Abstract

To the Editor: We read with great interest the paper titled “Review of Cerebrospinal Fluid Physiology and Dynamics: A Call for Medical Education Reform.”1 The classic theory of cerebrospinal fluid (CSF) circulation presupposes that CSF is produced in the choroid plexus and then circulates from the ventricles along the subarachnoid spaces to be reabsorbed at the level of the dural sinuses through the pacchionian granulations. This paradigm has been challenged by the studies of Bulat–Klarika–Oreskovic2,3 according to which CSF, driven by osmotic and hydrostatic forces, is continuously produced and absorbed in the entire CSF system. The last hypothesis is well integrated into the recent description of the “glymphatic system,” a wide perivascular pathway supporting CSF and interstitial fluid exchange.4,5 Basal cisternostomy has been proposed as a novel treatment for severe brain trauma (sTBI), based on the idea that sTBI produces an impairment of CSF circulation using the perivascular network, leading to a shift of fluid toward the parenchyma, now referred to as CSF-shift oedema that finally results in brain swelling.6 The opening of basal cisterns (often clogged by subarachnoid blood) could restore this circulation, thereby alleviating the brain oedema. Our group has developed an interest in the application of cisternostomy in the setting of surgery for sTBI.7,8 We believe that our clinical experience with TBI surgery strongly supports the modern theories focusing on the existence of an extensive perivascular pattern that communicates with the cisternal subarachnoid space. The results from our clinical series showed that cisternostomy contributed effectively to the treatment of raised intracranial hypertension after sTBI. This surgical maneuver, in most cases, provides remarkable brain relaxation and continued cisternal drainage (approximately for 1 week), prevented the worsening and allowed the resolution of brain oedema, and in most cases obviated the need for prolonged ventilation and treatment with mannitol, hypertonic saline, or hypothermia.7 In comparison, the previous gold standard namely hemicraniectomy only provided increase space for the prolapse of the brain outside the confines of the cranium and did not address the brain edema to any degree. Another observation that seems to support this hypothesis is the huge quantity of CSF (approximately 200 mL/day) that can be drained through the cisternal drain in these patients. The fact that this large quantity of CSF is obtained because of the perivascular network (that is in communication with the basal cisterns) needs to be proved clinically, although there are several laboratory studies that indicate it quite well.9 One of the main criticisms to this promising surgical technique is that CSF can also be drained from the ventricles. However, it is widely acknowledged in common neurosurgical practice that external ventricular drainage rarely provides enough CSF (like the cisternal drain), quite frequently malfunctions and is often insufficient in the control of raised intracranial hypertension in sTBI.10 The effects of cisternal drainage in terms of control of intracranial pressure and outcome in the few series published to date attest to its utility in sTBI when compared with the decompressive craniectomy.11 These observations lends credence to the fascinating idea that cisternal drainage could ultimately address the issue of brain edema, although further clinical research needs to be performed across larger patient cohorts. Fundamental to the application of cisternostomy in general neurosurgical practice is an acceptance of the basic CSF physiology as proposed by Atchley et al.1 In addition, further clinical studies in this field has the potential of developing clinical interventions along these lines for a host of neurological pathologies including chronic hydrocephalus, aneurysmal subarachnoid hemorrhage, and even neurodegenerative disease.

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