Research Article

Cerebrospinal fluid influx drives acute ischemic tissue swelling

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Science  13 Mar 2020:
Vol. 367, Issue 6483, eaax7171
DOI: 10.1126/science.aax7171

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  • Cerebrospinal fluid influx contributes to brain edema formation: A further rationale for cisternostomy
    • Giovanni Grasso, Neurosurgeon, Section of Neurosurgery, Department of Biomedicine, Neurosciences and Advanced Diagnostics (BiND), University of Palermo, Palerm
    • Other Contributors:
      • Iype Cherian, Neurosurgeon, Institute of Neurosciences, Nobel Medical College and Teaching Hospital, Biratnagar, Nepal

    In their research article “Cerebrospinal fluid influx drives acute ischemic tissue swelling” (13 March 2020) Mestre and collaborators have demonstrated that cerebrospinal fluid (CSF) can provide an alternative source of ischemic edema (1). Glymphatic inflow of CSF appears to be the primary initial event driving tissue swelling. This finding open new avenues in our current understanding of edema formation in the setting of numerous brain pathologies including traumatic brain injury (TBI).
    In this regard, we have already proposed the same mechanism of brain swelling during TBI where an increase in pressure into the subarachnoid space, secondary to traumatic subarachnoid hemorrhage, would result in a rapid shift of CSF from the cisterns into the brain parenchyma, through the paravascular spaces, resulting in an increase of the water content of the brain (2-4). This mechanism of brain swelling, termed as “CSF-shift edema”, promoted by a pressure gradient, leads to an increase in pressure inside the paravascular spaces and the interstitium of the brain, disturbing the functions of the paravascular system with implications in secondary brain injury (5-7).
    In their perspective Moss and Williams (8) (13 March 2020) pose a challenging question: Can CSF-induced edema be therapeutically targeted? The question is relevant and answers cannot be too far behind. Cisternostomy, an emerging surgical treatment, would reverse the direction of the “CSF-shift”, allowing a decreas...

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    Competing Interests: Both authors described extensively the technique. IC is the pioneer in cisternostomy.
  • RE: Toward the Core Fact of Cerebral Swelling
    • Chongjie Cheng, Neurosurgeon, Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, China
    • Other Contributors:
      • Miao Wei, Radiologist, Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, China
      • Fajin Lv, Radiologist, Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, China
      • Xiaochuan Sun, Neurosurgeon, Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, China

    For human patients of diverse brain injuries, the most devastating result of cerebral edema is elevated ICP, or even brain herniation. Till now, no anti-vasogenic/cytotoxic edema drugs have passed the whole clinical assessments [1], and hypertonic agents and decompression surgery are still the last resorts to this emergency.
    The latest research by H. Mestre et al. brought inspiring and attractive findings [2]. By means of advanced radiological measurements, dynamic monitoring of water movement was achieved in vivo. Quite solid data verified that the early brain edema was driven by CSF influx into perivascular space, following ischemic spreading depolarization. Prevention of spreading depolarization and vasoconstriction might be future targets in edema control.
    Here we show our deep concern on its clinical significance. In the current study, no T2-hyperintense was observed in the hyperacute phase (15-25 min) after MCAO, nor the follow-up T2-weighted images were shown. In clinical practice, apparent T2-weighted abnormalty is difficult to detect until 8-12 hours post-stroke,with high false-negative rate within 24 hours [3]. In other words, early cerebral edema is comparatively mild and can hardly lead to symptomatic deterioration. Subsequently, the cerebral edema will peak at 2 to 4 days after onset [4], when patients frequently suffer from brain swelling. Without extended investigation till the peak phase (24 hours maximum here), we’re blind about how much contri...

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    Competing Interests: None declared.
  • An interesting phenomenon is captured during cerebral hematoma evacuation.
    • Wei Chen, Neurosurgeon, West China Hospital, Sichuan University
    • Other Contributors:
      • Lu Ma, Neurosurgeon, West China Hospital, Sichuan University
      • Chao You, Neurosurgeon, West China Hospital, Sichuan University

    Stroke is a life-threatening illness of global importance, with a poor prognosis and few proven treatments (1, 2). As a heterogeneous disease, insights into the underlying molecular mechanisms of stroke help identify the cause and develop treatment strategies. In a recent issue of Science, Mestre et al (3) renewed our understanding of post-stroke edema by showing cerebrospinal fluid surrounding the brain enters the tissue within minutes of an ischemic insult along perivascular flow channels. They found that the process was initiated by ischemic spreading depolarizations along with subsequent vasoconstriction, which in turn enlarged the perivascular spaces and doubled glymphatic inflow speeds (3). This finding prompts us to recall an interesting phenomenon that had been encountered in our clinical practice. A 38-year-old male was referred to our hospital with left basal ganglia hemorrhage. Notably, blend sign with both hypo- and hyper- attenuating regions was detected within hematoma (Fig. 1A). Before emergency microsurgical evacuation, the hematoma cavity puncture was performed. Other than active bleeding, relatively transparent fluid was captured (Fig. 1B and Movie 1). This clinical phenomenon and similar pattern were observed in additional patients (Fig. 1, C and D). Blend sign, a novel promise radiologic marker identified on non-enhanced computed tomography in patients with spontaneous intracerebral hemorrhage, has significance in predicting hematoma expansion (4, 5). I...

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    Competing Interests: None declared.

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