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Purpose of ReviewTo discuss the neurological complications of dengue virus (DENV) infection and their pathogenesis.Recent FindingsInclude recognition of the four different serotypes of DENV and their epidemiology as well as recognition of the expanded dengue syndrome encompassing multisystem involvement in the severe form of the disease including involvement of the central nervous system (CNS). DENV is a neurotropic virus with the ability to infect the supporting cells of the CNS. Neural injury during the acute stage of the infection results from direct neuro-invasion and/or the phenomenon of antibody-dependent enhancement, resulting in plasma leakage and coagulopathy. Immune mechanisms have been implicated in the development of the delayed neurological sequelae through molecular mimicry. A myriad of neurological syndromes has been described as a result of the involvement of the CNS, the peripheral nervous system (PNS), or both.SummaryNeurological manifestations in DENV infection are increasingly being recognized, some of which are potentially fatal if not treated promptly. DENV encephalopathy and encephalitis should be considered in the differential diagnosis of other acute febrile encephalopathies, autoimmune encephalitides, and in cases of encephalopathy/encephalitis related to SARS-CoV2 infection, especially in dengue-endemic areas. Acute disseminated encephalomyelitis (ADEM) may be occasionally encountered. Clinicians should be knowledgeable of the expanded dengue syndrome characterized by the concurrent compromise of cardiac, neurological, gastrointestinal, renal, and hematopopoietic systems. Isolated cranial nerve palsies occur rather uncommonly and are often steroid responsive. These neuropathies may result from the direct involvement of cranial nerve nuclei or nerve involvement or may be immune-mediated. Even if the diagnosis of dengue is confirmed, it is absolutely imperative to exclude other well-known causes of isolated cranial nerve palsies. Ischemic and hemorrhagic strokes may occur following dengue fever. The pathogenesis may be beyond the commonly observed thrombocytopenia and include cerebral vasculitis. Involvement of ocular blood vessels may cause maculopathy or retinal hemorrhages. Posterior reversible encephalopathy syndrome (PRES) is uncommon and possibly related to dysregulated cytokine release phenomena. Lastly, any patient developing acute neuromuscular weakness during the course or within a fortnight of remission from dengue fever must be screened for acute inflammatory demyelinating polyneuropathy (AIDP), hypokalemic paralysis, or acute myositis. Rarely, a Miller–Fisher-like syndrome with negative anti-GQ1b antibody may develop.

The development of long-term symptoms of coronavirus disease 2019 (COVID-19) more than four weeks after primary infection, termed “long COVID” or post-acute sequela of COVID-19 (PASC), can implicate persistent neurological complications in up to one third of patients and present as fatigue, “brain fog”, headaches, cognitive impairment, dysautonomia, neuropsychiatric symptoms, anosmia, hypogeusia, and peripheral neuropathy. Pathogenic mechanisms of these symptoms of long COVID remain largely unclear; however, several hypotheses implicate both nervous system and systemic pathogenic mechanisms such as SARS-CoV2 viral persistence and neuroinvasion, abnormal immunological response, autoimmunity, coagulopathies, and endotheliopathy. Outside of the CNS, SARS-CoV-2 can invade the support and stem cells of the olfactory epithelium leading to persistent alterations to olfactory function. SARS-CoV-2 infection may induce abnormalities in innate and adaptive immunity including monocyte expansion, T-cell exhaustion, and prolonged cytokine release, which may cause neuroinflammatory responses and microglia activation, white matter abnormalities, and microvascular changes. Additionally, microvascular clot formation can occlude capillaries and endotheliopathy, due to SARS-CoV-2 protease activity and complement activation, can contribute to hypoxic neuronal injury and blood–brain barrier dysfunction, respectively. Current therapeutics target pathological mechanisms by employing antivirals, decreasing inflammation, and promoting olfactory epithelium regeneration. Thus, from laboratory evidence and clinical trials in the literature, we sought to synthesize the pathophysiological pathways underlying neurological symptoms of long COVID and potential therapeutics.

Purpose of ReviewTo discuss the neurological complications and pathophysiology of organ damage following malaria infection.Recent FindingsThe principal advancement made in malaria research has been a better understanding of the pathogenesis of cerebral malaria (CM), the most dreaded neurological complication generally caused by Plasmodium falciparum infection. However, no definitive treatment has yet been evolved other than the use of antimalarial drugs and supportive care. The development of severe cerebral edema in CM results from two distinct pathophysiologic mechanisms. First, the development of “sticky” red blood cells (RBCs) leads to cytoadherence, where red blood cells (RBCs) get stuck to the endothelial walls and between themselves, resulting in clogging of the brain microvasculature with resultant hypoxemia and cerebral edema. In addition, the P. falciparum-infected erythrocyte membrane protein 1 (PfEMP1) molecules protrude from the raised knob structures on the RBCs walls and are in themselves made of a combination of human and parasite proteins in a tight complex. Antibodies to surfins, rifins, and stevors from the parasite are also located in the RBC membrane. On the human microvascular side, a range of molecules involved in host–parasite interactions, including CD36 and intracellular adhesion molecule 1, is activated during interaction with other molecules such as endothelial protein C receptor and thrombospondin. As a result, an inflammatory response occurs with the dysregulated release of cytokines (TNF, interleukins 1 and 10) which damage the blood–brain barrier (BBB), causing plasma leakage and brain edema. This second mechanism of CNS injury often involves multiple organs in adult patients in endemic areas but remains localized only to the central nervous system (CNS) among African children.SummaryNeurological sequelae may follow both P. falciparum and P. vivax infections. The major brain pathology of CM is brain edema with diffuse brain swelling resulting from the combined effects of reduced perfusion and hypoxemia of cerebral neurons due to blockage of the microvasculature by parasitized RBCs as well as the neurotoxic effect of released cytokines from a hyper-acute immune host reaction. A plethora of additional neurological manifestations have been associated with malaria, including posterior reversible encephalopathy syndrome (PRES), reversible cerebral vasoconstriction syndrome (RCVS), malarial retinopathy, post-malarial neurological syndrome (PMNS), acute disseminated encephalomyelitis (ADEM), Guillain-Barré syndrome (GBS), and cerebellar ataxia. Lastly, the impact of the COVID-19 pandemic on worldwide malaria control programs and the possible threat from co-infections is briefly discussed.

Background Influenza is a common contagious respiratory virus that primarily causes respiratory tract infections. Neurological complications associated with influenza have also been reported, mainly in pediatric populations, and may be fatal. Methods A descriptive study evaluated pediatric patients who were diagnosed with severe influenza‐associated neurological complications at the Tropical Pediatrics Center—Vietnam National Children's Hospital from October 2022 to February 2024. Results In this study involving 20 patients, 80% of children were under 5 years old; 70% of patients had a history of good health. All patients had not received an influenza vaccination within 12 months. The median time from onset to neurological symptoms was 1 day. The most common neurological complication was encephalitis (16/20 patients) with symptoms included altered consciousness and seizures. Most patients had elevated levels of ALT (60%), AST (90%), LDH (94%), and ferritin (69%) in serum. The imaging of brain damage on MRI and CT scans varied in patterns and locations. There was no difference in the timing of methylprednisolone treatment within and after 48 h. The mortality rate was 20%, with 45% of patients experiencing severe sequelae. Conclusions IANCs are severe with damage to both white matter and central gray matter and can occur in healthy children, emphasizing the importance of vaccination to reduce the risk.

Background Influenza is a known respiratory and potential neurotropic virus. This study aimed to determine the prevalence and outcomes of influenza‐related neurological complications among hospitalized children. Methods All medical records of hospitalized children aged <18 years old diagnosed with influenza at a tertiary care hospital in Bangkok were retrospectively reviewed. Influenza infection was confirmed by rapid antigen or reverse transcription polymerase chain reaction tests. Neurological characteristics and clinical outcomes were analyzed using the Pediatric Cerebral Performance Category Scale. Results From 2013 to 2018, 397 hospitalized children with a median age of 3.7 years (interquartile range [IQR]: 1.6–6.9) were included. The prevalence of neurological complications, including seizure or acute encephalopathy, was 16.9% (95% confidence interval [CI]: 13.3–20.9). Influenza A and B were identified in 73.1% and 26.9% of the patients, respectively. Among 39 (58.2%) acute symptomatic seizure cases, 25 (37.3%) children had simple febrile seizures, 7 (10.4%) had repetitive seizures, and 7 (10.4%) had provoked seizures with pre‐existing epilepsy. For 28 (41.8%) encephalopathy cases, the clinical courses were benign in 20 (29.9%) cases and severe in 8 (11.9%) cases. Ten (14.9%) children needed intensive care monitoring, and 62 (93.5%) fully recovered to their baselines at hospital discharge. Predisposing factors to the neurological complications included a history of febrile seizure (adjusted odds ratio [aOR]: 20.3; 95% CI: 6.6–63.0), pre‐existing epilepsy (aOR: 3.6; 95% CI: 1.3–10.2), and a history of other neurological disorders (aOR: 3.5; 95% CI: 1.2–10.2). Conclusions One fifth of hospitalized children with influenza had neurological complications with a favorable outcome. Children with pre‐existing neurological conditions were at higher risk for developing neurological complications.

Guillain-Barré syndrome (GBS) is a peripheral nervous system disease caused by an immune-mediated inflammatory mechanism, usually triggered by a previous infectious process or vaccine; its typical presentation is a rapid and progressive bilateral limb hyposthenia, associated with sensory deficits and reduction or absence of osteotendinous reflexes. However, also autonomic nervous system can be involved with heart rate fluctuations, blood pressure instability, pupillary dysfunction, and urinary retention. Since the beginning of COVID-19 pandemic, GBS has been reported among neurological complications of SARS-CoV-2 infection, although etiopathological mechanisms still have to be clearly defined. We report the case of a 79-year-old man with multiple comorbidities, including diabetes, who was affected by SARS-CoV-2 interstitial pneumonia and developed dysautonomic symptoms after 10 days of hospitalization. A neurological evaluation was performed, and GBS was considered as a possible cause of the clinical manifestations. This hypothesis was confirmed by electrophysiological study and further supported, ex-juvantibus , by the satisfactory response to immunoglobulin treatment. In our opinion, this case of pure dysautonomic presentation of GBS in a SARS-CoV-2 positive patient is relevant because it suggests to consider GBS upon SARS-CoV-2 infection even if the symptoms have uncommon characteristics (e.g., pure vegetative manifestations) and if there are confounding factors which could lead to a misdiagnosis (e.g., old age, SARS-CoV-2 infection consequences and diabetes).

Background Delirium is one of the most common neurological complications after cardiac surgery. The purpose of our study was to assess the relationship between perioperative blood pressure variability (BPV) and postoperative delirium (POD) in the patients undergoing cardiac surgery. Methods Adult patients received cardiac surgery and stayed in Cardiovascular Intensive Care Unit (ICU) for more than 24 h after surgery during the study period between June 2019 and December 2022 were included in this study. Baseline characteristics, perioperative hemodynamic variables and postoperative laboratory results of the cardiac patients were collected and analyzed. Perioperative BPV was quantified by calculating the standard deviation (SD) and average real variability (ARV) of blood pressure. Assessment of delirium was based on the mental status of the patients and CAM-positive. The relationship between perioperative BPV and POD was analyzed by LASSO and logistic regression using R (R package, 4.3.2). Results The incidence of POD was 15.0% (324/2164) in the patients receiving cardiac surgery, and the average day for POD occurred at day 3 after surgery. Patients with POD had statistically lower levels of intraoperative mean blood pressure ( P  = 0.015) and blood pressure ARV ( P  < 0.001) as well as mean blood pressure at 24 h postoperatively ( P  = 0.003) when compared to those without. Whereas, ARV for systolic blood pressure (8.64 vs. 7.91 mmHg, P  < 0.001), diastolic blood pressure (4.00 vs. 3.77 mmHg, P  = 0.014) and mean blood pressure (5.23 vs. 4.94 mmHg, P  = 0.001) at 24 h postoperatively was significantly higher in the patients with POD than those without. LASSO regression and further logistic regression revealed that intraoperative blood pressure ARV (OR:0.92, P  < 0.001), mean central venous pressure (OR:1.05, P  = 0.048) and ARV of systolic blood pressure (OR:1.17, P  = 0.002) at 24 h postoperatively were independent risk factors for POD. Conclusions Perioperative ARV, especially postoperative high ARV exposure, was associated with POD in the patients receiving cardiac surgery. Maintaining a relatively stable blood pressure after cardiac surgery might be beneficial to avoid POD in those patients.

Purpose Neurological complications are among the most frightening risks in spine surgery. Intraoperative neuromonitoring (IONM) aims to quickly detect changes in the patient’s neurology, allowing for actions that can reverse neurological deficits before they become irreversible. A checklist was proposed in 2014 in response to changes in neuromonitoring for correcting deformities in spine surgery; however, it was designed specifically for procedures on stable spines, which are different from oncological and degenerative spine surgery. The goal of this project is to provide a checklist for oncological and degenerative spine surgery to improve the quality of surgical treatment and patient’s safety. Methods To revise and implement the existing checklist a study group of 27 people was created, including: 8 surgeons from five hospitals, 7 anesthetists, 7 IONM operators and 5 operating room nurses. To achieve consensus the Delphi method was used with 2 surveys and 3 consensus rounds, which occurred from February 2022 to February 2023, when the new checklist was approved. Results Initial survey and Round I : 22 items of the existing checklist considered appropriate. Thirty new items proposed, focusing particularly on unstable spine procedures. Second survey and Round II : 28 items considered suitable; 24 items deemed as unnecessary. Round III and final survey : discussion about the participants’ experience with the new checklist. One item was added: “Evaluate D-Wave response (if applicable)” and the final version of the checklist was approved. Conclusion A new checklist based on IONM changes during oncological and degenerative spine surgery was created. Its implementation can potentially improve surgical results and patient’s safety in spine surgery.

Neurological manifestations and complications in coronavirus disease-2019 (COVID-19) patients are frequent. Prior studies suggested a possible association between neurological complications and fatal outcome, as well as the existence of potential modifiable risk factors associated to their occurrence. Therefore, more information is needed regarding the incidence and type of neurological complications, risk factors, and associated outcomes in COVID-19. This is a pre-planned secondary analysis of the international multicenter observational study of the COVID-19 Critical Care Consortium (which collected data both retrospectively and prospectively from the beginning of COVID-19 pandemic) with the aim to describe neurological complications in critically ill COVID-19 patients and to assess the associated risk factors, and outcomes. Adult patients with confirmed COVID-19, admitted to Intensive Care Unit (ICU) will be considered for this analysis. Data collected in the COVID-19 Critical Care Consortium study includes patients' pre-admission characteristics, comorbidities, severity status, and type and severity of neurological complications. In-hospital mortality and neurological outcome were collected at discharge from ICU, and at 28-days. The COVID-19 Critical Care Consortium main study and its amendments have been approved by the Regional Ethics Committee of participating sites. No further approval is required for this secondary analysis. ACTRN12620000421932.

Purpose Diagnostic cerebral digital subtraction angiography (DSA) is an invasive examination that involves catheterization of the major supra-aortic arterial trunks and evaluation of intracranial vessels for diagnostic purposes. Although considered the gold standard method for investigating cerebrovascular diseases, DSA carries measurable and potentially serious complication rates. This report describes the frequency of neurological and non-neurological complications of DSA performed in five hospitals in the state of São Paulo, Brazil, and analyzes them in different disease subgroups. It has a special focus on thromboembolic cerebral complications. Methods We retrospectively reviewed clinical records of all adult patients who underwent DSAs between January 2019 and December 2022. Demographic variables, DSA reports, CT/MRI reports, and clinical follow-up notes were reviewed. Results Twenty-four patients experienced some type of complication among 2,457 diagnostic DSAs (0.97%). Thromboembolic complications were recorded in 9 patients (0.36%), and access site hematomas larger than 5 cm were registered in six patients (0.24%). There was a statistical trend for thromboembolic complications in patients with cervical and/or intracranial atherosclerosis (p = 0.07), but age was not associated with them (p = 0.93). Patients who received heparin had lower rates of embolic complications than those who did not receive it, but there was no statistically significant difference (p = 0.17). Intravenous administration of heparin showed a trend toward significance with groin hematoma (p = 0.10). Conclusion Diagnostic catheter DSAs have low complication rates.