Vinchon et al. report on nine cases of progressive myelopathy due to meningeal thickening many years after initial insertion of a ventricular peritoneal shunt. The condition that they have described is characterized by an unrelenting progressive quadriparesis that does not seem to be benefited significantly by surgical decompression. In all children, the initial shunt insertion was placed in infancy between 1 and 6.6 months. All but one patient had neonatal meningitis, and the other patient presented with post-shunt meningitis at 2 months of age. In addition, four patients had additional episodes of shunt infection. The findings suggest that cerebrospinal fluid (CSF) infection, in the face of ventricular shunting in infancy, may be a pre-disposing factor to the later development of this specific problem. This condition has been reported previously in nonneurosurgical literature as a rare complication of neonatal meningitis [1, 2]. In the prior reported cases, all patients had a ventriculoperitoneal (VP) shunt in addition to the meningitis, but shunting as a predisposing factor was not discussed. The focus in those reports was on the prior meningitis, whereas in this report, the focus is more on the prior shunting. It is interesting that this complication has not received attention in the neurosurgical literature. The development of a severe progressive quadriparesis in most of these children represented a severe deterioration in neurologic function. Such patients would certainly return to see their neurosurgeon for further investigation of the problem. In this case series, the problem was diagnosed at a median age of 12.8 years with a range of 5.7 to 20.4 years. Thus, most of the patients would have developed the problem at a time when the neurosurgeons involved in the care of the child, even if we assume that they were pediatric neurosurgeons specifically, would have been involved in the continuous follow-up of these children. Could it be that the diagnosis of this shunt-related problem is obscured by the fact that many of these children have “cerebral palsy” and already have some degree of underlying quadriparesis because of brain injury? The degree of disability that these patients exhibited in infancy and childhood, and that subsequently evolved, is not described in sufficient detail to evaluate the extent, rapidity, or functional impact of the clinical syndrome that the authors are reporting, nor is the information provided sufficient detail to determine anatomical localization. A progressive quadriparesis might be interpreted as having to do with brain dysfunction due to uncontrolled hydrocephalus, shunt malfunction, medications, or chronic infection rather than spinal cord dysfunction. Spinal magnetic resonance imaging scans may not be done, and the diagnosis would therefore be missed. This certainly is a reasonable possibility. We think that the authors have provided an important contribution to the neurosurgical literature, and neurosurgeons looking after children with shunted hydrocephalus will now be looking for this possible diagnosis in any child who develops progressive quadriparesis after a shunt procedure, especially if there has been prior CSF infection. Childs Nerv Syst (2007) 23:847–848 DOI 10.1007/s00381-007-0347-0