Cochlear Implant Electrode Choice in Challenging Surgical Cases: Malformation, Residual Hearing, Ossification, or Reimplantation

Abstract

Purpose of Review

The limits of cochlear implantation candidacy have been expanding over the last decade and recent studies show that patients with inner ear anomalies, significant residual hearing, ossified cochlea, or far advanced otosclerosis can benefit from implant. The cochlear implant companies are coming up with various electrode designs. The purpose of this study is to review the factors that can affect the choice of electrode array in the expanding indications of cochlear implantation and suggest some surgical tips.

Recent Findings

A comprehensive preoperative evaluation is crucial. Detailed audiologic examination and radiologic assessment of inner ear structures with high-resolution computed tomography and/or magnetic resonance imaging is necessary. The choice of electrode array should be made regarding the type of cochlea in the presence of inner ear anomalies. If the patient has residual hearing in low-frequencies, electrode array and surgical insertion technique should be as atraumatic as possible to protect apical part of the cochlea. Appropriate selection of electrodes and surgical techniques are necessary if the cochlea is obstructed by fibrosis or ossified. The surgeon also should consider the possibility of reimplantation in the future and select the initial electrode after comprehensive evaluation.

Summary

There is a diversity of electrode arrays for different indications. The selection of the most accurate electrode depends on the audiological tests, etiology of hearing loss, and cochlear anatomy. Surgeon must be prepared preoperatively for various clinical situations and unexpected surgical circumstances. One should keep in mind that making the right electrode choice will impact the outcomes of unusual or challenging cases.

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IgG4-related disease: with emphasis on the biopsy diagnosis of autoimmune pancreatitis and sclerosing cholangitis

Abstract

In 2011, chronic fibroinflammatory processes occurring simultaneously or metachronously in various organs and associated with elevated IgG4 serum levels and/or tissue infiltration with IgG4-positive plasma cells have been recognized as manifestations of a systemic disorder called IgG4-related disease (IgG4-RD). The histologic key findings are lymphoplasmacytic infiltration rich in IgG4-positive plasma cells combined with storiform fibrosis and obliterative phlebitis. Among the organs mainly affected by IgG4-RD are the pancreas and the extrahepatic bile ducts. The pancreatic and biliary alterations have been described under the terms autoimmune pancreatitis (AIP) and sclerosing cholangitis, respectively. These diseases are currently more precisely called IgG4-related pancreatitis (or type 1 AIP to distinguish it from type 2 AIP that is unrelated to IgG4-RD) and IgG4-related sclerosing cholangitis (IgG4-related SC). Clinically and grossly, both diseases commonly imitate pancreatic and biliary adenocarcinoma, tumors that are well known for their dismal prognosis. As IgG4-RD responds to steroid treatment, making a resection of a suspected tumor unnecessary, a biopsy is often required to establish the preoperative diagnosis. This review discusses the morphologic spectrum of IgG4-related pancreatitis and IgG4-related SC and focuses on the biopsy relevant histologic features for the diagnosis and differential diagnosis of these diseases.

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Plasma IL-8 signature correlates with pain and depressive symptomatology in patients with Burning Mouth Syndrome: results from a pilot study

Abstract

Background

Burning mouth syndrome (BMS) is a neuropathic orofacial pain condition of unknown aetiology that encompasses intra-oral burning pain without abnormal clinical findings. Psychological, neural and inflammatory processes are associated with BMS pathogenesis. Currently, studies characterising plasma cytokine/chemokine profiles with pain and depression in BMS patients are lacking. Considering that inflammation is associated with the pathophysiology of BMS, and that inflammation is closely associated with pain and depression, we aimed to correlate depressive symptomatology and oral cavity pain with plasma cytokine/chemokine signatures in a cohort of patients with BMS.

Methods

In the present study, plasma protein levels of Th1 cytokines (IFN-γ, IL-2, IL-12p70, TNF-α), Th2 cytokines (IL-4, IL-10, IL-6, IL-13), and the chemokine IL-8, were assessed in BMS patients (n = 10) and healthy volunteers (n = 10), using pro-inflammatory-10-plex assays. Clinical histories, alongside self-rated oral cavity pain intensities and depressive symptomatology were assessed using a visual analogue scale (VAS) and the 16-item Quick Inventory of Depressive Symptomatology (QIDS-SR₁₆) questionnaires, respectively.

Results

We present evidence that BMS is associated with increased depressive symptomatology and enhanced oral cavity pain. Plasma isolated from BMS patients display enhanced expression of the pro-inflammatory chemokine IL-8, when compared to plasma from healthy individuals. Plasma IL-8 signature correlates with pain and depressive symptomatology in the study cohort.

Conclusions

Overall, these findings indicate that plasma IL-8 profiles are dysregulated in BMS and that modulation of IL-8 production in the disorder may be a tool in the management of BMS symptomatology.

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Characterization of CD45RO+ Memory T Lymphocytes in Keloid Disease

Abstract

Background

Memory T cells, a highly effective subset of T lymphocytes, have been reported to be involved in many inflammatory skin disorders. However, the potential role of memory T cells in keloid disease (KD) remains unclear.

Objectives

Due to their important role in regulating inflammation, we investigated the characteristics of CD45RO⁺ memory T cells (mT) in KD.

Methods

Primary cutaneous cells were isolated from keloid scars and normal skin by enzymic digestion. Combined with peripheral blood mononuclear cells (PBMCs) isolated from a related blood sample, flow cytometry was applied to identify the phenotypic and functional abnormalities of memory T cells in KD.

Results

We observed that the majority of T lymphocytes in keloid scars had the memory phenotype, and a greater number of the CD8⁺ mT in keloid scars produced lower levels of TNF-α. This abnormal cytokine production was even more distinct in FOXP3^-CD8^- mT, with lower TNF-α production and enhanced IFN-γ production. Furthermore, FOXP3⁺CD8^- mT in keloid scars were abnormal, including showing reduced CD25 and CTLA-4 expression and IL-10 production. In addition, a significant decrease in the number of CD4⁺CD25^highFOXP3⁺ regulatory T cells was identified in patients with multiple keloid scars. We also found that there was significantly increased infiltration of CD103⁺CD8⁺ mT in keloid scars.

Conclusions

Our findings preliminarily elucidate the abnormalities of CD45RO⁺ memory T cells in keloid scars and provide early evidence that a disrupted T cell response contributes to the progression of KD.

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Impaired Langerhans’ cell migration in psoriasis is due to an altered keratinocyte phenotype induced by interleukin-17

Abstract

Psoriasis is a common skin condition driven by increased expression of interleukin (IL)-17. Langerhans' cells (LC) are epidermal dendritic cells that regulate cutaneous immune responses. Within uninvolved skin of patients with psoriasis, LC display impaired migration from the epidermis. Here the role of keratinocytes (KC) in the regulation of LC function, and the response of KC to IL-17 has been investigated. Keratinocytes were cultured from the uninvolved skin of psoriasis patients and healthy individuals with or without IL-17 treatment and the conditioned medium examined for its ability to alter LC function in an ex vivo human skin explant model. Furthermore, we examined the effect of IL-17 on LC mobilisation in psoriasis by neutralising IL-17 in the same skin explant model. We found that conditioned medium from psoriasis KC inhibited LC migration in healthy skin. Moreover, conditioned medium from healthy KC treated with IL-17 also inhibited healthy LC migration. Finally, neutralising IL-17 in psoriasis skin resulted in enhanced LC migration. Collectively, these data suggest that an altered KC secretome, driven by increased expression of IL-17, is responsible for impaired LC migration in uninvolved skin of patients with psoriasis.

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Squamous cell carcinoma arising from a keratocystic odontogenic tumor: a case report

The term "primary intraosseous squamous cell carcinoma" was introduced in 2005 by the World Health Organization with three subcategories. Squamous cell carcinoma arising from the lining of an odontogenic cyst ...

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Evidence of the efficacy and safety of house dust mite subcutaneous immunotherapy in elderly allergic rhinitis patients: a randomized, double-blind placebo-controlled trial

Allergen specific immunotherapy (AIT) in elderly patients is controversial, and there is still little evidence supporting the safety and efficacy of this treatment in this population. The study objective was t...

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