Post-TBI Insomnia Linked to White Matter and Connectivity Changes

Insomnia after traumatic brain injury (TBI) is linked to altered axonal integrity in cortico-subcortical white matter tracts, according to results published in Sleep Medicine Reviews.

Sleep disturbances, including difficulty falling asleep, poor sleep quality, and excessive daytime sleepiness, affect between 30% and 70% of individuals after TBI, with insomnia and hypersomnia being the most common sleep-wake disturbances reported in both acute and chronic phases. To better understand the neurological basis of these problems, researchers at Johns Hopkins University School of Medicine reviewed 21 studies published through 2023. These studies examined structural and functional neuroimaging in 3176 patients with TBI (mean age, 39.6 years; 66% men) and 396 controls (mean age, 42.9 years; 72.2% men). Neuroimaging occurred on average 41.4 months after injury.

Computed tomography (CT) studies showed mixed results. Some found that intracranial hemorrhage was associated with longer sleep duration and fewer insomnia symptoms. However, most acute intracranial abnormalities were not reliable predictors of self-reported insomnia, as 4 of 5 CT studies found no significant association.

The results of our review identified several distinct neuroimaging correlates of post-TBI sleep disturbances, with important implications for future research.

Magnetic resonance imaging (MRI) studies were more consistent. Across diffusion tensor imaging studies, all 6 that assessed fractional anisotropy (FA) found that lower FA, a measure of reduced axonal integrity, was associated with greater self-reported sleep disturbance. Lower FA in projection and association tracts correlated with higher Pittsburgh Sleep Quality Index (PSQI) scores and increased daytime sleepiness.

Resting-state functional connectivity was also related to sleep outcomes. In 3 studies, weaker connectivity between the left parahippocampal gyrus and regions including the caudate, cerebellum, frontal gyri, and precuneus was associated with poorer sleep quality. Stronger connectivity in cognitive control and attention networks was linked to less daytime sleepiness.

Other neuroimaging findings included reduced hippocampal and rostral anterior cingulate blood flow in patients with greater sleep impairment. Quantitative electroencephalography studies (n=3) showed decreased delta and increased beta spectral power during nonrapid eye movement and rapid eye movement sleep, primarily within 6 months post-injury, though sample sizes were small. One randomized trial of 26 patients with mild-to-moderate TBI found that right prefrontal repetitive transcranial magnetic stimulation improved self-reported sleep disturbance, reducing PSQI scores by an average of 3.5 points compared with sham stimulation.

Study limitations include heterogeneity in TBI severity and small sample sizes.

The study authors concluded, “The results of our review identified several distinct neuroimaging correlates of post-TBI sleep disturbances, with important implications for future research.”