from Section 2 - Clinical Neurosurgical Diseases
Published online by Cambridge University Press: 04 January 2024
Hydrocephalus affects 1/1000 births and is treated using neurosurgical cerebrospinal fluid(CSF) diversion techniques with high complication and failure rates. Recent data on the pathogenesis of acute post-hemorrhagic hydrocephalus(PHH) have implicated an acute Toll-like receptor(TLR4)-dependent hypersecretory response of the choroid plexus epithelium(CPe), the site of highly regulated CSF production and part of the blood–CSF barrier. Post-infectious hydrocephalus(PIH) is the most common form of hydrocephalus worldwide and shares multiple features with PHH, including TLR4-regulated CSF cytokines and immune cells. We introduce the concept of “inflammatory hydrocephalus”, and argue this may more precisely convey the shared pathogenic mechanisms and potential therapeutic vulnerabilities of PHH/PIH than the current concept of “secondary hydrocephalus.” This change of emphasis could shift our view of PHH/PIH from that of lifelong neurosurgical disorders to one of preventable neuroinflammatory conditions. In addition to attenuating acute CPe hypersecretion, early targeting of TLR4 may prevent inflammation-induced brain damage resulting in scarring, obstruction, and poor long-term neurodevelopmental outcomes.
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