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Hearing Disorders: HELP
Articles by Jaina Negandhi
Based on 3 articles published since 2010
(Why 3 articles?)
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Between 2010 and 2020, Jaina Negandhi wrote the following 3 articles about Hearing Disorders.
 
+ Citations + Abstracts
1 Review Auditory neuropathy spectrum disorder (ANSD) and cochlear implantation. 2015

Harrison, Robert V / Gordon, Karen A / Papsin, Blake C / Negandhi, Jaina / James, Adrian L. ·Department of Otolaryngology - HNS, Program in Neuroscience and Mental Health, The Hospital for Sick Children, 555 University Ave, Toronto, Ontario, Canada M5G 1X8; Department of Otolaryngology - Head and Neck Surgery, University of Toronto, 190 Elizabeth Street, Toronto, Ontario, Canada MG5 2N2. Electronic address: rvh@sickkids.ca. · Department of Otolaryngology - HNS, Program in Neuroscience and Mental Health, The Hospital for Sick Children, 555 University Ave, Toronto, Ontario, Canada M5G 1X8; Department of Otolaryngology - Head and Neck Surgery, University of Toronto, 190 Elizabeth Street, Toronto, Ontario, Canada MG5 2N2. · Department of Otolaryngology - HNS, Program in Neuroscience and Mental Health, The Hospital for Sick Children, 555 University Ave, Toronto, Ontario, Canada M5G 1X8. ·Int J Pediatr Otorhinolaryngol · Pubmed #26545793.

ABSTRACT: We discuss issues related to cochlear implantation in children with auditory neuropathy spectrum disorder (ANSD). We describe the varied nature of this disease category including the numerous potential causes of auditory neuropathy. The most prevalent etiology for infants with ANSD is associated with prolonged neonatal intensive care unit (NICU) stay. We discuss the potential contribution of cochlear hypoxia to this etiology. The second part of this review describes in detail our own experience at the Hospital for Sick Children in Toronto, with cochlear implantation of children diagnosed with ANSD. We outline the detection, diagnosis, and referral routes for our patients. We provide an overview of our "standard operation procedures" regarding candidacy, and discuss some of the special considerations that need to be applied to children with ANSD. This includes decisions to implant children with better audiometric thresholds that are standard in non-ANSD patients, concerns about the possibility of spontaneous remission and the appropriate timing of implantation. Finally we review an extensive published literature in outcomes after cochlear implantation (CI) in ANSD. This is not a systematic review but rather an exercise to distill out some important reoccurring themes and the general consensus of opinion to date. Our conclusion is that the hearing loss category ANSD, together with its numerous co-morbidities, is far too heterogeneous to make definitive statements about prognosis with CI.

2 Article Remodelling at the calyx of Held-MNTB synapse in mice developing with unilateral conductive hearing loss. 2014

Grande, Giovanbattista / Negandhi, Jaina / Harrison, Robert V / Wang, Lu-Yang. ·Corresponding Author L.-Y. Wang, The Hospital for Sick Children, 555 University Ave, Toronto, Ontario, Canada M5G 1X8.  luyang.wang@utoronto.ca. ·J Physiol · Pubmed #24469075.

ABSTRACT: Structure and function of central synapses are profoundly influenced by experience during developmental sensitive periods. Sensory synapses, which are the indispensable interface for the developing brain to interact with its environment, are particularly plastic. In the auditory system, moderate forms of unilateral hearing loss during development are prevalent but the pre- and postsynaptic modifications that occur when hearing symmetry is perturbed are not well understood. We investigated this issue by performing experiments at the large calyx of Held synapse. Principal neurons of the medial nucleus of the trapezoid body (MNTB) are innervated by calyx of Held terminals that originate from the axons of globular bushy cells located in the contralateral ventral cochlear nucleus. We compared populations of synapses in the same animal that were either sound deprived (SD) or sound experienced (SE) after unilateral conductive hearing loss (CHL). Middle ear ossicles were removed 1 week prior to hearing onset (approx. postnatal day (P) 12) and morphological and electrophysiological approaches were applied to auditory brainstem slices taken from these mice at P17-19. Calyces in the SD and SE MNTB acquired their mature digitated morphology but these were structurally more complex than those in normal hearing mice. This was accompanied by bilateral decreases in initial EPSC amplitude and synaptic conductance despite the CHL being unilateral. During high-frequency stimulation, some SD synapses displayed short-term depression whereas others displayed short-term facilitation followed by slow depression similar to the heterogeneities observed in normal hearing mice. However SE synapses predominantly displayed short-term facilitation followed by slow depression which could be explained in part by the decrease in release probability. Furthermore, the excitability of principal cells in the SD MNTB had increased significantly. Despite these unilateral changes in short-term plasticity and excitability, heterogeneities in the spiking fidelity among the population of both SD and SE synapses showed similar continuums to those in normal hearing mice. Our study suggests that preservations in the heterogeneity in spiking fidelity via synaptic remodelling ensures symmetric functional stability which is probably important for retaining the capability to maximally code sound localization cues despite moderate asymmetries in hearing experience.

3 Article Resting neural activity patterns in auditory brainstem and midbrain in conductive hearing loss. 2012

Harrison, Robert V / Negandhi, Jaina. ·Auditory Science Laboratory, Department of Otolaryngology-HNS, Hospital for Sick Children, ON, Canada. rvh@sickkids.ca ·Acta Otolaryngol · Pubmed #22339503.

ABSTRACT: CONCLUSIONS: Conductive hearing loss (CHL) lowers resting neural activity patterns in the auditory periphery. Such reductions of peripheral auditory activity may influence the developing central brain during early postnatal years when the system is still highly plastic. OBJECTIVES: A common cause of CHL in young children is otitis media; if chronic and/or episodic there may be a risk to speech and language development. In this clinical context we have investigated changes in neural activity patterns in the brainstem and midbrain in an animal model of CHL. METHODS: In a mouse model, a 50-60 dB CHL was produced by blocking the ear canals. We quantified resting neural activity patterns in the cochlear nucleus and inferior colliculus using c-fos immuno-labelling. This experimental group was compared with normal-hearing controls and with animals with bilateral cochlear ablation. RESULTS: Subjects with CHL had a statistically significant reduction in c-fos-labelled cells in the cochlear nucleus and central nucleus of the inferior colliculus compared with normal controls. This decreased c-fos expression suggests a change in resting neural activity generated at the inner hair cell synapse, leading to a reduction in activity levels in the ascending auditory pathways.