Epilepsy and migraine are chronic neurological disorders, characterized by recurrent episodes with an absence of symptoms. Neuroinflammation is thought to be an adaptive response caused by noxious stimuli such as infection, injury, and tissue stress, and plays an essential role in the pathogenesis of epilepsy and migraine, indicating the use of novel therapeutic strategies. In addition, inflammatory mediators could contribute diagnostic, prognostic, and predictive biomarkers for epilepsy and migraine, which would enable the stratification of patients in future clinical studies.
Migraine is thought to be a complex neurogenic inflammatory disorder, but the pathophysiology is still not fully understood. In the context of migraine, neurogenic neuroinflammation refers to inflammatory responses in the central and peripheral parts of the trigeminal nervous system due to neuronal activity. Various cytokines, including tumor necrosis factor (TNF), interleukin 1 (IL-1), and adiponectin, have been implicated in inflammation, modulation of pain thresholds, trigeminal fiber sensitisation, and ultimately migraine triggering. Neurogenic neuroinflammation also plays a critical role in the pathogenesis of epilepsy. Several studies have shown that seizures can produce activation of neuroinflammation, which in turn may be involved in the progression of epileptogenesis. Recent studies have demonstrated abnormal levels of plasma inflammatory and neurotrophic markers in patients with epilepsy, independent of the underlying etiology, suggesting that such biomarkers may be a consequence rather than a cause of epilepsy. Further understanding of the neuroinflammatory mechanisms of epilepsy and migraine identifies cellular and molecular targets for new mechanistic therapies that can overcome the limitations of current drugs that can only be symptomatically controlled. We would like to focus on the available evidence that biomarkers of inflammation have pathogenic value and could be therapeutic targets to explore immunomodulatory and anti-neuroinflammatory treatments for epilepsy and migraine.
We welcome submissions of original research and review of the following topics:
1. Neuroinflammation of migraine attacks
2. Neuroinflammation of epileptic seizures
3. Neuroinflammation of the comorbidity of epilepsy and migraine.
4. Potential biomarkers of inflammation and therapeutic targets
Epilepsy and migraine are chronic neurological disorders, characterized by recurrent episodes with an absence of symptoms. Neuroinflammation is thought to be an adaptive response caused by noxious stimuli such as infection, injury, and tissue stress, and plays an essential role in the pathogenesis of epilepsy and migraine, indicating the use of novel therapeutic strategies. In addition, inflammatory mediators could contribute diagnostic, prognostic, and predictive biomarkers for epilepsy and migraine, which would enable the stratification of patients in future clinical studies.
Migraine is thought to be a complex neurogenic inflammatory disorder, but the pathophysiology is still not fully understood. In the context of migraine, neurogenic neuroinflammation refers to inflammatory responses in the central and peripheral parts of the trigeminal nervous system due to neuronal activity. Various cytokines, including tumor necrosis factor (TNF), interleukin 1 (IL-1), and adiponectin, have been implicated in inflammation, modulation of pain thresholds, trigeminal fiber sensitisation, and ultimately migraine triggering. Neurogenic neuroinflammation also plays a critical role in the pathogenesis of epilepsy. Several studies have shown that seizures can produce activation of neuroinflammation, which in turn may be involved in the progression of epileptogenesis. Recent studies have demonstrated abnormal levels of plasma inflammatory and neurotrophic markers in patients with epilepsy, independent of the underlying etiology, suggesting that such biomarkers may be a consequence rather than a cause of epilepsy. Further understanding of the neuroinflammatory mechanisms of epilepsy and migraine identifies cellular and molecular targets for new mechanistic therapies that can overcome the limitations of current drugs that can only be symptomatically controlled. We would like to focus on the available evidence that biomarkers of inflammation have pathogenic value and could be therapeutic targets to explore immunomodulatory and anti-neuroinflammatory treatments for epilepsy and migraine.
We welcome submissions of original research and review of the following topics:
1. Neuroinflammation of migraine attacks
2. Neuroinflammation of epileptic seizures
3. Neuroinflammation of the comorbidity of epilepsy and migraine.
4. Potential biomarkers of inflammation and therapeutic targets
