About this Research Topic
Neuropathic pain is a common syndrome in demyelinating diseases. For example, in Multiple Sclerosis (MS), 80% of patients suffer chronic pain; in Guillain–Barré syndrome (GBS), 70%-90% of cases report persistent pain; in Optic Neuritis (ON), pain with eye movement is a significant symptom of disease attack. Pain in demyelinating conditions could be caused by either the direct effects of nerve injury or the result of paralysis and prolonged immobilization. Therefore, pain syndromes need to be defined in each disorder based on the underlying pathophysiology. So far, in animal research, demyelinating pain has been considered an unimportant aspect of disease and has been overlooked. However recently, new demyelinating models reveal cellular and molecular mechanisms that initiate a new era of pain research in demyelinating disorders. Characterizing the mechanism underlining demyelinating pain will help develop new pain management therapy in clinics and improve the understanding of demyelinating disorders.
The aim of this Research Topic is
• to collect papers from clinicians to characterize demyelinating disease-associated pain in patients, thus providing clinical features of the disease-dependent pain in patients. This will highlight the biomedical issues posed and the necessity for basic research questions to be answered.
• to collect papers from laboratory researchers about pain behavior changes in demyelinating disease models. This article collection will provide a platform for communication for basic researchers in both pain and demyelinating disease fields.
• to synergize clinical and laboratory research to further understanding of these pain syndromes and improve therapy and management in these patients.
We welcome the submission of manuscripts including, but not limited to, the following topics:
• Clinical features of demyelinating disease-associated pain and its relationship with other disease-associated syndromes:
- Chronic pain associated with multiple sclerosis (MS), neuromyelitis Optica (NMO), optic neuritis (ON), transverse myelitis, and acute disseminated encephalomyelitis (ADEM), etc.
- The effect of pain management in these patients with the clinical outcomes in these patients, and the prospective mechanism, such as demyelinating induced neuronal hyperactivity, inflammation, muscle/joint dysfunctions, etc.
• Chronic pain in demyelinating animal models, and the laboratory evidence of cellular and molecular mechanism underlying the pain. The animal models include but not restricted to:
- Immune-Mediated Demyelination (EAE model)
- Auto-antibody induced demyelination(AQP4-IgG and MOG-IgG induced demyelination)
- Viral models of CNS demyelination (TMEV, MHV, and SFV)
- Toxic induced demyelination (TNFa, cuprizone, LPS, and LPC).
• We particularly encourage translational medicine-related research.
Keywords: demyelination, chronic pain, clinical feature, animal model, pain management
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.