Abstract
BackgroundMild traumatic brain injury (mTBI) has a higher prevalence (more than 50%) of developing chronic posttraumatic headache (CPTH) compared with moderate or severe TBI. However, the underlying neural mechanism for CPTH remains unclear. This study aimed to investigate the inflammation level and cortical volume changes in patients with acute PTH (APTH) and further examine their potential in identifying patients who finally developed CPTH at follow-up.MethodsSeventy-seven mTBI patients initially underwent neuropsychological measurements, 9-plex panel of serum cytokines and MRI scans within 7 days post-injury (T-1) and 54 (70.1%) of patients completed the same protocol at a 3-month follow-up (T-2). Forty-two matched healthy controls completed the same protocol at T-1 once.ResultsAt baseline, mTBI patients with APTH presented significantly increased GM volume mainly in the right dorsal anterior cingulate cortex (dACC) and dorsal posterior cingulate cortex (dPCC), of which the dPCC volume can predict much worse impact of headache on patients’ lives by HIT-6 (β = 0.389, P = 0.007) in acute stage. Serum levels of C-C motif chemokine ligand 2 (CCL2) were also elevated in these patients, and its effect on the impact of headache on quality of life was partially mediated by the dPCC volume (mean [SE] indirect effect, 0.088 [0.0462], 95% CI, 0.01–0.164). Longitudinal analysis showed that the dACC and dPCC volumes as well as CCL2 levels had persistently increased in patients developing CPTH 3 months postinjury.ConclusionThe findings suggested that structural remodelling of DMN brain regions were involved in the progression from acute to chronic PTH following mTBI, which also mediated the effect of inflammation processes on pain modulation.Trial registrationClinicalTrial.gov ID: NCT02868684; registered 16 August 2016.
Highlights
Traumatic brain injury (TBI) is a major global public health problem that affects 50 million people each year, and it is estimated that about half the world’s population will have one or more TBIs over their lifetime [1, 2]
Our recent study found that acute posttraumatic headache (PTH) (APTH) following Mild traumatic brain injury (mTBI) led to the disrupted functional connectivity between the periaqueductal grey (PAG) and default mode network (DMN)
In the acute phase (2.39 ± 1.47 days, range: 0–6 days), a seventy-seven patients were divided into two subgroups: 1) mTBI + APTH, 60 individuals with APTH after mTBI, 2) mTBI – APTH, 17 individuals with mTBI without headache
Summary
Traumatic brain injury (TBI) is a major global public health problem that affects 50 million people each year, and it is estimated that about half the world’s population will have one or more TBIs over their lifetime [1, 2]. Mild TBI (mTBI) is identified as one of the most vulnerable risk to develop chronic PTH (CPTH) (prevalence rate: 72.7%–77.9%), compared with much server cases (moderate or severe TBI, prevalence rate: 29.3%–34.9%) [6]. Our recent study found that acute PTH (APTH) following mTBI led to the disrupted functional connectivity between the periaqueductal grey (PAG) and default mode network (DMN). This pain-related cognitive dysregulation may partially due to the over-attention on brain injury-related symptom. Mild traumatic brain injury (mTBI) has a higher prevalence (more than 50%) of developing chronic posttraumatic headache (CPTH) compared with moderate or severe TBI. The underlying neural mechanism for CPTH remains unclear. This study aimed to investigate the inflammation level and cortical volume changes in patients with acute PTH (APTH) and further examine their potential in identifying patients who developed CPTH at follow-up
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