One of the well reported but difficult to manage symptoms of spinal cord injury (SCI) is neurogenic lower urinary tract dysfunction (NLUTD). The type of NLUTD is variable based on location and extent of injury. SCI affects more males and NLUTD is especially debilitating for men with incomplete injury. This review summarizes the anatomical basis of NLUTD in SCI and discusses current diagnostic and management strategies that are being utilized clinically. The last two sections address new innovations and emerging discoveries with the goal of increasing scientific interest in improving treatment options for people with SCI. Areas warranting further investigation are pinpointed to address current gaps in knowledge and/or appropriate technology.

Objective Post-traumatic epilepsy is a devastating complication of traumatic brain injury that has no targeted pharmacological therapy. Previous literature has explored the role of the c-Jun N-terminal kinase (JNK) pathway in epilepsy and the creation of epileptogenic foci by reactive astrogliosis; however, the relationship between reactive astrogliosis and the c-Jun N-terminal kinase signaling pathway in the development of post-traumatic epilepsy has not been thoroughly examined. Methods Four experimental groups, consisting of c57/b16 male mice, were examined: (1) control, (2) traumatic brain injury of graded severity (mild, moderate, severe), (3) sub-convulsive kainic acid alone without traumatic brain injury (15 mg/kg i.p.), and (4) sub-convulsive kainic acid administered 72 h after moderate traumatic brain injury. Modified Racine scale from 1 to 72 h and total beam breaks at 72 h were used to assess seizure activity. Immunohistochemistry and western blot were utilized to examine astrogliosis (GFAP), microglia activation (IBA-1), and phosphorylated JNK in prefrontal cortex samples collected from the contracoup side at 72 h post-injury. Results Astrogliosis, measured by GFAP, was increased after traumatic brain injury and increased commensurately based on the degree of injury. Mice with traumatic brain injury demonstrated a four-fold increase in phosphorylated JNK: p < 0.001. Sub-convulsive kainic acid administration did not increase seizure activity nor phosphorylation of JNK in mice without traumatic brain injury; however, sub-convulsive kainic acid administration in mice with moderate traumatic brain injury did increase phosphorylated JNK. Seizure activity was worse in mice, with traumatic brain injury, administered kainic acid than mice administered kainic acid. Conclusions Reactive astrocytes may have dysfunctional glutamate regulation causing an increase in phosphorylated JNK after kainic acid administration. Future studies exploring the effects of JNK inhibition on post-traumatic epilepsy are recommended.

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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 ongoing 2022 monkeypox virus outbreak has disproportionately impacted men who have sex with men and is associated with an increased frequency of atypical symptoms. The impetus for this outbreak is currently unknown. Experts suggest it may be related to the cessation of routine smallpox vaccination globally and biological changes in the monkeypox virus itself. Human monkeypox infection is classically associated with a fever prodrome followed by the eruption of small macules at the site of inoculation and when disseminating. The lesions then develop into a papule within 1–2 days and turn it a vesicle that pustulate with central umbilication within 5–7 days. They may ulcerate as they heal but will eventually begin to scab and new skin will form which often leaves a hyperpigmented or pitting scar. The overall process can take 2–3 weeks to heal entirely depending on the immune status of the host and other factors, such as antiviral treatment and previous vaccination. Primary inoculation of the monkeypox virus in the perianal region can lead to the development of single or multiple vesiculopustular lesions. They can appear similar to other sexually transmitted infections which could lead to a misdiagnosis. We present two separate cases of human monkeypox infection in men who have sex with men and concomitant human immunodeficiency virus (HIV) disease who both presented for anogenital lesions and proctitis who were successfully treated with tecovirimat. Treatment with tecovirimat has been shown to reduce symptoms and duration of illness. However, the unique features of the 2022 monkeypox virus outbreak necessitate further research to better understand the efficacy of this antiviral in the current monkeypox outbreak.

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Objective This narrative review of the literature concerns persistent headache attributed to past non‐traumatic subarachnoid hemorrhage (SAH), based off demographic and clinical features, what are pathophysiologic mechanisms by which these headaches occur, which medical and interventional treatments have the most evidence for pain alleviation, and what pre‐clinical evidence is there for emerging treatments for these patients. Background Following initial stabilization and treatment of spontaneous SAH, most commonly due to aneurysmal rupture, headache in the immediate inpatient setting and persisting after discharge are an important cause of morbidity. These headaches often receive heterogenous treatment of uncertain efficacy, and the risk factors and pathophysiology of their development has received little study. Methods A narrative review of current literature discussing post‐SAH headache was conducted using a literature search in PubMed with search term combinations including “post subarachnoid hemorrhage pain”, “subarachnoid hemorrhage headache”, and “post subarachnoid hemorrhage headache”. Clinical studies mentioning headache after SAH and/or treatment in the abstract/title were included through March, 2022. Results and Conclusion Post‐SAH headaches are shown to decrease quality of life, have a multi‐modal pathophysiology in their occurrence, and only a select few medications (reviewed herein) have been demonstrated to have efficacy in alleviation of these headaches, while also harboring possible risks including vasospasm and re‐bleeding. An effective treatment paradigm of these headaches will include trials of evidence‐based therapeutics, rapid reduction of opioid medications if not effective, and consideration of multi‐modal pain control strategies including nerve blocks.

The placement of cervical and intracranial stents requires the administration of antiplatelet drugs to prevent thromboembolic complications. Ticagrelor has emerged as the most widely used alternative in clopidogrel non-responders owing to its potent antiplatelet effects. Because ticagrelor does not require hepatic activation, many neurointerventionalists choose to forgo laboratory testing of platelet inhibition. In rare instances, patients may not achieve adequate platelet inhibition following ticagrelor administration. In this paper we review the mechanism of action of ticagrelor and its use in cerebrovascular procedures. We present two cases of ticagrelor non-responsiveness from two high-volume cerebrovascular centers, discuss their management, and propose an algorithm for managing ticagrelor non-responsiveness.