Hydrocephalus is a neurological disorder characterized by abnormal dilation of the ventricular system, resulting from impaired cerebrospinal fluid (CSF) circulation. Its pathophysiology involves complex disturbances in CSF production, flow, and absorption. Post-hemorrhagic hydrocephalus represents a particularly complex form, where disrupted CSF circulation and intracranial pressure imbalance play central roles. Recent studies have identified the glymphatic system and meningeal lymphatic vessels (mLV) as important alternative pathways for CSF clearance, and metabolic waste removal. After intracranial hemorrhage, free hemoglobin triggers oxidative stress, that downregulates aquaporin-4 expression in astrocytes, while iron deposition induces endothelial ferroptosis in mLV. These processes jointly impair glymphatic drainage and mLV clearance function, exacerbating ventricular pressure. Emerging evidence suggests that dysfunction of the glymphatic and meningeal lymphatic systems may act not only as a secondary consequence but also as an early driving factor in hydrocephalus development, challenging traditional pathophysiological models. Future research should integrate clinical and animal studies to clarify the role of intracranial lymphatic pathways in hydrocephalus and explore their potential as therapeutic targets.