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Migraine Pain (migraine + pain)

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Medical Sciences	100%

Selected Abstracts

Migraine Pain and Nociceptor Activation,Where Do We Stand?

HEADACHE, Issue 5 2010
Dan Levy PhD
The mechanisms underlying the genesis of migraine pain remain enigmatic largely because of the absence of any identifiable cephalic pathology. Based on numerous indirect lines of evidence, 2 nonmutually exclusive hypotheses have been put forward. The first theorizes that migraine pain originates in the periphery and requires the activation of primary afferent nociceptive neurons that innervate cephalic tissues, primarily the cranial meninges and their related blood vessels. The second maintains that nociceptor activation may not be required and that the headache is promoted primarily as a result of abnormal processing of sensory signals in the central nervous system. This paper reviews the evidence leading to these disparate theories while siding with the primacy of nociceptor activation in the genesis migraine headache. The paper further examines the potential future use of established human models of migraine for addressing the origin of migraine headache. [source]

Migraine Pain,Intracranial or Extracranial?

HEADACHE, Issue 10 2007
Elliot Shevel MD
No abstract is available for this article. [source]

Brain Imaging in Migraine Research

HEADACHE, Issue 9 2010
David Borsook MD
Understanding the pathophysiology and pharmacology of migraine has been driven by astute clinical observations, elegant experimental medicine studies, and importantly by studying highly effective anti-migraine agents in the laboratory and the clinic. Significant progress has been made in the use of functional brain imaging to compliment observational studies of migraine phenotypes by highlighting pathways within the brain that may be involved in predisposition to migraine, modulating migraine pain or that could be sensitive to pharmacological or behavioral therapeutic intervention (Fig. 1). In drug discovery, molecular imaging approaches compliment functional neuroimaging by visualizing migraine drug targets within the brain. Molecular imaging enables the selection and evaluation of drug candidates by confirming that they engage their targets sufficiently at well tolerated doses to test our therapeutic hypotheses. Figure 1.,. Imaging and defining the migraine brain disease state: from anatomy to chemical entities (targets) to functional systems (function and pathways) (from Borsook et al31 with permission, Nature Publishing Group). Migraine is a progressive disorder. Developing our knowledge of where drugs act in the brain and of how the brain is altered in both episodic migraine (interictal state and ictal state) and chronic migraine are important steps to understanding why there is such differential responsiveness to therapeutics among migraine patients and to improving how they are evaluated and treated. [source]

Migraine Pain and Nociceptor Activation,Where Do We Stand?

Middle Meningeal Artery Dilatation in Migraine

HEADACHE, Issue 10 2009
Dip MFOS, Elliot Shevel BDS, MB BCh
Objective., To show that migraine pain is not related to dilatation of the dural meningeal arteries. Background., The origin of the pain in migraine has not yet been adequately explained and remains the subject of vigorous debate. Current theories implicate changes in the trigeminovascular system, which is defined as comprising the large intracranial vessels, and in particular, the dural meningeal vessels, the dura mater, and their neural connections. Methods., The anatomical relationships of the dural meningeal arteries to the dura mater and the inner surface of the calvarium are described. Results., The dural meningeal arteries lie in grooves in the inner table of the calvarium, are encased in the unyielding fibrous dura mater, and are consequently unable to dilate. Conclusion., The pain of migraine is not related to dilatation of the dural meningeal arteries. [source]

Early Intervention With Almotriptan Improves Sustained Pain-free Response in Acute Migraine

HEADACHE, Issue 10 2003
Ninan T. Mathew MD
Objective.,To determine whether treatment of migraine with almotriptan, when pain intensity is mild, improves 1- and 2-hour pain-free and sustained pain-free rates compared with treatment when pain intensity is moderate or severe. Methods.,This was a post hoc analysis derived from an open-label, multicenter, long-term study of the safety, tolerability, and efficacy of almotriptan 12.5 mg. Patients who met International Headache Society criteria for migraine with or without aura were eligible. Patients were instructed to take a single dose of almotriptan 12.5 mg at the onset of a migraine attack. Rescue medication could be taken if migraine pain had not disappeared at 2 hours. A second dose of almotriptan 12.5 mg could be taken if head pain recurred within 24 hours of the initial dose. Patients reported the intensity of pain at baseline and at 1 and 2 hours postmedication using a 4-point scale: no pain, mild, moderate, or severe pain. They also reported recurrence of pain (return of moderate or severe pain within 2 to 24 hours of taking the study medication) and use of rescue medication. Rescue medication consisted of supplemental analgesics taken for pain relief at 2 to 24 hours postdose. Ergotamines and other 5-HT1B/1D agonists were excluded as rescue medications. Based on these patient-reported end points, sustained pain-free rates, defined as pain-free at 2 hours with no recurrence from 2 to 24 hours and no use of rescue medication, were calculated. Results.,A higher proportion of migraine attacks of mild intensity were pain-free at 1 hour (35.3%) compared with attacks of moderate or severe intensity (7.5%) (P < .001). Two-hour pain-free rates also were significantly higher with mild intensity pain (76.9%) compared to moderate or severe intensity (43.9%) (P < .001). In addition, recurrence rates and use of rescue medication were reduced when attacks were treated during mild pain. Recurrence was 12.9% for mild pain versus 25.0% for moderate or severe pain (P < .001), and use of rescue medication was 9.4% for mild pain versus 17.2% for moderate or severe pain (P < .001). Sustained pain-free rates were nearly twice as high when attacks were treated during mild intensity pain (66.6%) compared with attacks treated during moderate or severe pain (36.6%) (P < .001). Conclusion.,Treatment with almotriptan 12.5 mg during migraine attacks of mild pain intensity improves 1- and 2-hour pain-free and sustained pain-free responses. [source]

Neurotoxins in the Neurobiology of Pain

HEADACHE, Issue 2003
Stephen D. Silberstein MD
Migraine is a common, chronic, incapacitating, neurovascular disorder that affects an estimated 12% of the population. Understanding the basic mechanisms of pain is important when treating patients with chronic pain disorders. Pain, an unpleasant sensory and emotional experience, is usually triggered by stimulation of peripheral nerves and often associated with actual or potential tissue damage. Peripheral nerve fibers transmit pain signals from the periphery toward the spinal cord or brain stem. The different diameter pain fibers (A and C) vary in the speed of conduction and the type of pain transmitted (eg, sharp versus dull). When stimulated, peripheral pain fibers carrying sensory input from the body enter at different layers of the dorsal horn, which is then propagated toward the thalamus via the spinothalamic tract within the spinal cord. Conversely, sensory input from the face does not enter the spinal cord but enters the brain stem via the trigeminal nerve. This review describes in detail the neurobiological mechanisms and pathways for pain sensation, with a focus on migraine pain. [source]

Evidence for Antinociceptive Activity of Botulinum Toxin Type A in Pain Management

HEADACHE, Issue 2003
K. Roger Aoki PhD
The neurotoxin, botulinum toxin type A, has been used successfully, in some patients, as an analgesic for myofascial pain syndromes, migraine, and other headache types. The toxin inhibits the release of the neurotransmitter, acetylcholine, at the neuromuscular junction thereby inhibiting striated muscle contractions. In the majority of pain syndromes where botulinum toxin type A is effective, inhibiting muscle spasms is an important component of its activity. Even so, the reduction of pain often occurs before the decrease in muscle contractions suggesting that botulinum toxin type A has a more complex mechanism of action than initially hypothesized. Current data points to an antinociceptive effect of botulinum toxin type A that is separate from its neuromuscular activity. The common biochemical mechanism, however, remains the same between botulinum toxin type A's effect on the motor nerve or the sensory nerve: enzymatic blockade of neurotransmitter release. The antinociceptive effect of the toxin was reported to block substance P release using in vitro culture systems.1 The current investigation evaluated the in vivo mechanism of action for the antinociceptive action of botulinum toxin type A. In these studies, botulinum toxin type A was found to block the release of glutamate. Furthermore, Fos, a product of the immediate early gene, c- fos, expressed with neuronal stimuli was prevented upon peripheral exposure to the toxin. These findings suggest that botulinum toxin type A blocks peripheral sensitization and, indirectly, reduces central sensitization. The recent hypothesis that migraine involves both peripheral and central sensitization may help explain how botulinum toxin type A inhibits migraine pain by acting on these two pathways. Further research is needed to determine whether the antinociceptive mechanism mediated by botulinum toxin type A affects the neuronal signaling pathways that are activated during migraine. [source]

an algorithmic approach. (Jefferson Headache Center, Thomas Jefferson University, Philadelphia, PA) Neurology 2000;55:S46,S52.

PAIN PRACTICE, Issue 2 2001
Stephen D. Silberstein
This article provided practical suggestions for treating migraine pain. It covered an overall wellness program including exercise, rest, good nutrition, and avoidance of headache triggers. The authors pointed out that simple analgesics or nonsteroidal anti-inflammatory drugs are often the first line of attack with combinations of analgesics and ergotamine preparations representing the second-line of attack for patients with infrequent attacks. For patients unlikely to respond to simpler treatments, other options were provided. Patients suggested for preventive therapy were those with 3 or more days of headache-related disability per month or with headache refractory to acute treatment. [source]

Defeating migraine pain with triptans: A race against the development of cutaneous allodynia

ANNALS OF NEUROLOGY, Issue 1 2004
Rami Burstein PhD
For many migraine patients, triptan therapy provides complete pain relief in some attacks but not in others. Here, we tested whether the success of triptan therapy is hindered in the presence of cutaneous allodynia (pain resulting from a nonnoxious stimulus to normal skin), a phenomenon we previously described develop gradually during the course of the migraine attack in more than 70% of patients. We studied migraine patients repeatedly on three visits to the clinic: in the absence of migraine (baseline), within the first hour of one attack, or at 4 hours from onset of another attack. Presence or absence of allodynia was determined based on differences between migraine and baseline pain thresholds to mechanical and thermal stimulation of periorbital skin. In 31 patients, we studied 34 migraine attacks that were associated with allodynia at the time of triptan treatment and 27 attacks that were not. Within 2 hours of triptan treatment, patients were rendered pain-free in 5 of 34 (15%) of allodynic attacks versus 25 of 27 (93%) of nonallodynic attacks. Treating migraine attacks 1 hour (early) or 4 hours (late) after the onset of pain was equally ineffective in inducing a pain-free state in the presence of allodynia, and equally effective in the absence of allodynia. For patients susceptible to allodynia during the attack, triptan therapy was by far more likely to provide complete pain relief if administered before rather than after the establishment of cutaneous allodynia. Patients who never developed allodynia were highly likely to be rendered pain-free by triptan therapy anytime after the onset of pain. We conclude that the probability of consistent pain-free outcome increases drastically if triptan therapy is vigilantly timed to precede any signs of cutaneous allodynia. Ann Neurol 2004;55:000,000 [source]