Protracted hypomobility in the absence of trigeminal sensitization after cortical spreading depolarization: Relevance to migraine postdrome. (November 2021)

• Record Type: Journal Article
• Authors: Shibata, Mamoru; Kitagawa, Satoshi; Tang, Chunghua; Unekawa, Miyuki; Kayama, Yohei; Shimizu, Toshihiko; Nakahara, Jin; Suzuki, Norihiro
• Is Part Of: Neuroscience research. Volume 172(2021)
• Page Start: 80
• Page End: 86
• Publication Date: 2021-11
• Subjects: CI Confidence intervals -- CSD Cortical spreading depolarization -- FWHM Full width at half maximum -- NF-κB Nuclear factor-kappa B; Migraine -- Cortical spreading depolarization -- Photophobia -- Physical activity -- Migraine postdrome -- Neurotropin®; Neurosciences -- Research -- Periodicals; Neurosciences -- Research -- Japan -- Periodicals; Neurology -- Periodicals; Neurosciences -- Periodicals; Neurosciences -- Recherche -- Périodiques; Neurosciences -- Recherche -- Japon -- Périodiques; Neurosciences -- Research; Japan; Periodicals; 612.8
• DOI: 10.1016/j.neures.2021.03.010
• Languages: English
• ISSNs: 0168-0102

Abstract

Graphical abstract: Cortical spreading depolarization (CSD) can cause prolonged hypoactivity and photophobia postdrome symptoms, which leads to protracted disability in migraine sufferers. Neurotropin® may relieve these disabling CSD-induced symptoms. The data at 24 h after CSD have been reported previously (Tang et al., 2020). Highlights: Cortical spreading depolarization causes prolonged deterioration of hypomotility. This is especially true for a light environment, which mimics migraine postdrome. At a dose used for neuropathic pain management, Neurotropin® relieved hypomobility. Our study has therapeutic relevance for postdromal/interictal migraine symptoms. Abstract: Migraine sufferers often exhibit photophobia and physical hypoactivity in the postdrome and interictal periods, for which no effective therapy currently exists. Cortical spreading depolarization (CSD) is a neural phenomenon underlying migraine aura. We previously reported that CSD induced trigeminal sensitization, photophobia, and hypomobility at 24 h in mice. Here, we examined the effects of CSD induction on light sensitivity and physical activity in mice at 48 h and 72 h. Trigeminal sensitization was absent at both time points. CSD-subjected mice exhibited significantly less ambulatory time in both light (P = 0.0074, the Bonferroni test) and dark (P = 0.0354, the Bonferroni test) zones than sham-operated mice at 72 h. CSD-subjected mice also exhibited a significantly shorter ambulatory distance in the light zone at 72 h than sham-operated mice (P = 0.0151, the Bonferroni test). Neurotropin® is used for the management of chronic pain disorders, mainly in Asian countries. The CSD-induced reductions in ambulatory time and distance in the light zone at 72 h were reversed by Neurotropin® at 0.27 NU/kg. Our experimental model seems to recapitulate migraine-associated clinical features observed in the postdrome and interictal periods. Moreover, Neurotropin® may be effective in ameliorating postdromal/interictal hypoactivity, especially in a light environment.