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.