We read with great interest the article by Bartoli et al, 1 recently published in Neurosurgery. We would like to share some remarks, highlighting several points that should be discussed to better understand the phenomena elegantly described by the authors. In the article, 1 28 cases of hydrocephalus after 549 procedures of foramen magnum decompression (5.1%) for Chiari malformation type 1 (CM1) are reported. Hydrocephalus was observed in a mean time of 2.2 ± 2.6 standard deviation (SD) months

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... ter a surgical procedure, and was treated with permanent cerebrospinal fluid (CSF) diversion in 82.1% (23 patients), endoscopic third ventriculostomy (ETV) in 3.5% (1 patient), temporary CSF shunting in 10.7% (3 patients), and conservative management with acetazolamide in only 1 patient (3.5%). The manuscript enhanced several mechanisms for explaining the etiology of hydrocephalus after foramen magnum decompression, including the exacerbation of a previous mild CSF disturbance (mild hydrocephalus or idiopathic intracranial hypertension); a slit-valve mechanism due to arachnoid tear with consequent CSF dynamic alteration or blood entering in the subarachnoid space, causing aseptic meningitis; fourth ventricle outlet obstruction caused by cerebellar descent or CSF accumulation in the subdural space for an arachnoid tear; and adhesive arachnoiditis at the level of the fourth ventricle following tonsillar resection or coagulation. The authors corroborated the hypothesis of multifactorial etiology of hydrocephalus, observing a high rate of resolution after CSF shunting, and 1 case of resolution after ETV only. We would like to add a distinct hypothesis on hydrocephalus etiology and ETV failure after foramen magnum decompression. First, prone position has been described to explain the mechanism of stoma occlusion caused by blood clot deposition after preoperative ETV in posterior fossa surgery (snow globe effect). 2 Although the snow globe effect refers to preoperative ETV, the same mechanism could be involved in the failure of ETV performed for the treatment of hydrocephalus secondary to foramen magnum decompression. Second, hydrocephalus etiology after posterior fossa tumor resection is obstructive immediately after tumor removal (suggesting the primary role of ETV for the treatment of early hydrocephalus after tumor resection), whereas it is related to postsurgical edema and scarring reaction in the posterior fossa during the subsequent phases. 3, 4 Similarly, the mechanism should be mentioned for the later hydrocephalus in most of the cases of ventricular dilatation after foramen magnum decompression, 2 as testified by the timing of occurrence observed by the authors, ranging between 1 wk and 8 mo. 1 Early hydrocephalus could be more responsive to ETV than later hydrocephalus, according to the etiological mechanism described for posterior fossa tumors. 2 Additionally, we would like to emphasize another theme that could be of interest: the type of duraplasty adopted. To date, controversies are raised concerning the allogeneic grafts related with a high rate of postoperative complications (such as hydrocephalus or infection), although no studies have shown the superiority of autologous or allogeneic materials for duraplasty in CM1 treatment. 5 Besides, we agree on the multifactorial hypothesis suggested by the authors, 1 because of the high rate of failure of ETV for this type of hydrocephalus, thus confirming that in most of the cases fourth ventricle outlets or acqueductal obstruction is not the main etiological mechanism. 3, 4 A fundamental consideration related to Chiari 1 etiology should be highlighted to better understand the main mechanism related with hydrocephalus occurrence. According to the Poretti, Reybaud, Milhroat, and Buel classifications of Chiari 1 malformations, the mechanisms involved in the etiology of the disease are structural anomalies of the skull base and abnormal segmentation of the cervical vertebral bodies. 4 These mechanisms could often lead to venous congestion with subsequent CSF dynamics alterations, confirming the major efficacy of CSF shunting on ETV for the treatment of hydrocephalus secondary to foramen magnum decompression. Summarizing, according to all the possible etiologies proposed by the authors and remarked in the present Letter, we believe that early hydrocephalus could be responsive to ETV. However, CSF shunting generally represents the best management of hydrocephalus for the higher rate of success related to the timing of its occurrence. Besides, in the presence of mild signs of hydrocephalus, a first conservative management with acetazolamide and corticosteroids to cover the possible etiology related to aseptic meningitis should be performed.