The following is a summary of “Association of Biomarkers of Neuronal Injury and Inflammation With Insomnia Trajectories After Traumatic Brain Injury: A TRACK-TBI Study,” published in the March 2024 issue of Neurology by Werner al.

Traumatic brain injury (TBI) frequently disrupts sleep, with insomnia impacting around a third of patients and hindering recovery.

Researchers conducted a retrospective study exploring whether higher levels of inflammatory markers in patients with TBI blood plasma at injury corresponded with greater sleep problems over the following year.

They enrolled participants from 18 level-1 trauma centers in the Transforming Research and Clinical Knowledge in Traumatic Brain Injury study(February 26, 2014, and August 8, 2018). GFAP, hs-CRP, S100b, NSE, and UCH-L1 plasma levels were obtained on days 1 (D1) and 14 (D14) post-TBI. The insomnia severity index was measured at 2 weeks, 3, 6, and 12 months post-injury. Participants’ insomnia patterns were identified using a model. Associations between biomarkers and these patterns were analyzed, adjusting for various factors.

The results showed that 2,022 patients with TBI were examined. The elevated D1 hsCRP levels were linked to persistent insomnia. For severe insomnia, the OR was 1.33 (1.11, 1.59), and for mild insomnia, it was 1.10 (1.02, 1.19) (P=0.002 and P=0.011, respectively). Likewise, increased D14 hsCRP levels were associated with persistent insomnia, showing an OR of 1.27 (1.02, 1.59) for severe insomnia (P=0.03). Interestingly, D1 GFAP levels were lower in individuals with persistent severe insomnia (median [Q1, Q3]: 154 [19, 445] pg/mL) compared to those with resolving mild insomnia (491 [154, 1,423], P<0.001) and persistent mild insomnia (344 [79, 1,287], P<0.001). Furthermore, D14 GFAP levels were also lower in individuals with persistent (11.8 [6.4, 19.4], P=0.001) and resolving (13.9 [10.3, 20.7], P=0.011) severe insomnia compared to resolving mild insomnia (20.6 [12.4, 39.6]). Consequently, an increase in D1 GFAP levels was associated with a reduced likelihood of having persistent severe insomnia (OR = 0.76 [95% CI 0.63–0.92], P=0.004) and persistent mild insomnia (OR = 0.88 [0.81, 0.96], P=0.003) compared to mild resolving insomnia. No significant differences were observed with other biomarkers.

Investigators found that elevated hs-CRP and, unexpectedly, lower GFAP in blood plasma were linked to poorer sleep outcomes following TBI, highlighting the need for further research into these markers’ role in guiding insomnia treatment after TBI.

Source: neurology.org/doi/10.1212/WNL.0000000000209269