Tympanic membrane perforations: the importance of etiology, size and location.

PURPOSE: The ability to predict the degree of a conductive hearing loss caused by a tympanic membrane perforation is important for every otologist, as it may require additional diagnostic tests and prevent unexpected intraoperative findings. The aim of this study was to correlate the various characteristics of a perforation (etiology, size, location, involvement of the manubrium or umbo) with the degree and frequency predominance of the consequent hearing loss. METHODS: A transversal study in a tertiary hospital center was conducted between July 2019 and December 2020. Fifty-eight patients with 65 tympanic perforations underwent a comprehensive medical and audiological evaluation, which included an otoendoscopy. An image processing software (ImageJ®) was used to measure the perforated area. The qualitative variables were etiology, affected quadrants, presence of myringosclerosis and involvement of umbo or manubrium of the malleus. The air-bone gap was measured at 250, 500, 1000, 2000 and 4000 Hz. Primary outcomes (mean air-bone gap and pure-tone average) were evaluated to find clinical factors associated with worse hearing. RESULTS: Data collected from 50 ears was included. Perforation size showed a positive statistically significant correlation with the air-bone gap (r = .508; p < .001) and pure-tone average (r = .375; p < .001). Higher air-bone gaps were found in perforations involving the posterior quadrants and the manubrium (p < .001 and p = .031, respectively). Inflammatory causes showed higher bone and air conduction pure-tone averages (p = .031 and p = .084, respectively) compared to traumatic or iatrogenic. An "inverted V" pattern of the air-bone gap, with the 2 kHz frequency being the least affected, was a consistent finding. However, it was not due to the Carhart's notch in bone conduction. CONCLUSION: The conductive hearing loss resulting from a tympanic membrane perforation is etiology, size and location-dependent, with higher losses occurring for inflammatory backgrounds, large perforations and when the posterior quadrants or the manubrium are involved. If the "inverted V" is absent, additional middle ear pathology should be investigated.

Platelet-derived growth factor (PDGF) and PDGF receptor expression and function in folliculostellate pituitary cells.

Homo- and heterodimers of platelet-derived growth factor-A (PDGF-A) and PDGF-B chains are involved through PDGF alpha- and beta-receptors in the growth regulation of multiple normal and tumoural cell types as well as in tumour neovascularization. Since little information is available on the impact of PDGF/PDGF receptors in normal and adenomatous pituitary, we studied the expression and action of this growth factor system in a variety of pituitary tumour cell lines and in rat anterior pituitary cell cultures. By RT-PCR, mRNA expression of PDGF-A and -B chains and of both receptors was found in rat pituitary and mouse folliculostellate TtT/GF pituitary tumour cells. Rat somatotroph MtT-S and mouse corticotroph AtT20 tumor cells expressed only a part of the PDGF/PDGF receptor components whereas mouse gonadotroph alphaT3-1 and rat lactosomatotroph GH3 pituitary tumour cells contained neither PDGF nor PDGF receptors. To further characterize the role of PDGF in TtT/GF cells, the effect of PDGF-AB and -BB on growth and vascular endothelial growth factor-A (VEGF-A) release was studied. Proliferation of TtT/GF cells was weakly but significantly stimulated by PDGF. Both in rat pituitary cell cultures and in TtT/GF cells, PDGF-AB and -BB strongly enhanced VEGF-A secretion. The PI3 kinase inhibitor LY 294002 blocked the increase in VEGF-A. Western immunoblotting confirmed the participation of key components of the PI3 kinase/Akt signal pathway (PDK1, Akt-Ser476) in PDGF-stimulated VEGF production. Thus the PDGF/PDGF receptor system is expressed in folliculostellate cells and is involved in VEGF regulation. Its role in endocrine pituitary tumour cell lines and pituitary adenomas need to be clarified in future studies.

A practical outcome scale for paediatric head injury.

Traumatic brain injury (TBI) is the commonest cause of acquired disability in childhood. A major obstacle to the evaluation of acute and rehabilitative therapies after TBI is the lack of simple descriptors of outcome. We developed the King's Outcome Scale for Childhood Head Injury (KOSCHI), as a specific paediatric adaptation of the original adult Glasgow Outcome Scale (GOS). The KOSCHI expands the five category GOS to provide increased sensitivity at the milder end of the disability range. The GOS category of "persistent vegetative state" was replaced by "vegetative". "Good recovery" was allocated two categories, in acknowledgement of the long term importance of relatively minor sequelae in a developing child. The scale was quick and easy to use. Inter-rater reliability studies show that even with such an apparently simple scale, some training may be required. The KOSCHI provides a practical scale for paediatric head injury which will enable clinicians to describe rate and extent of recovery, and evaluate the effects of service and research interventions.