Altered Corticobrainstem Connectivity during Spontaneous Fluctuations in Pain Intensity in Painful Trigeminal Neuropathy.

Autor: Meylakh N; School of Medical Sciences (Neuroscience), Brain and Mind Centre, University of Sydney, Sydney, New South Wales 2050, Australia., Crawford LS; School of Medical Sciences (Neuroscience), Brain and Mind Centre, University of Sydney, Sydney, New South Wales 2050, Australia., Mills EP; School of Medical Sciences (Neuroscience), Brain and Mind Centre, University of Sydney, Sydney, New South Wales 2050, Australia., Macefield VG; Department of Neuroscience, Monash University, Melbourne, Victoria 3800, Australia., Vickers ER; School of Medical Sciences (Neuroscience), Brain and Mind Centre, University of Sydney, Sydney, New South Wales 2050, Australia., Macey PM; UCLA School of Nursing and Brain Research Institute, University of California, Los Angeles, California 90095., Keay KA; School of Medical Sciences (Neuroscience), Brain and Mind Centre, University of Sydney, Sydney, New South Wales 2050, Australia., Henderson LA; School of Medical Sciences (Neuroscience), Brain and Mind Centre, University of Sydney, Sydney, New South Wales 2050, Australia luke.henderson@sydney.edu.au.
Jazyk: angličtina
Zdroj: ENeuro [eNeuro] 2024 Jul 25; Vol. 11 (7). Date of Electronic Publication: 2024 Jul 25 (Print Publication: 2024).
DOI: 10.1523/ENEURO.0522-23.2024
Abstrakt: Chronic neuropathic pain can result from nervous system injury and can persist in the absence of external stimuli. Although ongoing pain characterizes the disorder, in many individuals, the intensity of this ongoing pain fluctuates dramatically. Previously, it was identified that functional magnetic resonance imaging signal covariations between the midbrain periaqueductal gray (PAG) matter, rostral ventromedial medulla (RVM), and spinal trigeminal nucleus are associated with moment-to-moment fluctuations in pain intensity in individuals with painful trigeminal neuropathy (PTN). Since this brainstem circuit is modulated by higher brain input, we sought to determine which cortical sites might be influencing this brainstem network during spontaneous fluctuations in pain intensity. Over 12 min, we recorded the ongoing pain intensity in 24 PTN participants and classified them as fluctuating ( n  = 13) or stable ( n  = 11). Using a PAG seed, we identified connections between the PAG and emotional-affective sites such as the hippocampal and posterior cingulate cortices, the sensory-discriminative posterior insula, and cognitive-affective sites such as the dorsolateral prefrontal (dlPFC) and subgenual anterior cingulate cortices that were altered dependent on spontaneous high and low pain intensity. Additionally, sliding-window functional connectivity analysis revealed that the dlPFC-PAG connection anticorrelated with perceived pain intensity over the entire 12 min period. These findings reveal cortical systems underlying moment-to-moment changes in perceived pain in PTN, which likely cause dysregulation in the brainstem circuits previously identified, and consequently alter the appraisal of pain across time.
Competing Interests: The authors declare no competing financial interests.
(Copyright © 2024 Meylakh et al.)
Databáze: MEDLINE