Materiały źródłowe

• #1 Migraine Headache: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1142556-overview

  The mechanisms of migraine remain incompletely understood. However, new technologies have allowed formulation of current concepts that may explain parts of the migraine syndrome. […] Migraine was previously considered to be a vascular phenomenon that resulted from intracranial vasoconstriction followed by rebound vasodilation. Currently, however, the neurovascular theory describes migraine as primarily a neurogenic process with secondary changes in cerebral perfusion associated with a sterile neurogenic inflammation. […] The neurovascular theory holds that a complex series of neural and vascular events initiates migraine. According to this theory, migraine is primarily a neurogenic process with secondary changes in cerebral perfusion. […] In 1944, Leao proposed the theory of cortical spreading depression (CSD) to explain the mechanism of migraine with aura. CSD is a well-defined wave of neuronal excitation in the cortical gray matter that spreads from its site of origin at the rate of 2-6 mm/min.

• #2 Migraine pathogenesis and state of pharmacological treatment options | BMC Medicine | Full Text

  https://bmcmedicine.biomedcentral.com/articles/10.1186/1741-7015-7-71

  Migraine is a largely inherited disorder of the brain characterized by a complex, but stereotypical, dysfunction of sensory processing. […] This review discusses the current pathophysiological concepts of migraine and migraine aura, such as a possible brainstem dysfunction and cortical spreading depression. […] The disorder was considered to be vascular in origin for much of the 20th century, although it was considered to be a disorder of the nervous system by 19th century luminaries. […] This view is supported by data which include the fact that: vasoactive intestinal peptide – a strong intracranial vasodilator – does not trigger migraine; intracranial vasodilatation also occurs secondary to experimental head pain stimulation, probably mediated by the trigeminal-parasympathetic reflex; and non-vasoconstrictor drugs, such as aspirin and calcitonin gene-related peptide (CGRP) receptor antagonists can abort migraine attacks.

• #3 Migraine Headache – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK560787/

  Migraine is a genetically influenced complex neurological disorder characterized by episodes of moderate-to-severe headaches, typically unilateral and frequently accompanied by nausea and heightened sensitivity to light and sound. […] Understanding the etiology of migraine headaches is crucial for effective diagnosis and treatment. Migraines are believed to result from a combination of genetic, environmental, and neurological factors. Research indicates that these headaches are linked to abnormal brain activity that affects nerve signals, chemicals, and blood vessels within the brain. […] Although not fully understood, the pathogenesis of migraine headaches involves multiple components of both the peripheral and central (CNS) nervous systems. This section describes some of the most well-understood concepts. According to the older vascular theory of migraine, headaches were thought to be produced by vasodilation and auras by vasoconstriction; however, this theory is no longer considered viable. Current theories suggest that multiple primary neuronal impairments lead to a series of intracranial and extracranial changes that cause migraines.

• #4 Pathophysiology, clinical manifestations, and diagnosis of migraine in adults – UpToDate

  https://www.uptodate.com/contents/pathophysiology-clinical-manifestations-and-diagnosis-of-migraine-in-adults/print

  Migraine is an episodic disorder, the centerpiece of which is a severe headache generally associated with nausea and/or light and sound sensitivity. It is one of the most common complaints encountered by neurologists in day-to-day practice. […] The pathophysiology, clinical manifestations, diagnosis, and complications of migraine will be reviewed here. […] The current state of knowledge suggests that a primary neuronal dysfunction leads to a sequence of changes intracranially and extracranially that account for migraine, including the four phases of premonitory symptoms, aura, headache, and postdrome. […] The once-popular vascular theory of migraine, which suggested that migraine headache was caused by the dilatation of blood vessels while the aura of migraine resulted from vasoconstriction, is no longer considered viable.

• #5 Headache – Wikipedia

  https://en.wikipedia.org/wiki/Headache

  Primary headaches are more difficult to understand than secondary headaches. The exact mechanisms which cause migraines, tension headaches and cluster headaches are not known. There have been different hypotheses over time that attempt to explain what happens in the brain to cause these headaches. […] Migraines are currently thought to be caused by dysfunction of the nerves in the brain. Previously, migraines were thought to be caused by a primary problem with the blood vessels in the brain. This vascular theory, which was developed in the 20th century by Wolff, suggested that the aura in migraines is caused by constriction of intracranial vessels (vessels inside the brain), and the headache itself is caused by rebound dilation of extracranial vessels (vessels just outside the brain). Dilation of these extracranial blood vessels activates the pain receptors in the surrounding nerves, causing a headache. The vascular theory is no longer accepted.

• #6 Migraine Headache – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK560787/

  Migraine is a genetically influenced complex neurological disorder characterized by episodes of moderate-to-severe headaches, typically unilateral and frequently accompanied by nausea and heightened sensitivity to light and sound. […] Understanding the etiology of migraine headaches is crucial for effective diagnosis and treatment. Migraines are believed to result from a combination of genetic, environmental, and neurological factors. Research indicates that these headaches are linked to abnormal brain activity that affects nerve signals, chemicals, and blood vessels within the brain. […] Although not fully understood, the pathogenesis of migraine headaches involves multiple components of both the peripheral and central (CNS) nervous systems. This section describes some of the most well-understood concepts. According to the older vascular theory of migraine, headaches were thought to be produced by vasodilation and auras by vasoconstriction; however, this theory is no longer considered viable. Current theories suggest that multiple primary neuronal impairments lead to a series of intracranial and extracranial changes that cause migraines.

• #7 Pathophysiology of Migraine | Science of Migraine

  https://www.scienceofmigraine.com/pathophysiology/phases-of-migraine

  Clinical evidence suggests that CGRP is involved in migraine pain. […] Neuropeptides may play a fundamental role in neurogenic inflammation, and peripheral and central sensitization of the trigeminovascular and other systems.1,18,32 […] Sensitization of primary nociceptors and central trigeminovascular neurons may contribute to allodynia in migraine.33-35 […] This suggests that altered sensory processing and brainstem structure may contribute to the severity of allodynia and hypersensitivity to the pain observed in migraine.4 […] The trigeminovascular system, which relays head pain signals to the brain, plays a key role in migraine pathophysiology and has components in the periphery (ie, outside the blood-brain barrier) as well as in the central nervous system (CNS) (ie, inside the blood-brain barrier).3,48-50

• #8 Migraine Headache: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1142556-overview

  Perivascular nerve activity also results in release of substances such as substance P, neurokinin A, calcitonin gene-related peptide, and nitric oxide, which interact with the blood vessel wall to produce dilation, protein extravasation, and sterile inflammation. […] A potential „migraine center” in the brainstem has been proposed, based on PET-scan results showing persistently elevated rCBF in the brainstem even after sumatriptan-produced resolution of headache and related symptoms. […] Once the CSD occurs on the surface of the brain, H+ and K+ ions diffuse to the pia mater and activate C-fiber meningeal nociceptors, releasing a proinflammatory soup of neurochemicals and causing plasma extravasation to occur. Therefore, a sterile, neurogenic inflammation of the trigeminovascular complex is present.

• #9 Migraine Headache: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1142556-overview

  Activation of the trigeminovascular system by CSD stimulates nociceptive neurons on dural blood vessels to release plasma proteins and pain-generating substances such as calcitonin gene-related peptide, substance P, vasoactive intestinal peptide, and neurokinin A. The resultant state of sterile inflammation is accompanied by further vasodilation, producing pain. […] The initial cortical hyperperfusion in CSD is partly mediated by the release of trigeminal and parasympathetic neurotransmitters from perivascular nerve fibers, whereas delayed meningeal blood flow increase is mediated by a trigeminal-parasympathetic brainstem connection. […] In addition, through a variety of molecular mechanisms, CSD upregulates genes, such as those encoding for cyclo-oxygenase 2 (COX-2), tumor necrosis factor alpha (TNF-alpha), interleukin-1beta, galanin, and metalloproteinases.

• #10 Pathophysiology of Migraine | Science of Migraine

  https://www.scienceofmigraine.com/pathophysiology/phases-of-migraine

  Migraine may occur as a result of a dysfunctional trigeminovascular system.11 […] Pain is experienced when trigeminovascular neurons are activated and relay the migraine pain signal from the periphery to the CNS.5 […] Repeated activation of the trigeminovascular system over time results in a state of nervous system hypersensitivity and sustained pain.5 […] The headache phase of migraine is associated with a distinct pathophysiology that may involve sensitization of the peripheral and central nervous system.8,26 […] There are several neuropeptides implicated in head pain and peripheral and central sensitization of the trigeminovascular system and other systems during the headache phase.1 […] Preclinical studies with PACAP and CGRP suggest that both neuropeptides may also play a role in photophobia or light sensitivity that may occur during the headache phase of a migraine attack.1 […] There are a number of new findings, again, related to the phases of the migraine attack and how these progress.6-9 […] The exact neurological events that underlie these different symptoms remain uncertain.1,34

• #11 Migraine Headache: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1142556-overview

  The mechanisms of migraine remain incompletely understood. However, new technologies have allowed formulation of current concepts that may explain parts of the migraine syndrome. […] Migraine was previously considered to be a vascular phenomenon that resulted from intracranial vasoconstriction followed by rebound vasodilation. Currently, however, the neurovascular theory describes migraine as primarily a neurogenic process with secondary changes in cerebral perfusion associated with a sterile neurogenic inflammation. […] The neurovascular theory holds that a complex series of neural and vascular events initiates migraine. According to this theory, migraine is primarily a neurogenic process with secondary changes in cerebral perfusion. […] In 1944, Leao proposed the theory of cortical spreading depression (CSD) to explain the mechanism of migraine with aura. CSD is a well-defined wave of neuronal excitation in the cortical gray matter that spreads from its site of origin at the rate of 2-6 mm/min.

• #12 Aura and the Mechanism of Migraine: The Next Treatment Target?

  https://www.neurologylive.com/view/aura-and-the-mechanism-of-migraine-the-next-treatment-target/1000

  The neurological symptoms of migraine aura are generally attributed to cortical spreading depression/depolarization, although that hypothesis does have its detractors. The question of whether CSD triggers migraine headache remains controversial. […] The varied presentations of migraine aura have contributed to the difficulty in characterizing underlying neurologic processes and their links to migraine headache, according to Dodick. […] The variable timing of aura and headache symptoms has challenged not only clinical beliefs but also the biological bases and sequence of physiological events underlying a migraine attack, he observed. […] Dodick described CSD as a self-propagating wave of transient neuronal depolarization, a form of intense neuronal excitation associated with reversible breakdown of ion homeostasis and transient depression of neuronal activity.

• #13 Aura and the Mechanism of Migraine: The Next Treatment Target?

  https://www.neurologylive.com/view/aura-and-the-mechanism-of-migraine-the-next-treatment-target/1000

  Neurons are depolarized by local elevations in extracellular potassium, and the disrupted cell membrane ionic gradients are marked by the influx of sodium and calcium and the release of glutamate. […] These ionic shifts result in neuronal swelling, reciprocal decrease in extracellular space, and dendritic beading, which in turn lead to the release of amino acids and neurotransmitters that further the spread of depolarization. […] Dodick suggested that initial accumulations of extracellular potassium occur as a result of repeated depolarization and repolarization of hyperexcitable neurons in the cortex, and the accumulation then further depolarizes the cells from which the potassium is released. […] He also pointed to evidence from animal studies that supports the proposition that CSD can activate trigeminal nociception and thereby trigger migraine headache.

• #14 Migraine Headache: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1142556-overview

  Activation of the trigeminovascular system by CSD stimulates nociceptive neurons on dural blood vessels to release plasma proteins and pain-generating substances such as calcitonin gene-related peptide, substance P, vasoactive intestinal peptide, and neurokinin A. The resultant state of sterile inflammation is accompanied by further vasodilation, producing pain. […] The initial cortical hyperperfusion in CSD is partly mediated by the release of trigeminal and parasympathetic neurotransmitters from perivascular nerve fibers, whereas delayed meningeal blood flow increase is mediated by a trigeminal-parasympathetic brainstem connection. […] In addition, through a variety of molecular mechanisms, CSD upregulates genes, such as those encoding for cyclo-oxygenase 2 (COX-2), tumor necrosis factor alpha (TNF-alpha), interleukin-1beta, galanin, and metalloproteinases.

• #15 Migraine Headache – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK560787/

  Neuropeptides believed to play a role in migraine pathogenesis include the following: Serotonin is released from the brainstem serotonergic nuclei and is thought to be involved in migraine; however, the exact mechanisms are still debated. […] CGRP is abundant in trigeminal ganglion neurons and released from the peripheral and central nerve terminals. CGRP is secreted within the trigeminal ganglion. Upon release from peripheral terminals, CGRP stimulates increased synthesis of nitric oxide and subsequent sensitization of trigeminal nerves. […] PACAP may also have a significant role in mediating migraine attacks, as its concentration is elevated during the attacks, and infusion of PACAP may trigger migraines in susceptible patients.

• #16 Migraine: Advances in the Pathogenesis and Treatment

  https://www.mdpi.com/2035-8377/15/3/67

  Calcitonin gene-related peptide (CGRP) is an incredibly potent neuropeptide comprised of 37 amino acids. It serves as a vasodilator and is produced within neurons located in both the peripheral and central nervous systems. This neuro-peptide binds to a complex heterodimer receptor, which is primarily composed of a class B G-protein coupled receptor, commonly referred to as CLR (calcitonin receptor-like receptor). Within the central nervous system, empirical research has identified elevated levels of CGRP in the blood and saliva of patients who experience certain headache disorders. Such disorders include migraine and cluster headaches, as well as neuralgias like trigeminal neuralgia, chronic paroxysmal hemicranias, and even rhinosinusitis. It is noteworthy that the levels of CGRP remain heightened during a migraine episode and continue to be elevated in-between these attacks for patients suffering from chronic migraine. Additionally, studies have revealed that exogenous infusions of CGRP can initiate a migraine episode. […]

• #17 Modern understanding of the pathophysiology of migraine | CnsBytes US

  https://www.cnsbytes.us/migraine/modern-understanding-of-the-pathophysiology-of-migraine/

  Trigeminal nerve endings contain vasoactive neuropeptides such as calcitonin gene-related peptide (CGRP), substance P, neurokinin A, and pituitary adenylate-cyclase activating peptide (PACAP). Activation of these neurons triggers the release of the neuropeptides, especially CGRP, leading to neurogenic inflammation, and vasodilation of dural and pial vessels. While vasodilation does not directly cause migraine, and neurogenic inflammation is unlikely to be a major migraine trigger, the latter may be involved in the sensitization of peripheral nociceptors. CGRP is also likely involved in central nociceptive sensitization. Although the exact mechanism of migraine onset remains to be elucidated, CGRP is clearly involved in modulating nociceptive input to the TCC. […] Several studies in the past two decades have shown that CGRP plays a key role in migraine pathogenesis. Clinical evidence supporting this conclusion includes: elevated levels of CGRP in the circulation during migraine attacks; development of migraine-like headaches after experimental injection of CGRP; and effectiveness of selective CGRP receptor antagonists in the treatment of migraine.

• #18 Migraine – Neurobiology and aetiology – Neurotorium

  https://neurotorium.org/slidedeck/migraine-neurobiology-and-aetiology/

  Migraine pathogenesis and the role of CGRP trigeminal ganglion […] Migraine pathogenesis and the role of CGRP trigeminal nucleus caudalis […] Migraine pathogenesis and the role of CGRP thalamus […] Migraine pathogenesis and the role of CGRP hypothalamus […] Evolving theories of migraine pathogenesis […] The vascular theory of migraine […] The vasculature and migraine symptoms […] Inflammation and the role of the immune system […] The role of CGRP in migraine […] Pharmacological targets for CGRP inhibition […] Structural changes from migraine attacks.

• #19 Migraine Headache – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK560787/

  Neuropeptides believed to play a role in migraine pathogenesis include the following: Serotonin is released from the brainstem serotonergic nuclei and is thought to be involved in migraine; however, the exact mechanisms are still debated. […] CGRP is abundant in trigeminal ganglion neurons and released from the peripheral and central nerve terminals. CGRP is secreted within the trigeminal ganglion. Upon release from peripheral terminals, CGRP stimulates increased synthesis of nitric oxide and subsequent sensitization of trigeminal nerves. […] PACAP may also have a significant role in mediating migraine attacks, as its concentration is elevated during the attacks, and infusion of PACAP may trigger migraines in susceptible patients.

• #20 Pathophysiology of Migraine | Science of Migraine

  https://www.scienceofmigraine.com/pathophysiology/phases-of-migraine

  Migraine may occur as a result of a dysfunctional trigeminovascular system.11 […] Pain is experienced when trigeminovascular neurons are activated and relay the migraine pain signal from the periphery to the CNS.5 […] Repeated activation of the trigeminovascular system over time results in a state of nervous system hypersensitivity and sustained pain.5 […] The headache phase of migraine is associated with a distinct pathophysiology that may involve sensitization of the peripheral and central nervous system.8,26 […] There are several neuropeptides implicated in head pain and peripheral and central sensitization of the trigeminovascular system and other systems during the headache phase.1 […] Preclinical studies with PACAP and CGRP suggest that both neuropeptides may also play a role in photophobia or light sensitivity that may occur during the headache phase of a migraine attack.1 […] There are a number of new findings, again, related to the phases of the migraine attack and how these progress.6-9 […] The exact neurological events that underlie these different symptoms remain uncertain.1,34

• #21 Migraine pathogenesis and state of pharmacological treatment options | BMC Medicine | Full Text

  https://bmcmedicine.biomedcentral.com/articles/10.1186/1741-7015-7-71

  Compared to other hypothesis on migraine neurobiology, dysfunction of such brainstem structures and networks could not only account for the somatosensory component of migraine (headache) but also for the auditory, olfactory and visual components. […] Migraine prevention is an important component of therapy aimed at reducing the attack frequency and severity. […] A potential mechanism is the inhibition of cortical spreading depression but, as noted above, the efficacy against cortical spreading depression does not necessarily predict the efficacy in treating migraine without aura. […] According to the pathophysiological concepts discussed above, these drugs most probably target the activity of modulatory circuits as well as the neuronal activity in afferent sensory pathways such as the trigeminal system.

• #22 Migraine Headache: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1142556-overview

  Perivascular nerve activity also results in release of substances such as substance P, neurokinin A, calcitonin gene-related peptide, and nitric oxide, which interact with the blood vessel wall to produce dilation, protein extravasation, and sterile inflammation. […] A potential „migraine center” in the brainstem has been proposed, based on PET-scan results showing persistently elevated rCBF in the brainstem even after sumatriptan-produced resolution of headache and related symptoms. […] Once the CSD occurs on the surface of the brain, H+ and K+ ions diffuse to the pia mater and activate C-fiber meningeal nociceptors, releasing a proinflammatory soup of neurochemicals and causing plasma extravasation to occur. Therefore, a sterile, neurogenic inflammation of the trigeminovascular complex is present.

• #23 Migraine: pathogenesis and pathophysiology | MedLink Neurology

  https://www.medlink.com/articles/migraine-pathogenesis-and-pathophysiology

  Migraine is prevalent and is one of the leading causes of disability worldwide. […] To tackle this condition and help the millions suffering worldwide, we must first understand the pathophysiology of migraine and how it is associated with the hypothalamus, cortical spreading depression, and the trigeminocervical complex. […] In recent years our understanding of the pathophysiology behind migraines has advanced (especially through functional imaging), leading us to put away old theories like the vascular theory and further evaluate involvement of the hypothalamus, cortical spreading depression, and the trigeminocervical complex in various migraine phases (premonitory, aura, headache, and postdrome). […] The hypothalamus is a key contributor to multiple migraine phases, including the premonitory phase, headache phase, postdrome phase, and chronic migraine.

• #24 Migraine: pathogenesis and pathophysiology | MedLink Neurology

  https://www.medlink.com/articles/migraine-pathogenesis-and-pathophysiology

  The hypothalamus is not only implicated in the premonitory phase but also in the headache phase. […] Imaging studies suggest that the anterior thalamus is associated with the premonitory phase and chronic migraine whereas the posterior hypothalamus is involved with the headache phase. […] The trigeminal pain system can shift to whats known as chronic migraine through a variety of factors including impaired modulation, peripheral sensitization, central sensitization, decreased threshold, and alterations in connectivity. […] Predominating theories about pathogenesis include: hypoxemia with an associated increase in hemoglobin and cardiac output (which can initiate CSD), an increase in trigger chemicals (like serotonin) that avoid pulmonary capillary filtration, and microemboli/microthrombi that are shunted to the brain from the venous circulation causing tiny infarctions (and therefore low blood flow and/or CSD).

• #25

  https://naturveda.fr/en/blogs/migraine/mechanism-of-the-migraine?srsltid=AfmBOoprEFts0-0QZOBrrc_GLw8fJHvdc2vPA7FazGMmx6oQhhSNoTbh

  Migraine evolves according to four phases which are: prodromes, migraine aura, headache and postdromes. […] The headache phase is the phase where the described pain in the head. In general this phase that we consider as migraine. It is the consequence of an inflammatory phenomenon at the level of the envelope which surrounds the brain: the meninges. Indeed it is not the brain that hurts directly, it is not innervated and is unable to feel pain. […] By various mechanisms, these triggering factors are integrated into the brain and particularly at the level of an area called the hypothalamus. […] We know that in the migraine patient, the hypothalamus has an increased activity. […] This state of excitement is found even between seizures. Therefore, in the migraine patient the hypothalamus needs constancy.

• #26

  https://naturveda.fr/en/blogs/migraine/mechanism-of-the-migraine?srsltid=AfmBOoprEFts0-0QZOBrrc_GLw8fJHvdc2vPA7FazGMmx6oQhhSNoTbh

  Migraine evolves according to four phases which are: prodromes, migraine aura, headache and postdromes. […] The headache phase is the phase where the described pain in the head. In general this phase that we consider as migraine. It is the consequence of an inflammatory phenomenon at the level of the envelope which surrounds the brain: the meninges. Indeed it is not the brain that hurts directly, it is not innervated and is unable to feel pain. […] By various mechanisms, these triggering factors are integrated into the brain and particularly at the level of an area called the hypothalamus. […] We know that in the migraine patient, the hypothalamus has an increased activity. […] This state of excitement is found even between seizures. Therefore, in the migraine patient the hypothalamus needs constancy.

• #27 Pathophysiology of Migraine | Science of Migraine

  https://www.scienceofmigraine.com/pathophysiology/phases-of-migraine

  Migraine may occur as a result of a dysfunctional trigeminovascular system.11 […] Pain is experienced when trigeminovascular neurons are activated and relay the migraine pain signal from the periphery to the CNS.5 […] Repeated activation of the trigeminovascular system over time results in a state of nervous system hypersensitivity and sustained pain.5 […] The headache phase of migraine is associated with a distinct pathophysiology that may involve sensitization of the peripheral and central nervous system.8,26 […] There are several neuropeptides implicated in head pain and peripheral and central sensitization of the trigeminovascular system and other systems during the headache phase.1 […] Preclinical studies with PACAP and CGRP suggest that both neuropeptides may also play a role in photophobia or light sensitivity that may occur during the headache phase of a migraine attack.1 […] There are a number of new findings, again, related to the phases of the migraine attack and how these progress.6-9 […] The exact neurological events that underlie these different symptoms remain uncertain.1,34

• #28 Migraine: Advances in the Pathogenesis and Treatment

  https://www.mdpi.com/2035-8377/15/3/67

  The phenomenon of central sensitization in individuals prone to migraine leads to heightened pain perception during a migraine, a condition known as cutaneous allodynia, and may contribute to the progression from episodic to chronic migraine. Approximately 65% of migraine sufferers develop cutaneous allodynia during individual headache episodes. Patients with allodynia experience the skin becoming painfully sensitive to stimuli that are normally harmless, such as a light touch. Developing ways to block or reverse central sensitization could potentially alleviate migraine pain and lower the likelihood of episodic migraine evolving into chronic migraine. […] […] The advent of neuroimaging technologies has brought significant advancements in our understanding of migraine mechanisms and has enabled us to pinpoint secondary structural and functional impacts resulting from migraine. Imaging conducted during a migraine episode has helped the scientific community progress from a strictly vascular understanding of migraine pathophysiology, to a neurovascular theory, and currently towards a central nervous system (CNS) model. […]

• #29 Migraine: Advances in the Pathogenesis and Treatment

  https://www.mdpi.com/2035-8377/15/3/67

  The phenomenon of central sensitization in individuals prone to migraine leads to heightened pain perception during a migraine, a condition known as cutaneous allodynia, and may contribute to the progression from episodic to chronic migraine. Approximately 65% of migraine sufferers develop cutaneous allodynia during individual headache episodes. Patients with allodynia experience the skin becoming painfully sensitive to stimuli that are normally harmless, such as a light touch. Developing ways to block or reverse central sensitization could potentially alleviate migraine pain and lower the likelihood of episodic migraine evolving into chronic migraine. […] […] The advent of neuroimaging technologies has brought significant advancements in our understanding of migraine mechanisms and has enabled us to pinpoint secondary structural and functional impacts resulting from migraine. Imaging conducted during a migraine episode has helped the scientific community progress from a strictly vascular understanding of migraine pathophysiology, to a neurovascular theory, and currently towards a central nervous system (CNS) model. […]

• #30 Current Understanding on Pain Mechanism in Migraine and Cluster Headache

  https://brieflands.com/articles/aapm-17559.html

  The clinical expression of first-order-neuron sensitization is the throbbing pain that characterizes migraine attacks. […] In CH, activation of the trigeminovascular system triggers autonomic manifestations through the trigeminal-autonomic reflex. […] Neurogenic inflammation refers to a neurally mediated inflammatory response in meningeal tissue characterised by vasodilatation, leakage of plasma protein from blood vessels and mast cell degranulation. […] The release of neuropeptides has been proposed as a pain mechanism in migraine and other primary headaches. […] The infusion of nitrovasodilators can trigger CH attacks similar to spontaneous attacks, suggesting a role for NO in nociceptive processes. […] Studies conducted by Kudrow et al. were the first to implicate the hypothalamus in the pathogenesis of CH with the demonstration of lower levels of testosterone during a bout. […] Neuroimaging further supports the role of the hypothalamus in CH. […] Imaging studies in CH have also implicated other brain areas that are generally associated with the pain matrix. […] Migraine and CH are neurovascular disorders with multiple processes and complex pathophysiologies.

• #31 Current Understanding on Pain Mechanism in Migraine and Cluster Headache

  https://brieflands.com/articles/aapm-17559.html

  Migraine and cluster headache are undoubtedly painful conditions. The respective pathogenesis of these two conditions is incompletely understood. […] There is evidence that the trigeminovascular system and neurogenic inflammation play important roles, together with certain areas of the brain, leading to these conditions being termed neurovascular headaches. […] The exact mechanism causing pain in both conditions is incompletely understood and more research needs to be undertaken in this area. […] In both migraine and CH, pain occurs as a result of activation of the trigeminovascular system. […] Migraine attacks are a manifestation of central and peripheral sensitization. […] The central sensitization hypothesis suggests an altered processing sensory signal in the brainstem, where the neurons of trigemino-cervical (TCC) system become hyperexcitable.

• #32 EXPLORING THE PATHOPHYSIOLOGY AND PATHOGENESIS OF MIGRAINE, AND THE PROMISING POTENTIAL OF HOMEOPATHIC MEDICINES

  https://www.linkedin.com/pulse/exploring-pathophysiology-pathogenesis-migraine-hospital-1h5gc

  Neurotransmitter Imbalance: Imbalances in neurotransmitters, particularly serotonin (5-HT), play a crucial role in migraine pathogenesis. Low levels of serotonin during a migraine attack can lead to the dilation of blood vessels and increased pain sensitivity. The exact mechanisms by which serotonin influences migraines are still under investigation. […] Pathogenesis: Migraine is initiated by genetic and environmental factors leading to CSD, activation of the trigeminovascular system, and neurotransmitter imbalances. […] Pathophysiology: The result is a series of physiological changes, including vasodilation, neurogenic inflammation, and central sensitization, manifesting as the characteristic symptoms of migraine such as throbbing headache, nausea, and aura.

• #33 EXPLORING THE PATHOPHYSIOLOGY AND PATHOGENESIS OF MIGRAINE, AND THE PROMISING POTENTIAL OF HOMEOPATHIC MEDICINES

  https://www.linkedin.com/pulse/exploring-pathophysiology-pathogenesis-migraine-hospital-1h5gc

  Neurotransmitter Imbalance: Imbalances in neurotransmitters, particularly serotonin (5-HT), play a crucial role in migraine pathogenesis. Low levels of serotonin during a migraine attack can lead to the dilation of blood vessels and increased pain sensitivity. The exact mechanisms by which serotonin influences migraines are still under investigation. […] Pathogenesis: Migraine is initiated by genetic and environmental factors leading to CSD, activation of the trigeminovascular system, and neurotransmitter imbalances. […] Pathophysiology: The result is a series of physiological changes, including vasodilation, neurogenic inflammation, and central sensitization, manifesting as the characteristic symptoms of migraine such as throbbing headache, nausea, and aura.

• #34 Migraine: Advances in the Pathogenesis and Treatment

  https://www.mdpi.com/2035-8377/15/3/67

  Biochemical research has revealed several metabolic irregularities in the synthesis of neuromodulators and neurotransmitters associated with migraine, particularly migraine without aura (MO). Alterations in the metabolic pathway of tyrosine, for example, lead to abnormal production of neurotransmitters like noradrenaline (NE) and dopamine (DA). This process results in an increase in the levels of trace amines, such as tyramine, octopamine, and synephrine. Such changes compromise mitochondrial function and elevate glutamate concentrations within the central nervous system (CNS). These imbalances in the neurotransmitter and neuromodulator levels within the dopaminergic and noradrenergic synapses of pain pathways could potentially activate the trigeminovascular system (TGVS), causing the release of the calcitonin gene-related peptide (CGRP). This chain of events is believed to directly trigger migraine attacks. […]

• #35 Pathogenesis of Migraine – Role of Neuromodulators — Lucia Zamorano, MD, PLC

  https://www.luciazamorano.com/pathogenesis-of-migraine-role-of-neuromodulators/

  The pathogenesis of migraine is still, today, a hotly debated issue. Recent biochemical studies report the occurrence in migraine of metabolic abnormalities in the synthesis of neurotransmitters and neuromodulators. These include a metabolic shift directing tyrosine metabolism toward the decarboxylation pathway, therein resulting in an unphysiological production of noradrenaline and dopamine along with increased synthesis of traces amines such as tyramine, octopamine, and synephrine. This biochemical alteration is possibly favored by impaired mitochondrial function and high levels of glutamate in the central nervous system (CNS) of migraine patients. […] The unbalanced levels of the neurotransmitters (dopamine and noradrenaline) and neuromodulators (eg, tyramine, octopamine, and synephrine) in the synaptic dopaminergic and noradrenergic clefts of the pain matrix pathways may activate, downstream, the trigeminal system that releases calcitonin gene-related peptide. This induces the formation of an inflammatory soup, the sensitization of first trigeminal neuron, and the migraine attack. In view of this, we propose that migraine attacks derive from a top-down dysfunctional process that initiates in the frontal lobe in a hyperexcitable and hypoenergetic brain, thereafter progressing downstream resulting in abnormally activated nuclei of the pain matrix.

• #36 Migraine: Advances in the Pathogenesis and Treatment

  https://www.mdpi.com/2035-8377/15/3/67

  Biomarkers, in the realm of medical and biological research, are defined as quantifiable indicators of biological conditions, representing either physical manifestations or results obtained from laboratory tests that correlate with biological processes. These markers have the potential to serve critical diagnostic or prognostic functions. A more explicit definition of biomarkers was proposed during a conference hosted by the US Food and Drug Administration. In this context, biomarkers are characterized as quantifiable attributes that can be objectively measured and assessed, providing insights into standard biological, pathological, or pharmacological processes. […] […] The markers of inflammation and oxidative stress have been associated with migraine in several studies. Proinflammatory cytokines, such as interleukin-1 (IL-1) and interleukin-6 (IL-6), have been implicated in this condition. It has been found that the level of IL-1α is elevated in the blood of children suffering from migraine with aura (MA). Similarly, adults with MA have been found to exhibit higher plasma levels of IL-1β during headache-free periods and early stages of attacks as compared to those suffering from migraine without aura (MO). The concentration of IL-6 is reported to increase during the initial two hours of a migraine attack. Additionally, the levels of IL-10 and tumor necrosis factor alpha (TNF-α) are also found to be elevated during these attacks. It is believed that other inflammatory markers associated with vascular dysfunction, such as homocysteine (Hcy) and matrix metalloproteinase-9 (MMP-9), are also elevated in the blood of individuals with migraine. […]

• #37 Migraine: Advances in the Pathogenesis and Treatment

  https://www.mdpi.com/2035-8377/15/3/67

  Biomarkers, in the realm of medical and biological research, are defined as quantifiable indicators of biological conditions, representing either physical manifestations or results obtained from laboratory tests that correlate with biological processes. These markers have the potential to serve critical diagnostic or prognostic functions. A more explicit definition of biomarkers was proposed during a conference hosted by the US Food and Drug Administration. In this context, biomarkers are characterized as quantifiable attributes that can be objectively measured and assessed, providing insights into standard biological, pathological, or pharmacological processes. […] […] The markers of inflammation and oxidative stress have been associated with migraine in several studies. Proinflammatory cytokines, such as interleukin-1 (IL-1) and interleukin-6 (IL-6), have been implicated in this condition. It has been found that the level of IL-1α is elevated in the blood of children suffering from migraine with aura (MA). Similarly, adults with MA have been found to exhibit higher plasma levels of IL-1β during headache-free periods and early stages of attacks as compared to those suffering from migraine without aura (MO). The concentration of IL-6 is reported to increase during the initial two hours of a migraine attack. Additionally, the levels of IL-10 and tumor necrosis factor alpha (TNF-α) are also found to be elevated during these attacks. It is believed that other inflammatory markers associated with vascular dysfunction, such as homocysteine (Hcy) and matrix metalloproteinase-9 (MMP-9), are also elevated in the blood of individuals with migraine. […]

• #38 Mechanisms of migraine as a chronic evolutive condition | The Journal of Headache and Pain | Full Text

  https://thejournalofheadacheandpain.biomedcentral.com/articles/10.1186/s10194-019-1066-0

  Although genetic factors may be involved in the evolutive processes of migraine, to date they failed to explain the pathophysiology of migraine and evolutive mechanisms. […] The physiological mechanisms that underlie the development of chronic migraine from its episodic form are not understood. […] Inflammation and central sensitization play a significant role in the evolutive mechanisms of chronic migraine.

• #39 Mechanism of traditional Chinese medicine in treating migraine: future | JPR

  https://www.dovepress.com/mechanism-of-traditional-chinese-medicine-in-treating-migraine-a-compr-peer-reviewed-fulltext-article-JPR

  The IL-1/COX2/PGE2 inflammatory pathway may be involved in the release of CGRP during trigeminovascular system activation in migraine. […] The BBB plays a crucial role in maintaining normal neuronal function. […] The change of BBB permeability associated with neuroinflammation is important when considering therapeutic strategies. […] Chinese herbs could be beneficial for the treatment of migraine by changing and regulating the BBB permeability. […] Massage can achieve analgesia by reducing substance P and cortisol levels, increasing 5-HT content, and relieving muscle tension.

• #40 Migraine – Wikipedia

  https://en.wikipedia.org/wiki/Migraine

  Migraine is believed to be caused by a mixture of environmental and genetic factors that influence the excitation and inhibition of nerve cells in the brain. […] The accepted hypothesis suggests that multiple primary neuronal impairments lead to a series of intracranial and extracranial changes, triggering a physiological cascade that leads to migraine symptomatology. […] Sensitization of trigeminal pathways is a key pathophysiological phenomenon in migraine. It is debatable whether sensitization starts in the periphery or in the brain. […] Cortical spreading depression, or spreading depression according to Leo, is a burst of neuronal activity followed by a period of inactivity, which is seen in those with migraine with aura. […] The exact mechanism of the head pain which occurs during a migraine episode is unknown. Some evidence supports a primary role for central nervous system structures (such as the brainstem and diencephalon), while other data support the role of peripheral activation (such as via the sensory nerves that surround blood vessels of the head and neck). […] Calcitonin gene-related peptides (CGRPs) have been found to play a role in the pathogenesis of the pain associated with migraine, as levels of it become elevated during an attack.

• #41 EXPLORING THE PATHOPHYSIOLOGY AND PATHOGENESIS OF MIGRAINE, AND THE PROMISING POTENTIAL OF HOMEOPATHIC MEDICINES

  https://www.linkedin.com/pulse/exploring-pathophysiology-pathogenesis-migraine-hospital-1h5gc

  The pathogenesis of migraine involves a complex interplay of genetic, environmental, and neurological factors that lead to the onset of a migraine attack. While the exact cause is not fully understood, the following key processes are involved: […] Genetic Predisposition: Migraine is known to have a genetic component, with a higher likelihood of occurrence in individuals with a family history of the condition. Certain genes related to neurotransmitter regulation and vascular function may predispose individuals to migraines. […] Triggering Factors: Various factors can trigger a migraine attack in susceptible individuals. These triggers might include stress, hormonal changes (such as menstruation), certain foods, alcohol, lack of sleep, or environmental factors like bright lights or strong smells.

• #42 EXPLORING THE PATHOPHYSIOLOGY AND PATHOGENESIS OF MIGRAINE, AND THE PROMISING POTENTIAL OF HOMEOPATHIC MEDICINES

  https://www.linkedin.com/pulse/exploring-pathophysiology-pathogenesis-migraine-hospital-1h5gc

  The pathogenesis of migraine involves a complex interplay of genetic, environmental, and neurological factors that lead to the onset of a migraine attack. While the exact cause is not fully understood, the following key processes are involved: […] Genetic Predisposition: Migraine is known to have a genetic component, with a higher likelihood of occurrence in individuals with a family history of the condition. Certain genes related to neurotransmitter regulation and vascular function may predispose individuals to migraines. […] Triggering Factors: Various factors can trigger a migraine attack in susceptible individuals. These triggers might include stress, hormonal changes (such as menstruation), certain foods, alcohol, lack of sleep, or environmental factors like bright lights or strong smells.

• #43 Mechanisms of migraine as a chronic evolutive condition | The Journal of Headache and Pain | Full Text

  https://thejournalofheadacheandpain.biomedcentral.com/articles/10.1186/s10194-019-1066-0

  Understanding the mechanisms of migraine remains challenging as migraine is not a static disorder, and even in its episodic form migraine remains an evolutive chronic condition. […] Considerable progress has been made in elucidating the pathophysiological mechanisms of migraine, associated genetic factors that may influence susceptibility to the disease, and functional and anatomical changes during the progression of a migraine attack or the transformation of episodic to chronic migraine. […] The mechanisms behind this evolutive process remain unknown, but genetic and epigenetic factors, inflammatory processes and central sensitization may play an important role. […] However, understanding disease mechanisms remains challenging as migraine is not a static disorder, and even in its episodic form migraine remains an evolutive chronic condition.

• #44 Mechanisms of migraine as a chronic evolutive condition | The Journal of Headache and Pain | Full Text

  https://thejournalofheadacheandpain.biomedcentral.com/articles/10.1186/s10194-019-1066-0

  Although genetic factors may be involved in the evolutive processes of migraine, to date they failed to explain the pathophysiology of migraine and evolutive mechanisms. […] The physiological mechanisms that underlie the development of chronic migraine from its episodic form are not understood. […] Inflammation and central sensitization play a significant role in the evolutive mechanisms of chronic migraine.

• #45 Headaches at the Back of Your Head: Causes, Pathogenesis, Symptoms, Diagnosis, and Treatment

  https://www.alleviatepainclinic.com/blog/comprehensive-guide-to-headaches-at-the-back-of-your-head-causes-pathogenesis-symptoms-diagnosis-and-treatment/

  Headaches at the back of the head can arise from various underlying causes. Understanding these causes is crucial for accurate diagnosis and effective treatment. Common causes include: […] The pathogenesis of headaches at the back of the head is complex and often related to the specific underlying cause. For example: […] Tension Headaches: These headaches are thought to result from muscle tension and changes in blood flow in the head and neck muscles. Psychological factors like stress and anxiety can contribute to their development. […] Cervicogenic Headaches: These headaches are primarily due to structural issues in the cervical spine. Arthritis, disc herniation, or trauma can lead to irritation of nerves or blood vessels, causing pain in the back of the head. […] Occipital Neuralgia: Occipital neuralgia is characterized by inflammation or irritation of the occipital nerves. This irritation can be due to trauma, compression, or other underlying conditions.

• #46 Headaches at the Back of Your Head: Causes, Pathogenesis, Symptoms, Diagnosis, and Treatment

  https://www.alleviatepainclinic.com/blog/comprehensive-guide-to-headaches-at-the-back-of-your-head-causes-pathogenesis-symptoms-diagnosis-and-treatment/

  Headaches at the back of the head can arise from various underlying causes. Understanding these causes is crucial for accurate diagnosis and effective treatment. Common causes include: […] The pathogenesis of headaches at the back of the head is complex and often related to the specific underlying cause. For example: […] Tension Headaches: These headaches are thought to result from muscle tension and changes in blood flow in the head and neck muscles. Psychological factors like stress and anxiety can contribute to their development. […] Cervicogenic Headaches: These headaches are primarily due to structural issues in the cervical spine. Arthritis, disc herniation, or trauma can lead to irritation of nerves or blood vessels, causing pain in the back of the head. […] Occipital Neuralgia: Occipital neuralgia is characterized by inflammation or irritation of the occipital nerves. This irritation can be due to trauma, compression, or other underlying conditions.

• #47 Headaches at the Back of Your Head: Causes, Pathogenesis, Symptoms, Diagnosis, and Treatment

  https://www.alleviatepainclinic.com/blog/comprehensive-guide-to-headaches-at-the-back-of-your-head-causes-pathogenesis-symptoms-diagnosis-and-treatment/

  Migraines and Cluster Headaches: The exact cause of these primary headaches is not fully understood, but they are believed to involve a combination of genetic, neurological, and vascular factors. […] Sinusitis: Sinus headaches at the back of the head are related to inflammation and pressure in the sinus cavities, which can refer pain to the head.

• #48 Current Understanding on Pain Mechanism in Migraine and Cluster Headache

  https://brieflands.com/articles/aapm-17559.html

  The clinical expression of first-order-neuron sensitization is the throbbing pain that characterizes migraine attacks. […] In CH, activation of the trigeminovascular system triggers autonomic manifestations through the trigeminal-autonomic reflex. […] Neurogenic inflammation refers to a neurally mediated inflammatory response in meningeal tissue characterised by vasodilatation, leakage of plasma protein from blood vessels and mast cell degranulation. […] The release of neuropeptides has been proposed as a pain mechanism in migraine and other primary headaches. […] The infusion of nitrovasodilators can trigger CH attacks similar to spontaneous attacks, suggesting a role for NO in nociceptive processes. […] Studies conducted by Kudrow et al. were the first to implicate the hypothalamus in the pathogenesis of CH with the demonstration of lower levels of testosterone during a bout. […] Neuroimaging further supports the role of the hypothalamus in CH. […] Imaging studies in CH have also implicated other brain areas that are generally associated with the pain matrix. […] Migraine and CH are neurovascular disorders with multiple processes and complex pathophysiologies.

• #49 Primary headache disorders: From pathophysiology to neurostimulation therapies

  https://pmc.ncbi.nlm.nih.gov/articles/PMC10106918/

  Primary headache disorders including migraine, cluster headache, and tension-type headache are among the most common disabling diseases worldwide. The unclear pathogenesis of primary headache disorders has led to high rates of misdiagnosis and limited available treatment options. […] Advances in functional neuroimaging, genetics, neurophysiology have indicated that cortical hyperexcitability, regional brain dysfunction, central sensitization and neuroplasticity changes play vital roles in the development of primary headache disorders. […] Advances in functional neuroimaging, neurophysiology and genetics have facilitated research on the pathophysiology and management of primary headache disorders. In this review, we have summarized some understanding of pathophysiology proposed to improve previous explanations, including vascular theory, trigeminovascular theory and neural theory.

• #50 Primary headache disorders: From pathophysiology to neurostimulation therapies

  https://pmc.ncbi.nlm.nih.gov/articles/PMC10106918/

  The findings of functional imaging studies, especially positron emission tomography (PET), have observed increase in regional cerebral blood flow in the rostral brainstem during migraine attacks, however the activation of brainstem still sustained even after sumatriptan treatments had relieved the nausea, phonophobia, and photophobia. […] It has been suggested that not only the midbrain and pons but also the hypothalamus is activated during migraine attacks. […] There are numerous evidences showing that the trigeminovascular system and neurogenic inflammation play important roles in the development process of migraine. However, the factors modulating susceptibility to attacks and the precise mechanisms triggering the initiation of attacks are still unclear. […] It is thought that CSD can activate the trigeminovascular system, but clinical studies remain to be conducted.

• #51 Modern understanding of the pathophysiology of migraine | CnsBytes US

  https://www.cnsbytes.us/migraine/modern-understanding-of-the-pathophysiology-of-migraine/

  In addition to nociceptive modulation and pain perception, CGRP is likely involved in other migraine phases and phenomena, such as photophobia and migraine aura. The mechanism through which CGRP causes migraine aura is believed to be related to its critical role in cortical spreading depression (CSD). […] With a better understanding of migraine pathophysiology, the focus of research has shifted to target-based approaches. In this context, the CGRP pathway has emerged as one of the primary mediators of migraine. In recent years, several monoclonal antibodies targeting the CGRP pathway have been studied and approved in select global regions for preventive treatment of episodic and chronic migraine. The development of new treatments targeting the CGRP pathway represents an exciting progress in the field of migraine prevention.

• #52 Migraine pathogenesis and state of pharmacological treatment options | BMC Medicine | Full Text

  https://bmcmedicine.biomedcentral.com/articles/10.1186/1741-7015-7-71

  The success of CGRP receptor antagonists and 5-HT1F receptor agonists reinforce a neurally-based approach to migraine and emphasize that migraine is a brain disorder. […] Migraine is a disorder of the brain characterized by a complex sensory dysfunction. Hence, therapeutic approaches with neural targets are most promising.

• #53 Mechanism of traditional Chinese medicine in treating migraine: future | JPR

  https://www.dovepress.com/mechanism-of-traditional-chinese-medicine-in-treating-migraine-a-compr-peer-reviewed-fulltext-article-JPR

  Acupuncture can inhibit CGRP by reducing NO release, activating CB1 receptors, and lowering levels of inflammatory factors. […] Acupuncture may provide additional potential benefits in neuronal sensitization by modulating neurotrophic factors and neurotransmitters; however, the evidence on how acupuncture affects neurotrophic factors and neurotransmitters is not clear. […] The mechanism of Chinese herbs in treating migraine involves the following aspects: 1) inhibiting the release and expression of CGRP neuropeptide; 2) suppressing inflammatory reactions such as inhibition of inflammatory factors and modulation of NF-B and nerve growth factor (NGF) signaling pathways; 3) changing the permeability of BBB. […] Studies have shown that acupuncture can alleviate neuroinflammation by reducing the release of trigeminal nerve-activating neuropeptides.

• #54 Migraine: pathogenesis and pathophysiology | MedLink Neurology

  https://www.medlink.com/articles/migraine-pathogenesis-and-pathophysiology

  The hypothalamus is not only implicated in the premonitory phase but also in the headache phase. […] Imaging studies suggest that the anterior thalamus is associated with the premonitory phase and chronic migraine whereas the posterior hypothalamus is involved with the headache phase. […] The trigeminal pain system can shift to whats known as chronic migraine through a variety of factors including impaired modulation, peripheral sensitization, central sensitization, decreased threshold, and alterations in connectivity. […] Predominating theories about pathogenesis include: hypoxemia with an associated increase in hemoglobin and cardiac output (which can initiate CSD), an increase in trigger chemicals (like serotonin) that avoid pulmonary capillary filtration, and microemboli/microthrombi that are shunted to the brain from the venous circulation causing tiny infarctions (and therefore low blood flow and/or CSD).

• #55 Migraine: Advances in the Pathogenesis and Treatment

  https://www.mdpi.com/2035-8377/15/3/67

  The phenomenon of central sensitization in individuals prone to migraine leads to heightened pain perception during a migraine, a condition known as cutaneous allodynia, and may contribute to the progression from episodic to chronic migraine. Approximately 65% of migraine sufferers develop cutaneous allodynia during individual headache episodes. Patients with allodynia experience the skin becoming painfully sensitive to stimuli that are normally harmless, such as a light touch. Developing ways to block or reverse central sensitization could potentially alleviate migraine pain and lower the likelihood of episodic migraine evolving into chronic migraine. […] […] The advent of neuroimaging technologies has brought significant advancements in our understanding of migraine mechanisms and has enabled us to pinpoint secondary structural and functional impacts resulting from migraine. Imaging conducted during a migraine episode has helped the scientific community progress from a strictly vascular understanding of migraine pathophysiology, to a neurovascular theory, and currently towards a central nervous system (CNS) model. […]

• #56 Stephen Silberstein, MD: Understanding the Mechanism of Migraine

  https://www.neurologylive.com/view/stephen-silberstein-md-understanding-the-mechanism-of-migraine

  Silberstein spoke about the new mechanism-based treatments that are revolutionary in changing the treatment landscape of migraine. […] We are now ending the era of misbelief and mistrust and moving onto the scientific proven therapies for the treatment of migraine. […] The migraine future is bright, as we have new drugs being developed that are mechanism-based, Stephen Silberstein, MD, Professor of Neurology, Thomas Jefferson University, and Director of the Jefferson Headache Center, told NeurologyLive in an interview. We now have an understanding of the mechanism of migraine and are working to target the mechanism themselves. […] The industry is now ending the era of misbelief and moving onto scientific proven therapies for the treatment of migraine.

• #57 Preventive Treatments | Complete list of Preventives Available in Canada, including Classes, Mechanisms of Action, and Side Effects – Migraine Canada

  https://migrainecanada.org/posts/the-migraine-tree/branches/preventive-treatments/migraine-preventives-classes-and-mechanism-of-action/

  There are several types of preventive medications and they act through different mechanisms in the brain to increase the migraine threshold (the limit your brain has for migraine occurrence) and make the brain less susceptible to triggers that result in a migraine attack. […] Preventive medications need to be taken at effective doses for several months. One month is never enough to make a decision. […] Migraine attacks often occur in cycles, with periods of increased frequency followed by times of relative calm. Various factors, such as less sleep, more stress, new medications, or hormonal changes, can trigger these episodes, but sometimes the reasons are unclear. […] Using migraine preventives can lead to a virtuous circle that may allow you to stop the drug. Its easier to adopt a healthy, migraine-friendly lifestyle when one is feeling better and life becomes more predictable.

• #58 Migraine pathogenesis and state of pharmacological treatment options | BMC Medicine | Full Text

  https://bmcmedicine.biomedcentral.com/articles/10.1186/1741-7015-7-71

  The success of CGRP receptor antagonists and 5-HT1F receptor agonists reinforce a neurally-based approach to migraine and emphasize that migraine is a brain disorder. […] Migraine is a disorder of the brain characterized by a complex sensory dysfunction. Hence, therapeutic approaches with neural targets are most promising.

• #59 Migraine pathogenesis and state of pharmacological treatment options | BMC Medicine | Full Text

  https://bmcmedicine.biomedcentral.com/articles/10.1186/1741-7015-7-71

  Compared to other hypothesis on migraine neurobiology, dysfunction of such brainstem structures and networks could not only account for the somatosensory component of migraine (headache) but also for the auditory, olfactory and visual components. […] Migraine prevention is an important component of therapy aimed at reducing the attack frequency and severity. […] A potential mechanism is the inhibition of cortical spreading depression but, as noted above, the efficacy against cortical spreading depression does not necessarily predict the efficacy in treating migraine without aura. […] According to the pathophysiological concepts discussed above, these drugs most probably target the activity of modulatory circuits as well as the neuronal activity in afferent sensory pathways such as the trigeminal system.

• #60 Headache – Wikipedia

  https://en.wikipedia.org/wiki/Headache

  Currently, most specialists think migraines are due to a primary problem with the nerves in the brain. Auras are thought to be caused by a wave of increased activity of neurons in the cerebral cortex (a part of the brain) known as cortical spreading depression followed by a period of depressed activity. Some people think headaches are caused by the activation of sensory nerves which release peptides or serotonin, causing inflammation in arteries, dura and meninges and also cause some vasodilation. Triptans, medications that treat migraines, block serotonin receptors and constrict blood vessels. […] Tension headaches are thought to be caused by the activation of peripheral nerves in the head and neck muscles. […] Cluster headaches involve overactivation of the trigeminal nerve and hypothalamus in the brain, but the exact cause is unknown.

• #61 What is the mechanism of Pizotifen?

  https://synapse.patsnap.com/article/what-is-the-mechanism-of-pizotifen

  Pizotifen is a medication primarily used in the prevention of migraine headaches and cluster headaches. Understanding its mechanism of action requires a dive into the complex neurophysiological processes involved in migraine pathophysiology and how Pizotifen interacts with various receptors in the brain. Pizotifen primarily functions as a serotonin antagonist. Serotonin, also known as 5-hydroxytryptamine (5-HT), plays a crucial role in the regulation of mood, appetite, and the vascular system, including cerebral blood vessels. During a migraine attack, there is a significant release of serotonin from platelets, which causes a sequence of reactions leading to the dilation and inflammation of blood vessels in the brain, contributing to the throbbing pain characteristic of migraines. […] Pizotifen works by blocking serotonin receptors, particularly the 5-HT2A and 5-HT2C receptors. By inhibiting these receptors, Pizotifen reduces the release of serotonin, thereby preventing the downstream vascular and inflammatory changes that lead to migraine headaches. This antagonistic action on serotonin receptors helps stabilize blood vessels and reduces the likelihood of migraine onset.

• #62 Stephen Silberstein, MD: Understanding the Mechanism of Migraine

  https://www.neurologylive.com/view/stephen-silberstein-md-understanding-the-mechanism-of-migraine

  Silberstein spoke about the new mechanism-based treatments that are revolutionary in changing the treatment landscape of migraine. […] We are now ending the era of misbelief and mistrust and moving onto the scientific proven therapies for the treatment of migraine. […] The migraine future is bright, as we have new drugs being developed that are mechanism-based, Stephen Silberstein, MD, Professor of Neurology, Thomas Jefferson University, and Director of the Jefferson Headache Center, told NeurologyLive in an interview. We now have an understanding of the mechanism of migraine and are working to target the mechanism themselves. […] The industry is now ending the era of misbelief and moving onto scientific proven therapies for the treatment of migraine.

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