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Anti-Migraine agents |
A migraine headache is
a form of vascular headache. Migraine headache is caused by a combination
of vasodilatation (enlargement of blood vessels) and the release of chemicals
from nerve fibers that coil around the blood vessels. During a migraine
attack, the temporal artery enlarges. (The temporal artery is an artery
that lies on the outside of the skull just under the skin of the temple.)
Enlargement of the temporal artery stretches the nerves that coil around
the artery and causes the nerves to release chemicals. The chemicals cause
inflammation, pain, and further enlargement of the artery. The increasing
enlargement of the artery magnifies the pain.
Migraine attacks commonly activate the sympathetic nervous system in the
body. The sympathetic nervous system is often thought of as the part of
the nervous system that controls primitive responses to stress and pain,
the so-called "fight or flight" response. The increased sympathetic
nervous activity in the intestine causes nausea, vomiting, and diarrhea.
Sympathetic activity also delays emptying of the stomach into the small
intestine and thereby prevents oral medications from entering the intestine
and being absorbed. The impaired absorption of oral medications is a common
reason for the ineffectiveness of medications taken to treat migraine
headaches. The increased sympathetic activity also decreases the circulation
of blood, and this leads to pallor of the skin as well as cold hands and
feet. The increased sympathetic activity also contributes to the sensitivity
to light and sound sensitivity as well as blurred vision.
Migraine afflicts 28 million Americans, with females suffering more frequently
(17%) than males (6%). Missed work and lost productivity from migraine
create a significant public burden. Nevertheless, migraine still remains
largely undertreated and underdiagnosed. Less than half the sufferers
are diagnosed by their doctors.
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IMIGRAN (IMITREX)
Generic name: Sumatriptan succinate
Manufacturer: Glaxo Wellcome (UK)
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Dosage |
Packing |
Price |
Pay now |
50 mg |
6 tab |
USD 66.00 |
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100 mg |
6 tab |
USD 107.00 |
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Medication therapies for migraine |
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Individuals with
occasional mild migraine headaches that do not interfere with daily activities
usually medicate themselves with over-the-counter (OTC, non-prescription)
pain relievers (analgesics). Many OTC analgesics are available. OTC analgesics
have been shown to be safe and effective for short-term relief of headache
(as well as muscle aches, pains, menstrual cramps , and fever) when used
according to the instructions on their labels.
There are two major classes of OTC analgesics: acetaminophen (Tylenol)
and non-steroidal anti-inflammatory drugs (NSAIDs). The two types of NSAIDs
are aspirin and non-aspirin. Examples of non-aspirin NSAIDs are ibuprofen
(Advil, Nuprin, Motrin IB, and Medipren) and naproxen (Aleve). Some NSAIDs
are available by prescription only. Prescription NSAIDs are usually prescribed
to treat arthritis and other inflammatory conditions such as bursitis,
tendonitis, etc. The difference between OTC and prescription NSAIDs may
only be the amount of the active ingredient contained in each pill. For
example, OTC naproxen (Aleve) contains 220 mg of naproxen per pill, whereas
prescription naproxen (Naprosyn) contains 375 or 500 mg of naproxen per
pill.
Acetaminophen reduces pain and fever by acting on pain centers in the
brain. Acetaminophen is well tolerated and generally is considered easier
on the stomach than NSAIDs. However, acetaminophen can cause severe liver
damage in high (toxic) doses or if used on a regular basis over extended
periods of time. In individuals who regularly consume moderate or large
amounts of alcohol, acetaminophen can cause serious damage to the liver
in lower doses that usually are not toxic. Acetaminophen also can damage
the kidneys when taken in large doses. Therefore, acetaminophen should
not be taken more frequently or in larger doses than recommended on the
label. For information, please read the Acetaminophen and Liver Damage
article.
NSAIDs relieve pain by reducing the inflammation that causes the pain
(They are called non-steroidal anti-inflammatory drugs or NSAIDs because
they are different from corticosteroids such as prednisone, prednisolone,
and cortisone which also reduce inflammation). Corticosteroids, though
valuable in reducing inflammation, have predictable and potentially serious
side effects, especially when used long-term. NSAIDs do not have the same
side effects that corticosteroids have.
Aspirin, Aleve, Motrin, and Advil all are NSAIDs and are similarly effective
in relieving pain and fever. The main difference between aspirin and non-aspirin
NSAIDs is their effect on platelets. Platelets are small particles in
the blood that cause blood clots to form. Aspirin prevents the platelets
from forming blood clots. Therefore, aspirin can increase bleeding by
preventing blood from clotting though it also can be used therapeutically
to prevent clots from causing heart attacks and strokes. The non-aspirin
NSAIDs also have anti-platelet effects, but their anti-platelet action
does not last as long as aspirin.
Aspirin, acetaminophen, and caffeine also are available combined in OTC
analgesics for the treatment of headaches. Examples of such combination
analgesics are Pain-aid, Excedrin, Fioricet, and Fiorinal.
Finding an effective analgesic or analgesic combination often is a process
of trial and error because individuals respond differently to different
analgesics. In general, a person should use the analgesic that has worked
in the past. This will increase the likelihood that an analgesic will
be effective and decrease the risk of side effects. |
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Articles on Anti-Migraine
agents |
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Am Fam Physician.
2005 Feb 15;71(4):717-24.
Management of cluster headache.
Beck E, Sieber WJ, Trejo R.
Department of Family and Preventive Medicine, University of California,
San Diego, La Jolla, California, USA. ebeck@ucsd.edu
Cluster headache, an excruciating, unilateral headache usually accompanied
by conjunctival injection and lacrimation, can occur episodically or chronically,
and can be difficult to treat. Existing effective treatments may be underused
because of underdiagnosis of the syndrome. Oxygen and sumatriptan have
been demonstrated to be effective in the acute treatment of cluster headaches.
Verapamil has been shown to be effective for prophylaxis. For cluster
headache completely refractory to all treatments, surgical modalities
and newer interventions such as the implantation of stereotactic electrodes
may be useful. Patients should be encouraged to avoid possible triggers
such as smoking or alcohol consumption, especially during the duster period.
The intensity of duster headache pain leads to ethical concerns among
researchers over the use of placebo, making randomized controlled trials
difficult. As new technology and genetic studies clarify the etiology
of duster headache, it is possible that more specific therapies will emerge.
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J Neurol. 2005 Mar
11.
The use of multiattribute decision models in evaluating triptan treatment
options in migraine.
Ferrari MD, Goadsby PJ, Lipton RB, Dodick DW, Cutrer FM, McCrory D, Williams
P.
Dept. of Neurology, Leiden University Medical Centre, 9600, 2300, RC Leiden,
The Netherlands, M.D.Ferrari@LUMC.NL.
BACKGROUND : The physician treating patients with migraine is now able
to choose from among seven triptans-almotriptan, eletriptan, frovatriptan,
naratriptan, rizatriptan, sumatriptan and zolmitriptan. These differ,
to greater or lesser degrees, on a range of clinical attributes important
for treatment selection. OBJECTIVE : To outline the basic principles of
Multiattribute Decision Making (MADM) and describe how one such method-TOPSIS
(Technique for Order Preference by Similarity to the Ideal Solution)-can
be applied to evaluate the currently available triptans. METHODS : In
an example application, summary data from a recent meta-analysis of 53
published and unpublished placebo-controlled trials of the oral triptans
were combined in TOPSIS models with computer-generated attribute importance
weights representing the entire range of possible values, That is, the
relative performance of the triptans was explored across all logically
possible combinations of relative importance of the treatment attributes
available from the meta-analysis, and uncertainty was assessed based on
the confidence intervals from the meta-analysis. RESULTS : When compared
across the entire range of values for relative attribute importance, almotriptan,
eletriptan and rizatriptan were more similar to a hypothetical ideal triptan
and were more likely to appear in the top three closest to the hypothetical
ideal, than were naratriptan, sumatriptan, and zolmitriptan. CONCLUSION
: Using the TOPSIS model, almotriptan, eletriptan and rizatriptan were
more likely to appear in the top three closest to the hypothetical ideal
triptan.
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Cephalalgia. 2003
Sep;23(7):504-10.
Placebo response in cluster headache trials: a review.
Nilsson Remahl AI, Laudon Meyer E, Cordonnier C, Goadsby PJ.
Department of Neurology at Karolinska Institutet, Huddinge University Hospital,
Sweden.
Probably because of its relative rarity as primary headache, there are
few well-controlled clinical trials on cluster headache (CH) patients.
Due to the severity of the pain, the placebo response in CH has been considered
to be small. During the eighties the first double-blind, placebo-controlled
trials were reported, and placebo responses demonstrated. Here we review
the placebo response in CH trials in order to assess its magnitude and
consider how future studies can be optimized. Six trials were identified
with a double-blind, placebo-controlled, cross-over design testing treatments
of acute CH. For those with a primary endpoint set to no or mild headache
the placebo responses varied from 7 to 42%. In five of seven prophylactic
trials, using a double-blind, placebo-controlled, parallel-group design,
the placebo was merely used to set a baseline for comparison. The placebo
responses were reported in only two trials. Here the response varies from
14 to 43%, the lowest value was reported using the strict endpoint; cessation
of headache attacks. We conclude that a placebo response exists in trials
of drugs on CH patients. Furthermore, this placebo response is of the
same magnitude as that seen in migraine studies. We recommend the use
of IHS guidelines when designing new trials. The possibility of a genuine
biological mechanism responsible for the placebo response is discussed.
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Int J Clin Pract.
1998 Nov-Dec;52(8):566-70.
New anti-migraine drugs: present and beyond the millennium.
Limmroth V, Diener HC.
Department of Neurology, University of Essen, Germany.
A fast growing new class of anti-migraine drugs has recently been introduced
for the acute treatment of migraine: the serotonin (5-HT) 1B/D-agonists.
Since the introduction of its first representative, sumatriptan, in 1993,
several new compounds of this class have been or are about to be approved.
The following review introduces this class of compounds and focuses on
indications, differences, advantages and disadvantages of each member.
It further discusses new indications of established drugs for the use
in migraine, including prophylaxis. For the use of analgesics and ergotamine,
the reader is referred to recent reviews.
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Headache. 1990 Jan;30(1
Suppl):5-11; discussion 24-8.
The pharmacology of current anti-migraine drugs.
Peroutka SJ.
Department of Neurology, Stanford University Medical Center, CA 94305.
The major finding of this analysis is that acute anti-migraine agents
(e.g., ergots, sumatriptan) share high affinity for 5-HT1D receptors.
This receptor appears to be present in certain intracranial blood vessels.
It is also found on nerve terminals where it inhibits the release of 5-HT
and other neurotransmitters. Theoretically, 5-HT1D receptor agonists may
acutely inhibit the release of vasoactive and/or pain-inducing substances
in the perivascular space. Conceivably, drugs acting at this receptor
would stop the progression of this perivascular process. In contrast,
a number of prophylactic anti-migraine drugs share a relatively high affinity
for 5-HT2 receptors in human brain. Although this receptor is also found
in certain blood vessels, it is present throughout the nervous system.
The receptor appears to mediate neuronal depolarizations at the cellular
level. No hypothesis, at present, readily explains the effectiveness of
prophylactic anti-migraine drugs based on this receptor. These data offer
a novel approach to the analysis of anti-migraine agents. Drugs could
be selected for use in clinical migraine studies based on their selectivity
for a specific 5-HT receptor subtype. "Pure" drugs could be
chosen which would essentially limit the number of possible sites of action
for the drugs. For example, an agent which displays both high affinity
and selectivity for 5-HT1D receptors could be clinically evaluated. Its
effectiveness, or lack thereof, would indicate the importance of the specific
5-HT receptor site in the pathogenesis of migraine. Further attempts to
determine a common mechanism of action for effective anti-migraine agents
should facilitate the elucidation of the pathogenesis of this neurological
syndrome.
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