Traumatic basal ganglia hematoma (TBGH) represents a rare but significantly consequential subset of traumatic brain injuries (TBIs), characterized by intracerebral hemorrhages within the basal ganglia region secondary to trauma. This review examines the epidemiology, clinical presentation, treatment modalities, and molecular mechanisms underlying TBGH, drawing insights from 19 relevant studies encompassing 137 patients. TBGH predominantly affects males, with road traffic accidents being the leading cause of injury. Clinical management varies, with conservative approaches favored in the majority of cases, while surgical intervention is considered for larger hematoma volumes. Prognostic outcomes are influenced by factors such as Glasgow Coma Scale (GCS) scores, with low GCS being associated with increased mortality and neurological deficits. Molecular mechanisms implicated in TBGH include disruption of the blood-brain barrier (BBB) integrity, leading to hematoma formation and subsequent secondary insults such as perihematomal edema. Ferroptosis, a novel iron-dependent form of programmed cell death, and prokinectins have been implicated in TBGH pathogenesis, offering potential therapeutic targets for future interventions. Early detection of intracranial hematomas through imaging modalities such as CT scans and Near-infrared spectroscopy (NIRS) is crucial for prompt intervention. Treatment strategies aim to limit hematoma expansion, reduce intracranial pressure, and minimize secondary injury complications. Future research should focus on refining management protocols tailored to TBGH, with a concerted effort to elucidate the underlying molecular mechanisms for improved patient outcomes. This review underscores the clinical significance of TBGH within the TBI spectrum and highlights the importance of continued research efforts in advancing our understanding and management of this condition.

Glioblastoma multiforme (GBM) presents a significant obstacle in the field of cancer therapy because of its aggressiveness and limited treatment options. Despite advances in surgical resection, radiation therapy, and chemotherapy, the median survival remains dishearteningly brief at 15 months. This review focuses on the mysterious Glioblastoma stem cells (GSCs), particularly those expressing the CD133 marker, acknowledged for their pivotal role in tumor growth and resistance to conventional therapies. The NOTCH signaling pathway emerges as a promising target. This review explores the NOTCH signaling pathway, a crucial regulator of GSCs, and evaluates inhibitors like gamma-secretase inhibitors (GSI), siRNA, and monoclonal antibodies. While recent trials suggest improved outcomes by integrating GSIs with standard treatments, the challenge persists in sparing CD133-positive cells. This review also emphasizes the role of Chk1 and Chk3 inhibitors in the reversal of radioresistance in CD133+ cells. In summary, this review explores the nuances of NOTCH signaling inhibition in GBM treatment, emphasizing precision in targeting the tumor microenvironment and addressing therapeutic resistance associated with CD133-positive cells.