Τετάρτη 7 Ιουνίου 2017

Morphometric evaluation of facial and vestibulocochlear nerves using magnetic resonance imaging: comparison of Menière's disease ears with normal hearing ears.

Morphometric evaluation of facial and vestibulocochlear nerves using magnetic resonance imaging: comparison of Menière's disease ears with normal hearing ears.

Eur Arch Otorhinolaryngol. 2017 Jun 05;:

Authors: Henneberger A, Ertl-Wagner B, Reiser M, Gürkov R, Flatz W

Abstract
Loss of neural structures (such as hair cells or neurones within the spiral ganglion) has been proposed to be involved in Menière's disease (MD) (Spoendlin et al. Acta oto-laryngologica Supplementum 499:1-21, 1; Merchant et al. Eur Arch Oto-Rhino-Laryngol Off J Eur Feder Oto-Rhino-Laryngol Soc (EUFOS) Affil German Soc Oto-Rhino-Laryngol Head Neck Surg 252(2):63-75, 2; Tsuji et al. Ann Otol Rhinol Laryngol Suppl 81:26-31, 3; Kariya, Otol Neurotol Off Publ Am Otol Soc Am Neurotol Soc Eur Acad Otol Neurotol 28(8):1063-1068, 4; Megerian Laryngoscope 115(9):1525-1535, 5) but this has yet to be confirmed. Therefore, the aim of this study was to investigate morphometric changes of VIIth and VIIIth cranial nerve in MD. MD is characterized by episodic vertigo, tinnitus, fluctuating hearing loss, and aural fullness. The exact pathophysiological mechanisms involved such as viral infections, autoimmune processes, genetic predisposition, cellular apoptosis, and oxidative stress are still not clear. Using a T2-weighted 3D-GE "constructive interference in steady state" (CISS) 3T magnetic resonance imaging (MRI) sequence, we evaluated the properties of the VIIth and VIIIth cranial nerves as they passed from the cerebellopontine angle to the inner ear modiolus. 21 patients with MD were examined along with 39 normal controls. Bidirectional nerve diameters and cross-sectional areas (CSA) were measured in a transverse plane. The comparison of study and control group showed statistically significant (P < 0.000595 after Bonferroni correction) differences between the CSA measurements. The facial, cochlear, superior vestibular, and inferior vestibular nerves (FN, CN, SVN, IVN) of MD patients were significantly larger than those of the control group, both on the MD-affected side and on the healthy side. Thus for example, the cochlear nerve CSA measurements were 0.69 ± 0.14 mm(2) (P < 0.0001) in the affected ears of the unilateral MD group, 0.70 ± 0.12 mm(2) (P < 0.0001) in the affected ears of the cohort including the bilateral MD group, 0.71 ± 0.13 mm(2) (P < 0.0001) in the non-affected ears of the MD patients, as compared to 0.46 ± 0.14 mm(2) in the control group. The perpendicular nerve diameters were found to vary according to site of measurement and type of measurement used. For example a statistically significant enlargement of the short diameter measurements of the SVN at the level of the meatus was found, but not of long diameter measurements at the same site. Although cellular death would theoretically be expected to lead to a decreased nerve thickness, our data showed a swelling of cranial nerves VII and VIII within the study group compared to our normal hearing control group. The similar reaction of the facial nerve supports mediator-based theories of MD pathophysiology.

PMID: 28584970 [PubMed - as supplied by publisher]



from #Audiology via ola Kala on Inoreader http://ift.tt/2rUddzT
via IFTTT

Noise trauma induced behavioral gap detection deficits correlate with reorganization of excitatory and inhibitory local circuits in the inferior colliculus and are prevented by acoustic enrichment.

Noise trauma induced behavioral gap detection deficits correlate with reorganization of excitatory and inhibitory local circuits in the inferior colliculus and are prevented by acoustic enrichment.

J Neurosci. 2017 Jun 05;:

Authors: Sturm JJ, Zhang-Hooks YX, Roos H, Nguyen T, Kandler K

Abstract
Hearing loss leads to a host of cellular and synaptic changes in auditory brain areas, which are thought to give rise to auditory perception deficits such as temporal processing impairments, hyperacusis, or tinnitus. However, little is known about possible changes in synaptic circuit connectivity that may underlie these hearing deficits. Here, we show that mild hearing loss as a result of brief noise exposure leads to a pronounced reorganization of local excitatory and inhibitory circuits in the mouse inferior colliculus. The exact nature of these reorganizations correlated with the presence or absence of the animals' impairments in detecting brief sound gaps, a commonly used behavioral sign for tinnitus in animal models. Mice with gap detection deficits showed a shift in the balance of synaptic excitation and inhibition that was present in both glutamatergic and GABAergic neurons, whereas mice without gap detection deficits showed stable excitation-inhibition balances. Acoustic enrichment with moderate intensity, pulsed white noise immediately following noise trauma prevented both circuit reorganization and gap detection deficits raising the possibility of using acoustic enrichment immediately after cochlear damage to prevent or alleviate the emergence central auditory processing deficits.SIGNIFICANCE STATEMENTNoise overexposure is a major cause of central auditory processing disorders including tinnitus, yet the changes in synaptic connectivity underlying these disorders remain poorly understood. Here we find that brief noise overexposure leads to distinct reorganizations of excitatory and inhibitory synaptic inputs onto glutamatergic and GABAergic neurons, and that the nature of these reorganizations correlates with animals' impairments in detecting brief sound gaps, which is often considered a sign of tinnitus. Acoustic enrichment immediately following noise trauma prevents circuit reorganizations as well as gap detection deficits, highlighting the potential for using sound therapy soon after cochlear damage to prevent the development of central processing deficits.

PMID: 28583912 [PubMed - as supplied by publisher]



from #Audiology via ola Kala on Inoreader http://ift.tt/2r4OOUs
via IFTTT

White noise after loud noise prevents hearing deficits in mice

Mild hearing loss from exposure to less than one hour of loud noise leads to a reorganization of circuits in a key midbrain structure of the auditory system in mice, finds new research published in...

from #Audiology via ola Kala on Inoreader http://ift.tt/2r0yEQw
via IFTTT

White noise after loud noise prevents hearing deficits in mice

Mild hearing loss from exposure to less than one hour of loud noise leads to a reorganization of circuits in a key midbrain structure of the auditory system in mice, finds new research published in...

from #Audiology via xlomafota13 on Inoreader http://ift.tt/2r0yEQw
via IFTTT

White noise after loud noise prevents hearing deficits in mice

Mild hearing loss from exposure to less than one hour of loud noise leads to a reorganization of circuits in a key midbrain structure of the auditory system in mice, finds new research published in...

from #Audiology via ola Kala on Inoreader http://ift.tt/2r0yEQw
via IFTTT