Cluster Headache Pathophysiology—A Disorder of Network Excitability?
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...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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MDPI AG
2021-09-01
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| Series: | Clinical and Translational Neuroscience |
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| Online Access: | https://www.mdpi.com/2514-183X/5/2/16 |
| _version_ | 1797519716632231936 |
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| author | Heiko Pohl Peter S. Sandor Lars Michels Andreas R. Gantenbein |
| author_facet | Heiko Pohl Peter S. Sandor Lars Michels Andreas R. Gantenbein |
| author_sort | Heiko Pohl |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-03-10T07:46:44Z |
| format | Article |
| id | doaj.art-b3788bcf091047df88b9f725ac594251 |
| institution | Directory Open Access Journal |
| issn | 2514-183X |
| language | English |
| last_indexed | 2024-03-10T07:46:44Z |
| publishDate | 2021-09-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Clinical and Translational Neuroscience |
| spelling | doaj.art-b3788bcf091047df88b9f725ac5942512023-11-22T12:36:46ZengMDPI AGClinical and Translational Neuroscience2514-183X2021-09-01521610.3390/ctn5020016Cluster Headache Pathophysiology—A Disorder of Network Excitability?Heiko Pohl0Peter S. Sandor1Lars Michels2Andreas R. Gantenbein3Department of Neurology, University Hospital Zurich, 8091 Zurich, SwitzerlandDepartment of Neurology, University Hospital Zurich, 8091 Zurich, SwitzerlandDepartment of Neuroradiology and Clinical Neuroscience Center, University Hospital Zurich, University of Zurich, 8091 Zurich, SwitzerlandDepartment of Neurology, University Hospital Zurich, 8091 Zurich, SwitzerlandPatients’ 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.https://www.mdpi.com/2514-183X/5/2/16sensitizationhomeostatic plasticitysynaptic scalingepilepsy |
| spellingShingle | Heiko Pohl Peter S. Sandor Lars Michels Andreas R. Gantenbein Cluster Headache Pathophysiology—A Disorder of Network Excitability? Clinical and Translational Neuroscience sensitization homeostatic plasticity synaptic scaling epilepsy |
| title | Cluster Headache Pathophysiology—A Disorder of Network Excitability? |
| title_full | Cluster Headache Pathophysiology—A Disorder of Network Excitability? |
| title_fullStr | Cluster Headache Pathophysiology—A Disorder of Network Excitability? |
| title_full_unstemmed | Cluster Headache Pathophysiology—A Disorder of Network Excitability? |
| title_short | Cluster Headache Pathophysiology—A Disorder of Network Excitability? |
| title_sort | cluster headache pathophysiology a disorder of network excitability |
| topic | sensitization homeostatic plasticity synaptic scaling epilepsy |
| url | https://www.mdpi.com/2514-183X/5/2/16 |
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