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Hearing loss due to brain tumour,is ringing ears a symptom of ms 2014,beaded earrings patterns native american 8a - PDF Review

Author: admin | 11.07.2015 | Category: One Ear Ringing

The eardrum (tympanic membrane) and the three small bones (ossicles) convert incoming sound into vibrations.
The fluid-filled inner ear (cochlea) contains highly sensitive hair cells that move in response to vibrations. The human ear is an intricate and delicately balanced structure of the body with which we are able to detect, differentiate, filter and identify sounds. Your hearing starts when your outer ear channels these sound waves down its auditory canal into your middle ear where sound is amplified. 2.  Children’s ears and hearing are more sensitive than adults allowing them to hear a greater variety of sounds. 4.   Earache is caused by too much fluid putting pressure on your eardrums which often happens if you are suffering from an infection, allergy or virus. Heteroplasmic mitochondrial DNA (mtDNA) defects are an important cause of neurological disease.
Patients harbouring pathological mtDNA mutations usually have a mixture of mutated and wild-type (normal) mtDNA (heteroplasmy). Fresh muscle was analysed histochemically and respiratory chain complex assays were carried out as described previously (Johnson and Barron, 1996; Taylor and Turnbull, 1997).
A detailed hearing history was taken from each patient and they were asked to complete an auditory questionnaire which included details of unilateral and bilateral hearing problems, the presence of tinnitus or vertigo and questions designed to identify a problem with auditory recruitment.
Pure tone audiometry using air and bone conduction was performed according to British Society of Audiology procedures (British Society of Audiology, 1981, 1985, 1986), in a sound-treated booth (IAC Acoustics, Middlesex, UK) using a clinical audiometer (GSI-16, Graystad, Cradely Heath, UK).
Brainstem auditory evoked responses were carried out in a sound-proofed room, using TDT (Tucker Davis Technologies, Calif., USA) SigGen and BioSig software for stimulus delivery and response acquisition, implemented using TDT hardware. Twenty-two patients underwent cranial MRI at 1.0 T (Siemens, Impact Expert, Siemens, Erlangen, Germany).
The auditory nerve transmits sound information from the hair cells to the hearing center of the brain. Here the sound waves hit your eardrum making it vibrate and the vibrations are then transmitted into the inner ear. Although hearing impairment is common in patients with mtDNA defects, the spectrum and pathophysiology of the hearing loss is not well characterized. The clinical features of mtDNA disease are diverse, ranging from asymptomatic or mildly affected individuals with signs limited to extraocular and skeletal muscle, to severely affected individuals who develop central neurological complications at a young age (Chinnery and Turnbull, 1997).

In vitro studies have shown that a heteroplasmic mtDNA defect is only expressed when the percentage level exceeds a critical threshold level (Larsson and Clayton, 1995). A priori, hearing impairment in mitochondrial disease might arise from end-organ dysfunction due to deficient energy release within the stria vascularis or hair cells, which are metabolically active structures.
The patients were selected on the basis of their genetic defect alone, irrespective of any known pre-existing hearing loss (Table 1). Total genomic DNA was extracted from blood and skeletal muscle and Southern blotting was carried out on skeletal muscle DNA (Moraes et al., 1989).
The overall responses were classified as present if after 260 averages the whole wave reproducibility was ?50% and there was a response in at least three of five frequency bands of at least 3 dB above the noise level. This is where the sound waves are converted into nerve impulses which travel to the hearing center in your brain due to the stimulation and movement of tiny hair-like nerve endings.  Your brain recognises and processes these nerve impulses and tells you what you are hearing. We therefore studied the relationship between cochlear and brainstem auditory function in 23 patients harbouring a range of different mtDNA mutations. The level of mutated mtDNA (mutation load) varies both between and within individuals with mtDNA disease (Lightowlers et al., 1997). However, patients with central neurological manifestations might also have a central component to their hearing loss.
The age-corrected mean hearing loss was defined as the measured mean loss at 500, 1000, 2000 and 4000 Hz minus the expected mean loss for a mixed gender, otologically unscreened population of that age, using data reported in the National Study of Hearing (Davis, 1995). Otoacoustic emissions were deemed to be absent when there were no discernible waves to click stimulation under the same stimulation and recording conditions.
Signals were recorded between the ipsilateral mastoid and vertex using the contralateral mastoid as the indifferent electrode. Based upon the pure tone audiogram, patients fell into three distinct groups: (i) normal hearing, (ii) mild to moderate predominantly high frequency hearing loss, and (iii) severe or profound hearing loss at all frequencies. Over 100 different deletions of mtDNA have been associated with disease (Schon et al., 1997).
This variability, coupled with tissue-specific differences in the threshold of expression, partly explains the diverse clinical phenotypes which are seen in patients harbouring the same mtDNA defect (Wallace, 1992a). In this study we therefore investigated the auditory function of 23 patients with a representative range of mtDNA defects.
An average of 2000 responses was carried out on each side at click rates of 8 Hz and 15 Hz.

Within this study group only certain genetic defects were associated with hearing loss, and for individuals harbouring the A3243G point mutation, the severity of the hearing loss correlated with the percentage level of mutated mtDNA (mutation load) in skeletal muscle. Ten of the patients harboured the same mtDNA point mutation, which allowed us to relate the degree of hearing loss to mutation load. Speech audiometry was performed on all subjects using recorded AB isophonemic word lists presented monaurally via earphones in a sound-treated booth. The presence of an emission in frequency regions where hearing levels exceed 30 dB was taken to suggest a possible non-cochlear hearing impairment. The 10 patients who had a moderate hearing loss or less had normal brainstem auditory evoked responses and MRI, but it was not possible to interpret the brainstem auditory evoked responses in 13 patients with severe hearing loss. In addition to pure tone and speech audiometry, subjects were systematically investigated with otoacoustic emissions, a sensitive indicator of cochlear dysfunction, as well as with correlates of central auditory processing: auditory brainstem evoked potentials and high-resolution structural imaging. Relative intensity was controlled by the audiometer, and one list of 10 words was presented at each test level and scored by phonemes correctly repeated. Latency of waves I–V and the amplitude ratio of waves V : I were measured by three independent observers and compared with established age-matched values (Abramovich, 1990).
Mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) is caused by a relatively common point mutation in the leucine (UUR) transfer RNA (tRNA) gene at position 3243 of the mtDNA L-strand (Goto et al., 1990). The maximum discrimination score and the best two average pure tone thresholds (of 500, 1000 and 2000 Hz) were compared to decide whether abnormal speech audiograms were indicative of sensory or neural hearing loss, and the half peak level elevation of the speech curve was inspected for agreement with the pure tone threshold (Priede and Coles, 1976). These findings are consistent with a predominantly cochlear origin for the hearing deficit, which is determined by the precise genetic defect and the percentage mutation load. Other point mutations are less common, such as the 8993 mutation which affects the ATPase 6 protein encoding gene, and is associated with neurogenic weakness with ataxia and retinitis pigmentosa (NARP) (Holt et al., 1990). Abnormally low maximum discrimination score or unexpectedly large half peak level elevation were regarded as evidence of possible neurological abnormality.

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