A PET study of photophobia during spontaneous migraine attacks

Denuelle, Marie; Boulloche, Nicolas; Payoux, Pierre; Fabre, Nelly; Trotter, Yves; Géraud, G

doi:10.1212/wnl.0b013e3182074a57

Cited by 154 publications

(132 citation statements)

References 33 publications

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“…PET radiotracer technology was used to measure changes in µORs availability with [ 11 C]carfentanil. When examined during the headache event, the brains of migraineurs are usually scanned following an attack trigger (e.g., glyceryl trinitrate, photostimulation) 16,17 , or under the technical demand of a specific evoked stimulus (e.g., pain, brush, light, and odor) [18][19][20] . All those studies corroborate the knowledge that the disorder is associated with cortical and subcortical hyperexcitability during the headache phase.…”

Section: Discussionmentioning

confidence: 99%

3D-Neuronavigation <em>In Vivo</em> Through a Patient's Brain During a Spontaneous Migraine Headache

DaSilva

Nascimento

Love³

et al. 2014

JoVE

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A growing body of research, generated primarily from MRI-based studies, shows that migraine appears to occur, and possibly endure, due to the alteration of specific neural processes in the central nervous system. However, information is lacking on the molecular impact of these changes, especially on the endogenous opioid system during migraine headaches, and neuronavigation through these changes has never been done. This study aimed to investigate, using a novel 3D immersive and interactive neuronavigation (3D-IIN) approach, the endogenous µ-opioid transmission in the brain during a migraine headache attack in vivo. This is arguably one of the most central neuromechanisms associated with pain regulation, affecting multiple elements of the pain experience and analgesia. A 36 year-old female, who has been suffering with migraine for 10 years, was scanned in the typical headache (ictal) and nonheadache (interictal) migraine phases using Positron Emission Tomography (PET) with the selective radiotracer [ 11 C]carfentanil, which allowed us to measure µ-opioid receptor availability in the brain (non-displaceable binding potential -µOR BP ND ). The short-life radiotracer was produced by a cyclotron and chemical synthesis apparatus on campus located in close proximity to the imaging facility. Both PET scans, interictal and ictal, were scheduled during separate mid-late follicular phases of the patient's menstrual cycle. During the ictal PET session her spontaneous headache attack reached severe intensity levels; progressing to nausea and vomiting at the end of the scan session. There were reductions in µOR BP ND in the pain-modulatory regions of the endogenous µ-opioid system during the ictal phase, including the cingulate cortex, nucleus accumbens (NAcc), thalamus (Thal), and periaqueductal gray matter (PAG); indicating that µORs were already occupied by endogenous opioids released in response to the ongoing pain. To our knowledge, this is the first time that changes in µOR BP ND during a migraine headache attack have been neuronavigated using a novel 3D approach. This method allows for interactive research and educational exploration of a migraine attack in an actual patient's neuroimaging dataset.

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Section: Discussionmentioning

confidence: 99%

3D-Neuronavigation <em>In Vivo</em> Through a Patient's Brain During a Spontaneous Migraine Headache

DaSilva

Nascimento

Love³

et al. 2014

JoVE

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“…Such description of photo-hypersensitivity suggests that the flow of nociceptive signals along the trigeminovascular pathway converges on the visual cortex and alters its responsiveness to visual stimuli. Indeed, the visual cortex appears to be hyperexcitable in migraineurs and may be the neural substrate of abnormal processing of light sensitivity [28]. Support on how meningeal pain could induce increased perception of light intensity, refers to light/durasensitive thalamic neurons located outside the VPM nucleus that project directly to the primary and secondary visual cortices [88; 91].…”

Section: Neural Substrate Of Migraine-type Photophobiamentioning

confidence: 99%

Migraine pathophysiology: Anatomy of the trigeminovascular pathway and associated neurological symptoms, cortical spreading depression, sensitization, and modulation of pain

Noseda

Burstein²

2013

Pain

733

634

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Scientific evidence support the notion that migraine pathophysiology involves inherited alteration of brain excitability, intracranial arterial dilatation, recurrent activation and sensitization of the trigeminovascular pathway, and consequential structural and functional changes in genetically susceptible individuals. Evidence of altered brain excitability emerged from clinical and preclinical investigation of sensory auras, ictal and interictal hypersensitivity to visual, auditory and olfactory stimulation, and reduced activation of descending inhibitory pain pathways. Data supporting the activation and sensitization of the trigeminovascular system include the progressive development of cephalic and whole-body cutaneous allodynia during a migraine attack. Also, structural and functional alterations include the presence of subcortical white mater lesions, thickening of cortical areas involved in processing sensory information, and cortical neuroplastic changes induced by cortical spreading depression. Here, we review recent anatomical data on the trigeminovascular pathway and its activation by cortical spreading depression, a novel understanding of the neural substrate of migraine-type photophobia, and modulation of the trigeminovascular pathway by the brainstem, hypothalamus and cortex.

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“…Most studies have assessed functional brain changes in response to experimentally induced noxious stimuli or during induced migraine attacks by nitric oxide donors, various other vasodilating chemicals or hypoxia (2)(3)(4)(5). PET recordings during spontaneous attacks have focused on brain stem and photophobia-related activations (6)(7)(8)(9)(10), but the central nervous system underpinnings of headache intensity were not assessed.…”

Section: Introductionmentioning

confidence: 99%

Resting state connectivity between default mode network and insula encodes acute migraine headache

et al. 2017

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Background: Previous functional MRI studies have revealed that ongoing clinical pain in different chronic pain syndromes is directly correlated to the connectivity strength of the resting default mode network (DMN) with the insula. Here, we investigated seed-based resting state DMN-insula connectivity during acute migraine headaches. Methods: Thirteen migraine without aura patients (MI) underwent 3 T MRI scans during the initial six hours of a spontaneous migraine attack, and were compared to a group of 19 healthy volunteers (HV). We evaluated headache intensity with a visual analogue scale and collected seed-based MRI resting state data in the four core regions of the DMN: Medial prefrontal cortex (MPFC), posterior cingulate cortex (PCC), and left and right inferior parietal lobules (IPLs), as well as in bilateral insula. Results: Compared to HV, MI patients showed stronger functional connectivity between MPFC and PCC, and between MPFC and bilateral insula. During migraine attacks, the strength of MPFC-to-insula connectivity was negatively correlated with pain intensity. Conclusion: We show that greater subjective intensity of pain during a migraine attack is associated with proportionally weaker DMN-insula connectivity. This is at variance with other chronic extra-cephalic pain disorders where the opposite was found, and may thus be a hallmark of acute migraine head pain.

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A PET study of photophobia during spontaneous migraine attacks

Cited by 154 publications

References 33 publications

3D-Neuronavigation <em>In Vivo</em> Through a Patient's Brain During a Spontaneous Migraine Headache

3D-Neuronavigation <em>In Vivo</em> Through a Patient's Brain During a Spontaneous Migraine Headache

Migraine pathophysiology: Anatomy of the trigeminovascular pathway and associated neurological symptoms, cortical spreading depression, sensitization, and modulation of pain

Resting state connectivity between default mode network and insula encodes acute migraine headache

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