Obstructive sleep apnea syndrome (OSAS) is the most common breathing-related sleep disorder. It is characterized by recurrent episodes of partial or complete airway obstruction during sleep, resulting in a reduction in or the total cessation of airflow, despite ongoing respiratory efforts, leading to oxygen desaturation and arousal. The purpose of this literature review is to evaluate the most common characteristics of this pathology, as well as to investigate the most effective treatment options, providing an update on the management of OSA patients.

(1) Background: In this study, we aimed to explore the regulatory mechanism of miR-124-3p microglial exosomes, as they were previously reported to modulate neuroinflammation and promote neuronal repair following traumatic brain injury (TBI). (2) Methods: Studies investigating the impact of microglial exosomal miRNAs, specifically miR-124-3p, on injured neurons and brain microvascular endothelial cells (BMVECs) in the context of TBI were reviewed. (3) Results: Animal models of TBI, in vitro cell culture experiments, RNA sequencing analysis, and functional assays were employed to elucidate the mechanisms underlying the effects of miR-124-3p-loaded exosomes on neuroinflammation and neuronal repair. Anti-inflammatory M2 polarization of microglia, mTOR signaling suppression, and BMVECs-mediated autophagy were reported as the main processes contributing to neuroprotection, reduced blood-brain barrier leakage, and improved neurologic outcomes in animal models of TBI. (4) Conclusions: Microglial exosomes, particularly those carrying miR-124-3p, have emerged as promising candidates for therapeutic interventions in TBI. These exosomes exhibit neuroprotective effects, attenuate neuroinflammation, and promote neuronal repair and plasticity. However, further research is required to fully elucidate the underlying mechanisms and optimize their delivery strategies for effective treatment in human TBI cases.

Background and objectives: Paragangliomas of the head and neck are rare, slow-growing neuroendocrine tumors, benign in their vast majority, but with a possibility of developing distant metastases. They show great inheritable character, and their behavior has proven to be unpredictable; therefore, they are considered malignant. Material and methods: This article aims to offer a more comprehensive presentation of the pathogenesis, epidemiology, diagnostic methods, imaging development, and treatment guidelines. We tried to bring together all the necessary data that, in our opinion, a head and neck practitioner should know when managing this type of tumor. Our main focus is on the most recent studies, with the purpose of a homogenous presentation of all current guidelines and approaches to this pathology. Results: Paragangliomas of the head and neck are still a disputed topic. One of the main reasons for that is their low incidence of 0.3 to 1 per 100,000 every year. The most frequent locations are the carotid body, the temporal bone, the jugular and mastoid foramen, and the vagal nerve. Their clinical presentation usually involves a painless lateral mass associated with symptoms such as hoarseness, hearing loss, tinnitus, and cranial nerve deficits. Up to 40% of them are inherited, mostly linked with mutations of succinate dehydrogenase complex. Imaging evaluation consists of CT and MRI, and new functional explorations such as ¹⁸F-FDA and ¹⁸F-FDG PET/CT, ¹⁸F-DOPA PET, ¹²³I-MIBG, and ⁶⁸Ga-DOTATE PET/CT. Measuring the catecholamine levels in the plasma and urine is mandatory, even though paragangliomas of the head and neck rarely display secretory behavior. Treatment mainly consists of surgery, with different approaches and techniques, but conservative management methods such as wait and scan, radiotherapy, proton therapy, and chemotherapy have proven their efficiency. The therapeutical decision lacks consensus, and current studies tend to recommend an individualized approach. Guidelines regarding long-term follow-up are still a matter of debate.

Persistent post-concussion syndrome (PPCS) is a complex and debilitating condition that can develop after head concussions or mild traumatic brain injury (mTBI). PPCS is characterized by a wide range of symptoms, including headaches, dizziness, fatigue, cognitive deficits, and emotional changes, that can persist for months or even years after the initial injury. Despite extensive research, the underlying mechanisms of PPCS are still poorly understood; furthermore, there are limited resources to predict PPCS development in mTBI patients and no established treatment. Similar to PPCS, the etiology and pathogenesis of functional neurological disorders (FNDs) are not clear neither fully described. Nonspecific multifactorial interactions that were also seen in PPCS have been identified as possible predispositions for FND onset and progression. Thus, we aimed to describe a functional overlay model of PPCS that emphasizes the interplay between functional and structural factors in the development and perpetuation of PPCS symptoms. Our model suggests that the initial brain injury triggers a cascade of physiological and psychological processes that disrupt the normal functioning of the brain leading to persistent symptoms. This disruption can be compounded by pre-existing factors, such as genetics, prior injury, and psychological distress, which can increase the vulnerability to PPCS. Moreover, specific interventions, such as cognitive behavioral therapy, neurofeedback, and physical exercise can target the PPCS treatment approach. Thus, the functional overlay model of PPCS provides a new framework for understanding the complex nature of this condition and for developing more effective treatments. By identifying and targeting specific functional factors that contribute to PPCS symptoms, clinicians and researchers can improve the diagnosis, management, and ultimately, outcomes of patients with this condition.

Deep neck infection is a pathology at the border of two specialties, otorhinolaryngology and maxillofacial surgery, and represents a medico-surgical emergency. In terms of its evolution, it can extend to the level of the thorax and result in mediastinitis, with difficult evolution and poor prognosis. The aims of this scoping review are to present the etiology, bacteriology, clinical manifestations, and diagnostics, as well as treatment, in light of the research published in the last 5 years on deep neck infection associated with descending necrotizing mediastinitis. The most common primary sources of deep neck infection are odontogenic and tonsillar. The other sources that are involved in deep neck infection are salivary glands, foreign bodies, malignancies, and iatrogenic causes after endoscopic maneuvers. The bacteriologic aspect is polymorphic, including both aerobic and anaerobic species. Complications that may appear include jugular vein thrombosis, airway obstruction, acute respiratory distress syndrome, sepsis, and disseminated intravascular coagulation. Timely diagnosis is important for ensuring the positive evolution of a deep neck infection. A CT scan is important for characterizing the nature of a deep neck lesion and identifying the spaces involved, and this method represents the gold standard for diagnosis of these lesions. Following the establishment of a definitive diagnosis, antibiotic therapy is initiated empirically, and is modified according to bacteriological exam results. The administration of antibiotics is an essential part of the treatment strategy for patients with a deep neck infection. Based on CT results, different surgical methods are applied under general anesthesia. The surgical strategy involves opening and draining the cervical spaces and debriding the necrotic tissue. In the cases of odontogenic causes, drainage and extraction of the infected teeth are performed. It is especially important to follow up on the dynamic progression of the patient. In the management of a deep neck infection associated with descending necrotizing mediastinitis, a multidisciplinary team is necessary.

(1) Background: Head and neck squamous cell carcinomas (HNSCCs) are some of the most frequent malignancies globally. Oncogenic viruses MCPyV, EBV and HPVs are recognized to be related to HNSCCs and skin cancers. There are no data from Romania regarding the involvement of herpes viruses and polyomaviruses in these types of cancer. We aim to evaluate the association of oncogenic viruses from Papillomaviridae, Herpesviridae, and Polyomaviridae families in HNSCCs and skin cancers. (2) Methods: A total of 26 fresh tumors (6/26 women) were tested for 67 viral agents using a multiplex PCR genotyping assay. (3) Results: A total of 23/26 (88.5%) samples were positive for one or more viruses. All the tested tumors were negative for any HPV (alpha or beta types). In total, we detected as positive samples: 16 (61.63%) EBV1, 12 (46.15%) HHV7, 8 (30.76%) MCV, 6 (23.07%) CMV and HHV6, 2 (7.69%) HHV8, 1 (3.8%) HPyV6 and EBV2. (4) Conclusions: We detected HPV-negative cases that are HPyV and HHV positive. In these fractions of HPV-negative HNSCCs cases, other oncogenic viruses may be involved, such as EBV1, MCV or CMV. Additional research is required for clarifying the natural history of these viruses in HNSCCs, as virus detection would have a decisive impact on diagnostic and decisional algorithms.