Recent research suggests that mild traumatic brain injury (TBI) may exert deleterious effects on endogenous pain modulatory function, potentially underlying the elevated risk for persistent headaches following injury. Accumulating research also shows race differences in clinical and experimental pain, with African Americans (AA) generally reporting more severe pain, worse pain modulation, and greater pain sensitivity compared with Caucasians. However, race differences in pain-related outcomes following mild TBI have rarely been studied. The purpose of this study was to explore race differences in endogenous pain modulation, pain sensitivity, headache pain, and psychological factors among AA and Caucasian individuals with mild TBI in the first month following injury compared with healthy controls and across time. Patients with mild TBI were recruited from local emergency department trauma centers. Sixty-three participants with mild TBI (AAs: = 23, Caucasians: = 40) enrolled in this study and completed study sessions at 1-2 weeks and 1-month post-injury. Forty-one mild-TBI-free control participants (AAs: = 11, Caucasians: = 30), matched on age and sex, completed one study session. Assessments included a Headache Survey, Pain Catastrophizing Scale, Center for Epidemiological Studies-Depression Scale (CES-D), and quantitative sensory testing (QST) to measure endogenous pain modulatory function. QST included conditioned pain modulation (CPM) to measure endogenous pain inhibitory function and temporal summation (TS) of pain and pressure pain thresholds (PPTs) of the head to measure pain sensitization and sensitivity. Two-way analysis of variance (ANOVA) was used to determine whether the outcome measures differed as a function of race, mild TBI, and time. Mediation analysis was used to explore potential mediators for the race differences in headache pain intensity. The results showed that AA participants with mild TBI reported significantly greater headache pain and pain catastrophizing and exhibited higher pain sensitivity and worse pain modulation on QST compared with Caucasian participants with mild TBI. These same race differences were not observed among the healthy TBI-free control sample. The mediation analyses showed complete mediation for the relation between race and headache pain intensity by pain catastrophizing at 1-2 weeks and 1-month post-injury. Overall, the results of this study suggest that AAs compared with Caucasians are characterized by psychological and pain modulatory profiles following mild TBI that could increase the risk for the development of intense and persistent headaches following injury.
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http://dx.doi.org/10.1089/neu.2022.0415 | DOI Listing |
J West Afr Coll Surg
August 2024
Neurosurgery Unit, Department of Surgery, Korle-Bu Teaching Hospital, Accra, Ghana.
Background: Traumatic brain injury (TBI) is one of the common causes of long-term disabilities, with about 10 million deaths annually.
Objectives: Our aim is to compare the severity and outcomes of TBI between motorcycle and car accident victims.
Materials And Methods: A prospective cohort study focusing on TBI patients.
Exp Neurol
December 2024
Department of Molecular Biology and Genetics, Faculty of Science, Istanbul University, Istanbul, Turkiye. Electronic address:
Growing evidence reveals that microglia activation and neuroinflammatory responses trigger cell loss in the brain. Histamine is a critical neurotransmitter and promotes inflammatory responses; thus, the histaminergic system is a potential target for treating neurodegenerative processes. JNJ-7777120, a histamine H4 receptor (HR) antagonist, has been shown to alleviate inflammation, brain damage, and behavioral deficits effectively, but there is no report on its role in brain trauma.
View Article and Find Full Text PDFEClinicalMedicine
September 2024
Department of Medicine, University of Cambridge, Cambridge, UK.
Background: Even patients with normal computed tomography (CT) head imaging may experience persistent symptoms for months to years after mild traumatic brain injury (mTBI). There is currently no good way to predict recovery and triage patients who may benefit from early follow-up and targeted intervention. We aimed to assess if existing prognostic models can be improved by serum biomarkers or diffusion tensor imaging metrics (DTI) from MRI, and if serum biomarkers can identify patients for DTI.
View Article and Find Full Text PDFEClinicalMedicine
December 2024
Division of Anaesthesia, University of Cambridge, Addenbrooke's Hospital, Cambridge, United Kingdom.
Background: Post-traumatic stress disorder (PTSD) and depression are common after mild traumatic brain injury (mTBI), but their biological drivers are uncertain. We therefore explored whether polygenic risk scores (PRS) derived for PTSD and major depressive disorder (MDD) are associated with the development of cognate TBI-related phenotypes.
Methods: Meta-analyses were conducted using data from two multicenter, prospective observational cohort studies of patients with mTBI: the CENTER-TBI study (ClinicalTrials.
Am J Emerg Med
December 2024
Warfighter Readiness, Performance, and Brain Health Project Management Office (WRPBH PMO), US Army Medical Materiel Development Activity (USAMMDA), 1430 Veterans Drive, Fort Detrick, MD 21702, USA.
Background: A glial fibrillary acidic protein (GFAP) and ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1) blood biomarker panel can reliably eliminate the need to perform a head computed tomography (CT) scan in selected patients with traumatic brain injury (TBI). Currently, this FDA cleared panel can be run both on a core laboratory platform or a hand-held single-sample point of care platform. This study examined test characteristics of the panel as analyzed on a core lab-based fast high-throughput platform.
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