Explore the vast range of titles available.

We report a case of severe tick-borne encephalitis in a pregnant woman, leading to a prolonged stay in the intensive care unit. She showed minor clinical improvement >6 months after her presumed infection. The patient was not vaccinated, although an effective vaccine is available and not contraindicated during pregnancy.

Background Many patients with traumatic brain injury (TBI) across all levels of severity experience persistent psycho‐emotional, cognitive, and somatic symptoms. Psychological network theory views disorders as intricate systems rather than discrete diseases. This study employs an exploratory network analysis method to uncover potential causal links among long‐term TBI symptoms. Methods We examined persistent symptoms using secondary data from 250 TBI patients undergoing an inpatient “brain check” procedure. We constructed two partial correlation networks: one for the entire sample and another for a mild TBI subgroup, each consisting of 14 symptoms and three covariates. The symptoms and their connections were visualized in network graphs to identify potential causal, and structural indicators and centrality indices were calculated. Results The analysis revealed two dense networks characterized by multiple complex connections. In the overall network, symptoms are clustered into psycho‐emotional and cognitive communities, with attention deficits serving as a crucial link between them. One finding was that self‐reported cognitive impairments do not align with objectively measured deficits. Within the mild TBI subgroup, PTSD emerges as a central node in the network. Conclusion Network analysis reveals the multidimensional and reciprocal nature of long‐term TBI symptoms. Attention deficits bridge cognitive and psycho‐emotional areas, whereas psycho‐emotional symptoms influence self‐perceived performance. Self‐reported cognitive impairments should be emphasized in therapy as they are linked rather to sleep, visual disturbances, and anxiety than to objective deficits. Network analysis is valuable for understanding TBI symptom complexity and exploring treatment options. Future research should utilize longitudinal designs to validate our findings. We analyzed persistent symptoms in 250 TBI patients using partial correlation networks. The main findings show that attention deficits link cognitive and psycho‐emotional domains, whereas psycho‐emotional symptoms greatly impact self‐perceived performance. We suggest network analysis as an effective method for understanding the complexity of TBI symptoms and identifying potential treatment options.

Recent studies elucidate that coronavirus disease 2019 (COVID‐19) patients may face a higher risk of cardiovascular complications. This study aimed to evaluate association of COVID‐19 with the risk of pulmonary embolism (PE) or deep vein thrombosis (DVT). This nationwide population‐based retrospective cohort study included Korean adult citizens between January 2021 and March 2022 from the Korea Disease Control and Prevention Agency COVID‐19 National Health Insurance Service cohort. The Fine and Gray's regression with all‐cause death as a competing event was adopted to evaluate PE and DVT risks after COVID‐19. This study included a total of 1,601,835 COVID‐19 patients and 14,011,285 matched individuals without COVID‐19. The risk of PE (adjusted hazard ratio [aHR], 6.25; 95% confidence interval [CI], 3.67–10.66; p < 0.001) and DVT (aHR, 3.05; 95% CI, 1.75–5.29; p < 0.001) was higher in COVID‐19 group in individuals without complete COVID‐19 vaccination. In addition, individuals with complete COVID‐19 vaccination still had a higher risk of COVID‐19‐related PE (aHR, 1.48; 95% CI, 1.15–1.88; p < 0.001). However, COVID‐19 was not a significant risk factor for DVT among those with complete COVID‐19 vaccination. COVID‐19 was identified as an independent factor that elevated PE and DVT risks, especially for individuals without complete COVID‐19 vaccination. COVID‐19 was associated with an increased risk of PE (aHR, 6.25; 95% CI, 3.67–10.66; p < 0.001) and DVT (aHR, 3.05; 95% CI, 1.75–5.29; p < 0.001) in unvaccinated participants. Even in those with complete COVID‐19 vaccination, a smaller but significant risk of PE was observed (aHR, 1.48; 95% CI, 1.15–1.88; p < 0.001). However, COVID‐19 did not increase DVT risk in those with complete vaccination.

Here, we present the case of an 81‐year‐old male patient, who was hospitalized for a severe form of COVID‐19. Transthoracic echocardiogram (TTE) performed 1 month after symptom onset was normal. Respiratory evolution was favourable, and the patient was discharged at Day 78. At 6 months, despite a good functional recovery, he presented pulmonary sequelae, and the TTE revealed a clear reduction of left ventricular ejection fraction (LVEF) and mild LV dilatation without cardiac symptoms. The cardiac magnetic resonance (CMR) using Lake Louise Criteria (LLC), T1 and T2 mapping showed focal infero‐basal LV wall oedema, elevated T1 and T2 myocardial relaxation times especially in basal inferior and infero‐lateral LV walls, and sub‐epicardial late gadolinium enhancement in those LV walls. The diagnosis of active myocarditis was raised especially based on TTE abnormalities and CMR LLC, T1 and T2 mapping. Currently, we are not aware of published reports of a 6 month post‐COVID‐19 active myocarditis.

Sepsis is a major cause of death in intensive care units worldwide. The acute phase of sepsis is often accompanied by sepsis-associated encephalopathy, which is highly associated with increased mortality. Moreover, in the chronic phase, more than 50% of surviving patients suffer from severe and long-term cognitive deficits compromising their daily quality of life and placing an immense burden on primary caregivers. Due to a growing number of sepsis survivors, these long-lasting deficits are increasingly relevant. Despite the high incidence and clinical relevance, the pathomechanisms of acute and chronic stages in sepsis-associated encephalopathy are only incompletely understood, and no specific therapeutic options are yet available. Here, we review the emergence of sepsis-associated encephalopathy from initial clinical presentation to long-term cognitive impairment in sepsis survivors and summarize pathomechanisms potentially contributing to the development of sepsis-associated encephalopathy.

In late December 2019, multiple atypical pneumonia cases resulted in severe acute respiratory syndrome caused by a pathogen identified as a novel coronavirus SARS-CoV-2. The most common coronavirus disease 2019 (COVID-19) symptoms are pneumonia, fever, dry cough, and fatigue. However, some neurological complications following SARS-CoV-2 infection include confusion, cerebrovascular diseases, ataxia, hypogeusia, hyposmia, neuralgia, and seizures. Indeed, a growing literature demonstrates that neurotropism is a common feature of coronaviruses; therefore, the infection mechanisms already described in other coronaviruses may also be applicable for SARS-CoV-2. Understanding the underlying pathogenetic mechanisms in the nervous system infection and the neurological involvement is essential to assess possible long-term neurological alteration of COVID-19. Here, we provide an overview of associated literature regarding possible routes of COVID-19 neuroinvasion, such as the trans-synapse-connected route in the olfactory pathway and peripheral nerve terminals and its neurological implications in the central nervous system.

We recently reported acute COVID-19 symptoms, clinical status, weight loss, multi-organ pathological changes, and animal death in a murine hepatitis virus-1 (MHV-1) coronavirus mouse model of COVID-19, which were similar to that observed in humans with COVID-19. We further examined long-term (12 months post-infection) sequelae of COVID-19 in these mice. Congested blood vessels, perivascular cavitation, pericellular halos, vacuolation of neuropils, pyknotic nuclei, acute eosinophilic necrosis, necrotic neurons with fragmented nuclei, and vacuolation were observed in the brain cortex 12 months post-MHV-1 infection. These changes were associated with increased reactive astrocytes and microglia, hyperphosphorylated TDP-43 and tau, and a decrease in synaptic protein synaptophysin-1, suggesting the possible long-term impact of SARS-CoV-2 infection on defective neuronal integrity. The lungs showed severe inflammation, bronchiolar airway wall thickening due to fibrotic remodeling, bronchioles with increased numbers of goblet cells in the epithelial lining, and bronchiole walls with increased numbers of inflammatory cells. Hearts showed severe interstitial edema, vascular congestion and dilation, nucleated red blood cells (RBCs), RBCs infiltrating between degenerative myocardial fibers, inflammatory cells and apoptotic bodies and acute myocyte necrosis, hypertrophy, and fibrosis. Long-term changes in the liver and kidney were less severe than those observed in the acute phase. Noteworthy, the treatment of infected mice with a small molecule synthetic peptide which prevents the binding of spike protein to its respective receptors significantly attenuated disease progression, as well as the pathological changes observed post-long-term infection. Collectively, these findings suggest that COVID-19 may result in long-term, irreversible changes predominantly in the brain, lung, and heart.

Arthropod-borne viruses or arbovirus, are most commonly associated with acute infections, resulting on various symptoms ranging from mild fever to more severe disorders such as hemorrhagic fever. Moreover, some arboviral infections can be associated with important neuroinflammation that can trigger neurological disorders including encephalitis, paralysis, ophthalmological impairments, or developmental defects, which in some cases, can lead to long-term defects of the central nervous system (CNS). This is well illustrated in Zika virus-associated congenital brain malformations but also in West Nile virus-induced synaptic dysfunctions that can last well beyond infection and lead to cognitive deficits. Here, we summarize clinical and mechanistic data reporting on cognitive disturbances triggered by arboviral infections, which may highlight growing public health issues spanning the five continents.

Introduction There are no published studies assessing the evolution of combined determination of the lung diffusing capacity for both nitric oxide and carbon monoxide (DL NO and DL CO ) 12 months after the discharge of patients with COVID-19 pneumonia. Methods Prospective cohort study which included patients who were assessed both 3 and 12 months after an episode of SARS-CoV-2 pneumonia. Their clinical status, health condition, lung function testings (LFTs) results (spirometry, DL NO -DL CO analysis, and six-minute walk test), and chest X-ray/computed tomography scan images were compared. Results 194 patients, age 62 years (P 25–75 , 51.5–71), 59% men, completed the study. 17% required admission to the intensive care unit. An improvement in the patients’ exercise tolerance, the extent of the areas of ground-glass opacity, and the LFTs between 3 and 12 months following their hospital discharge were found, but without a decrease in their degree of dyspnea or their self-perceived health condition. DL NO was the most significantly altered parameter at 12 months (19.3%). The improvement in DL NO -DL CO mainly occurred at the expense of the recovery of alveolar units and their vascular component, with the membrane factor only improving in patients with more severe infections. Conclusions The combined measurement of DL NO -DL CO is the most sensitive LFT for the detection of the long-term sequelae of COVID-19 pneumonia and it explain better their pathophysiology.