Serum Interleukin-1 Beta is Increased in Cluster Headache

Martelletti, Paolo; Granata, M; Giacovazzo, M

doi:10.1046/j.1468-2982.1993.1305343.x

Cited by 42 publications

(48 citation statements)

References 17 publications

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“…The immunoinflammatory system takes part in modulating the mechanisms giving rise to migraine, possibly by the intermediation of cytokines that are broadly expressed by several cells Review Lovati, D'Amico, Raimondi, Mariani & Bertora of the CNS, including the neurons that are considered to mediate pain in neurovascular inflammation [55]. Activation of the immune system has been identified in CH in which an increase in IL-1 b, in particular during the ictal phase, can be found [56].…”

Section: Cytokinesmentioning

confidence: 99%

Sleep and headache: a bidirectional relationship

Lovati¹,

D’Amico²,

Raimondi³

et al. 2010

Expert Review of Neurotherapeutics

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Sleep and pain perception are two phylogenetically well-conserved functions, strictly influenced by environmental and psychological factors, and are able to interact reciprocally both in physiological and pathological situations. Sleep and head-pain perception share the involvement of several structures, such as the thalamus, the hypothalamus and brainstem nuclei, including the locus coeruleus and raphe nuclei. There ais clinical evidence indicating that sleep disorders can precede the appearance of certain headaches and that head pain, especially when frequent, can, in turn, affect sleep quality. In the present work the anatomy, physiology and pathology of sleep and head-pain perception will be reviewed with the aim of highlighting the points of contact and possible unifying treatment strategies.

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Section: Cytokinesmentioning

confidence: 99%

Sleep and headache: a bidirectional relationship

Lovati¹,

D’Amico²,

Raimondi³

et al. 2010

Expert Review of Neurotherapeutics

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“…Furthermore, recombinant IL-2 and interferon-β were found to counteract this peripheral downregulation 47–49. In a later work, Martelletti et al observed that the serum IL-1β level was significantly higher in ECH patients compared to HCs, intraictally as well as postictally 50. In addition, intraictal concentrations were higher than postictal values.…”

Section: Moa Of Cervical Vns In Cluster Headache (Human and Preclinicmentioning

confidence: 91%

Spotlight on cervical vagus nerve stimulation for the treatment of primary headache disorders: a review

Lendvai

Maier

Scheele

et al. 2018

JPR

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ObjectivesCervical noninvasive vagus nerve stimulation (nVNS) emerged as an adjunctive neuromodulation approach for primary headache disorders with limited responsiveness to pharmacologic and behavioral treatment. This narrative review evaluates the safety and efficacy of invasive and noninvasive peripheral nerve stimulation of the cervical branch of the vagal nerve (afferent properties) for primary headache disorders (episodic/chronic migraine [EM/CM] and cluster headache [ECH/CCH]) and provides a brief summary of the preclinical data on the possible mechanism of action of cervical vagus nerve stimulation (VNS) and trigemino-nociceptive head pain transmission.Materials and methodsA systematic search of published data was performed in PubMed for randomized controlled trials (RCTs) and prospective cohort clinical studies assessing the efficacy/safety and cost-effectiveness of cervical VNS in primary headache disorders and related preclinical studies.ResultsThree RCTs were identified for ECH/CCH (ACT-1, ACT-2 and PREVA), one RCT for migraine (EVENT) and several prospective cohort studies and retrospective analyses for both headache disorders. In ACT-1, a significantly higher response rate, a higher pain-free rate and a decrease in mean attack duration were found in nVNS-treated ECH/CCH patients compared to sham stimulation. ACT-2 confirmed these findings (e.g., significantly higher pain-free attacks, pain severity decline and increased responder-rate [defined as ≥50% reduction]). The PREVA study demonstrated the superiority of adjunctive nVNS to standard care alone and observed a significantly higher attack reduction (p=0.02) and responder rate (defined as ≥50% reduction). For CM, the EVENT study assessed a significantly higher frequency of decline in the open-label phase. Mostly transient mild/moderate adverse events were recorded, and no severe device-related adverse events occurred.ConclusionCervical nVNS represents a novel, safe and efficient adjunctive treatment option for primary headache disorders. In particular, preliminary observations suggest enhanced nVNS responsiveness in favor of episodic subtypes (EM and ECH). However, preclinical studies are urgently warranted to dissect the mechanism of action.

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“…Orbital phlebography [20] and gallium single photon emission computerized tomography scans [21] have suggested inflammation in the cavernous sinus ipsilateral to CH pain during cluster periods. Inflammatory mediators can be detected in cerebrospinal fluid [22] and blood (eg, interleukin-1β) [23] during CH periods and CH attacks and an increase in some restricted subsets of circulating leukocytes (eg, Leu7+, LeuM3+) has been detected specifically during CH attacks [24]. Other evidence for a dysimmune process in CH comes from genotyping of major histocompatibility complex genes.…”

Section: Pathophysiologic Rationale For the Therapeutic Efficacy Of Cmentioning

confidence: 99%

Corticosteroid treatment in cluster headache: Evidence, rationale, and practice

Shapiro

2005

Current Science Inc

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The use of corticosteroids in the treatment of cluster headache (CH) is commonplace and has been a mainstay of clinical practice for this indication for 50 years. The published evidence supporting this practice is weak, with no methodologically rigorous or large-scale controlled trials executed. Nonetheless, the clinical experiences of practitioners and the conclusion of investigators provide a clear signal of benefit from corticosteroid use in CH. The pathophysiologic explanation for this beneficial effect is unknown, but corticosteroid influences on inflammatory, hypothalamic-pituitary-adrenal, histaminergic, and opioid systems have been proposed. Best-practice parameters are unclear, but the professional consensus is that corticosteroids generally are effective for arresting CH attacks, only if administered in relatively high doses, and that safety concerns warrant courses of 4 weeks or less. Concomitant use of other prophylactic agents for CH in addition to corticosteroids usually is advisable because attacks often recur when the corticosteroid dose is tapered.

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Serum Interleukin-1 Beta is Increased in Cluster Headache

Cited by 42 publications

References 17 publications

Sleep and headache: a bidirectional relationship

Sleep and headache: a bidirectional relationship

Spotlight on cervical vagus nerve stimulation for the treatment of primary headache disorders: a review

Corticosteroid treatment in cluster headache: Evidence, rationale, and practice

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