Cluster Headache Pathophysiology—A Disorder of Network Excitability?

Clinical and Translational Neuroscience

Peter S. Sandor¹  Heiko Pohl¹  Andreas R. Gantenbein¹  Lars Michels² 

[1] Department of Neurology, University Hospital Zurich, 8091 Zurich, Switzerland;Department of Neuroradiology and Clinical Neuroscience Center, University Hospital Zurich, University of Zurich, 8091 Zurich, Switzerland;

关键词: sensitization;    homeostatic plasticity;    synaptic scaling;    epilepsy;   

DOI  :  10.3390/ctn5020016

来源: DOAJ

【 摘 要 】

Patients’ accounts of cluster headache attacks, ictal restlessness, and electrophysiological studies suggest that the pathophysiology involves Aδ-fibre nociceptors and the network processing their input. Continuous activity of the trigeminal autonomic reflex throughout the in-bout period results in central sensitization of these networks in many patients. It is likely that several factors force circadian rhythmicity upon the disease. In addition to sensitization, circadian changes in pain perception and autonomic innervation might influence the excitability of the trigeminal cervical complex. Summation of several factors influencing pain perception might render neurons vulnerable to spontaneous depolarization, particularly at the beginning of rapid drops of the pain threshold (“summation headache”). In light of studies suggesting an impairment of short-term synaptic plasticity in CH patients, we suggest that the physiologic basis of CH attacks might be network overactivity—similarly to epileptic seizures. Case reports documenting cluster-like attacks support the idea of distinct factors being transiently able to induce attacks and being relevant in the pathophysiology of the disorder. A sustained and recurring proneness to attacks likely requires changes in the activity of other structures among which the hypothalamus is the most probable candidate.

【 授权许可】

Unknown