Aneurysmal subarachnoid hemorrhage is an acute cerebrovascular disease with high disability and mortality. We intended to explore the association between levels of erythrocytes in cerebrospinal fluid at different times of hemorrhage and the outcome of patients. One retrospective study including 216 patients with aneurysmal subarachnoid hemorrhage undergoing surgeries in the First Affiliated Hospital of Yangtze University from January 2020 to July 2023 was carried. The univariable analysis and multivariable logistic regression analysis were used for factors associated with poor outcome. The level of erythrocytes in cerebrospinal fluid on the 1st postoperative day in patients with poor outcome was 311 × 103/µL, significantly higher than patients with good outcome (108 × 103/µL), P < .001. The level of erythrocytes in cerebrospinal fluid on 7th postoperative day was 86.5 × 103/µL, also significantly higher than patients with good outcome (26.0 × 103/µL). The multivariable logistic regression analysis results showed that erythrocytes in cerebrospinal fluid on the 1st postoperative day (≥177 × 103/µL) and on the 7th postoperative day (≥53.5 × 103/µL) were possibly associated with poor outcome in aneurysmal subarachnoid hemorrhage patients. Treatment with tranexamic acid and continuous lumbar drainage did not result in a decrease of erythrocytes in cerebrospinal fluid. Higher erythrocytes in cerebrospinal fluid on the 1st and 7th postoperative days were associated with poor outcome in aneurysmal subarachnoid hemorrhage patients.
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http://dx.doi.org/10.1097/MD.0000000000040027 | DOI Listing |
Zhonghua Er Ke Za Zhi
January 2025
Department of Rheumatology and Immunology, Children's Hospital Affiliated to Capital Institute of Pediatrics, Beijing100020, China.
J Clin Med
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Department of Neurology, Christian-Doppler University Hospital, Paracelsus Medical University, Centre for Cognitive Neuroscience, Ignaz Harrer Str. 79, 5020 Salzburg, Austria.
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Department of Microbiology, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India.
Neurobiol Dis
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Department of Medical Biosciences, Clinical Chemistry, Umeå University, SE-901 85 Umeå, Sweden. Electronic address:
Mutations in superoxide dismutase-1 (SOD1) are a cause of hereditary amyotrophic lateral sclerosis (ALS) through a gain-of-function mechanism involving unfolded mutant SOD1. Intrathecal gene therapy using the antisense-oligo-nucleotide drug tofersen to reduce SOD1 expression delays disease progression and has recently been approved in the United States and the European Union. However, the discovery of children homozygous for inactivating SOD1 mutations developing the SOD1 Deficiency Syndrome (ISODDES) with injury to the motor system suggests that a too low SOD1 antioxidant activity may be deleterious in humans.
View Article and Find Full Text PDFPediatr Rheumatol Online J
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Division of Rheumatology, Department of Pediatrics, Faculty of Medicine Vajira Hospital, Navamindradhiraj University, Bangkok, 10300, Thailand.
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