Subarachnoid hemorrhage (SAH) is most commonly seen in patients over 55 years of age and often results in a loss of many productive years. SAH has a high mortality rate, and survivors often suffer from early and secondary brain injuries. Understanding the pathophysiology of the SAH is crucial in identifying potential therapeutic agents. One promising target for the diagnosis and prognosis of SAH is circulating microRNAs, which regulate gene expression and are involved in various physiological and pathological processes. In this review, we discuss the potential of microRNAs as a target for diagnosis, treatment, and prognosis in SAH.

Chemotherapy as an adjuvant therapy that has largely failed to significantly improve outcomes for aggressive brain tumors; some reasons include a weak blood brain barrier penetration and tumor heterogeneity. Recently, there has been interest in designing effective ways to deliver chemotherapy to the tumor. In this review, we discuss the mechanisms of focused chemotherapies that are currently under investigation. Nanoparticle delivery demonstrates both a superior permeability and retention. However, thus far, it has not demonstrated a therapeutic efficacy for brain tumors. Convection-enhanced delivery is an invasive, yet versatile method, which appears to have the greatest potential. Other vehicles, such as angiopep-2 decorated gold nanoparticles, polyamidoamine dendrimers, and lipid nanostructures have demonstrated efficacy through sustained release of focused chemotherapy and have either improved cell death or survival in humans or animal models. Finally, focused ultrasound is a safe and effective way to disrupt the blood brain barrier and augment other delivery methods. Clinical trials are currently underway to study the safety and efficacy of these methods in combination with standard of care.

Traumatic optic neuropathy is one of the causes of visual loss caused by blunt or penetrating head trauma and is classified as both direct and indirect. Clinical history and examination findings usually allow for the diagnosis of traumatic optic neuropathy. There is still controversy surrounding the management of traumatic optic neuropathy; some physicians advocate observation alone, while others recommend steroid therapy, surgery, or both. In this entry, we tried to highlight traumatic optic neuropathy’s main pathophysiologic mechanisms with the most available updated treatment. Recent research suggests future therapies that may be helpful in traumatic optic neuropathy cases.

Traumatic brain injury (TBI) results from external biomechanical forces that cause structural and physiological disturbances in the brain, leading to neuronal, axonal, and vascular damage. TBIs are predominantly mild (65%), with moderate (10%) and severe (25%) cases also prevalent. TBI significantly impacts health, increasing the risk of neurodegenerative diseases such as dementia, post injury. The initial phase of TBI involves acute disruption of the blood–brain barrier (BBB) due to vascular shear stress, leading to ischemic damage and amyloid-beta accumulation. Among the acute cerebrovascular changes after trauma are early progressive hemorrhage, micro bleeding, coagulopathy, neurovascular unit (NVU) uncoupling, changes in the BBB, changes in cerebral blood flow (CBF), and cerebral edema. The secondary phase is characterized by metabolic dysregulation and inflammation, mediated by oxidative stress and reactive oxygen species (ROS), which contribute to further neurodegeneration. The cerebrovascular changes and neuroinflammation include excitotoxicity from elevated extracellular glutamate levels, coagulopathy, NVU, immune responses, and chronic vascular changes after TBI result in neurodegeneration. Severe TBI often leads to dysfunction in organs outside the brain, which can significantly impact patient care and outcomes. The vascular component of systemic inflammation after TBI includes immune dysregulation, hemodynamic dysfunction, coagulopathy, respiratory failure, and acute kidney injury. There are differences in how men and women acquire traumatic brain injuries, how their brains respond to these injuries at the cellular and molecular levels, and in their brain repair and recovery processes. Also, the patterns of cerebrovascular dysfunction and stroke vulnerability after TBI are different in males and females based on animal studies.

Primary pulmonary lymphoma (PPL) is a rare entity with the most common presentation as mediastinal lymphadenopathy. The most common form of PPL is Mucosa-Associated Lymphoid Tissue Lymphoma (MALToma) which is an extranodal B-cell lymphoma originating from the mucosal layers involving different organs such as the gastrointestinal tract as well as the lung. Herein, we present a case of a 51-year-old woman with progressive dyspnea for 6 months and no prior medical history. The computed tomography (CT scan) revealed bilateral multifocal consolidation and ground-glass opacities as well as interlobular septal thickening. Bronchoscopy was normal and CT-guided biopsy of lung consolidations was conclusive of MALToma. Complete extrapulmonary evaluations inducing bone marrow aspiration were unremarkable. The primary pulmonary MALToma is an extremely rare entity that presents with non-specific symptoms and a wide variety of CT findings such as mediastinal, hilar lymphadenopathy, and single or multiple lung nodules ranging from 2 to 8 cm. the disease has a favorable prognosis, so prompt diagnosis is essential.