Cluster headache, hypothalamus, and orexin

Holland, Philip R.; Goadsby, PJ

doi:10.1007/s11916-009-0025-x

Cited by 82 publications

(61 citation statements)

References 58 publications

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“…Using positron emission tomography, a previous study reported increased cerebral blood flow bilaterally in the hypothalamus during an acute attack in migraine patients (Denuelle et al, 2007). However, the exact role of hypothalamic (dys)functions in migraine has not yet been entangled and should be addressed in further studies (Alstadhaug, 2009;Holland and Goadsby, 2009).…”

Section: Discussionmentioning

confidence: 96%

Trigeminal Nociceptive Transmission in Migraineurs Predicts Migraine Attacks

Stankewitz¹,

Aderjan²,

Eippert³

et al. 2011

J. Neurosci.

245

221

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Several lines of evidence suggest a major role of the trigeminovascular system in the pathogenesis of migraine. Using functional magnetic resonance imaging (fMRI), we compared brain responses during trigeminal pain processing in migraine patients with those of healthy control subjects. The main finding is that the activity of the spinal trigeminal nuclei in response to nociceptive stimulation showed a cycling behavior over the migraine interval. Although interictal (i.e., outside of attack) migraine patients revealed lower activations in the spinal trigeminal nuclei compared with controls, preictal (i.e., shortly before attack) patients showed activity similar to controls, which demonstrates that the trigeminal activation level increases over the pain-free migraine interval. Remarkably, the distance to the next headache attack was predictable by the height of the signal intensities in the spinal nuclei. Migraine patients scanned during the acute spontaneous migraine attack showed significantly lower signal intensities in the trigeminal nuclei compared with controls, demonstrating activity levels similar to interictal patients. Additionally we found-for the first time using fMRI-that migraineurs showed a significant increase in activation of dorsal parts of the pons, previously coined "migraine generator." Unlike the dorsal pons activation usually linked to migraine attacks, the gradient-like activity following nociceptive stimulation in the spinal trigeminal neurons likely reflects a raise in susceptibility of the brain to generate the next attack, as these areas increase their activity long before headache starts. This oscillating behavior may be a key player in the generation of migraine headache, whereas attack-specific pons activations are most likely a secondary event.

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Section: Discussionmentioning

confidence: 96%

Trigeminal Nociceptive Transmission in Migraineurs Predicts Migraine Attacks

Stankewitz¹,

Aderjan²,

Eippert³

et al. 2011

J. Neurosci.

245

221

View full text Add to dashboard Cite

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“…It contains sensory, motor and autonomic fibers, of which only the parasympathetic nerves synapse in the ganglion. Its implication in the pathophysiology of CH is well recognized (11,87,88).…”

Section: Spgmentioning

confidence: 99%

Neurostimulation in cluster headache: A review of current progress

2013

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Purpose of review: Neurostimulation has emerged as a viable treatment for intractable chronic cluster headache. Several therapeutic strategies are being investigated including stimulation of the hypothalamus, occipital nerves and sphenopalatine ganglion. The aim of this review is to provide an overview of the rationale, methods and progress for each of these. Latest findings: Results from a randomized, controlled trial investigating sphenopalatine ganglion stimulation have just been published. Reportedly the surgery is relatively simple and it is apparently the only therapy that provides relief acutely. Summary: The rationale behind these therapies is based on growing evidence from clinical, hormonal and neuroimaging studies. The overall results are encouraging, but unfortunately not all patients have benefited. All the mentioned therapies require weeks to months of stimulation for a prophylactic effect to occur, suggesting brain plasticity as a possible mechanism, and only stimulation of the sphenopalatine ganglion has demonstrated an acute, abortive effect. Predictors of effect for all modes of neurostimulation still need to be identified and in the future, the least invasive and most effective strategy must be preferred as first-line therapy for intractable chronic cluster headache.

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“…Recently, Steinberg and colleagues [12] showed elevated levels of NO metabolites in the cerebrospinal fluid of patients with CH both during and between CH cycles. There also is recent interest in the role of orexin A and B, both hypothalamic neuropeptides in CH pathogenesis [13]. Monda et al [14] noted that CSD alters the hyperthermic effects of orexin A in rats, suggesting at least some direct or indirect interaction between CSD and orexin.…”

Section: Aura Pathogenesis In Cluster Headachementioning

confidence: 99%

Cluster Headache with Aura

Rozen¹

2010

Curr Pain Headache Rep

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Aura was not recognized as a clinical symptom of cluster headache until fairly recently, but studies now have indicated that upwards of 20% of patients with cluster headache may have aura, the same percentage of migraine sufferers who have aura. This paper looks at the epidemiology of cluster headache with aura, suggests possible roles of cortical spreading depression in cluster headache pathogenesis, and looks at the clinical/diagnostic implications of aura in cluster headache sufferers.

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Cluster headache, hypothalamus, and orexin

Cited by 82 publications

References 58 publications

Trigeminal Nociceptive Transmission in Migraineurs Predicts Migraine Attacks

Trigeminal Nociceptive Transmission in Migraineurs Predicts Migraine Attacks

Neurostimulation in cluster headache: A review of current progress

Cluster Headache with Aura

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