The innate and adaptive immune systems are critical in defense against pathogens and ensuring homeostasis. The central nervous system (CNS) was initially considered to be impermeable to immune cells due to the blood–brain barrier. However, this has now been debunked, with modern research delineating immune cell trafficking within the CNS, ensuring constant immune surveillance. However, these defenses may be breached in infections, which trigger an inflammatory cascade causing tissue damage. In addition, autoimmune conditions and genetic mutations may also lead to sustained proinflammatory molecule release causing significant CNS damage. Ensuing brain injury from most immune triggers is varied but may be associated with common patterns by virtue of a shared immune driver. MRI plays an important role in identifying these conditions and further enables understanding of their pathophysiology as well as their spatial predilection in the brain. In this review, we discuss basic immunology, the major CNS barriers to infections as well as the current understanding of selected pediatric infections and inflammatory processes.

Severe acute respiratory syndrome coronavirus 2, the virus that causes coronavirus disease-2019, has been associated with an increased risk for ischemic and hemorrhagic stroke. As data emerge about the underlying mechanisms, it is important to synthesize current knowledge to improve effective treatment options. In this review, we highlight the known pathophysiology, discuss the relationship between ischemic and hemorrhagic stroke, and address emerging implications for patient management. The information here is compiled to be a user-friendly, quick guide to help practitioners select management options for these patients.

The Milwaukee protocol has been attributed to survival in rabies encephalitis despite a lack of scientific evidence supporting its therapeutic measures. We have reviewed the literature with reference to specific treatment recommendations made within the protocol. Current literature fails to support an important role for excitotoxicity and cerebral vasospasm in rabies encephalitis. Therapies suggested in the Milwaukee protocol include therapeutic coma, ketamine infusion, amantadine, and the screening/prophylaxis/management of cerebral vasospasm. None of these therapies can be substantiated in rabies or other forms of acute viral encephalitis. Serious concerns over the current protocol recommendations are warranted. The recommendations made by the Milwaukee protocol warrant serious reconsideration before any future use of this failed protocol.

Background: Cranioplasty encompasses various cranial reconstruction techniques that are used following craniectomy due to stroke or trauma. Despite classical infectious signs, symptoms, and radiologic findings, however, the diagnosis of infection following cranioplasty can be elusive, with the potential to result in definitive treatment delay. We sought to determine if fever or leukocytosis at presentation were indicative of infection, as well as to identify any factors that may limit its applicability. Methods: Following institutional review board approval, a retrospective cohort of 239 patients who underwent cranioplasty following craniectomy for stroke or trauma was established from 2001-2011 at a single center (Massachusetts General Hospital). Analysis was then focused on those who developed a surgical site infection, as defined by either frank intra-operative purulence or positive intra-operative cultures, and subsequently underwent operative management. Results: In 27 total cases of surgical site infection, only two had a fever and four had leukocytosis at presentation. This yielded a false-negative rate for fever of 92.6% and for leukocytosis of 85.2%. In regard to infectious etiology, 22 (81.5%) cases generated positive intra-operative cultures, with Propionibacterium acnes being the most common organism isolated. Median interval to infection was 99 days from initial cranioplasty to time of infectious presentation, and average follow-up was 3.4 years. Conclusions: The utilization of fever and elevated white blood cell count in the diagnosis of post-cranioplasty infection is associated with a high false-negative rate, making the absence of these features insufficient to exclude the diagnosis of infection.