Although many approaches have been tried in the attempt to reduce the devastating impact of stroke, tissue plasminogen activator for thromboembolic stroke is the only proved, effective acute stroke treatment to date. Vasopressin, an acute-phase reactant, is released after brain injury and is partially responsible for the subsequent inflammatory response via activation of divergent pathways. Recently there has been increasing interest in vasopressin because it is implicated in inflammation, cerebral edema, increased intracerebral pressure, and cerebral ion and neurotransmitter dysfunctions after cerebral ischemia. Additionally, copeptin, a byproduct of vasopressin production, may serve as a promising independent marker of tissue damage and prognosis after stroke, thereby corroborating the role of vasopressin in acute brain injury. Thus, vasopressin antagonists have a potential role in early stroke intervention, an effect thought to be mediated via interactions with aquaporin receptors, specifically aquaporin-4. Despite some ambiguity, vasopressin V1a receptor antagonism has been consistently associated with attenuated secondary brain injury and edema in experimental stroke models. The role of the vasopressin V2 receptor remains unclear, but perhaps it is involved in a positive feedback loop for vasopressin expression. Despite the encouraging initial findings we report here, future research is required to characterize further the utility of vasopressin antagonists in treatment of stroke.

BackgroundElevated intracranial pressure from cerebral edema is the major cause of early mortality in acute stroke. Current treatment strategies to limit cerebral edema are not particularly effective. Some novel anti-edema measures have shown promising early findings in experimental stroke models. Vasopressin antagonism in stroke is one such target which has shown some encouraging preliminary results. The aim of this report is to highlight the potential use of vasopressin antagonism to limit cerebral edema in patients after acute stroke.Case presentationA 57-year-old Caucasian man with new onset diplopia was diagnosed with vertebral artery aneurysm extending into the basilar circulation. He underwent successful elective vertebral artery angioplasty and coiling of the aneurysm. In the immediate post-operative period there was a decline in his neurological status and brain imaging revealed new midbrain and thalamic hemorrhage with surrounding significant brain edema. Treatment with conventional anti-edema therapy was initiated with no significant clinical response after which conivaptan; a mixed vasopressin antagonist was started. Clinical and radiological evaluation following drug administration showed rapid clinical improvement without identification of significant adverse effects.ConclusionsThe authors have successfully demonstrated the safety and efficacy of using mixed vasopressin antagonist in treatment of stroke related brain edema, thereby showing its promise as an alternative anti-edema agent. Preliminary findings from this study suggest mixed vasopressin antagonism may have significant utility in the management of cerebral edema arising from cerebrovascular accident. Larger prospective studies are warranted to explore the role of conivaptan in the treatment of brain edema and neuroprotection.

Purpose. To describe a case of postoperative scleritis caused by a novel strain of Nocardia resistant to linezolid and trimethoprim-sulfamethoxazole (TMP-SMX). Methods. Case report of a patient with microbiologically proven scleritis due to Nocardia asteroides. Results. The patient presented with pain, redness, and nodules on the sclera three months following pterygium excision with mitomycin C and amniotic membrane placement. As no response was noted with empiric treatment for bacterial scleritis, debridement was performed. The cytopathology report showed gram positive filamentous bacteria. A presumptive diagnosis of Nocardia scleritis was made and therapy was initiated based on a literature review on treatments for Nocardia infections. Cultures returned growing Nocardia asteroides. Antibiotic sensitivity testing revealed resistance to linezolid and TMP-SMX which are the traditional drugs of choice for Nocardia. The patient was treated with amikacin and imipenem as well as extensive debridement with pedicle grafts. The patient's scleritis resolved with a good visual outcome. Conclusions. Cultures should be obtained in all cases of necrotizing scleritis in patients with a recent history of conjunctival surgery to rule out unusual organisms such as Nocardia. Although literature states that resistance to linezolid and TMP-SMX is rare in Nocardia, sensitivity testing can be useful in unresponsive cases.

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