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Primary intraosseous meningiomas (PIOMs) are a rare subset of meningiomas, comprising fewer than 1% of all such tumors. Furthermore, PIOMs presenting as osteogenic lesions that invade both the dura and subcutaneous tissue are extremely rare. Unlike intracranial meningiomas, diagnosing and treating PIOMs are challenges due to their insidious clinical behavior and a lack of clear radiological diagnostic criteria. We report the case of a 60-year-old female with headache and a slightly outward protrusion of the parietal region of the skull. CT showed an osteogenic lesion in the right parietal bone. MR imaging indicated mild to moderate homogeneous enhancement with an intense dural reaction. The suggested clinical diagnosis was lymphoma, so we performed a skull biopsy, which revealed an intraosseous benign meningioma. A precise resection strategy was planned with a neuronavigation system accompanied by a one-step customized titanium mesh cranioplasty. The lesion was completely removed, and pathological analysis confirmed a meningothelial meningioma (WHO Grade I) of intraosseous layer origin invading the dura mater and subcutaneous tissue. This case highlights the need for an initial biopsy when the lesion is difficult to diagnose on imaging. Complete resection should be attempted to minimize the risk of recurrence.

In rare cases, chronic subdural hematoma can be a complication following cranioplasty implantation. Therefore, it can develop spontaneously or after a trauma in the underlying site of a duroplasty and represent, if compression of the brain structures, a life-threatening condition. In case of a patient with cranioplasty in polyetheretherketone (PEEK), performing a burr hole on prosthesis can represent, although unusual, an effective and safe technique for evacuation of the chronic subdural hematoma, avoiding the need to remove the prosthesis itself. Nevertheless, a rare and insidious prosthesis infection can occur, even after years.

Rheumatic diseases, such as osteoarthritis and rheumatoid arthritis, affect over 750 million people worldwide and contribute to approximately 40% of chronic pain cases. Inflammation and tissue damage contribute to pain in rheumatic diseases, but pain often persists even when inflammation/damage is resolved. Mechanisms that cause this persistent pain are still unclear. Mitochondria are essential for a myriad of cellular processes and regulate neuronal functions. Mitochondrial dysfunction has been implicated in multiple neurological disorders, but its role in sensory processing and pain in rheumatic diseases is relatively unexplored. This review provides a comprehensive understanding of how mitochondrial dysfunction connects inflammation and damage-associated pathways to neuronal sensitization and persistent pain. To provide an overall framework on how mitochondria control pain, we explored recent evidence in inflammatory and neuropathic pain conditions. Mitochondria have intrinsic quality control mechanisms to prevent functional deficits and cellular damage. We will discuss the link between neuronal activity, mitochondrial dysfunction and chronic pain. Lastly, pharmacological strategies aimed at reestablishing mitochondrial functions or boosting mitochondrial dynamics as therapeutic interventions for chronic pain are discussed. The evidence presented in this review shows that mitochondria dysfunction may play a role in rheumatic pain. The dysfunction is not restricted to neuronal cells in the peripheral and central nervous system, but also includes blood cells and cells at the joint level that may affect pain pathways indirectly. Pre-clinical and clinical data suggest that modulation of mitochondrial functions can be used to attenuate or eliminate pain, which could be beneficial for multiple rheumatic diseases.

To study the long-term treatment outcome of vestibular paroxysmia (VP).

Neuropathic pain (NP) caused by a lesion or disease of the somatosensory nervous system is a common chronic pain condition that has a major impact on quality of life. However, NP pathogenesis remains unclear. The purpose of this study was to identify differentially expressed genes (DEGs) and specific and meaningful gene targets for the diagnosis and treatment of NP.

Splenic torsion is a rare cause of abdominal pain that may develop due to laxity or absence of the ligaments that stabilize the spleen. A torsioned spleen may present with an acute abdomen clinically and may require urgent surgical intervention. We aimed to discuss three pediatric cases who applied to our clinic with acute abdomen symptoms after splenic torsion and their treatment approaches. Case 1: A 10-year-old female patient presented with complaints of progressive abdominal pain and non-bilious vomiting. On examination, there was abdominal tenderness and palpable fullness in the left lower quadrant. Imaging methods were compatible with splenic torsion. Laparoscopic splenectomy was performed. Case 2: A 4-year-old girl presented with complaints of abdominal pain and non-bilious vomiting. On examination, diffuse tenderness in the abdomen and defense-rebound were positive. Imaging methods were compatible with splenic torsion. On exploration, it was observed that the spleen was torsioned in different directions around the double pedicle. Splenectomy was performed. Case 3: A 5-year-old male patient was operated in another hospital with the complaint of abdominal pain, with the diagnosis of acute appendicitis, with open surgery. However, there was no improvement in the patient's symptoms after surgery. The patient was consulted to our clinic on the 5th post-operative day. Imaging methods were found to be compatible with splenic torsion. Laparoscopic splenectomy was performed. In the pediatric population, splenic torsion can cause acute or chronic abdominal pain of unknown cause. Splenopexy should be the first goal of treatment in torsion, but splenectomy is the only treatment option in complicated cases and laparoscopy can be used safely even in complicated cases.

The magnitude of the cost of chronic pain has been a matter of concern in many countries worldwide. The high prevalence, the cost it implies for the health system, productivity, and absenteeism need to be addressed urgently. Studies have begun describing this problem in Chile, but there is still a debt in highlighting its importance and urgency on contributing to chronic pain financial coverage. This study objective is to estimate the expected cost of chronic pain and its related musculoskeletal diseases in the Chilean adult population. We conducted a mathematical decision model exercise, Markov Model, to estimate costs and consequences. Patients were classified into severe, moderate, and mild pain groups, restricted to five diseases: knee osteoarthritis, hip osteoarthritis, lower back pain, shoulder pain, and fibromyalgia. Data analysis considered a set of transition probabilities to estimate the total cost, sick leave payment, and productivity losses. Results show that the total annual cost for chronic pain in Chile is USD 943,413,490, corresponding an 80% to the five diseases studied. The highest costs are related to therapeutic management, followed by productivity losses and sick leave days. Low back pain and fibromyalgia are both the costlier chronic pain-related musculoskeletal diseases. We can conclude that the magnitude of the cost in our country's approach to chronic pain is related to increased productivity losses and sick leave payments. Incorporating actions to ensure access and financial coverage and new care strategies that reorganize care delivery to more integrated and comprehensive care could potentially impact costs in both patients and the health system. Finally, the impact of the COVID-19 pandemic will probably deepen even more this problem.

Herpes zoster (HZ) is a localized, painful cutaneous eruption that occurs upon reactivation of the herpes virus. Postherpetic neuralgia (PHN) is the most common chronic complication of HZ. In this study, we examined the metabolomic and proteomic signatures of disease progression in patients with HZ and PHN. We identified differentially expressed metabolites (DEMs), differentially expressed proteins (DEPs), and key signaling pathways that transition from healthy volunteers to the acute or/and chronic phases of herpetic neuralgia. Moreover, some specific metabolites correlated with pain scores, disease duration, age, and pain in sex dimorphism. In addition, we developed and validated three optimal predictive models (AUC > 0.9) for classifying HZ and PHN from healthy individuals based on metabolic patterns and machine learning. These findings may reveal the overall metabolomics and proteomics landscapes and proposed the optimal machine learning predictive models, which provide insights into the mechanisms of HZ and PHN.

In this research, we examine and identify the implications of Adverse Childhood Experiences (ACEs) on a range of health outcomes, with particular focus on a number of mental health disorders. Many previous studies observed that traumatic childhood events are linked to long-term adult diseases using the standard Adverse Childhood Experience Questionnaire. The study cohort was derived from the Healthy Nevada Project, a volunteer-based population health study in which each adult participant is invited to take a retrospective questionnaire that includes the Adverse Childhood Experience Questionnaire, the 12-item Short Form Survey measuring quality of life, and self-reported incidence of nine mental disorders. Using participant's cross-referenced electronic health records, a phenome-wide association analysis of 1,703 phenotypes and the incidence of ACEs examined links between traumatic events in childhood and adult disease. These analyses showed that many mental disorders were significantly associated with ACEs in a dose-response manner. Similarly, a dose response between ACEs and obesity, chronic pain, migraine, and other physical phenotypes was identified. An examination of the prevalence of self-reported mental disorders and incidence of ACEs showed a positive relationship. Furthermore, participants with less adverse childhood events experienced a higher quality of life, both physically and mentally. The whole-phenotype approach confirms that ACEs are linked with many negative adult physical and mental health outcomes. With the nationwide prevalence of ACEs as high as 67%, these findings suggest a need for new public health resources: ACE-specific interventions and early childhood screenings.

Generalized pruritus can be the manifestation of many dermatologic and systemic diseases. However, it has been reported infrequently in the literature as a consequence of hyperferritinemia. We report the case of a 70-year-old male presenting to dermatology due to generalized pruritus in the absence of a rash, who was subsequently found to have a significantly elevated serum ferritin and transferrin saturation with otherwise normal iron studies. Hereditary hemochromatosis was ruled out on genetic testing; however, etiologies of secondary iron overload including alcohol use disorder and non-alcoholic fatty liver disease were present. The patient had minimal relief of his pruritus with topical corticosteroids, oral prednisone, and moisturizers. The only successful treatment was phlebotomy which resulted in complete resolution of his long-standing pruritus. We present the fifth case of generalized pruritus associated with hyperferritinemia, treated successfully with phlebotomy.