Bedside parameters may help predict chronic post-traumatic head and neck pain

1. Key predictors of chronic pain following motor vehicle collisions include elevated levels of acute post-traumatic stress symptoms (PTSS), high pain catastrophizing scores, lower pressure pain thresholds on QST, specific genetic markers related to catechol-O-methyltransferase (COMT) and adrenergic receptor function, as well as elevated IL-6. 

Evidence Rating Level: 2 (Good)

Study Rundown: Chronic head and neck pain following motor vehicle collisions (MVC) often emerges in patients who initially only presented with minor injuries. The cause of this chronic pain has been hypothesized to be due to either psychological or neurobiological factors or a multifactorial phenomenon encompassing both causes. This prospective cohort study aimed to identify factors contributing to the development of chronic pain in patients aged 18-65 years old who were involved in MVCs and sustained minor to moderate injuries. They evaluated these patients for 1 year using qualitative questionnaires (post-traumatic stress symptoms (PTSS), pain catastrophizing scores, quantitative sensory testing), genetic testing (catechol-O-methyltransferase (COMT) and adrenergic receptor), and inflammatory markers (e.g., IL-6). They found both psychological and neurobiological factors were independently contributing to the development of chronic pain post-MVC. This highlights the importance of multimodal analysis for predicting and managing chronic pain in patients following traumatic injuries. The findings advocate for early multidisciplinary interventions—including psychological counseling and pharmacologic strategies aimed at reducing central sensitization or inflammation.  

Click to read the study in PAIN

Relevant Reading: Traumatic brain injury: progress and challenges in prevention, clinical care, and research 

In-Depth [prospective cohort study]: This prospective cohort study aimed to investigate early predictors of chronic head and neck pain six months post-MVC and to evaluate the role of psychological and physiological factors, using a biopsychosocial framework. A total of 948 patients presenting to emergency departments within 24 hours of an MVC were enrolled. Inclusion criteria were focused on individuals aged 18 to 65 with no major injuries, allowing for the evaluation of those with typical “whiplash” injuries. Participants were given structured assessments including psychological questionnaires, quantitative sensory testing (QST), genotyping, and blood sampling for inflammatory markers. Pain outcomes were assessed at 6 weeks, 6 months, and 1 year post-MVC. The primary outcome was defined as moderate to severe head and neck pain at 6 months.

Out of the initial cohort, 873 participants completed the 6-month follow-up. Approximately 25% reported moderate to severe chronic head and neck pain at 6 months. Key predictors of chronic pain included elevated levels of acute post-traumatic stress symptoms (PTSS), high pain catastrophizing scores, lower pressure pain thresholds on QST, and specific genetic markers related to catechol-O-methyltransferase (COMT) and adrenergic receptor function. Elevated levels of pro-inflammatory cytokines, particularly interleukin-6 (IL-6), were also predictive of persistent pain.

As psychological factors such as acute PTSS and pain catastrophizing were shown to be strong, independent predictors of chronic post-traumatic pain, this study highlights the presence of a multifactorial model for the development of chronic post-traumatic pain. This shows the importance of early psychological assessment and intervention. Acute stress responses may sensitize central pain pathways, contributing to long-term pain experiences even in the absence of ongoing tissue damage.

In parallel, neurobiological factors played a significant role. QST revealed that individuals with heightened central sensitization responses (e.g., lower pressure pain thresholds) were at higher risk of chronic pain, supporting the central sensitization theory. Additionally, the study identified a correlation between COMT haplotypes and pain outcomes. The COMT gene regulates catecholamine breakdown, and variations associated with decreased enzymatic activity may lead to heightened pain sensitivity and reduced capacity for stress modulation. Similarly, polymorphisms in the adrenergic receptor gene were associated with altered sympathetic nervous system reactivity and increased risk of persistent pain. Additionally, elevated IL-6 in the acute phase was an independent predictor of chronic pain, suggesting that early systemic inflammation may contribute to prolonged pain states through sustained nociceptive signaling or modulation of central nervous system processing.

The key strength of this study its multifactorial approach of examining biological, psychological, and sensory factors concurrently. This model allows for the identification of individuals at high risk for chronic pain using a combination of early biomarkers, potentially paving the way for personalized prevention strategies.

Image: PD

©2025 2 Minute Medicine, Inc. All rights reserved. No works may be reproduced without expressed written consent from 2 Minute Medicine, Inc. Inquire about licensing here. No article should be construed as medical advice and is not intended as such by the authors or by 2 Minute Medicine, Inc.