There is significant inter-individual variability in the prevalence and severity of cisplatin-induced ototoxicity, which is greatly influenced by genetic and non-genetic factors that predispose the patient to the development of hearing loss. Currently, the focus should be on identifying patients who are more likely to develop ototoxicity based on genetic and non-genetic factors, as therapies to combat ototoxicity are limited or still under study. The severity of hearing loss and the time of its onset may be influenced by certain genetic polymorphisms or the dose administered, age, sex, diet, the administration of other drugs with ototoxic potential, and association with radiotherapy of the head and neck. Knowing the risk factors allows the doctor to manage each case in a personalized manner, preventing hearing damage, especially in the long term. With the help of PubMed and Scopus, we searched for relevant studies documenting the genetic and non-genetic risk in patients treated with cisplatin. This review article is a synthesis of the literature that points out the importance of these factors, encouraging genetic screening and improving quality of life in patients treated with cisplatin.

Although cisplatin plays a vital role in chemotherapy protocols, its impact on hearing should not be overlooked. The ototoxic effects of cisplatin can lead to hearing loss. Childhood hearing loss can significantly impact various aspects of development. Understanding the mechanism of cisplatin-induced ototoxicity is crucial due to its high level of complexity. The process involves multiple interconnected steps, ranging from cisplatin absorption to its interaction with the cellular antioxidant defense system, nuclear DNA, mitochondria, and the cytokine cascade. Each of these interactions contributes to the overall pathophysiology of ototoxicity and is closely interrelated. Based on these, various hypotheses and conclusions were outlined, and we tried to analyze them as broadly as possible. Knowledge of these mechanisms has given rise to promising avenues and otoprotection strategies to combat ototoxicity. Although there is only one drug approved by the FDA (Food and Drug Administration), there are numerous drugs that target the mechanisms presented, but that need more evidence to be able to be used safely. In addition to these, the role of the multidisciplinary team should not be neglected and protocols should be established for periodic follow-up of patients treated with cisplatin to prevent hearing loss. This narrative review aims to point out all the aspects presented, based on the analysis of the literature and the conclusions drawn over time. We have selected the articles of interest and analyzed the studies that have obtained promising results to bring an overview of how cisplatin acts at the cochlear level, what can be done to combat these mechanisms, what solutions exist now and how we can prevent hearing loss.

Malignant laryngeal tumor occupies an important place among ENT malignancies, representing 26% of head and neck cancers. The control of the disease and especially the quality of life are parameters often overlooked. The term "quality of life", has social impact too. The aim of this retrospective, observational study, is to evaluate the quality of life of patients with laryngeal tumors and the social impact in patients after the radiotherapy or radiochemotherapy. The group of study included 52 patients, diagnosed with histopathologically confirmed laryngeal tumors. The evaluation of the quality of life was done before and after surgery and during the radiotherapy and chemotherapy, weekly, for 8 weeks. The tools used to assess the quality of life, were the questionnaires EORTC QLQ-30 version 3.0, and EORTC QLQ 35. EORTC QLQ-30 version 3.0 showed a low score on scales such fatigue, pain and sleep problems, from the beginning of therapy. The symptoms that appeared during the treatment, with statistical significance were: fatigue, nausea / vomiting, pain and appetite problems. EORTC QLQ-35 signals from the beginning of therapy problems with the senses, voice, social life, cough, which increase in severity as the radiation dose increases. At the end of treatment, pain scales, senses, social life and dry mouth were affected. In conclusion, the patients with laryngeal tumors present an important degradation of the quality of life and social integration after the treatment and radiotherapy or chemoradiotherapy, situation that we must take into account in the therapeutic plan.

Background: Disability progression in multiple sclerosis (MS) is increasingly recognized as a consequence of large-scale brain network disruption rather than isolated regional damage. Although diffusion tensor imaging (DTI) is the reference method for assessing structural connectivity, its limited availability restricts widespread clinical application. There is therefore a critical need for alternative approaches capable of capturing network-level alterations using routinely acquired MRI data. Objective: This study aimed to determine whether synthetic structural connectivity matrices derived from standard regional volumetric MRI can capture clinically meaningful network alterations in MS and predict subsequent functional progression, particularly upper limb decline. Methods: Regional brain volumetry was obtained from routine T1-weighted MRI using an automated, clinically approved volumetric pipeline. Synthetic structural connectivity matrices were generated by integrating principles of structural covariance, distance-dependent connectivity, and disease-specific vulnerability patterns. Graph-theoretical network metrics were extracted to characterize global and regional topology. Machine learning models including logistic regression, support vector machines, random forests, and gradient boosting were trained to predict clinical progression defined by worsening on the 9-Hole Peg Test. Dimensionality reduction was performed using principal component analysis, and model performance was evaluated using balanced accuracy, AUC-ROC, and resampling-based validation. Feature importance analyses were conducted to identify network vulnerability patterns. Results: Synthetic connectivity networks exhibited biologically plausible properties, including preserved but attenuated small-world organization. Global efficiency showed a strong inverse correlation with disability severity (EDSS). Patients with clinical progression demonstrated marked reductions in network integration and segregation, alongside increased characteristic path length. Machine learning models achieved robust prediction of upper limb functional decline, with ensemble-based methods performing best (balanced accuracy > 80%, AUC-ROC up to 0.85). A limited subset of connections accounted for a disproportionate share of predictive power, predominantly involving frontoparietal associative networks, thalamocortical pathways, and inter-hemispheric connections. In a longitudinal subset, network-level alterations preceded measurable clinical deterioration by several months. Conclusions: Synthetic structural connectivity derived from routine volumetric MRI captures clinically relevant network-level disruption in multiple sclerosis and enables accurate prediction of functional progression. By bridging network neuroscience with widely accessible imaging data, this framework provides a pragmatic alternative for connectomic analysis when diffusion imaging is unavailable and supports a network-based understanding of disease evolution in MS.