Nordstrom, Charles W

Background: Influenza-associated encephalopathy, encephalitis, and acute necrotizing encephalopathy (ANE) are rare but potentially life-threatening neurological complications of influenza. Adult cases remain poorly characterized because the available literature is largely limited to isolated case reports and small case series. Methods: A PRISMA-guided scoping review of the MEDLINE database was conducted through 31 May 2026. Published adult cases of influenza-associated encephalopathy, encephalitis, and ANE were identified and analyzed for demographic characteristics, clinical presentation, neuroimaging findings, treatment, and outcomes. Results: Eighty-three adult cases reported between 1958 and 2026 were included. The mean age was 45.6 ± 17.8 years, and 57.8% were male. Two-thirds did not have any underlying comorbidities. Neurological symptoms developed a mean of 4.6 days after influenza onset, with influenza A accounting for 80.7% of infections. Fever (91.6%), altered mental status (86.7%), and seizures (36.1%) were the most common manifestations. Encephalitis was the predominant presentation (44.5%), followed by encephalopathy (31.3%) and ANE (24.1%). MRI most frequently demonstrated cerebral hemispheric lesions (53.0%) and bilateral thalamic involvement (36.4%), while EEG abnormalities were reported in 69.6% of patients. Overall mortality was 22.9%, highest among patients with ANE (45.0%). Among survivors, 28.9% experienced persistent neurological sequelae. Conclusions: Influenza-associated encephalopathy, encephalitis, and ANE are rare in adults but are associated with substantial morbidity and mortality. This review represents the largest adult cohort reported to date and provides important insights into the clinical spectrum, neurodiagnostic findings, and outcomes of these uncommon complications. This review highlights significant gaps in knowledge and the need for collaborative multicenter studies to improve the diagnosis, treatment, and outcome of these severe complications of influenza infection.

Background: Acute transverse myelitis (ATM) is an inflammatory disorder of the spinal cord with heterogeneous etiologies, including autoimmune, infectious, paraneoplastic, and drug-induced causes. Tumor necrosis factor-alpha (TNF-α) inhibitors have been infrequently associated with inflammatory central nervous system events, including transverse myelitis. TNF-inhibitor-associated myelitis typically presents with short-segment lesions, a normal brain MRI, and partial responsiveness to corticosteroids. Longitudinally extensive transverse myelitis (LETM) and steroid-refractory cases are uncommon. Case Presentation: A 39-year-old woman with psoriatic arthritis treated with etanercept for two years presented with subacute progressive bilateral lower-extremity sensory loss and weakness. MRI revealed a T2 hyperintense spinal cord lesion extending from T11 to L1 with gadolinium enhancement, consistent with transverse myelitis, while brain MRI was normal. Cerebrospinal fluid analysis showed lymphocytic pleocytosis, elevated protein, oligoclonal bands, and increased kappa free light chains. Extensive infectious, metabolic, paraneoplastic, and autoimmune testing, including aquaporin-4 and MOG antibodies, was negative. Despite high-dose intravenous corticosteroids and the discontinuation of etanercept, the patient experienced clinical worsening with lesion expansion, meeting criteria for LETM, and developed urinary retention. She subsequently underwent plasma exchange, resulting in radiologic improvement and moderate clinical recovery. Conclusions: This case highlights an atypical presentation of TNF-inhibitor-associated myelitis characterized by a biphasic course, longitudinally extensive spinal cord involvement, steroid refractoriness, and responsiveness to plasma exchange. These features suggest either an unusually severe TNF-inhibitor-related inflammatory phenotype or a TNF-inhibitor-triggered antibody-mediated demyelinating process. Reports of TNF-inhibitor-associated myelitis evolving into longitudinally extensive, steroid-refractory disease remain limited, and this presentation may broaden the recognized clinical spectrum of TNF-α-related CNS inflammatory events. Close neurologic follow-up and heightened awareness of severe CNS complications associated with TNF-α inhibitors are warranted.

Abstract Background Jamestown Canyon virus (JCV) is an emerging arboviral pathogen transmitted by mosquitoes in the United States and Canada. It is associated with neuroinvasive diseases and a wide spectrum of clinical presentations. Methods A retrospective chart review was conducted at the Mayo Clinic Health System in Northwest Wisconsin from January 2018 to December 2024, analyzing data from 12 hospitalized patients diagnosed with JCV infection. This study aimed to characterize the clinical, laboratory, imaging, and outcome profiles of the disease. The cohort included individuals aged 19 to 75 years, predominantly male (75%), with all patients reporting outdoor activity and 75% being pet owners. Results Only 27% of the patients recalled a mosquito bite. Among the cohort, 2 patients acquired an infection during the first trimester of pregnancy and subsequently delivered healthy infants. Coinfections with Borrelia burgdorferi were found in 33% of cases, while 16.7% of cases were seropositive to La Crosse virus. Magnetic resonance imaging of the brain was obtained in 5 patients and was nonspecific. Cerebrospinal fluid analysis demonstrated lymphocytic or monocytic pleocytosis in all cases where the test was performed. Conclusions All patients experienced clinical improvement, with only 1 developing lingering neurological symptoms in the form of brain fog. This study highlights the clinical heterogeneity of JCV infections and underscores the importance of including JCV in the differential diagnosis for patients residing in or traveling from endemic areas.

Background: Anaplasma phagocytophilum is an emerging tick-borne zoonotic pathogen that typically causes mild infections, which are often successfully managed in outpatient settings. Immunosuppression associated with splenectomy is a well-documented risk factor for severe infections from pathogens such as Babesia microti and encapsulated bacteria. However, splenectomy has not previously been identified as a risk factor for severe anaplasmosis. Case Presentation: This report describes a rare case of severe anaplasmosis complicated by multiorgan failure in a patient who had undergone splenectomy several decades earlier. The clinical course was notable for pneumonia, acute respiratory distress syndrome, acute kidney injury, rhabdomyolysis, atrial fibrillation, and possible myocarditis. Despite the severity of the presentation, prompt initiation of doxycycline led to recovery, albeit with a significantly prolonged hospital stay. Conclusions: Patients with splenectomy might be more likely to develop a serious form of Anaplasmosis infection such as multiorgan failure. Clinicians in tick-borne endemic areas should be aware that non-specific symptoms can indicate anaplasmosis.

Background and Objectives: Angioedema is a non-pitting edema of the submucosal layer which can be acquired or inherited and usually presents with hives. Intestinal angioedema is rare and can mimic other acute gastrointestinal disorders. It is typically associated with a lack or dysfunction of C1-inhibitor, with a small number of cases having normal C1-inhibitor function. We present a rare case of chronic recurrent intestinal angioedema in a patient with normal C1-inhibitor function who did not respond to icatibant therapy. Case presentation: A 56-year-old woman presented with 3 days of abdominal pain, nausea, vomiting, and diarrhea. She denied a history of allergies and reported a 30-year history of similar episodes requiring hospitalization. Initial evaluation demonstrated normal C4 and C1 esterase inhibitor function with negative gastrointestinal bacterial and viral panel. A CT of the abdomen and pelvis demonstrated acute diffuse bowel thickening and prominent mesenteric lymph nodes. MRI demonstrated inflammation of the small and large bowel. EGD and colonoscopy findings were normal. She was diagnosed with intestinal angioedema and started on icatibant without significant improvement. Her symptoms resolved after 3 days of supportive therapy and resolution of inflammation was noted on imaging. She was discharged home with allergy and immunology follow-up. Conclusions: Intestinal angioedema is under-recognized and presentation can overlap with other pathologies of the GI tract. Extensive work up is needed during the first episode of an attack and complement levels should be checked in all patients. Appropriate classification is important as it dictates therapy. However, ambiguous cases like ours sometimes cannot be classified into any specific category.