Abstract
Traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH) are major contributors to morbidity and mortality. Following the initial insult, patients may deteriorate due to secondary brain damage. The underlying molecular and cellular cascades incorporate components of the innate immune system. There are different approaches to assess and monitor cerebral inflammation in the neuro intensive care unit. The aim of this narrative review is to describe techniques to monitor inflammatory activity in patients with TBI and SAH in the acute setting. The analysis of pro- and anti-inflammatory cytokines in compartments of the central nervous system (CNS), including the cerebrospinal fluid and the extracellular fluid, represent the most common approaches to monitor surrogate markers of cerebral inflammatory activity. Each of these compartments has a distinct biology that reflects local processes and the cross-talk between systemic and CNS inflammation. Cytokines have been correlated to outcomes as well as ongoing, secondary injury progression. Alongside the dynamic, focal assay of humoral mediators, imaging, through positron emission tomography, can provide a global in vivo measurement of inflammatory cell activity, which reveals long-lasting processes following the initial injury. Compared to the innate immune system activated acutely after brain injury, the adaptive immune system is likely to play a greater role in the chronic phase as evidenced by T-cell-mediated autoreactivity toward brain-specific proteins. The most difficult aspect of assessing neuroinflammation is to determine whether the processes monitored are harmful or beneficial to the brain as accumulating data indicate a dual role for these inflammatory cascades following injury. In summary, the inflammatory component of the complex injury cascade following brain injury may be monitored using different modalities. Using a multimodal monitoring approach can potentially aid in the development of therapeutics targeting different aspects of the inflammatory cascade and improve the outcome following TBI and SAH.
Highlights
Pathophysiology of Brain InjuryTraumatic brain injury (TBI) and aneurysmal subarachnoid hemorrhage (SAH) are common neurological conditions [1, 2] associated with extensive morbidity and mortality [3, 4]
Many of the patients who survive these phenomena deteriorate days later from delayed ischemic neurological deficit (DIND), which is responsible for poor outcomes or death in up to 30% of patients with SAH
Similar to the findings identified in the review on TBI, the studies reporting on the analysis of cytokines via MD and cerebrospinal fluid (CSF) in aneurysmal SAH cytokine can be found in the parent systematic review, included in this Research Topic in Frontiers in Neurology (Zeiler et al, 2017, II submitted)
Summary
Traumatic brain injury (TBI) and aneurysmal subarachnoid hemorrhage (SAH) are common neurological conditions [1, 2] associated with extensive morbidity and mortality [3, 4]. Some groups have correlated cytokine concentrations measured in blood/plasma in the acute and chronic setting of patients with TBI and SAH to functional outcome [46,47,48] This suggests that, while these mediators may represent non-brain-specific inflammatory activity, systemic inflammation is triggered by brain injury, potentially having long-term sequelae such as stimulating an acute-phase response in the liver [49]. Claassen and coworkers found an association between the inflammatory response following SAH (TNF-receptor 1 and high-sensitivity C-reactive protein) and the presence of seizures [129] Several reviews covering this field have been published, and all do suggest a strong link between neuroinflammatory cascades, increased excitotoxicity, and epileptogenesis in the aftermath of brain injury [130, 131]. In some cases cytokines have partially overlapping functions, each cytokine has a unique role, pattern
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