The role of calcitonin gene-related peptide and substance P in the pathogenesis of dialysis headache.

AIM: The present study aims to establish the role of serum CGRP and SP levels in the disease pathophysiology in patients with dialysis headache not accompanied by primary or secondary headaches, and also whether there is a correlation between these vasoactive peptides and the severity of headache. METHOD: This study was designed as prospective and multicenter. A total of 30 dialysis headache patients and 30 patients without headache as the control group in the Nephrology outpatient clinics which implement similar dialysis procedures were included in the study. Blood samples were taken from all the patients before hemodialysis, and post-hemodialysis samples were collected. CGRP and SP contents in serum samples were measured using the ELISA method with detection kits. RESULTS: A total of 60 patients were included in the study with 17 female and 13 male patients in the dialysis headache group and 18 female and 12 male patients in the control group, and there were no significant differences in sex and age between the groups. CGRP levels in the headache group were found to be significantly higher compared with the control group both before and after hemodialysis. Furthermore, pre-hemodialysis CGRP levels were significantly higher than post-hemodialysis CGRP levels in both the headache and control groups. Serum SP levels in the headache group were found to be higher compared with the control group both before and after hemodialysis, there was no significant difference between the groups. Even though SP levels in both groups decreased after hemodialysis, there was again no significant difference between the groups. No correlation was found between the patients' severity of headache and serum CGRP and SP levels. CONCLUSION: This study concludes that CGRP and SP, even though the latter is not statistically significant, play a role in the pathophysiology of the dialysis headache, and further studies with a larger and more specific patient population may reveal the relationship between the neuropeptides and dialysis headache more clearly.

The effect of sleep disorders on quality of life in patients with epilepsy: A multicenter study from Turkey.

OBJECTIVE: We aimed to investigate sleep disorders in patients with epilepsy (PWE) and to investigate the effects of sleep disorders on quality of life. METHODS: In our multicenter study conducted in Turkey, 1358 PWE were evaluated. The demographic and clinical data of the patients were recorded. The Insomnia Severity Index (ISI), Epworth Sleepiness Scale (ESS), Pittsburgh Sleep Quality Index (PSQI), Beck Depression Inventory (BDI), and Quality of Life in Epilepsy Inventory-10 (QOLIE-10) were administered. RESULTS: The mean age of 1358 patients was 35.92 ±â€¯14.11 (range, 18-89) years. Seven hundred fifty-one (55.30 %) were women. Some 12.7 % of the patients had insomnia (ISI > 14), 9.6 % had excessive daytime sleepiness (ESS > 10), 46.5 % had poor sleep quality (PSQI > 5), and 354 patients (26.1 %) had depressive symptoms (BDI > 16). The mean QOLIE-10 score was 22.82 ±â€¯8.14 (10-48). Resistant epilepsy was evaluated as the parameter with the highest risk affecting quality of life Adjusted odds ratio (AOR = 3.714; 95 % confidence interval (CI): [2.440-5.652] < 0.001)). ISI (AOR = 1.184; 95 % CI: [1.128-1.243]; p < 0.001), ESS (AOR = 1.081; 95 % CI: [1.034-1.130]; p < 0.001), PSQI (AOR = 0.928; 95 % CI: [0.867 - 0.994]; p = 0.034), BDI (AOR = 1.106; 95 % CI: [1.084-1.129]; p < 0.001), epilepsy duration (AOR = 1.023; 95 % CI: [1.004-1.041]; p = 0.014), were determined as factors affecting quality of life. SIGNIFICANCE: Sleep disorders are common in PWE and impair their quality of life. Quality of life can be improved by controlling the factors that may cause sleep disorders such as good seizure control, avoiding polypharmacy, and correcting the underlying mood disorders in patients with epilepsy.

Increased neuropil antibody prevalence in COVID-19 patients with acute ischemic stroke.

OBJECTIVES: COVID-19 infection is associated with an increased risk of acute ischemic stroke (AIS). Although the underlying mechanisms are largely unknown, autoimmunity has been implicated as a potential role player. METHODS: To investigate the presence and clinical impact of neuronal cell surface antibodies in COVID-19 associated AIS, patients with COVID-19 pneumonia and AIS (n = 30), COVID-19 pneumonia without AIS (n = 32) and AIS without COVID-19 infection (n = 27) were recruited. Serum anti-neuronal antibodies directed against well-characterized and novel cell surface antibodies were evaluated by cell-based assays and indirect immunohistochemistry, respectively. RESULTS: None of the recruited patients displayed well-characterized neuronal cell surface antibodies. Ten patients in the COVID-19 pneumonia with AIS group and three patients in the COVID-19 pneumonia without AIS group exhibited antibodies to neuropil of hippocampus and cerebellum. Neuropil-antibody positive patients showed trends towards milder clinical severity and reduced blood levels of inflammation factors. CONCLUSION: Our results confirm the presence of neuropil antibodies in patients with COVID-19 infection and identify a putative antibody-driven association between AIS and COVID-19. The antigenic targets and potential pathogenic action of these antibodies need to be further explored.

Increased serum citrullinated histone H3 levels in COVID-19 patients with acute ischemic stroke.

Background and purpose: Prevalence of acute ische-mic stroke (AIS) is increased in patients with coronavirus disease 2019 (COVID-19). A proposed hypothesis is increased virus-induced propensity to hypercoagulation resulting in arterial thrombosis. Our aim was to provide evidence regarding the involvement of neutrophil extracellular trap (NET) formation (NETosis) in COVID-19 related AIS. Methods: Twenty-six consecutively enrolled COVID-19+ pneumonia patients with AIS, 32 COVID-19+ pneumonia patients without AIS and 24 AIS patients without COVID-19 infection were included to the study. Clinical characteristics of recruited patients were collected. Serum levels of citrullinated histone H3 (H3Cit; a factor of NETosis), IL-8 and C5a (mediators associated with NETosis) were measured by ELISA (enzyme-linked immunosorbent assay). Results: H3Cit levels were significantly higher in COVID-19+ AIS patients, whereas all study groups showed comparable IL-8 and C5a levels. There were no significant differences among etiological subgroups of AIS patients with or without COVID-19. AIS patients with COVID-19 showed relatively increased white blood cell, lymphocyte, neutrophil, D-dimer, C-reactive protein and procalcitonin levels than control groups. H3Cit levels did not correlate with clinical/prognostic features and inflammation parameters. H3Cit and IL-8 levels were correlated in COVID-19 patients without stroke but not in COVID-19 positive or negative AIS patients. Conclusion: Increased levels of inflammation parameters and H3Cit in COVID-19 related AIS suggest that NETosis may cause susceptibility to arterial thrombosis. However, H3Cit levels do not correlate with clinical severity measures and inflammation parameters diminishing the prognostic biomarker value of NETosis factors. Moreover, the link between IL-8 and NETosis appears to be abolished in AIS.

COVID-19-associated Isolated Cortical Vein Thrombosis: Detection of SARS-CoV-2 in CSF.

COVID-19 has been associated with central nervous system manifestations; however, cerebral venous thrombosis is rarely reported. A 34-year-old woman was admitted to the hospital with headache and recurrent seizures; she was recently discharged after COVID-19 pneumonia. Cranial magnetic resonance imaging and magnetic resonance venography showed cortical vein thrombosis in the right frontal lobe. SARS-CoV-2 RNA was detected in cerebrospinal fluid analysis. The patient was anticoagulated and put on antiepileptics. The most probable mechanism underlying the venous thrombosis is COVID-19-associated hypercoagulability. However, the relation between the viral RNA in cerebrospinal fluid analysis and the thrombosis is controversial.

A Case of HaNDL with Low Cerebrospinal Fluid Level of Neurofilament Light Chain.

Diagnosis of the syndrome of headache and neurological deficits with cerebrospinal fluid (CSF) lymphocytosis (HaNDL) is based on clinical features, and no diagnostic biomarkers are available. We present a case presenting with characteristic features of HaNDL and an MRI lesion in the splenium of corpus callosum. CSF neurofilament light chain (NFL) levels were assessed in this patient together with 7 additional HaNDL patients, 18 multiple sclerosis (MS) patients, and 15 primary headache patients. Both HaNDL and primary headache patients showed significantly lower NFL levels than MS patients. Our results suggest that increased CSF levels of NFL and neuroaxonal loss are not characteristic features of HaNDL. Neurological disorders mimicking HaNDL often present with increased levels of NFL, and thus CSF measurement of NFL might be useful in differential diagnosis of HaNDL.