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Purpose: To describe the presentation of lacrimal gland secretions mimicking a positive Seidel test following combined complex cataract surgery and endocyclophotocoagulation (ECP). Observation: The patient presented with a posterior subcapsular cataract (PSC) most likely secondary to chronic steroid use for a history of chemical burns from a firework injury in 2019. This injury resulted in symblepharon formation and limbal stem cell deficiency. He also developed glaucoma secondary to steroid response and angle structure damage. On postoperative day 1 (POD 1) after combined cataract surgery and ECP, the patient's paracentesis was Seidel positive and aqueous suppression was started. On postoperative week 1 (POW 1), the paracentesis was Seidel negative; however, it was noted at this visit that there were 3 pinpoint areas in the superotemporal conjunctiva that were Seidel positive. Digital pressure did not worsen the leak. Ultrasound biomicroscopy (UBM) was performed at POW 2.5 and showed lacrimal gland ducts in the superotemporal conjunctiva. Given this, it is likely that the “Seidel positive” finding was not due to aqueous humor leakage, but secretions from lacrimal gland tissue that may have been dragged more anteriorly due to conjunctiva scarring, thus producing a false positive Seidel sign. Conclusion & importance: This case highlights a false positive Seidel sign in the context of an eye with a complex ocular history and recent surgery. Clinicians should recognize that a false positive Seidel sign is possible if normal lacrimal gland anatomy has been disturbed.

Purpose: Immunizations have long been pivotal in preventing diseases like HZ (herpes zoster), caused by VZV (varicella zoster virus). This study aims to evaluate the efficacy and safety of the RZV (recombinant zoster vaccine) compared to the ZVL (zoster vaccine live) and to report rare adverse events following RZV administration. Observation: Herein, we report an unusual case of a 59-year-old man who developed a V1-limited rash with a positive HZ PCR (polymerase chain reaction) test following administration of RZV in the United States. Conclusion: The development of RZV has significantly improved the prevention of HZ compared to ZVL. Nevertheless, rare adverse events, such as dermatomal reactions, underscore the importance of ongoing monitoring and research into the immunomodulatory effects of RZV. Physicians should continue to administer the RZV to patients but be cognizant that reactivation may rarely subsequently occur. Case Presentation: The patient with a history of benign prostatic hyperplasia was treated at an outside hospital two days after receiving the RZV complaining of paresthesia and a rash on his nasolacrimal area and forehead. The patient presented to the ED (emergency department), 9 days post-vaccination due to persistence of his symptoms despite use of amoxicillin, valacyclovir, and an unidentified eye drop. The dose of valacyclovir was increased, and he completed 1 g TID (three times a day) PO (per orally) for 10 days with subsequent resolution of symptoms. A positive PCR test confirmed the diagnosis of HZ. Topical mupirocin ointment was initiated and the patient was referred for ophthalmologic evaluation.

Non-traumatic subarachnoid hemorrhage (SAH) affects an estimated 30,000 people each year in the United States, with an overall mortality of ~30%. Most cases of SAH result from a ruptured intracranial aneurysm, require long hospital stays, and result in significant disability and high fatality. Early brain injury (EBI) and delayed cerebral vasospasm (CV) have been implicated as leading causes of morbidity and mortality in these patients, necessitating intense focus on developing preclinical animal models that replicate clinical SAH complete with delayed CV. Despite the variety of animal models currently available, translation of findings from rodent models to clinical trials has proven especially difficult. While the explanation for this lack of translation is unclear, possibilities include the lack of standardized practices and poor replication of human pathophysiology, such as delayed cerebral vasospasm and ischemia, in rodent models of SAH. In this review, we summarize the different approaches to simulating SAH in rodents, in particular elucidating the key pathophysiology of the various methods and models. Ultimately, we suggest the development of standardized model of rodent SAH that better replicates human pathophysiology for moving forward with translational research.

Interleukin-10 (IL-10) is an important anti-inflammatory cytokine expressed in response to brain injury, where it facilitates the resolution of inflammatory cascades, which if prolonged causes secondary brain damage. Here, we comprehensively review the current knowledge regarding the role of IL-10 in modulating outcomes following acute brain injury, including traumatic brain injury (TBI) and the various stroke subtypes. The vascular endothelium is closely tied to the pathophysiology of these neurological disorders and research has demonstrated clear vascular endothelial protective properties for IL-10. In vitro and in vivo models of ischemic stroke have convincingly directly and indirectly shown IL-10-mediated neuroprotection; although clinically, the role of IL-10 in predicting risk and outcomes is less clear. Comparatively, conclusive studies investigating the contribution of IL-10 in subarachnoid hemorrhage are lacking. Weak indirect evidence supporting the protective role of IL-10 in preclinical models of intracerebral hemorrhage exists; however, in the limited number of clinical studies, higher IL-10 levels seen post-ictus have been associated with worse outcomes. Similarly, preclinical TBI models have suggested a neuroprotective role for IL-10; although, controversy exists among the several clinical studies. In summary, while IL-10 is consistently elevated following acute brain injury, the effect of IL-10 appears to be pathology dependent, and preclinical and clinical studies often paradoxically yield opposite results. The pronounced and potent effects of IL-10 in the resolution of inflammation and inconsistency in the literature regarding the contribution of IL-10 in the setting of acute brain injury warrant further rigorously controlled and targeted investigation.