Neuroprotection: Surgical approaches in traumatic brain injury

Abstract

Background: This review is centered on the pivotal role of surgical interventions within the comprehensive management of traumatic brain injury (TBI). Surgical strategies are indispensable components of TBI care, encompassing primary injury management and the alleviation of secondary injury processes, including the handling of intracranial hemorrhages (ICHs), contusions, and mass lesions.

Methods: A systematic review was carried out by searching databases including PubMed, Embase, and Scopus. The inclusion criteria involved studies discussing surgical strategies for TBI, with a focus on primary injury management, ICHs, contusions, and mass lesions. More recent articles were prioritized, and data were synthesized to assess the impact of surgical interventions on TBI outcomes.

Results: The evolution of surgical technologies has heralded a transformation in TBI management. These advancements encompass minimally invasive procedures, neuroimaging-guided surgeries, and robotic-assisted techniques, all geared toward optimizing patient outcomes.

Conclusion: Surgical interventions within TBI care present unique challenges, such as timing considerations, patient selection criteria, and postoperative care. This review underscores the critical significance of multidisciplinary collaboration among neurosurgeons, neurologists, and critical care specialists. Such collaboration is essential to tailor surgical strategies to the individualized needs of patients. Moreover, the review highlights emerging trends in TBI surgery and underscores the ongoing imperative of research endeavors aimed at refining surgical protocols and ultimately enhancing patient outcomes.

Keywords: Cisternostomy; Decompressive craniectomy; Intracranial hemorrhages; Neuroimaging-guided surgeries; Traumatic brain injury.

Figure 1:

Immune response following traumatic brain injury (TBI): (i-ii) following TBI, the primary mechanical injury can include meningeal contusion, axonal shearing, and cerebrovascular injury, culminating in meningeal and neuronal cell death, as well as microglial and astrocytic activation. (iii) Such neuronal injury and glial engagement generate chemokines, cytokines, and reactive oxygen species, along with the release of damage-associated molecular patterns (DAMPs), setting off an inflammatory response. (iv) In the presence of DAMPs, phagocytic microglia engage in debris clearance and synthesize neurotrophic agents. Sustained stimulation of these pathways induces subsequent injury through leukocyte recruitment, which initially aids in the removal of tissue debris. (v) Subsequently, it contributes to the progression of inflammation and disruption of the blood–brain barrier (BBB). The cytotoxic edema and compromised BBB integrity bring to an elevation of the intracranial pressure, leading to decreased cerebral blood flow, thereby intensifying hypoxia and disrupting the cerebral energy supply. Consequently, this cascade drives further neuronal depletion, propelling a self-perpetuating cycle of neuroinflammation and neurodegeneration. (vi) These progressive pathological modifications culminate in neurological dysfunction and deficits in motor, cognitive, and emotional functions. TBI also induces alterations in the autonomic nervous system (ANS), which monitors and regulates DAMPs, consequently eliciting both cerebral and peripheral immune responses. (vii) Activation of the sympathetic ANS culminates in the peripheral discharge of catecholamines (epinephrine and norepinephrine), which suppress the systemic immune responses of macrophages through the cholinergic anti-inflammatory pathway (CAO), thereby mitigating systemic inflammation. (viii) Furthermore, the release of catecholamines and glucocorticoids through the hypothalamic-pituitary-adrenal axis governs the functional behavior of systemic immune cells after TBI. (ix) The cellular immune response to traumatic brain injury involves an increase in leukocytosis and ROS generation, progresses through phagocytosis, and shifts from pro-inflammatory to anti-inflammatory states, potentially leading to immune dysfunction and immunosuppression. Abbreviations: ICP (increased intracranial pressure), CBF (cerebral blood flow), HPA (hypothalamic-pituitary-adrenal), ROS (reactive oxygen species). Image created with BioRender.com.

Figure 2:

This figure illustrates the Glasgow coma scale (GCS), a vital neurological assessment tool, as it pertains to traumatic brain injury (TBI). The GCS quantifies the patient’s level of consciousness based on eye, verbal, and motor responses, aiding clinicians in gauging TBI severity and guiding treatment decisions. Image created with BioRender.com.

Figure 3:

This figure delineates the criteria for surgical intervention across common traumatic brain injury scenarios. Specific clinical and radiological criteria guide the decision to opt for surgery.[4,5,28,64,69] Abbreviations: GCS (Glasgow Coma Scale), cSDH (chronic subdural hematoma), ICS (intracranial suppuration)