Messoud Ashina

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Messoud Ashina
Messoud Ashina-0919.png
Born(1965-12-29)29 December 1965
Baku, Azerbaijan
Education University of Copenhagen, Azerbaijan Medical University
Medical career
Profession Neurologist
Institutions University of Copenhagen; Rigshospitalet
AwardsRoche Prize for Scientific Achievements in Neurology,
GlaxoSmithKline Research Prize,
Mogens Fog Prize,
Monrad-Krohns Prize
TÜBA Academy Prize
KFJ Prize

Messoud Ashina (born December 29, 1965) is a Danish-Azerbaijani neurologist and neuroscientist. [1] [2] He is currently Professor of Neurology at the University of Copenhagen and Senior Consultant of Neurology at Copenhagen University Hospital - Rigshospitalet. He leads the Human Migraine Research Unit at the Danish Headache Center, Copenhagen University Hospital - Rigshospitalet. [1] Ashina is also Director of the Danish Knowledge Center on Headache Disorders and Past President of the International Headache Society. [3] [4] As of 2024, Ashina is ranked as the world's leading expert on headache disorders by Expertscape. [5]

Contents

Education

Ashina earned his medical degree at the age 22 from Azerbaijan Medical University in 1988. [1] [6] He later received his PhD and D.M.Sc. degrees at University of Copenhagen and completed his residency in neurology at Copenhagen University Hospitalet - Rigshospitalet. [1]

Personal life

Messoud Ashina was born on December 29, 1965, in Baku, Azerbaijan. [6] His father, Rustam Ashina was an architect, while his mother, Nelli Hajiyeva, is a retired biologist. [1]

He lives in Copenhagen and is married to Camilla Ashina who is a dentist. [6] They have two children.

Research

Ashina is an acclaimed neuroscientist and considered one of the most prolific contributors to headache sciences. [5] His academic works focus on migraine, [7] which is a ubiquitous neurological disorder that affects more than one billion people worldwide. [8] Ashina and his research lab have been key figures in the development and refinement of human provocation models that can be used to map signaling pathways underlying migraine pathogenesis and to identify novel drug targets. [7] [9] [10] In these provocation models, endogenous signaling molecules or other hypothesized 'trigger' agents are used to induce migraine attacks in people with migraine, whereas healthy volunteers most often develop no more than a mild headache. [7]

In his early work, Ashina and colleagues discovered that intravenous infusion of pituitary adenylate cyclase-activating polypeptide-38 (PACAP-38) induced migraine attacks in people with migraine. [11] He then showed that PACAP infusion caused migraine attacks accompanied by a long-lasting dilation of cranial blood vessels. [12] This contrasted findings using the closely related vasoactive intestinal polypeptide (VIP), which elicited mild headache (but not migraine) and only a short-lasting vasodilation. [12] Upon extending the infusion duration of VIP, Ashina discovered that VIP now induced migraine attacks accompanied by long-lasting vasodilation. [13] This led to the hypothesis that prolonged dilation of cranial arteries might contribute to the pathogenesis of migraine and other headache disorders. [14] Of note, promising phase II trial results have been announced on the effectiveness of a PACAP-targeted drug for migraine prevention. [15]

Ashina has, in addition to PACAP and VIP, identified other peptidergic drug targets for migraine and related headache disorders. These include adrenomedullin, amylin, and specific prostaglandins; all of which have been shown to induce migraine attacks in people with migraine. [16] [17] [18] [19] Efforts are ongoing for developing novel drugs directed against the signaling of these migraine-inducing peptides.

Ashina has also posited that accumulation of intracellular cyclic adenosine monophosphate (cAMP) must play an important role in migraine pathogenesis because the intracellular effects of PACAP receptor-binding are mediated by cAMP-dependent signaling pathways. [11] This was confirmed by Ashina's lab when oral administration of cilostazol - a blocker of cAMP degradation - induced migraine attacks in people with migraine without aura. [20] Ashina later hypothesized that downstream effects of cAMP-mediated migraine attacks were likely to involve opening of potassium channels. [7] This hypothesis has been supported by experimental data from provocation studies, in which Ashina and colleagues demonstrated that openers of adenosine-triphosphate (ATP)-sensitive potassium channels and large conductance calcium-activated potassium channels induced migraine attacks in people with migraine without aura. [9] [21] [22] Furthermore, Ashina and colleagues have also found that intravenous infusion of an ATP-sensitive potassium channel opener appears to be a potent inducer of migraine attacks with aura in people with migraine with aura. [23]

Publications

Ashina has authored over 450 papers, abstracts and book chapters, including more than 400 registered publications in PubMed (1997-2024). [24] He is the editor of the book 'Pathophysiology of Headaches'. His overall citation index is 20,142 (13,278 since 2018), and he has an H-index of 82 (65 since 2019). [25]

Related Research Articles

<span class="mw-page-title-main">Migraine</span> Disorder resulting in recurrent moderate-severe headaches

Migraine is a genetically influenced complex neurological disorder characterized by episodes of moderate-to-severe headache, most often unilateral and generally associated with nausea and light and sound sensitivity. Other characterizing symptoms may include nausea, vomiting, cognitive dysfunction, allodynia, and dizziness. Exacerbation of headache symptoms during physical activity is another distinguishing feature. Up to one-third of migraine sufferers experience aura: a premonitory period of sensory disturbance widely accepted to be caused by cortical spreading depression at the onset of a migraine attack. Although primarily considered to be a headache disorder, migraine is highly heterogenous in its clinical presentation and is better thought of as a spectrum disease rather than a distinct clinical entity. Disease burden can range from episodic discrete attacks, consisting of as little as several lifetime attacks, to chronic disease.

<span class="mw-page-title-main">Headache</span> Pain in the head, neck, or face

Headache, also known as cephalalgia, is the symptom of pain in the face, head, or neck. It can occur as a migraine, tension-type headache, or cluster headache. There is an increased risk of depression in those with severe headaches.

A medication overuse headache (MOH), also known as a rebound headache, usually occurs when painkillers are taken frequently to relieve headaches. These cases are often referred to as painkiller headaches. Rebound headaches frequently occur daily, can be very painful and are a common cause of chronic daily headache. They typically occur in patients with an underlying headache disorder such as migraine or tension-type headache that "transforms" over time from an episodic condition to chronic daily headache due to excessive intake of acute headache relief medications. MOH is a serious, disabling and well-characterized disorder, which represents a worldwide problem and is now considered the third-most prevalent type of headache. The proportion of patients in the population with Chronic Daily Headache (CDH) who overuse acute medications ranges from 18% to 33%. The prevalence of medication overuse headache (MOH) varies depending on the population studied and diagnostic criteria used. However, it is estimated that MOH affects approximately 1-2% of the general population, but its relative frequency is much higher in secondary and tertiary care.

<span class="mw-page-title-main">Visual snow syndrome</span> Visual impairment

Visual snow syndrome (VSS) is a form of visual hallucination that is characterized by the perception of small, flickering dots throughout the entire visual field. It is present in all conditions of illumination. The dots remain individual and do not clump together or change in size. Visual snow exists in one of two forms: the pulse type and the broadband type.

<span class="mw-page-title-main">Triptan</span> Class of pharmaceutical drugs

Triptans are a family of tryptamine-based drugs used as abortive medication in the treatment of migraines and cluster headaches. This drug class was first commercially introduced in the 1990s. While effective at treating individual headaches, they do not provide preventive treatment and are not considered a cure. They are not effective for the treatment of tension–type headache, except in persons who also experience migraines. Triptans do not relieve other kinds of pain.

<span class="mw-page-title-main">Aura (symptom)</span> Symptom of epilepsy and migraine

An aura is a perceptual disturbance experienced by some with epilepsy or migraine. An epileptic aura is a seizure.

<span class="mw-page-title-main">Scintillating scotoma</span> Visual aura associated with migraine

Scintillating scotoma is a common visual aura that was first described by 19th-century physician Hubert Airy (1838–1903). Originating from the brain, it may precede a migraine headache, but can also occur acephalgically, also known as visual migraine or migraine aura. It is often confused with retinal migraine, which originates in the eyeball or socket.

<span class="mw-page-title-main">Calcitonin gene-related peptide</span> Peptide hormone in animals

Calcitonin gene-related peptide (CGRP) is a member of the calcitonin family of peptides consisting of calcitonin, amylin, adrenomedullin, adrenomedullin 2 (intermedin) and calcitonin‑receptor‑stimulating peptide. Calcitonin is mainly produced by thyroid C cells whilst CGRP is secreted and stored in the nervous system. This peptide, in humans, exists in two forms: CGRP alpha, and CGRP beta. α-CGRP is a 37-amino acid neuropeptide and is formed by alternative splicing of the calcitonin/CGRP gene located on chromosome 11. β-CGRP is less studied. In humans, β-CGRP differs from α-CGRP by three amino acids and is encoded in a separate, nearby gene. The CGRP family includes calcitonin (CT), adrenomedullin (AM), and amylin (AMY).

<span class="mw-page-title-main">Sporadic hemiplegic migraine</span> Medical condition

Sporadic hemiplegic migraine (SHM) is a form of hemiplegic migraine headache isolated cases of which are observed. It is a rare disease. It is considered to be a separate type of migraine.

<span class="mw-page-title-main">Pituitary adenylate cyclase-activating peptide</span> Protein-coding gene in the species Homo sapiens

Pituitary adenylate cyclase-activating polypeptide also known as PACAP is a protein that in humans is encoded by the ADCYAP1 gene. pituitary adenylate cyclase-activating polypeptide is similar to vasoactive intestinal peptide. One of its effects is to stimulate enterochromaffin-like cells. It binds to vasoactive intestinal peptide receptor and to the pituitary adenylate cyclase-activating polypeptide receptor.

<span class="mw-page-title-main">Cortical spreading depression</span> Type of evoked potential

Cortical spreading depression (CSD) or spreading depolarization (SD) is a wave of electrophysiological hyperactivity followed by a wave of inhibition. Spreading depolarization describes a phenomenon characterized by the appearance of depolarization waves of the neurons and neuroglia that propagates across the cortex at a velocity of 1.5–9.5 mm/min.

The classification of all headaches, including migraines, is organized by the International Headache Society, and published in the International Classification of Headache Disorders (ICHD). The current version, the ICHD-3 beta, was published in 2013.

Preventive treatment of migraine can be an important component of migraine management. Such treatments can take many forms, including everything from surgery, taking certain drugs or nutritional supplements, to lifestyle alterations such as increased exercise and avoidance of migraine triggers.

The trigeminovascular system (TVS) refers to neurons and their axonal projections within the trigeminal nerve that project to the cranial meninges and meningeal blood vessels residing on the brain's surface. The term, introduced in 1983 denotes also the neuropeptides contained within axons that are released into the meninges to target vessels and surrounding cells.

Migraine treatment may be either prophylactic (preventive) or abortive (rescue). Prevention is better than cure, so the ideal treatment goal is to prevent migraine attacks. Because migraine is an exceedingly complex condition, there are various preventive treatments which have their effect by disrupting different links in the chain of events that occur during a migraine attack. As rescue treatments also target and disrupt different processes occurring during migraine, these are summarized, with their relative merits and demerits.

Migraine is often hereditary. It is estimated that 60% of migraine cases are caused by genetics. The role of natural selection in the development of migraines is not known. Fitness-impairing disorders, including migraines, tend to disappear as a result of natural selection, and their frequency decreases to near the rate of spontaneous mutation. However, it is estimated that migraines affect 15-20% of the population and is increasing. This could suggest that a central nervous system (CNS) susceptible to severe, intermittent headache has been linked to an important survival or reproductive advantage. Five possible evolutionary explanations exist: i) migraine as a defence mechanism, ii) migraine as a result of conflicts with other organisms, iii) migraine as a result of novel environmental factors, iv) migraine as a compromise between genetic harms and benefits, and v) headache as a design constraint. These considerations allow the treatment and prevention of migraine to be approached from an evolutionary medicine perspective.

A migrainous infarction is a rare type of ischaemic stroke which occurs in correspondence with migraine aura symptoms. Symptoms include headaches, visual disturbances, strange sensations and dysphasia, all of which gradually worsen causing neurological changes which ultimately increase the risk of an ischaemic stroke. Typically, women under the age of 45 who experience migraine with aura (MA) are at the greatest risk for developing migrainous infarction, especially when combined with smoking and use of oral contraceptives.

Menstrual migraine is the term used to describe both true menstrual migraines and menstrually related migraines. About 7%–14% of women have migraines only at the time of menstruation. These are called true menstrual migraines. Most female migraineurs experience migraine attacks throughout the menstruation cycle with an increased number perimenstrually, these are referred to as menstrually related or menstrually triggered migraine.

<span class="mw-page-title-main">Martin Lauritzen</span> Danish neuroscientist and researcher

Martin Johannes Lauritzen is a Danish neuroscientist. He is a Professor of Translational Neurobiology at the Department of Neuroscience, University of Copenhagen, Denmark and also a Professor of Clinical Neurophysiology at the Department of Neurophysiology, Rigshospitalet.

<span class="mw-page-title-main">Recurrent painful ophthalmoplegic neuropathy</span> Medical condition

Recurrent painful ophthalmoplegic neuropathy (RPON), previously known as ophthalmoplegic migraine (OM), is a rare neurological disorder that is characterized by repeated headache attacks and reversible ipsilateral paresis of one or more ocular cranial nerves (CN). Oculomotor nerve (CNIII) is by far the most common cranial nerve involves in RPON, while abducens nerve (CNVI) and trochlear nerve (CNIV) involvements are also reported. Globally, RPON was estimated to have an annual incidence rate of 0.7 per million as of 1990, no further epidemiological studies have been conducted. It occurs more often in children and females.

References

  1. 1 2 3 4 5 "Messoud Ashina". www.rigshospitalet.dk. Retrieved 2021-05-19.
  2. ↑ "Messoud Ashina". The Lancet Neurology. 12 (5): 432. 2013-05-01. doi:10.1016/S1474-4422(13)70097-8. ISSN   1474-4422. S2CID   54299949.
  3. ↑ "videnscenterforhovedpine.dk" (in Danish). Retrieved 2021-05-19.
  4. ↑ "Meet the President". International Headache Society. Retrieved 2021-05-19.
  5. 1 2 "Headache: Worldwide - Expertscape.com". expertscape.com. Retrieved 2021-05-19.
  6. 1 2 3 Bundgaard, Bente (2021-04-29). "Fra Kaukasus til København". Dagens Medicin (in Danish). Retrieved 2021-05-19.
  7. 1 2 3 4 Ashina, Messoud (2020-11-04). "Migraine". New England Journal of Medicine. 383 (19): 1866–1876. doi:10.1056/NEJMra1915327. PMID   33211930. S2CID   227078662.
  8. ↑ Ashina, Messoud; Katsarava, Zaza; Do, Thien Phu; Buse, Dawn C.; Pozo-Rosich, Patricia; Özge, Aynur; Krymchantowski, Abouch V.; Lebedeva, Elena R.; Ravishankar, Krishnamurthy; Yu, Shengyuan; Sacco, Simona (2021-04-17). "Migraine: epidemiology and systems of care". The Lancet. 397 (10283): 1485–1495. doi:10.1016/S0140-6736(20)32160-7. ISSN   0140-6736. PMID   33773613. S2CID   232359483.
  9. 1 2 Ashina, Messoud; Terwindt, Gisela M.; Al-Karagholi, Mohammad Al-Mahdi; Boer, Irene de; Lee, Mi Ji; Hay, Debbie L.; Schulte, Laura H.; Hadjikhani, Nouchine; Sinclair, Alexandra J.; Ashina, Håkan; Schwedt, Todd J. (2021-04-17). "Migraine: disease characterisation, biomarkers, and precision medicine". The Lancet. 397 (10283): 1496–1504. doi:10.1016/S0140-6736(20)32162-0. hdl: 1887/3276377 . ISSN   0140-6736. PMID   33773610. S2CID   232359490.
  10. ↑ Ashina, Messoud; Hansen, Jakob Møller; á Dunga, Bára Oladóttir; Olesen, Jes (December 2017). "Human models of migraine — short-term pain for long-term gain". Nature Reviews Neurology. 13 (12): 713–724. doi:10.1038/nrneurol.2017.137. ISSN   1759-4766. PMID   28984313. S2CID   7546339.
  11. 1 2 Schytz, Henrik Winther; Birk, Steffen; Wienecke, Troels; Kruuse, Christina; Olesen, Jes; Ashina, Messoud (January 2009). "PACAP38 induces migraine-like attacks in patients with migraine without aura". Brain. 132 (1): 16–25. doi: 10.1093/brain/awn307 . ISSN   1460-2156. PMID   19052139.
  12. 1 2 Amin, Faisal Mohammad; Hougaard, Anders; Schytz, Henrik W.; Asghar, Mohammad S.; Lundholm, Elisabet; Parvaiz, Arushma I.; de Koning, Patrick J. H.; Andersen, Malene R.; Larsson, Henrik B. W.; Fahrenkrug, Jan; Olesen, Jes; Ashina, Messoud (March 2014). "Investigation of the pathophysiological mechanisms of migraine attacks induced by pituitary adenylate cyclase-activating polypeptide-38". Brain. 137 (3): 779–794. doi:10.1093/brain/awt369. ISSN   1460-2156. PMID   24501094.
  13. ↑ Pellesi, Lanfranco; Al-Karagholi, Mohammad Al-Mahdi; De Icco, Roberto; Coskun, Hande; Elbahi, Fatima Azzahra; Lopez-Lopez, Cristina; Snellman, Josefin; Hannibal, Jens; Amin, Faisal Mohammad; Ashina, Messoud (2021-08-06). "Effect of Vasoactive Intestinal Polypeptide on Development of Migraine Headaches: A Randomized Clinical Trial". JAMA Network Open. 4 (8): e2118543. doi:10.1001/jamanetworkopen.2021.18543. ISSN   2574-3805. PMC   8346940 . PMID   34357396.
  14. ↑ Ashina, Messoud (2020-11-05). Ropper, Allan H. (ed.). "Migraine". New England Journal of Medicine. 383 (19): 1866–1876. doi:10.1056/NEJMra1915327. ISSN   0028-4793. PMID   33211930. S2CID   227078662.
  15. ↑ "Lundbeck announces positive phase II Proof of Concept results with Lu AG09222 in migraine prevention". News Powered by Cision. 2023-04-19. Retrieved 2024-02-21.
  16. ↑ Ghanizada, Hashmat; Al-Mahdi Al-Karagholi, Mohammad; Arngrim, Nanna; Mørch-Rasmussen, Mette; Walker, Christopher S.; Hay, Debbie L.; Ashina, Messoud (2021-05-18). "Effect of Adrenomedullin on Migraine-Like Attacks in Patients With Migraine: A Randomized Crossover Study". Neurology. 96 (20): e2488–e2499. doi:10.1212/WNL.0000000000011930. ISSN   0028-3878. PMID   33827963. S2CID   233183405.
  17. ↑ Ghanizada, Hashmat; Al-Karagholi, Mohammad Al-Mahdi; Walker, Christopher S.; Arngrim, Nanna; Rees, Tayla; Petersen, Jakeb; Siow, Andrew; Mørch-Rasmussen, Mette; Tan, Sheryl; O'Carroll, Simon J.; Harris, Paul; Skovgaard, Lene Theil; Jørgensen, Niklas Rye; Brimble, Margaret; Waite, Jayme S. (June 2021). "Amylin Analog Pramlintide Induces Migraine-like Attacks in Patients". Annals of Neurology. 89 (6): 1157–1171. doi:10.1002/ana.26072. ISSN   0364-5134. PMC   8486152 . PMID   33772845.
  18. ↑ Wienecke, T; Olesen, J; Ashina, M (February 2010). "Prostaglandin I 2 (epoprostenol) triggers migraine-like attacks in migraineurs". Cephalalgia. 30 (2): 179–190. doi:10.1111/j.1468-2982.2009.01923.x. ISSN   0333-1024. PMID   19614689. S2CID   10838594.
  19. ↑ Antonova, Maria; Wienecke, Troels; Olesen, Jes; Ashina, Messoud (August 2012). "Prostaglandin E 2 induces immediate migraine-like attack in migraine patients without aura". Cephalalgia. 32 (11): 822–833. doi:10.1177/0333102412451360. ISSN   0333-1024. PMID   22718556.
  20. ↑ Guo, Song; Olesen, Jes; Ashina, Messoud (November 2014). "Phosphodiesterase 3 inhibitor cilostazol induces migraine-like attacks via cyclic AMP increase". Brain. 137 (11): 2951–2959. doi: 10.1093/brain/awu244 . ISSN   1460-2156. PMID   25161294.
  21. ↑ Al-Karagholi, Mohammad Al-Mahdi; Hansen, Jakob Møller; Guo, Song; Olesen, Jes; Ashina, Messoud (2019-09-01). "Opening of ATP-sensitive potassium channels causes migraine attacks: a new target for the treatment of migraine". Brain. 142 (9): 2644–2654. doi: 10.1093/brain/awz199 . ISSN   0006-8950. PMID   31292608.
  22. ↑ Al-Mahdi Al-Karagholi, Mohammad; Ghanizada, Hashmat; Waldorff Nielsen, Cherie Amalie; Skandarioon, Camilla; Snellman, Josefin; Lopez-Lopez, Cristina; Hansen, Jakob Møller; Ashina, Messoud (2021-02-17). "Opening of BKCa channels causes migraine attacks: a new downstream target for the treatment of migraine". Pain. 162 (10): 2512–2520. doi:10.1097/j.pain.0000000000002238. ISSN   0304-3959. PMID   34252916. S2CID   233954463.
  23. ↑ Al-Karagholi, Mohammad Al-Mahdi; Ghanizada, Hashmat; Nielsen, Cherie Amalie Waldorff; Hougaard, Anders; Ashina, Messoud (2021-03-26). "Opening of ATP sensitive potassium channels causes migraine attacks with aura". Brain. 144 (8): 2322–2332. doi: 10.1093/brain/awab136 . ISSN   0006-8950. PMID   33768245.
  24. ↑ "PubMed.com - Messoud Ashina".
  25. ↑ "Google Scholar - Messoud Ashina".
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