanic membrane retractions do not cause any symptoms. Some cause hearing loss by restricting sound-induced vibrations of the eardrum. Permanent conductive hearing loss can be caused by erosion of the ossicles (hearing bones). Discharge from the ear often indicates that the retraction pocket has developed into a cholesteatoma.
In aviation and underwater diving, alternobaric vertigo is dizziness resulting from unequal pressures being exerted between the ears due to one Eustachian tube being less patent than the other.
Tympanic membrane retraction describes a condition in which a part of the eardrum lies deeper within the ear than its normal position.
The eardrum comprises two parts, the pars tensa, which is the main part of the eardrum, and the pars flaccida, which is a smaller part of the eardrum located above the pars tensa. Either or both of these parts may become retracted. The retracted segment of eardrum is often known as a retraction pocket. The terms "atelectasis" or sometimes "adhesive otitis media" can be used to describe retraction of a large area of the pars tensa.
Tympanic membrane retraction is fairly common and has been observed in one quarter of a population of British school children. Retraction of both eardrums is less common than having a retraction in just one ear. It is more common in children with cleft palate. Tympanic membrane retraction also occurs in adults.
Attempts have been made to categorise the extent of tympanic membrane retraction though the validity of these classifications is limited.
Enlarged adenoids can become nearly the size of a ping pong ball and completely block airflow through the nasal passages. Even if enlarged adenoids are not substantial enough to physically block the back of the nose, they can obstruct airflow enough so that breathing through the nose requires an uncomfortable amount of work, and inhalation occurs instead through an open mouth. Adenoids can also obstruct the nasal airway enough to affect the voice without actually stopping nasal airflow altogether.
Nasal blockage is determined by at least two factors: 1) the size of the adenoids, and 2) the size of the nasal pharynx passageway.
The adenoid usually reaches its greatest size by about age 5 years or so, and then fades away ("atrophies") by late childhood - generally by the age of 7 years. The lymphoid tissue remains under the mucosa of the nasopharynx, and could be seen under a microscope if the area was biopsied, but the mass is so reduced in size that the roof of the nasopharynx becomes flat rather than mounded. Just as the size of the adenoids is variable between individuals, so is the age at which adenoids atrophy.
The symptoms caused by enlarged adenoids are mostly due to "where" this lymphoid tissue is located. The adenoids are in the midline of the nasopharynx, and the Eustachian tubes open from either ear to the right and left of them. In children with excessive middle ear infections and chronic middle ear fluid, there is a high bacterial count in the adenoids as compared to children without problematic otitis media, even if the size of the adenoids is small. The adenoids in these cases provides a reservoir of pathogenic bacteria that cause ear infections and subsequent middle ear effusions (fluid).
The nasopharynx lies right above the throat. Splashes of excessive "drip" from infected adenoids may land directly on the vocal cords. Although the larynx and vocal cords do not ordinarily become infected from adenoiditis, their mucosa does become irritated. The vocal cords are extremely sensitive to touch, and any fluid drops falling on them cause an irresistible urge to cough. Adenoiditis therefore is one of the causes of cough.
Perforation of the eardrum leads to conductive hearing loss, which is usually temporary. Other symptoms may include tinnitus, earache or a discharge of mucus.
Adenoid hypertrophy (or enlarged adenoids) is the unusual growth ("hypertrophy") of the adenoid tonsil first described by the Danish physician Wilhelm Meyer (1824-1895) in Copenhagen in 1868. He described that a long term adenoid hypertrophy will cause an obstruction of the nasal airways. These will lead to a dentofacial growth anomaly that was defined as "adenoid facies" (see long face syndrome).
There is very little lymphoid tissue in the nasopharynx of young babies; humans are born without substantial adenoids. The mat of lymphoid tissue called adenoids starts to get sizable during the first year of life. Just how big the adenoids become is quite variable between individual children.
The general term for disorders of the velopharyngeal valve is velopharyngeal dysfunction (VPD). It includes three subterms: velopharyngeal insufficiency, velopharyngeal inadequacy, and velopharyngeal mislearning.
- Velopharyngeal insufficiency can be caused by an anatomical abnormality of the throat. It occurs in children with a history of cleft palate or submucous cleft, who have short or otherwise abnormal vela. Velopharyngeal insufficiency can also occur after adenoidectomy.
- Velopharyngeal incompetence is a defective closure of the velopharyngeal valve due to its lack of speed and precision. It is caused by a neurologic disorder or injury (e.g. cerebral palsy or traumatic brain injury).
- Sometimes children present no abnormalities yet still have hypernasal speech: this can be due to velopharyngeal mislearning, indicating that the child has been imitating or has never learned how to use the valve correctly.
Hypernasal speech (also hyperrhinolalia or open nasality; medically known as Rhinolalia aperta from Latin "rhinolalia": "nasal speech" and "aperta": "open") is a disorder that causes abnormal resonance in a human's voice due to increased airflow through the nose during speech. It is caused by an open nasal cavity resulting from an incomplete closure of the soft palate and/or velopharyngeal sphincter. In normal speech, nasality is referred to as nasalization and is a linguistic category that can apply to vowels or consonants in a specific language. The primary underlying physical variable determining the degree of nasality in normal speech is the opening and closing of a velopharyngeal passageway between the oral vocal tract and the nasal vocal tract. In the normal vocal tract anatomy, this opening is controlled by lowering and raising the velum or soft palate, to open or close, respectively, the velopharyngeal passageway.
The majority (98%) of patients with cholesteatoma have ear discharge or hearing loss or both in the affected ear.
Other more common conditions, such as otitis externa, may also present with these symptoms, but cholesteatoma is much more serious and should not be overlooked. If a patient presents to a doctor with ear discharge and hearing loss, the doctor should consider the patient to have cholesteatoma until the disease is definitely excluded.
Other less common symptoms (all less than 15%) of cholesteatoma may include: pain, balance disruption, tinnitus, ear ache, headaches and bleeding from the ear. There can also be facial nerve weakness.
Balance symptoms in the presence of a cholesteatoma raises the possibility that the cholesteatoma is eroding the balance organs, which form part of the inner ear.
On initial inspection, an ear canal full of discharge may be all that is visible. Until the doctor has cleaned the ear and inspected the entire tympanic membrane, cholesteatoma cannot be either confirmed or excluded.
Once the debris is cleared, cholesteatoma can give rise to a number of appearances. If there is significant inflammation, the tympanic membrane may be partially obscured by an aural polyp. If there is less inflammation, the cholesteatoma may present the appearance of 'semolina' discharging from a defect in the tympanic membrane. The posterior and superior parts of the tympanic membrane are most commonly affected. If the cholesteatoma has been dry, the cholesteatoma may present the appearance of 'wax over the attic'. The attic is just above the ear drum.
The patient may commonly also have clinical signs of conductive hearing loss. Less frequently, there may be signs of imbalance or facial weakness.
If untreated, a cholesteatoma can eat into the three small bones located in the middle ear (the malleus, incus and stapes, collectively called ossicles), which can result in nerve deterioration, deafness, imbalance and vertigo. It can also affect and erode, through the enzymes it produces, the thin bone structure that isolates the top of the ear from the brain, as well as lay the covering of the brain open to infection with serious complications (rarely even death due to brain abscess and septicemia).
Both the acquired as well as the congenital types of the disease can affect the facial nerve that extends from the brain to the face and passes through the inner and middle ear and leaves at the anterior tip of the mastoid bone, and then rises to the front of the ear and extends into the upper and lower face.
Neoplasm should be considered in any patient presenting with NLD obstruction.In patients with an atypical presentation, including younger age and male gender, further workup is appropriate. Bloody punctal discharge or lacrimal sac distension above the medial canthal tendon is also highly suggestive of neoplasm.
The condition is characterised by aversive reactions to feeding and oral stimulation including Co-Symptoms. It can occur one week after tube insertion.
- Food refusal/Head turning
- Loss of appetite/disinterest
- Oversensitivity for touching, smelling, tasting food
- Nausea
- Gagging
- Retching
- Vomiting
- Anxiety attacks
Granulomatous disease, including sarcoidosis, granulomatosis with polyangiitis, and midline granuloma, may also lead to NLD obstruction.
A perforated eardrum or punctured eardrum is a rupture or perforation (hole) of the eardrum which can occur as a result of otitis media (ear infection), trauma (e.g. by trying to clean the ear with sharp instruments), explosion, loud noise or surgery (accidental creation of a rupture). Flying with a severe cold can also cause perforation due to changes in air pressure and blocked eustachian tubes resulting from the cold. This is especially true on landing.
Conductive hearing loss occurs when there is a problem conducting sound waves anywhere along the route through the outer ear, tympanic membrane (eardrum), or middle ear (ossicles).
This type of hearing loss may occur in conjunction with sensorineural hearing loss (mixed hearing loss) or alone.
Fluid accumulation is the most common cause of conductive hearing loss in the middle ear, especially in children. Major causes are ear infections or conditions that block the eustachian tube, such as allergies or tumors. Blocking of the eustachian tube leads to decreased pressure in the middle ear relative to the external ear, and this causes decreased motion of both the ossicles and the tympanic membrane.
- acute or serous otitis media
- otitis media with effusion or 'glue ear'
- Perforated eardrum
- Chronic suppurative otitis media (CSOM)
- Cholesteatoma
- Otosclerosis, abnormal growth of bone in or near the middle ear
- middle ear tumour
- ossicular discontinuity as a consequence of infection or temporal bone trauma
- Congenital malformation of the ossicles. This can be an isolated phenomenon or can occur as part of a syndrome where development of the 1st and 2nd branchial arches is seen such as in Goldenhar syndrome, Treacher Collins syndrome, branchio-oto-renal syndrome etc.
- Barotrauma unequal air pressures in the external and middle ear. This can temporarily occur, for example, by the environmental pressure changes as when shifting altitude, or inside a train going into a tunnel. It is managed by any of various methods of ear clearing manoeuvres to equalize the pressures, like swallowing, yawning, or the Valsalva manoeuvre. More severe barotrauma can lead to middle ear fluid or even permanent sensorineural hearing loss.
Ear pain can be caused by disease in the external or middle ear(because of infection), or inner ear, but the three are indistinguishable in terms of the pain experienced.
External ear pain may be:
- Mechanical: trauma, foreign bodies such as hairs, insects or cotton buds.
- Infective (otitis externa): "Staphylococcus", "Pseudomonas", "Candida", herpes zoster, or viral Myringitis. (See Otitis externa)
Middle ear pain may be:
- Mechanical: barotrauma (often iatrogenic), Eustachian tube obstruction leading to acute otitis media.
- Inflammatory / infective: acute otitis media, mastoiditis.
Cholesteatomas occur in two basic classifications: Acquired cholesteatomas, which are more common, are usually caused by pathological alteration of the ear drum leading to accumulation of keratin within the middle ear. Congenital cholesteatomas are usually middle ear epidermal cysts that are identified deep within an intact ear drum.
Tube dependency refers to the process in which an individual becomes dependent on a feeding tube for nutrition. While the term technically refers to any individual who requires enteral feeding for nutrition, some practitioners specifically use this term for patients, primarily children, who are medically capable of eating by mouth but have been unable to wean from a feeding tube due to non-medical causes, which may be behavioral, sensory, or motoric in nature.
Ménière's is characterized by recurrent episodes of vertigo, hearing loss and tinnitus; episodes may be accompanied by headache and a feeling of fullness in the ears.
People may also experience additional symptoms related to irregular reactions of the autonomic nervous system. These symptoms are not symptoms of Meniere's disease per se, but rather are side effects resulting from failure of the organ of hearing and balance, and include nausea, vomiting, and sweating—which are typically symptoms of vertigo, and not of Ménière's. This includes a sensation of being pushed sharply to the floor from behind.
Sudden falls without loss of consciousness (drop attacks) may be experienced by some people.
It is characterized by nodular thickening of the tunica muscularis of the narrow (isthmic) portion of the Fallopian tube. In severe cases, it leads to complete obliteration of the tubal lumen. It is uncommonly bilateral.
Ear pain, also known as otalgia , is pain in the ear. Primary ear pain is pain that originates inside the ear. Referred ear pain is pain that originates from outside the ear.
Ear pain is not always associated with ear disease. It may be caused by several other conditions, such as impacted teeth, sinus disease, inflamed tonsils, infections in the nose and pharynx, throat cancer, and occasionally as a sensory aura that precedes a migraine.
Individuals with Treacher Collins syndrome often have both cleft palate and hearing loss, in addition to other disabilities. Hearing loss is often secondary to absent, small, or unusually formed ears (microtia), and commonly results from malformations of the middle ear. Researchers have found that most patients with Treacher Collins syndrome have symmetric external ear canal abnormalities and symmetrically dysmorphic or absent ossicles in the middle ear space. Inner ear structure is largely normal. Most patients show a moderate hearing impairment or greater, and the type of loss is generally a conductive hearing loss. Patients with Treacher Collins syndrome exhibit hearing losses similar to those of patients with malformed or missing ossicles (Pron "et al.", 1993).