Acute-Onset Blindness in a Patient Diagnosed With Myelin Oligodendrocyte Glycoprotein Antibody Disease (MOG-AD): A Case Report.

Myelin oligodendrocyte glycoprotein antibody disease (MOG-AD) poses a diagnostic challenge, often masquerading as other neurological disorders such as multiple sclerosis and aquaporin-4-positive neuromyelitis optica spectrum disorder. The deceptive clinical similarities demand a nuanced approach to differentiate these conditions effectively. This entails an extensive evaluation encompassing a meticulous medical history, advanced magnetic resonance imaging (MRI), cerebrospinal fluid analysis, and serum studies. In this context, we present a compelling case involving a 28-year-old Hispanic female with a history of migraine headache. She sought medical attention due to acute peripheral vision loss, ultimately diagnosed as MOG-AD through a comprehensive clinical assessment coupled with specific diagnostic tests. This case underscores the critical importance of precision in diagnostic procedures to ensure accurate identification and subsequent tailored treatment for MOG-AD, avoiding potential pitfalls associated with its resemblance to other neurological disorders.

Examining the Efficacy of Antimicrobial Therapy in Preventing the Development of Postinfectious Glomerulonephritis: A Systematic Review and Meta-Analysis.

Postinfectious glomerulonephritis (PIGN) is an immune-mediated acute glomerulonephritis classically seen weeks after infection with Streptococcus pyogenes, although other infectious etiologies have emerged. While it has become increasingly rare in industrialized regions, it continues to affect children in developing countries. There has been debate as to why incidence rates are declining, including the possibility of improved initial treatment of bacterial infections. The ability of antimicrobial therapy in preventing PIGN as infectious sequelae, however, has not been comprehensively assessed. As varying evidence from published studies exists, the objective of this meta-analysis is to determine if antimicrobial therapy utilized to treat an initial infection has an effect in reducing the development of PIGN in humans. EMBASE, MEDLINE, and CENTRAL were searched using a comprehensive terminology strategy. From an initial search that returned 337 publications, 9 articles were included for analysis. Eight studies showed an incidence of PIGN after antimicrobial use ranging from 0.05% to 10% with a mean standardized difference (MSD) of 0.03 (0.01-0.06). Three studies showed an occurrence of PIGN without antibiotic use ranging from 1% to 13% with an MSD of 0.06 (-0.09-0.21). Our findings suggest that antimicrobial treatment for the initial infection may help diminish the development of PIGN. Although Streptococcus pyogenes infections are generally treated aggressively to prevent rheumatic fever, these findings may help further support the early treatment of bacterial infections to prevent postinfectious sequelae, especially as we consider other infectious etiologies of PIGN antimicrobial resistance.

Spinal Cord Injury in Rats Dysregulates Diurnal Rhythms of Fecal Output and Liver Metabolic Indicators.

Spinal cord injury (SCI) dysregulates metabolic homeostasis. Metabolic homeostasis is optimized across the day by the circadian system. Despite the prevalence of metabolic pathologies after SCI, post-SCI circadian regulation of metabolism remains understudied. Here, we hypothesized that SCI in rats would disrupt circadian regulation of key metabolic organs, leading to metabolic dysregulation. Female and male Sprague-Dawley rats received moderate thoracic (T)-9 contusion SCI (or sham surgery). First, SCI disrupted diurnal rhythms in two metabolic behaviors: fecal production and food intake rhythms were ablated acutely. SCI also expedited whole-gut transit time. In parallel, acute SCI increased plasma glucose. Diurnal glucose storage-release cycles regulated by the liver were disrupted by SCI, which also increased liver glucose metabolism messenger RNAs (mRNAs). Further, SCI disrupted liver clock gene expression and suppressed inflammatory gene rhythms. Together, our novel data suggest that SCI disrupts typical metabolic and circadian function. Improving post-SCI metabolic function could enhance recovery of homeostasis.

Journal Club: MRI reveals acute inflammation in cortical lesions during early MS.

Early multiple sclerosis is characterized by immune-associated demyelination of CNS axons. In a recent Neurology® article, Maranzano et al. evaluated MRI scans of patients with early multiple sclerosis to study the evolution of leukocortical lesions. Their novel data suggest that acute inflammation after blood-brain barrier leakage may contribute to gray matter cortical lesions in early multiple sclerosis.

Spinal Cord Injury in Rats Disrupts the Circadian System.

Spinal cord injury (SCI) perturbs many physiological systems. The circadian system helps maintain homeostasis throughout the body by synchronizing physiological and behavioral functions to predictable daily events. Whether disruption of these coordinated daily rhythms contributes to SCI-associated pathology remains understudied. Here, we hypothesized that SCI in rats would dysregulate several prominent circadian outputs including glucocorticoids, core temperature, activity, neuroinflammation, and circadian gene networks. Female and male Sprague Dawley rats were subjected to clinically relevant thoracic 9 moderate contusion SCI (or laminectomy sham surgery). Diurnal measures-including rhythms of plasma corticosterone (CORT), body temperature, and activity (using small implanted transmitters), and intraspinal circadian and inflammatory gene expression-were studied prior to and after surgery. SCI caused overall increases and disrupted rhythms of the major rodent glucocorticoid, CORT. Presurgery and sham rats displayed expected rhythms in body temperature and activity, whereas rats with SCI had blunted daily rhythms in body temperature and activity. In parallel, SCI disrupted intraspinal rhythms of circadian clock gene expression. Circadian clock genes can act as transcriptional regulators of inflammatory pathways. Indeed, SCI rats also showed dysregulated rhythms in inflammatory gene expression in both the epicenter and distal spinal cord. Our data show that moderate SCI in rats causes wide-ranging diurnal rhythm dysfunction, which is severe at acute time points and gradually recovers over time. Normalizing post-SCI diurnal rhythms could enhance the recovery of homeostasis and quality of life.

Exploring acute-to-chronic neuropathic pain in rats after contusion spinal cord injury.

Spinal cord injury (SCI) causes chronic pain in 65% of individuals. Unfortunately, current pain management is inadequate for many SCI patients. Rodent models could help identify how SCI pain develops, explore new treatment strategies, and reveal whether acute post-SCI morphine worsens chronic pain. However, few studies explore or compare SCI-elicited neuropathic pain in rats. Here, we sought to determine how different clinically relevant contusion SCIs in male and female rats affect neuropathic pain, and whether acute morphine worsens later chronic SCI pain. First, female rats received sham surgery, or 150kDyn or 200kDyn midline T9 contusion SCI. These rats displayed modest mechanical allodynia and long-lasting thermal hyperalgesia. Next, a 150kDyn (1s dwell) midline contusion SCI was performed in male and female rats. Interestingly, males, but not females showed SCI-elicited mechanical allodynia; rats of both sexes had thermal hyperalgesia. In this model, acute morphine treatment had no significant effect on chronic neuropathic pain symptoms. Unilateral SCIs can also elicit neuropathic pain that could be exacerbated by morphine, so male rats received unilateral T13 contusion SCI (100kDyn). These rats exhibited significant, transient mechanical allodynia, but not thermal hyperalgesia. Acute morphine did not exacerbate chronic pain. Our data show that specific rat contusion SCI models cause neuropathic pain. Further, chronic neuropathic pain elicited by these contusion SCIs was not amplified by our course of early post-trauma morphine. Using clinically relevant rat models of SCI could help identify novel pain management strategies.