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Sensorineural Hearing Loss

Sensorineural Hearing Loss is a type of hearing impairment caused by damage to the inner ear or auditory nerve.
It is characterized by a reduction in sound sensitivity and clarity, making it difficult to hear and understand speech.
This condition can result from a variety of factors, including noise exposure, aging, genetic factors, and certain medical conditions.
Effective management of Sensorineural Hearing Loss often involves the use of hearing aids, cochlear implants, or other assistive devices to improve auditory function and enhance quality of life.
Reseach in this area focuses on understanding the underlying mechanisms, developing better diagnostic tools, and improving treatment options to address this common and often debilitating form of hearing loss.

Most cited protocols related to «Sensorineural Hearing Loss»

This study was approved by the National Institute of Child Health and Human Development Institutional Review Board. Consent and, when appropriate, assent were obtained. A clinical severity scale was developed to ascertain clinical symptoms in nine major and eight minor clinical areas (Table I). Four of the domains (Ambulation, Fine Motor Skills, Speech, and Swallowing) were modified from the disability scale developed by Iturriaga et al [Iturriaga et al., 2006 (link)]. The scoring of each domain was designed to allow a score to be derived from a comprehensive clinical evaluation. A Likert-like scale was used to assign nine major domain scores of 0–5 and eight minor domain scores of 0–2. Clinical experience was used to weight the various scales. Summation of all 17 domains yielded total possible scores that range from 0–61, with a higher score indicating more severe clinical impairment. A comprehensive medical history form was developed to document both the clinical history of current patients and to serve as a guide in extraction of data from medical records. To be scored, seizures, cataplexy, and narcolepsy had to be definitive and not questionable. For the swallowing domain, one point was scored if the patient had a history of cough while eating. Additional points were added if the patient had intermittent or consistent dysphagia with either liquids or solids. Hearing loss refers to sensorineural hearing loss and not hearing loss secondary to conductive defects. The diagnosis of NPC was established by either biochemical testing or mutation analysis. All patients have NPC1 by either molecular or complementation group testing. Two patient groups were studied. The first group consisted of 18 NPC patients (current cohort) who were enrolled in an observational study at the National Institutes of Health Clinical Center (NIH CC) between August 2006 and September 2007 (Table II). The second patient cohort consisted of 19 NPC patients (historical cohort) for whom we had sufficient medical records to generate at least three scores at different time points. Medical records were reviewed for 36 patients followed at the NIH CC by other investigators between 1972 and 2005. Of the 36 previous NIH CC patients with a diagnosis of NPC, 16 patients had three or more NIH admissions with adequate documentation to generate a severity score. Of the current patients, patient 1 had previous NIH admissions for which records were available and patients 13 and 15 had sufficient outside medical records from which we could derive longitudinal data.
Publication 2009
Cardiac Conduction System Disease Cataplexy Cough Deglutition Disorders Diagnosis Disabled Persons Ethics Committees, Research Hearing Impairment Motor Skills Mutation Narcolepsy Niemann-Pick Disease, Type C1 Patients Seizures Sensorineural Hearing Loss Speech
Neonates with symptomatic congenital CMV disease, with or without CNS involvement, were eligible for enrollment. Given the rarity of this disease, 40 study sites participated, and each was anticipated to contribute only a few study participants. All the study participants had CMV detected in urine or throat-swab specimens by means of culture, shell-vial culture, or polymerase-chain-reaction assay. Symptomatic disease was defined as one or more of the following: thrombocytopenia, petechiae, hepatomegaly, splenomegaly, intrauterine growth restriction, hepatitis, or CNS involvement such as microcephaly, intracranial calcifications, abnormal cerebrospinal fluid indexes, chorioretinitis, sensorineural hearing loss, or the detection of CMV DNA in cerebrospinal fluid. Eligible participants had a gestational age of 32 weeks or more, were 30 days of age or less, and weighed at least 1800 g at the initiation of therapy.
The institutional review board at each study center approved the study protocol. After written informed consent was obtained from the parent or legal guardian, all participants received valganciclovir (at a dose of 16 mg per kilogram of body weight, orally twice daily) for 6 weeks.15 (link) Participants then underwent randomization in a 1:1 ratio to receive either continued valganciclovir or placebo for 4.5 months. The dose of the study medication was adjusted monthly for growth. Study drugs (oral valganciclovir and placebo) were provided by Hoffmann–La Roche, which had no role in the study design or data analyses or in the writing of the manuscript or the decision to submit it for publication. Study personnel and the participants’ families were unaware of the randomization assignments.
The primary end point prespecified in the protocol was the change in hearing in the better ear (“best-ear” hearing), from baseline to the 6-month follow-up.13 (link) Secondary end points prespecified in the protocol included the change in total-ear hearing (i.e., hearing in one or both ears that could be evaluated) from baseline to follow-up at 6, 12, and 24 months; change in best-ear hearing from baseline to follow-up at 12 and 24 months; neurologic impairment at 12 and 24 months; and adverse events leading to the permanent discontinuation of therapy. Tertiary end points included the correlation of viral load in whole blood with audiologic and neurodevelopmental outcomes, adverse events related to the study medication, and characterization of blood concentrations of ganciclovir.
Publication 2015
Biological Assay BLOOD Body Weight Cerebrospinal Fluid Chorioretinitis Congenital Cytomegalovirus Infection Ethics Committees, Research Fetal Growth Retardation Ganciclovir Gestational Age Hepatitis A Infant, Newborn Legal Guardians Microcephaly Parent Petechiae Pharynx Physiologic Calcification Placebos Polymerase Chain Reaction Rare Diseases Sensorineural Hearing Loss Therapeutics Thrombocytopenia Urine Valganciclovir
We recruited families with twin children aged between 6;0 and 11;11 years, whose first language at home was English. We aimed for an over-representation of twin pairs in which one or both twins had language or literacy problems that might be indicative of DLD. Families were recruited via fliers sent to primary schools around the UK, advertisements on our group’s website and via twins’ clubs. The initial flier was worded as follows: ‘We are looking for sets of twins to participate in a new study investigating factors underlying children’s language difficulties. We want to test twins with and without language problems (language-impaired, typically-developing, or one twin of each)’. Head teachers were asked to forward information sheets about the study to parents of twin children. We aimed to recruit 180 pairs selected on the basis of having language or literacy problems (60 MZ, 60 DZ opposite sex and 60 DZ same sex), and 60 unselected pairs (20 of each type). In practice, self-selection of those volunteering to take part meant that the latter group tended to come from relatively highly educated backgrounds, and could not be regarded as representative of the general population. The flow chart in Fig. 1 shows the numbers of participant children at different stages of selection. Parents and caregivers of 194 twin pairs volunteered for the study, yielding 134 children who met our criteria for DLD, and 190 children who met criteria as typically developing (TD). See the Data Analysis section below for criteria.
Children were excluded from the sample if they met any of the following criteria: WASI nonverbal ability (performance IQ) more than two SDs below the population mean; diagnosis of autism spectrum disorder (ASD) in one or both twins; sensorineural hearing loss or failure of a hearing test on the day of testing; and brain injury or a serious medical condition affecting one or both twins. In order to test our main hypothesis that DLD was related to cerebral laterality as measured by fTCD, it was necessary to exclude individuals in a second stage of exclusions if we did not obtain useable fTCD data from them, defined as fewer than 12 accepted trials. We also excluded participants with extreme laterality indices (above 10 or below −10); 3 individuals were excluded based on this criterion. Useable fTCD data were obtained from 107 (80%) of the children with DLD, and 156 (82%) of the TD children.
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Publication 2018
Autism Spectrum Disorders Brain Injuries Child Diagnosis factor A Functional Laterality Head Hearing Tests Parent Sensorineural Hearing Loss Twins

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Publication 2014
BaseLine dental cement Child Diet, Formula Electrocardiogram Electrocardiography, 12-Lead Epistropheus Ethics Committees, Research Females Fingers Males Rate, Heart Sensorineural Hearing Loss
The leading symptom of VP is recurrent spontaneous attacks of vertigo. The diagnosis is generally straightforward because of the characteristic brief duration (from seconds up to one minute), the frequently recurring attacks of vertigo and the response to a treatment with carbamazepine or oxcarbazepine. There are only a few other disorders which may present with this leading symptom:

Menière’s disease: duration of the attacks from 20 min to 12 hours, low- to medium-frequency sensorineural hearing loss (>30 dB, <2000 Hz) [28 (link)].

Tumarkin’s otolithic crisis (“vestibular drop attacks”). These sudden falls are usually not accompanied by vertigo and occur most often in patients with known Menière’s disease, typically while standing, whereas in VP the attacks occur in any body positions.

Paroxysmal brainstem attacks with vertigo, dysarthria or ataxia (after stroke or in MS) may be difficult to distinguish, as they also respond to low doses of sodium-channel blockers. It was shown that they may be caused by a brainstem lesion due to MS plaques or lacunar infarctions [27 (link)], which also leads to ephaptic discharges of neighboring fibers of the brainstem paths. In such cases the use of MRI with thin brainstem slices is useful for establishing the diagnosis.

Vestibular migraine [26 (link)]: officially the duration of the attacks is 5 min to 72 hours, current or previous history of migraine, most attacks being accompanied by other migrainous symptoms. In vestibular migraine, short spells of vertigo may be induced by changes of head or body position when patients are motion sensitive during an episode of vestibular migraine.

Vertebrobasilar transient ischemic attacks: vertigo frequently occurs in isolation in this condition [33 (link)].

Panic attacks: according to DSM-5, the diagnostic criteria for a panic attack include a discrete period of intense fear or discomfort, in which four (or more) of the following symptoms develop abruptly and reach a peak within minutes: feeling dizzy, unsteady, lightheaded, or faint; nausea or abdominal distress; palpitations, and/or accelerated heart rate; sweating; trembling or shaking; sensations of shortness of breath or being smothered; feeling of choking; chest pain or discomfort; de-realization or depersonalization; fear of losing control or going insane; sense of impending death; paresthesias; chills or hot flashes. Panic attacks are often longer than typical attacks of VP. It may be helpful to ask the patient which of the symptoms come first to differentiate between the two.

Perilymph fistula: The cardinal symptoms of perilymph fistula (and superior canal dehiscence syndrome) are attacks of vertigo caused by changes in pressure, for example, by coughing, pressing, sneezing, lifting, or loud noises and accompanied by illusory movements of the environment (oscillopsia) and instability of posture and gait with or without hearing disorders. The attacks, which can last seconds to days, may also occur during changes in the position of the head (e.g., when bending over) and when experiencing significant changes in altitude (e.g., mountain tours, flights) [6 ].

Episodic ataxia type 2: the duration of the attacks varies from several minutes to hours and more than 90% of the patients have cerebellar signs, in particular gaze-evoked nystagmus and downbeat nystagmus [20, 40 (link)]. The onset of manifestations after the age of 20 is unusual. The much rarer episodic ataxia type 1 is another differential diagnosis. It is characterized by recurrent attacks of ataxia, dizziness and visual blurring, provoked by abrupt postural changes, emotion, vestibular stimulation and lasting minutes. These patients also have neuromyotonia, i.e. continuous spontaneous muscle fiber activity [19 (link)].

Epilepsy with vestibular aura: Vestibular auras can manifest with short attacks of vertigo and nystagmus. Vestibular aura with additional symptoms, so-called non-isolated vestibular aura, is much more prevalent than isolated vestibular aura, which is rare. Vestibular aura is primarily associated with temporal lobe seizures. Isolated vestibular aura spells often last only a few seconds, but longer spells are also reported [41 (link)].

Other differential diagnoses are characterized by recurrent attacks of vertigo that are induced by certain maneuvers. These differential diagnoses include BPPV, central positional vertigo/nystagmus, “rotational vertebral artery occlusion syndrome” (RVAOS), orthostatic hypotension, or rarely cysts or tumors in the cerebello-pontine angle [1, 24 (link)]. In BPPV the attacks are induced by changes of head or body position relative to gravity, and the diagnosis can be proven by the diagnostic positional maneuvers. However, if they are negative, VP remains an important differential diagnosis. In central positional/positioning nystagmus the positioning maneuvers induce a similar nystagmus in different head positions [9 (link)]. In RVAOS the attacks are induced by rotation of the head either to the right or left, and diagnosis is proven by angiography. Similar to VP the symptoms are also caused by an excitation of the peripheral vestibular system [38 (link)]. In orthostatic hypotension the symptoms occur when the patient stands up and may be associated with vertigo and downbeat nystagmus; the key to this diagnosis is measurement of supine and orthostatic blood pressure [11 (link)].
Publication 2016
Abdomen Angiography Ataxia Benign Paroxysmal Positional Vertigo Blood Pressure Brain Stem Carbamazepine Cerebellum Cerebrovascular Accident Chest Pain Chills Cyst Dental Occlusion Depersonalization Diagnosis Differential Diagnosis Drop Attack Dysarthria Dyspnea Emotions Epilepsy Epilepsy, Temporal Lobe Episodic Ataxia, Type 1 Episodic Ataxia, Type 2 Fear Fibrosis Fistula Gravity Head Hot Flashes Hypotension, Orthostatic Illusions Infarction, Lacunar Isaacs' Syndrome Migraine Disorders Movement Muscle Tissue Nausea Neoplasm Metastasis Otoconia Oxcarbazepine Panic Attacks Paresthesia Pathologic Nystagmus Patients Perilymph Pontine Tumors Positional Nystagmus Positional Vertigo Pressure Rate, Heart Senile Plaques Sensorineural Hearing Loss Sodium Channel Blockers Superior Semicircular Canal Dehiscence Syncope Transient Ischemic Attack Vertebral artery syndrome Vertigo Vestibular Labyrinth Vestibular System

Most recents protocols related to «Sensorineural Hearing Loss»

Forty children (21 males, mean age  ±  standard deviation (SD): 5.09  ±  3.79
years old) with sensorineural hearing loss who received their first CI in our
hospital from September 2018 to June 2020 were included in this study. These
children were right-handed according to an assessment with the Edinburgh
Handedness Inventory (Oldfield, 1971 (link)). They started to use hearing aids at a mean age of
2.30  ±  1.21 years old, and had used hearing aids with a mean duration of
2.79  ±  3.26 years and for at least 4 h per day in their daily life. These
children had auditory responses to environmental sounds during the initial
period of hearing aid fitting. To confirm the effectiveness of hearing aid
fitting in the daily life, their auditory performance was reexamined by the
Meaningful Auditory Integration Scale (MAIS) and Categories of Auditory
Performance (CAP) at least every 8 months. The MAIS includes 10 questions
reflecting children's confidence in hearing devices, auditory sensitivity and
ability to connect sounds with meaning. The highest score is 40 and indicates
the best performance for meaningful sound use in everyday situations. The CAP is
an eight-score hierarchical scale that evaluates receptive auditory abilities
and ranges from no awareness of environmental sounds (1 score) to telephone use
with a familiar talker (8 scores). When hearing aid outcomes were poor and the
ABR thresholds estimated by the click and 500-Hz tone burst were above 90 dB
nHL, the hearing-impaired child received a CI. Before the CI surgery, the ABR,
40-Hz auditory evoked potential, multi-frequency steady state potential (MFSSP),
distortion product otoacoustic emission (DPOAE) and acoustic impedance had been
performed to confirm profound sensorineural hearing loss (hearing threshold ≥90
dB nHL). The 40-Hz auditory evoked potential (Lynn et al., 1984 (link)) and MFSSP (Johnson & Brown,
2005
) tests were performed for hearing threshold estimation using the
500-Hz tone burst and sinusoidally amplitude modulated tones (1, 2 and 4 kHz),
respectively. Only 24 children finished the pure-tone audiometry and their
unaided pure tone averages (averaged over 0.25, 0.5, 1, 2, 4 and 8 kHz) were
above 90 dB HL. Participants who had a mental disability, intracranial lesions
or head trauma were excluded from this study. Of children in our study, 20 had
IEMs assessed by computerized tomography (CT) and magnetic resonance imaging
(MRI) according to previously published criteria (Sennaroglu & Bajin, 2017 (link)).
Detailed information for all children is provided in Table 1. All procedures performed in
this study involving human participants were in accordance with the ethical
standards of the institutional and/or national research committee and with the
1964 Helsinki declaration and its later amendments or comparable ethical
standards. The protocols and experimental procedures in the present study were
reviewed and approved by the Anhui Provincial Hospital Ethics Committee. Each
participant's guardians provided written informed consent.
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Publication 2023
Acoustics Adult Audiometry, Pure-Tone Auditory Evoked Potentials Awareness Child Craniocerebral Trauma Disabled Persons Ethics Committees, Clinical Hearing Aids Homo sapiens Hypersensitivity Legal Guardians Males Meaningful Use Medical Devices Mycobacterium avium Complex Only Child Operative Surgical Procedures Otoacoustic Emissions, Spontaneous Sensorineural Hearing Loss Sound X-Ray Computed Tomography
The study protocol was scheduled within two time-points: the first step at birth in the Neonatal Department and the second step within 3 months-old in the Audiology Department. All neonates underwent NHS by means of otoacoustic emissions (OAE) at birth [21 ]. For this test, a Madsen AccuScreen device (Natus® Medical Incorporated, Taastrup, Denmark) was used. As usual, results were binary for each ear, “pass” in the case of the presence of an OAE response in both ears, and “refer” in the case of a repeated unclear unilateral or bilateral response.
Then, within the third month of life, every newborn was evaluated in the Audiology Department, where otoscopy, ABR and impedance tests were performed bilaterally. ABR was recorded during spontaneous sleep, using Medelec® Synergy software. Acoustic wide range click stimuli of 21 pps were applied by headphones. Action potentials were detected using vertex-mastoid ipsilateral derivations. At least two runs were obtained at any stimulus intensity and compared to each other, in order to assess waveform repeatability. The exam was conducted presenting medium intensity stimuli, then decreasing gradually until the V wave peak threshold was obtained; lastly, a high intensity stimulus was presented to detect wave’ latencies. With regards to ABR results, the following parameters were evaluated: identification of I, III and V wave peaks at different stimulus intensity and their replicability; identification of V wave threshold expressed in dB nHL; measurements of peak latencies of I, III and V waves expressed in ms; interaural difference of V wave latency (IT-5) expressed in ms.
Thresholds of V wave identification ≤30 dB nHL, without pathological delay of latency, were considered indicative of normal results.
An acoustic immittance test was conducted in order to rule-out potential overestimations of the auditory threshold caused by middle or external ear dysfunctions. A Madsen Zodiac device (Natus® Medical Incorporated, Denmark) at 1000 Hz probe tone frequency was used to test acoustic immittance. Tympanograms were classified according to the Jerger classification and acoustic reflex (AR) measures were taken using the same instrument [23 (link)].
All families with normal results were invited, as usual practice for children at risk for hearing loss, to take their children to the hospital for repeat audiological evaluation at the age of 1 year. Basically, all children underwent visual reinforcement audiometry (VRA) using a two-channel diagnostic audiometer (Piano Plus VRA, Audiology and Balance, Inventis Srl, Padova, Italy) and an immittance test.
The severity of sensorineural hearing loss was defined according to the WHO classification: mild (≥26 to <40 dB), moderate (≥41 to <55 dB), moderate-severe (≥56 to <70 dB), severe (≥71 to <90 dB) and profound (>90 dB) [24 ].
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Publication 2023
Acoustics Action Potentials Audiometry Child Childbirth Diagnosis Ear External Ear Hearing Impairment Infant, Newborn Medical Devices Otoacoustic Emissions, Spontaneous Otoscopy Process, Mastoid Reflex, Acoustic Reinforcement, Psychological Sensorineural Hearing Loss Sleep
At the conclusion of the home visit, a trial randomisation website will be accessed for concealed study group assignment. An independent data manager generates a computer-generated randomisation sequence stratified for age (<2 years vs 2 years and above), AOM laterality (unilateral vs bilateral) and AOM baseline antibiotic prescribing (yes vs no). Children will be randomly allocated to either (1) lidocaine hydrochloride 5 mg/g (Otalgan) ear drops one to two drops up to six times daily for a maximum of 7 days24
25 with usual care (oral analgesics, with/without antibiotics); or (2) usual care. Analgesic ear drops will be provided by the study team. These drops should not be used in children with a tympanic membrane perforation or ventilation tube as they carry a risk of inner ear damage causing hearing loss or tinnitus. These children will therefore be excluded, as well as those with ear wax obscuring visualisation of the tympanic membrane. Parents of children allocated to the intervention group are expressly instructed to stop applying the drops if their child develops ear discharge.
The study team will notify the GP about the result of the randomisation. The local pharmacist will be notified in case the child is allocated to the analgesic ear drops, in order to check any known sensitivities/allergies and any interactions (with current or future drugs). Any treatment decisions other than the use of analgesic ear drops, that is, antibiotics and oral analgesics, will be left to the GP’s discretion in both groups. To those allocated to the intervention group, the study physician will not provide any treatment advice other than instructions about the use of analgesic ear drops. To those allocated to the control group, the study physician will not provide any treatment advice.
During follow-up, parents and GPs will be encouraged to manage AOM symptoms according to current clinical practice guidance on AOM in children issued by the Dutch College of General Practitioners. Lidocaine ear drops are currently not recommended in this guideline due to the lack of evidence.23
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Publication 2023
Analgesics Antibiotics Antibiotics, Antitubercular Cerumen Child Functional Laterality General Practitioners Hypersensitivity Lidocaine Lidocaine Hydrochloride Parent Patient Discharge Pharmaceutical Preparations Physicians Sensorineural Hearing Loss Tinnitus Tympanic Membrane Tympanic Membrane Perforation
Children aged 1–6 years presenting to primary care with AOM23 and parent-reported ear pain in 24 hours prior to enrolment will be eligible for trial participation. Children with (suspected) tympanic membrane perforation or ventilation tube (as they carry a risk of inner ear damage causing hearing loss or tinnitus after application of lidocaine drops), ear wax obscuring visualisation of the tympanic membrane or those who are very unwell or require hospitalisation will be excluded. Detailed inclusion and exclusion criteria are listed in box 1.
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Publication 2023
Cerumen Child Earache Lidocaine Parent Primary Health Care Sensorineural Hearing Loss Tinnitus Tympanic Membrane Tympanic Membrane Perforation
A retrospective review was conducted to assess the patterns of attendance for referred patients to the cochlear implantation candidacy evaluation and adherence to recommended post‐activation visits as a function of age, travel time to the CI center, and SES. The procedures were approved by the study site's Institutional Review Board (IRB#: 09‐2328).
The query included data for adults referred to the CI center for their first cochlear implantation candidacy evaluation between April 2017 and July 2019. Patients in consideration for revision surgery or second‐side evaluation were excluded to control for additional factors that may influence attendance to the cochlear implantation evaluation appointment and adherence to the recommended post‐activation follow‐up. More recent data (i.e., after 2019) were excluded due to the confounding nature and implications of variables introduced by the COVID‐19 pandemic. The query was limited to data for patients residing in North Carolina for consistency of criteria used to determine county‐level socioeconomic and geographic data. The query included the following data: age at time of referral, insurance/payer type, zip code, county, and referral source (e.g., primary care physician, ENT physician, audiologist). For the patients who attended the cochlear implantation candidacy evaluation, the type of candidate was grouped by the audiologic findings, including conventional criteria (i.e., bilateral moderate‐to‐profound sensorineural hearing loss [SNHL]), expanded indications (i.e., unilateral moderate‐to‐profound SNHL or asymmetric SNHL), or not a candidate. If surgery was pursued, the duration of time between device activation and the initial post‐activation follow‐up visit was calculated. Patients who did not attend the initial evaluation were classified as “Did Not Attend” and were not grouped based on audiologic findings. Patients who met the cochlear implantation candidacy criteria and decided not to pursue cochlear implantation were classified as “Did Not Pursue” and by their respective audiologic candidate type.
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Publication 2023
Adult Audiologist COVID 19 Implantations, Cochlear Medical Devices Operative Surgical Procedures Otolaryngologist Patients Primary Care Physicians Repeat Surgery Sensorineural Hearing Loss

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The ALGO 2e is a diagnostic device designed for the screening of newborn hearing. It is a compact, portable unit that measures otoacoustic emissions, a physiological response from the inner ear, to assess hearing function. The ALGO 2e provides objective and reliable results to support early identification of hearing loss in infants.
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More about "Sensorineural Hearing Loss"

Sensorineural hearing impairment, nerve deafness, inner ear damage, cochlear hearing loss, auditory neuropathy, and high-frequency hearing loss are all terms used to describe sensorineural hearing loss (SNHL).
This type of hearing impairment is caused by damage to the delicate structures within the inner ear, such as the hair cells or auditory nerve, which are responsible for converting sound waves into electrical signals that the brain can interpret.
SNHL can result from a variety of factors, including exposure to loud noises, aging, genetic disorders, certain medical conditions (e.g., Ménière's disease, otosclerosis, or acoustic neuroma), and ototoxic medications.
Symptoms of SNHL often include difficulty hearing soft sounds, understanding speech in noisy environments, and perceiving high-pitched voices or sounds.
Diagnosis of SNHL typically involves a comprehensive audiological evaluation, which may include pure-tone audiometry (using an audiometer), speech testing, and possibly imaging studies like CT scans or MRI.
Treatment options for SNHL can include the use of hearing aids, cochlear implants, assistive listening devices, and in some cases, surgical interventions.
Ongoing research in this field focuses on developing better diagnostic tools, such as the ALGO 2e or ALGO 3 systems, and improving treatment strategies, including the use of genetic therapies and stem cell-based approaches.
Software like ORBIS, SPSS, and Stata are often utilized in data analysis and study design.
Additionally, the QIAamp DSP DNA Blood Mini Kit may be employed in genetic research related to SNHL.
By understanding the underlying mechanisms and advancing treatment options, researchers and clinicians aim to improve the quality of life for individuals affected by this common and often debilitating form of hearing loss.