Showing posts with label trigger. Show all posts
Showing posts with label trigger. Show all posts

Sunday, September 2, 2012

Stop migraines before they start

http://www.health.harvard.edu/newsletters/Harvard_Health_Letter/2012/August/stop-migraines-before-they-start?utm_source=health&utm_medium=pressrelease&utm_campaign=health0812


Take advantage of proven therapies.
If you are a migraine sufferer, then you undoubtedly long for something, anything, to keep these painful episodes from recurring. Migraines affect about 15% of the adult population, but only a relatively small percentage of those people take advantage of preventive medications.
Migraine prevention guidelines released earlier this year by the American Academy of Neurology and the American Headache Society note that about 38% of people who have migraines could benefit from preventive medications, but less than a third of those people actually utilize these treatments. Dr. Lee Schwamm, vice chairman of the Department of Neurology at Massachusetts General Hospital, suggests that one explanation may be that these drugs must be taken every day to be effective, even though migraines might only be "an intermittent problem."
"The evidence shows that the more often you have to take a medicine, the less likely you are to take it faithfully," says Dr. Schwamm. "If you don't have the symptom right away when you skip a dose, then you are even more likely to skip doses." He adds that the expense of some pills also may diminish compliance.
The mystery of migraines
The mystery of migraines
These are three current theories about what causes migraine pain.

What causes migraines?

The cause of migraine headaches is still not completely understood. Nerve fibers that have endings on blood vessels in the brain become extra sensitive to pain. Every heartbeat creates extra pressure on the blood vessel walls. The supersensitive nerve endings turn this into a throbbing headache. Why the nerve endings are sensitized is not known. Migraines also are influenced, in part, by genetics. Diet, exercise, hormones, sleep, and other illnesses or medications can all play a role in when and how a migraine hits.

Preventive medications

Drugs listed in the new guidelines include the antiseizure drugs divalproex (Depakote), valproate (Depacon), and topiramate (Topamax), along with the beta blockers metoprolol, propranolol, and timolol. The herbal remedy butterbur was also listed as an effective prevention option for some migraineurs, people who experience migraine headaches.
Dr. Schwamm notes that all of these medicines have side effects, which may also play a part in their underuse. "Because topiramate has a side effect of weight loss, some patients are more compliant with this drug," he says. The antiseizure medicines listed above used to prevent migraines can reduce concentration and may cause some drowsiness. Beta blockers can slow heart rate, cause low blood pressure, and in some cases cause depression or sexual dysfunction. Check with your doctor about side effects.
"These drugs can reduce the frequency and severity of migraine attacks, and may require different doses over time to achieve these benefits," says Dr. Schwamm. "They must be taken daily. They are different from pain-relieving medicines—drugs that halt a migraine once it has started."
The pain-relieving medicines used most often are over-the-counter medications such as aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) and prescription drugs such as Fiorinal or Fioricet, or a class of medicines called triptans. These medicines can be quite effective at stopping a migraine, but they are not helpful for preventing migraines, according to Dr. Schwamm.

Personalized migraine prevention

Migraine prevention, however, does not always require medications. "Good sleep hygiene, attention to diet and exercise, and reducing stress are all very effective strategies, but are not always sufficient to prevent disabling attacks," says Dr. Schwamm.
Knowing your migraine triggers can also help you cut down on the frequency of attacks. Items such as chocolate, caffeine, and alcohol are known triggers for some. The causes of migraines are all very individual.
If you suspect that chocolate, for example, is a trigger for you, Dr. Schwamm suggests experimenting to see if it's true and whether a small amount of chocolate is safe to eat. "Try a nibble of chocolate and then see if a headache predictably follows," he advises. "Increase the dose daily until you discover that you either get migraines reproducibly, or you get to eat yummy chocolate whenever you want. Repeat this process for other potential provocative foods."
Caffeine has a causal relationship with headaches. Abrupt cessation of caffeine triggers migraines in many people, as does the abrupt withdrawal of commonly prescribed pain-relieving medicines such as NSAIDs or prescription medications such as Fiorinal or Fioricet, which contain caffeine.
In addition, Dr. Schwamm says it is very helpful to record when your migraines occur and what was going on that day. Include details such as what you were doing when the headache started, what your day had been like (stressful, sedentary, active, etc.), if you were hungry, when you ate last, if you had a fever or other symptoms, and, for women, at what point in in your menstrual cycle the headache occurred. He also suggests rating your symptoms as mild, moderate, or severe, and noting how long the migraine lasted.

Thursday, July 14, 2011

What initiates a migraine attack? Conclusions from four longitudinal studies of quantitative EEG and steady-state visual-evoked potentials in migraineurs.

Acta Neurol Scand: 2011: 124 (Suppl. 191): 56–63. © 2011 John Wiley & Sons A/S.

Bjørk M, Stovner LJ, Hagen K, Sand T.
Objectives – Quantitative electroencephalograpic (QEEG) frequency spectra and steady-state visual-evoked potentials (SSVEP) are indicators of corticothalamic excitability (e.g., arousal). Increased interictal excitability is suggested to be an important element in the migraine pathophysiology. In this paper, we summarize our results from four studies of QEEG and SSVEP recordings in migraineurs interictally and in the days before an attack with the intention to shed light on attack-initiating mechanisms.
Material and methods – Thirty-two healthy controls, 33 migraineurs without and eight with aura each had three EEGs with photic stimulation on different days. Using the patient headache diaries, we classified the recordings as interictal, preictal, ictal, or post-ictal retrospectively. Interictal recordings were compared pairwise with attack-related EEGs from the same patient as well as with control EEGs. We also correlated clinical variables with the QEEG and SSVEP data.
Results – Between attacks, we found increased relative theta activity and attenuated medium-frequency photic responses in migraineurs without aura compared with those in controls. Within 36 h before the attack, slow and asymmetric EEG activity developed. Increased trigger sensitivity and photophobia correlated with higher theta power and depressed photic responses. Attack duration, migraine history duration, and pain intensity were associated with EEG slowing.
Conclusions – A general tendency toward EEG slowing and depression of photic responses characterized the migraine group. This pattern was also related to increased severity of symptoms. A change in cortical activity occurred within 36 h before attacks. Our results indicate that thalamocortical hypoexcitability is associated with attack initiation and sensory hypersensitivity in migraine.

Wednesday, July 6, 2011

What initiates a migraine attack? Conclusions from four longitudinal studies of quantitative EEG and steady-state visual-evoked potentials in migraineurs.

Acta Neurol Scand: 2011: 124 (Suppl. 191): 56–63. © 2011 John Wiley & Sons A/S.
Bjørk M, Stovner LJ, Hagen K, Sand T. 


Objectives – Quantitative electroencephalograpic (QEEG) frequency spectra and steady-state visual-evoked potentials (SSVEP) are indicators of corticothalamic excitability (e.g., arousal). Increased interictal excitability is suggested to be an important element in the migraine pathophysiology. In this paper, we summarize our results from four studies of QEEG and SSVEP recordings in migraineurs interictally and in the days before an attack with the intention to shed light on attack-initiating mechanisms.


Material and methods – Thirty-two healthy controls, 33 migraineurs without and eight with aura each had three EEGs with photic stimulation on different days. Using the patient headache diaries, we classified the recordings as interictal, preictal, ictal, or post-ictal retrospectively. Interictal recordings were compared pairwise with attack-related EEGs from the same patient as well as with control EEGs. We also correlated clinical variables with the QEEG and SSVEP data.


Results – Between attacks, we found increased relative theta activity and attenuated medium-frequency photic responses in migraineurs without aura compared with those in controls. Within 36 h before the attack, slow and asymmetric EEG activity developed. Increased trigger sensitivity and photophobia correlated with higher theta power and depressed photic responses. Attack duration, migraine history duration, and pain intensity were associated with EEG slowing.


Conclusions – A general tendency toward EEG slowing and depression of photic responses characterized the migraine group. This pattern was also related to increased severity of symptoms. A change in cortical activity occurred within 36 h before attacks. Our results indicate that thalamocortical hypoexcitability is associated with attack initiation and sensory hypersensitivity in migraine.

Wednesday, February 24, 2010

Sleep and Headache

Current Treatment Options in Neurology 1092-8480 (Print) 1534-3138 (Online)Jeanetta C. Rains1 and J. Steven Poceta2

(1) Center for Sleep Evaluation, Elliot Hospital, One Elliot Way, Manchester, NH 03103, USA
(2) Scripps Clinic Sleep Center and Division of Nematology, 10666 North Torrey Pines Road, La Jolla, CA 92037, USA 


Published online: 14 February 2010

Opinion statement Headache has been linked to a wide range of sleep disorders that may impact headache management. There are no evidence-based guidelines, but the authors believe that literature supports the following clinical recommendations: 1. Diagnose headache according to standardized criteria. Specific diagnoses are associated with increased risk for specific sleep and psychiatric disorders.
2. Collect sleep history in relation to headache patterns. Screening questionnaires and prediction equations are cost-effective.
3. Rule out sleep apnea headache in patients with awakening headache or higher-risk headache diagnoses (cluster, hypnic, chronic migraine, and chronic tension-type headache); patients with signs and symptoms of obstructive sleep apnea warrant polysomnography and treatment according to sleep medicine practice guidelines. There is no evidence for suspending conventional headache treatment in suspected or confirmed cases of sleep apnea. Treatment of sleep apnea with CPAP may improve or resolve headache in a subset of patients. The impact on sleep apnea headache of other treatments for sleep apnea (eg, oral appliances, surgery, weight loss) is largely untested. At a minimum, sedative-hypnotic drugs should be avoided in suspected apneics until the sleep apnea is treated.
4. Among patients with migraine and tension-type headache, insomnia is the most common sleep complaint, reported by one half to two thirds of clinic patients. Patients who suffer from chronic migraine or tension-type headache may benefit from behavioral sleep modification. Pharmacologic treatment may be considered on a case-by-case basis, with hypnotics, anxiolytics, or sedating antidepressants used to manage insomnia, tailoring treatment to the symptom pattern.
5. Individuals with chronic headache are at increased risk for psychiatric disorders. Assessment for depression and anxiety may be warranted when either insomnia or hypersomnia is present. Psychiatric symptoms affect the choice of sedating versus alerting versus neutral pharmacologic agents for headache.
6. All headache patients, particularly those with episodic migraine and tension-type headaches, may benefit from inclusion of sleep variables in trigger management.

Wednesday, November 25, 2009

How triggers trigger acute migraine attacks: A hypothesis

Medical Hypotheses
Volume 73, Issue 5, Pages 633-866 (November 2009)
Ambar Chakravarty, Department of Neurology, Vivekananda Institute of Medical Science, 1E 1202, Avishikta II, Calcutta 700 078, India (Tel.: +91 33 24843283.)

Summary 
  A trigger is an integral part of any acute migraine attack. In this article, the author argues that triggers, identifiable or not, must be present in all attacks of migraine headache. It is hypothesized that triggers, internal or external, induce the onset of cortical spreading depression (CSD) in a pre-existing hyper-excitable cortex of a migraine brain, initiating the process of pain generation.
The author hypothesizes on a second site of action of triggers at the level of trigeminal nuclear complex (TNC) in brain stem, the cell station of second order neuron pathway for migraine pain transmission to the sensory cortex.
The author suggests existence of a hypothetical ‘gate’ at TNC level where incoming trigeminal migraine pain impulses would ‘compete’ with descending inhibitory signals from brain stem pain modulatory neurons, to get entry into the central nervous system. The author draws analogy with the ‘gate control’ mechanism operative at the dorsal horn level for spinally transmitted somatic and visceral pain. It is suggested that the hypothetical ‘gate’ at TNC level is controlled by activity of 5HT receptors, thus supporting the concept of an additional site of action of triptans in aborting acute migraine pain.
The suggested hypothesis on mechanism of action of triggers, offers theoretical basis for efficacy of currently available pharmacologic and non-pharmacologic therapies for abortive and prophylactic treatment of migraine.

Monday, September 21, 2009

Neurological mechanisms of migraine: potential of the gap-junction modulator tonabersat in prevention of migraine.

Durham PL, Garrett FG.
Center for Biomedical and Life Sciences, Missouri State University, Springfield, MO 65897, USA. pauldurham@missouristate.edu

Migraine is a neurovascular disorder characterized by recurrent episodic headaches, and is caused by abnormal processing of sensory information due to peripheral and/or central sensitization. The exact pathophysiological mechanism underlying migraine is not fully understood; however, cortical spreading depression (CSD) is thought to provide the basis for migraine aura and may serve as a trigger of migraine pain. CSD depends on neuronal-glial cell communication, which is mediated by intercellular transfer of messengers through connexin-containing gap junctions, as well as messengers released into the extracellular space by non-junctional connexin-containing hemichannels. These processes are believed to be important in peripheral sensitization within the trigeminal ganglion and to lead to central sensitization. The novel benzopyran compound tonabersat binds selectively to a unique site in the brain. In preclinical studies, tonabersat markedly reduced CSD and CSD-associated events and inhibited gap-junction communication between neurons and satellite glial cells in the trigeminal ganglion. Together, these findings suggest that tonabersat should have clinical application in preventing migraine attacks.

Cephalalgia. 2009 Nov;29 Suppl 2:1-6

Friday, September 4, 2009

Blame Your Migraine on the Weather

Blame Your Migraine on the Weather

(Ivanhoe Newswire)

A large-scale study confirms what some migraine sufferers have suspected for years; the weather can play a role in their headaches.The research, led by a team at Beth Israel Deaconess Medical Center (BIDMC), looks at more than 7,000 patients and how environmental conditions, including the weather and air pollution influence headache pain. The findings demonstrate that higher temperatures and lower barometric pressure contribute to severe headaches.The study’s first author and BIDMC physician Dr. Kenneth Mukammal recommends patients sit down with their doctors to identify the triggers that lead to their headache symptoms. Dr. Mukammal adds that even though the weather can't be altered, doctors might be able to prescribe medication that can be administered to help avert the onset of weather-related headaches.

SOURCE: Neurology, March 2009