Presence of ventriculoperitoneal and lumbar shunts stimulate long lasting non-inflammatory changes in the cerebrospinal fluid distinct from the response to bacterial infection

Ventriculoperitoneal (VP) shunts are effective at relieving hydrocephalus but are prone to malfunction. There are two hypotheses as to how shunts may malfunction independently of mechanical failure or blockage by debris from initial placement. The first is that the presence of a foreign object results in cells migrating into and colonising the shunt. The second is that the shunts contain either small numbers of live bacteria or residual bacterial products from manufacture or handling, triggering an inflammatory response that attracts cells to the site which go on to cause malfunctions. The presence of bacteria can be difficult to definitively rule in or out, given that they are capable of forming biofilms which poses challenges for isolation and microbiological culture. In this study, we measured 91 soluble immunological molecules and 91 soluble neurological molecules in CSF of patients with VP shunts and compared them to both patients without shunts and those with bacterial infection to determine whether there is an ongoing inflammatory response to shunting. We find that shunts elicit a soluble signature of neural wound healing and cell migration proteins that is distinct from the inflammatory signature of patients with neurological infection. This appears to represent a long-term response, persisting for at least 5 years in one patient