Abstract
BackgroundPost-traumatic headache (PTH) is one of the most frequent symptoms following mild traumatic brain injury (mTBI). Neuroimaging studies implicate hypothalamic function connectivity (FC) disruption as an important factor in pain disorders. However, it is unknown whether there are alterations in the hypothalamus-based resting state FC within PTH following mTBI at the acute stage and its relationship with headache symptom measurement.MethodsForty-four mTBI patients with PTH, 27 mTBI patients without PTH and 43 healthy controls who were well matched for age, gender, and years of education were enrolled in this study. All participants underwent resting-state functional magnetic resonance imaging (fMRI) scanning as well as headache symptom measurement and cognitive assessment. Hypothalamic resting state networks were characterized by using a standard seed-based whole-brain correlation method. The bilateral hypothalamic FC was compared among the three groups. Furthermore, the correlations between hypothalamic resting state networks and headache frequency, headache intensity and MoCA scores was investigated in mTBI patients with PTH using Pearson rank correlation.ResultsCompared with mTBI patients without PTH, mTBI patients with PTH at the acute stage presented significantly decreased left hypothalamus-based FC with the right middle frontal gyrus (MFG) and right medial superior frontal gyrus (mSFG), and significantly decreased right hypothalamus-based FC with the right MFG. Decreased FC of the right MFG was significantly positively associated with headache frequency and headache intensity (r = 0.339, p = 0.024; r = 0.408, p = 0.006, respectively). Decreased FC of the right mSFG was significantly positively associated with headache frequency and headache intensity (r = 0.740, p < 0.0001; r = 0.655, p < 0.0001, respectively).ConclusionOur data provided evidence of disrupted hypothalamic FC in patients with acute mTBI with PTH, while abnormal FC significantly correlated with headache symptom measurement. Taken together, these changes may play an essential role in the neuropathological mechanism of mTBI patients with PTH.
Highlights
Post-traumatic headache (PTH) is one of the most frequent symptoms following mild traumatic brain injury
Whole patients with mild traumatic brain injury (mTBI) vs healthy controls Compared with healthy controls, all whole patients with mTBI demonstrated significantly reduced function connectivity (FC) between the left hypothalamus and left fusiform gyrus, left Rolandic operculum, and right middle frontal gyrus (MFG) as well as reduced FC between the left hypothalamus and right medial superior frontal gyrus (Fig. 1, Table 2)
All whole patients with mTBI exhibited significantly decreased FC between the right hypothalamus and right MFG and right postcentral gyrus as well as decreased FC between the right hypothalamus and left mTBI patients with PTH vs healthy controls; mTBI patients without PTH Compared with mTBI patients without PTH, mTBI patients with PTH showed a significant FC reduction between the left hypothalamus and right medial superior frontal gyrus (mSFG) and right MFG as well as decreased FC between the right hypothalamus and right MFG (Fig. 2, Table 3)
Summary
Post-traumatic headache (PTH) is one of the most frequent symptoms following mild traumatic brain injury (mTBI). Neuroimaging studies implicate hypothalamic function connectivity (FC) disruption as an important factor in pain disorders. It is unknown whether there are alterations in the hypothalamus-based resting state FC within PTH following mTBI at the acute stage and its relationship with headache symptom measurement. Following mTBI, patients frequently suffer lifelong disabilities, including post-traumatic headache (PTH), depression, insomnia, dizziness and hypomnesia. Persistent post traumatic injury (PPTH) may sometimes be underestimated because many patients never go to the hospital to obtain headache medication, which leads to long-lasting disability and imposes major burdens on society. The underlying pathophysiologic mechanisms of PTH following mTBI are poorly understood
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