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 (PHH) 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 (mLVs) as important alternative pathways for CSF clearance, facilitating the removal of CSF and metabolic waste. After intracranial hemorrhage, free hemoglobin triggers oxidative stress, which downregulates aquaporin-4 (AQP4) expression in astrocytes, while iron deposition induces ferroptosis in mLVs endothelial cells. These processes jointly reduce glymphatic drainage efficiency and impair CSF and interstitial fluid clearance. In addition, inflammatory activation and CSF pathway obstruction further compromise the clearance function of mLVs, exacerbating ventricular pressure and accelerating hydrocephalus progression. 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.