The severe impact of aneurysmal subarachnoid hemorrhage (aSAH) is often followed by a prolonged, critical phase in which any decompensation of the fragile cerebral homeostasis can leave further, permanent damage. The neurological deterioration resulting from this decompensation has been summarized under the term “delayed cerebral ischemia (DCI)”. Its etiology has historically been limited to the presence of large-vessel vasospasm. Only after failure of trials trying to achieve better clinical outcome by reducing vasospasm has the understanding of DCI evolved to that of a multifactorial process, including disturbed cerebral autoregulation, cortical spreading depolarization, microthrombosis and neurotoxicity besides macro- and microvasospasm. However, the understanding of these single pathways has not yet formed into a chronologically and clinically comprehensible concept that would allow to clearly identify DCI in individual patients and pinpoint its exact location, its temporal evolution or the dominating pathomechanism.
This gap in knowledge is problematic for the proper diagnosis and treatment of DCI. DCI is diagnosed with a neurological deterioration not attributable to other causes, but diagnosis remains difficult in unconscious patients. If diagnosed, the cornerstones of current rescue treatment are hemodynamic augmentation of cerebral perfusion (induced hypertension) followed by pharmacological or mechanical vasodilation (balloon angioplasty, intravenous or intraarterial single or continuous application of vasodilating agents), which are still based on the presence of vasospasm and have been utilized in this form for decades without major breakthroughs. Due to lack of evidence, the practical execution of rescue treatment is highly divergent regarding indication, type, timing, duration or monitoring of treatment efficacy. Newer forms of rescue treatment targeting other components of DCI are presently not available. In summary, there is a pressing need to make rescue treatment for DCI more effective.
In this Research Topic, we welcome manuscripts - research article, brief research article, review, and mini-review - on rescue treatment for DCI including, but not limited to:
• DCI diagnosis, timing and indication for rescue treatment
• new insights on current rescue treatment
• new forms or combinations of rescue treatment, with particular emphasis on the presumed multifactorial etiology of DCI
• monitoring treatment efficacy, e.g. with multimodality neuromonitoring
The severe impact of aneurysmal subarachnoid hemorrhage (aSAH) is often followed by a prolonged, critical phase in which any decompensation of the fragile cerebral homeostasis can leave further, permanent damage. The neurological deterioration resulting from this decompensation has been summarized under the term “delayed cerebral ischemia (DCI)”. Its etiology has historically been limited to the presence of large-vessel vasospasm. Only after failure of trials trying to achieve better clinical outcome by reducing vasospasm has the understanding of DCI evolved to that of a multifactorial process, including disturbed cerebral autoregulation, cortical spreading depolarization, microthrombosis and neurotoxicity besides macro- and microvasospasm. However, the understanding of these single pathways has not yet formed into a chronologically and clinically comprehensible concept that would allow to clearly identify DCI in individual patients and pinpoint its exact location, its temporal evolution or the dominating pathomechanism.
This gap in knowledge is problematic for the proper diagnosis and treatment of DCI. DCI is diagnosed with a neurological deterioration not attributable to other causes, but diagnosis remains difficult in unconscious patients. If diagnosed, the cornerstones of current rescue treatment are hemodynamic augmentation of cerebral perfusion (induced hypertension) followed by pharmacological or mechanical vasodilation (balloon angioplasty, intravenous or intraarterial single or continuous application of vasodilating agents), which are still based on the presence of vasospasm and have been utilized in this form for decades without major breakthroughs. Due to lack of evidence, the practical execution of rescue treatment is highly divergent regarding indication, type, timing, duration or monitoring of treatment efficacy. Newer forms of rescue treatment targeting other components of DCI are presently not available. In summary, there is a pressing need to make rescue treatment for DCI more effective.
In this Research Topic, we welcome manuscripts - research article, brief research article, review, and mini-review - on rescue treatment for DCI including, but not limited to:
• DCI diagnosis, timing and indication for rescue treatment
• new insights on current rescue treatment
• new forms or combinations of rescue treatment, with particular emphasis on the presumed multifactorial etiology of DCI
• monitoring treatment efficacy, e.g. with multimodality neuromonitoring
