Noise-induced hearing loss in the context of "Hearing loss"

Audio feedback (also known as acoustic feedback, howlround in the UK, or simply as feedback) is a positive feedback situation that may occur when an acoustic path exists between an audio output (for example, a loudspeaker) and its audio input (for example, a microphone or guitar pickup). In this example, a signal received by the microphone is amplified and passed out of the loudspeaker. The sound from the loudspeaker can then be received by the microphone again, amplified further, and then passed out through the loudspeaker again. The frequency of the resulting howl is determined by resonance frequencies in the microphone, amplifier, and loudspeaker, the acoustics of the room, the directional pick-up and emission patterns of the microphone and loudspeaker, and the distance between them. The principles of audio feedback were first discovered by Danish scientist Søren Absalon Larsen, hence it is also known as the Larsen effect.

Feedback is almost always considered undesirable when it occurs with a singer's or public speaker's microphone at an event using a sound reinforcement system or PA system. Audio engineers typically use directional microphones with cardioid pickup patterns and various electronic devices, such as equalizers and, since the 1990s, automatic feedback suppressors, to prevent feedback, which detracts from the audience's enjoyment of the event and may damage equipment or hearing.

In excitotoxicity, nerve cells suffer damage or death when the levels of otherwise necessary and safe neurotransmitters such as glutamate become pathologically high, resulting in excessive stimulation of receptors. For example, when glutamate receptors such as NMDA receptors or AMPA receptors encounter excessive levels of the excitatory neurotransmitter, glutamate, significant neuronal damage might ensue. Different mechanisms might lead to increased extracellular glutamate concentrations, e.g. reduced uptake by glutamate transporters (EAATs), synaptic hyperactivity, or abnormal release from different neural cell types. Excess glutamate allows high levels of calcium ions (Ca) to enter the cell. Ca influx into cells activates a number of enzymes, including phospholipases, endonucleases, and proteases such as calpain. These enzymes go on to damage cell structures such as components of the cytoskeleton, membrane, and DNA. In evolved, complex adaptive systems such as biological life it must be understood that mechanisms are rarely, if ever, simplistically direct. For example, NMDA, in subtoxic amounts, can block glutamate toxicity and induce neuronal survival. In addition to abnormally high neurotransmitter concentrations, also elevation of the extracellular potassium concentration, acidification and other mechanisms may contribute to excitotoxicity.

Excitotoxicity may be involved in cancers, spinal cord injury, stroke, traumatic brain injury, hearing loss (through noise overexposure or ototoxicity), and in neurodegenerative diseases of the central nervous system such as multiple sclerosis, Alzheimer's disease, amyotrophic lateral sclerosis (ALS), Parkinson's disease, alcoholism, alcohol withdrawal or hyperammonemia and especially over-rapid benzodiazepine withdrawal, and also Huntington's disease. Other common conditions that cause excessive glutamate concentrations around neurons are hypoglycemia. Blood sugars are the primary energy source for glutamate removal from inter-synaptic spaces at the NMDA and AMPA receptor site. Persons in excitotoxic shock must never fall into hypoglycemia. Patients should be given 5% glucose (dextrose) IV drip during excitotoxic shock to avoid a dangerous build up of glutamate. When 5% glucose (dextrose) IV drip is not available high levels of fructose are given orally. Treatment is administered during the acute stages of excitotoxic shock along with glutamate receptor antagonists. Dehydration should be avoided as this also contributes to the concentrations of glutamate in the inter-synaptic cleft and "status epilepticus can also be triggered by a build up of glutamate around inter-synaptic neurons."

A hearing protection device, also known as a HPD, is an ear protection device worn in or over the ears while exposed to hazardous noise and provide hearing protection to help prevent noise-induced hearing loss. HPDs reduce the level of the noise entering the ear. HPDs can also protect against other effects of noise exposure such as tinnitus and hyperacusis. There are many different types of HPDs available for use, including earmuffs, earplugs, electronic hearing protection devices, and semi-insert devices.

The use of the HPD without individual selection, training and fit testing does not significantly reduce the risk of hearing loss. For example, one study covered more than 19 thousand workers, some of whom usually used hearing protective devices, and some did not use them at all. There was no statistically significant difference in the risk of noise-induced hearing loss.

Sensorineural hearing loss (SNHL) is a type of hearing loss in which the root cause lies in the inner ear, sensory organ (cochlea and associated structures), or the vestibulocochlear nerve (cranial nerve VIII). SNHL accounts for about 90% of reported hearing loss. SNHL is usually permanent and can be mild, moderate, severe, profound, or total. However, if the loss happened suddenly, and very recently, Prednisone and other treatments may reverse the loss (See SSHL below). Various other descriptors can be used depending on the shape of the audiogram, such as high frequency, low frequency, U-shaped, notched, peaked, or flat.

Sensory hearing loss often occurs as a consequence of damaged or deficient cochlear hair cells. Hair cells may be abnormal at birth or damaged during the lifetime of an individual. There are both external causes of damage, including infection, and ototoxic drugs, as well as intrinsic causes, including genetic mutations. A common cause or exacerbating factor in SNHL is prolonged exposure to environmental noise, or noise-induced hearing loss. Exposure to a single very loud noise, such as a gunshot or bomb blast, can cause noise-induced hearing loss. Using headphones at high volume over time, or being in loud environments regularly, such as a loud workplace, sporting events, concerts, and using noisy machines, can also be a risk for noise-induced hearing loss.

Hearing loss is a partial or total inability to hear. Hearing loss may be present at birth or acquired at any time afterwards. Hearing loss may occur in one or both ears. In children, hearing problems can affect the ability to acquire spoken language. In adults, it can create difficulties with social interaction and at work. Hearing loss can be temporary or permanent. Hearing loss related to age usually affects both ears and is due to cochlear hair cell loss. In some people, particularly older people, hearing loss can result in isolation and loneliness.

Hearing loss may be caused by a number of factors, including: genetics, ageing, exposure to noise, some infections, birth complications, trauma to the ear or brain, and certain medications or toxins. A common condition that results in hearing loss is chronic ear infections. Certain infections during pregnancy, such as cytomegalovirus, syphilis and rubella, may also cause hearing loss in the child. Hearing loss is diagnosed when hearing testing finds that a person is unable to hear 25 decibels in at least one ear. Testing for poor hearing is recommended for all newborns. Hearing loss can be categorized as minimal/slight (15 to 25 dB), mild (25 to 40 dB), moderate (41 to 55 dB), moderate-severe (56 to 70 dB), severe (71 to 90 dB), or profound (greater than 90 dB). There are three main types of hearing loss: conductive hearing loss, sensorineural hearing loss, and mixed hearing loss.