Background: Impaired cerebrovascular reactivity following moderate/severe traumatic brain injury (TBI) has emerged as a key potential driver of morbidity and mortality. However, the major contributions to the literature so far have been solely focused on single point measures of long-term outcome. Therefore, it remains unknown whether cerebrovascular reactivity impairment, during the acute phase of TBI, is associated with failure to improve in outcome across time.
Methods: Cerebrovascular reactivity was measured using three intracranial pressure-based surrogate metrics. For each patient, % time spent above various literature-defined thresholds was calculated. Patients were dichotomized based on outcome transition into Improved vs Not Improved between 1 and 3 months, 3 and 6 months, and 1 and 6 months, based on the Glasgow Outcome Scale-Extended (GOSE). Univariate and multivariable logistic regression analyses were performed, adjusting for the International Mission for Prognosis and Analysis of Clinical Trials (IMPACT) variables.
Results: Seventy-eight patients from the Winnipeg Acute TBI Database were included in this study. On univariate logistic regression analysis, higher % time with cerebrovascular reactivity metrics above clinically defined thresholds was associated with a lack of clinical improvement between 1 and 3 months and 1 and 6 months post injury (p < 0.05). These relationships held true on multivariable logistic regression analysis.
Conclusion: Our study demonstrates that impaired cerebrovascular reactivity, during the acute phase of TBI, is associated with failure to improve clinically over time. These preliminary findings highlight the significance that cerebrovascular reactivity monitoring carries in outcome recovery association in moderate/severe TBI.
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http://dx.doi.org/10.1007/s00701-022-05366-9 | DOI Listing |
J Biophotonics
January 2025
Britton Chance Center for Biomedical Photonics-MoE Key Laboratory for Biomedical Photonics, Huazhong University of Science and Technology, Wuhan, China.
Diabetes mellitus (DM), a chronic metabolic disorder that adversely affects the blood-brain barrier (BBB) and microglial function in the central nervous system (CNS), contributing to neuronal damage and neurodegenerative diseases. However, the underlying molecular mechanisms linking diabetes to BBB dysfunction and microglial dysregulation remain poorly understood. Here, we assessed the impacts of diabetes on BBB and microglial reactivity and investigated its mechanisms.
View Article and Find Full Text PDFJ Neuropathol Exp Neurol
January 2025
Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, United States.
In modern war theaters, exposures to blast overpressures are one of the most common causes of brain injury. These pervasive events result in acute and chronic cerebrovascular degenerative processes. Using a rat model of blast-induced mild traumatic brain injury, we identified intramural periarterial hematomas as early primary acute lesions induced by blast exposures.
View Article and Find Full Text PDFJ Ultrasound
January 2025
Clinical Unit of Neurology, Department of Medicine, Surgery and Health Sciences, University Hospital and Health Services of Trieste, ASUGI, University of Trieste, Strada di Fiume, 447, 34149, Trieste, Italy.
Introduction: Post-stroke cognitive impairment (PSCI) and dementia affect short- and long-term outcome after stroke and can persist even after recover from a physical handicap. The process underlying PSCI is not yet fully understood. Transcranial Doppler ultrasound (TCD) is a feasible method to investigate cerebrovascular aging or dementia, through the pulsatility index (PI), the cerebrovascular reactivity (e.
View Article and Find Full Text PDFJ Cereb Blood Flow Metab
January 2025
Neurovascular Research Laboratory, Faculty of Life Sciences and Education, University of South Wales, Pontypridd, UK.
To what extent sildenafil, a selective inhibitor of the type-5 phosphodiesterase modulates systemic redox status and cerebrovascular function during acute exposure to hypoxia remains unknown. To address this, 12 healthy males (aged 24 ± 3 y) participated in a randomized, placebo-controlled crossover study involving exposure to both normoxia and acute (60 min) hypoxia (Fi = 0.14), followed by oral administration of 50 mg sildenafil and placebo (double-blinded).
View Article and Find Full Text PDFNutrients
January 2025
Department of Obstetrics and Gynaecology, Semmelweis University, Üllői Street 78/a, 1082 Budapest, Hungary.
Background/objectives: Both hyperandrogenism (HA) and vitamin D deficiency (VDD) can separately lead to impaired vascular reactivity and ovulatory dysfunction in fertile females. The aim was to examine the early interactions of these states in a rat model of PCOS.
Methods: Four-week-old adolescent female rats were divided into four groups: vitamin D (VD)-supplemented ( = 12); VD-supplemented and testosterone-treated ( = 12); VDD- ( = 11) and VDD-and-testosterone-treated ( = 11).
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