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However, preventative therapy may also be given for less frequent but very disabling symptoms.
It is reasonable to consider a preventive medicine when:
Symptoms are interfering significantly with work, school or social life
Symptoms are occurring at least once a week
Although it is not officially endorsed, the use of a preventive medicine can be helpful to confirm a suspected diagnosis.
Since many migraine disorders are more chronic, treatment with preventive agents often offers the best relief to sufferers, but finding an agent that has tolerable side effects and is effective involves a trial and error process. It is usually most effective and safe to trial one medicine at a time, although some medications work well together in low doses.
These drugs were first used for many other medical purposes, such as prevention of high blood pressure, depression or epilepsy. These medicines act on the transmission of information in our nervous system and, at the low doses needed for preventing migraine, they usually have little or no other effects.
There are no firm rules on how any particular medication should be used. The Food and Drug Administration (FDA) has approved only four of these drugs for prevention of migraine: propanolol, timolol, divalproex sodium (Depakote) and topiramate (Topamax), but that does not mean that there has not been a great deal of research and success with a much larger number of migraine preventive drugs.
A beta blocker or calcium channel antagonist may be more appropriate for a patient with hypertension, while a tricyclic antidepressant may benefit a migraine patient who is depressed or having difficulty sleeping.
These medicines should be started at a low dose to minimize side effects. The dose should be regularly increased in small amounts until an ideal dose is reached.
Many medicines need be taken for 4-12 weeks to know if it works or not. Discuss with your physician the option to discontinue any medication that causes an unpleasant side effect.
Migraine preventative treatments often do not completely prevent all migraine symptoms, but they aim to reduce the frequency and severity of symptoms.
You need to discuss with your health professional issues about pregnancy, weight, sleep disturbances, blood pressure and more.
If a preventative treatment works well, that medication can then be continued for several months (usually 6-12 months). With better symptom control one may want to wean down the dose. When stopping a preventive medicine, there is a risk of the headaches returning. It is unusual for migraine frequency suddenly to bounce back again during weaning down. Migraine illness varies during a lifetime and the use of preventive medication may have to be adjusting for those variations.
This information is NOT intended to endorse drugs or recommend therapy. While these reviews might be helpful, they are not a substitute for the expertise, skill, knowledge and judgment of healthcare practitioners in patient care. Only your doctor can decide which medications are right for you. Never stop, start or change the way you use a prescription medicine without first consulting your doctor.
This beta-adrenergic blocking drug may suppress the central catecholaminergic system by inhibiting norepinephrine release, reducing neuronal activity and excitability, stabilizing cell membranes and inhibiting nitric oxide production. Altogether the effects make the brain less reactive.
Low blood pressure (dizziness and lightheadedness, cold fingers and feet)
Sexual dysfunction (decreased libido and function)
Worsen asthma (limits use in young adults)
Vivid dreams and nightmares
It is extremely important not to stop the drug abruptly. Lower dose when combined with Rizatriptan (Maxalt). Some evidence suggests that people with migraines who have had a stroke should avoid beta-blockers.
Although not FDA-approved for migraine, several different agents including: Verapamil, Flunarizine (not available in the United States), Nimodipine, Nifedipine, Cyclandelate, and Nicardipine.
Calcium-channel blockers most likely act by suppressing nitric oxide. The drug decreases calcium influx, resulting in decreased activity of neural nitric oxide synthase and lower production of nitric oxide. Calcium-channel blockers can also suppress the neurovascular inflammation by inhibiting the release of vasoactive neuropeptide release and suppressing trigeminal nerve activation.
A current strategy in migraine prevention is the suppression of cortical spreading depression. Animal models show that prolonged treatment with Topiramate or Amitriptyline, as well as Beta-blockers, Valproate, or Methysergide, reduced the number of cortical spreading depressions.
For more detailed information on Verapamil’s mechanism of action see drugfx.com.
The most common side effects are related to reducing the pumping mechanism of the heart:
Low blood pressure
Atrioventricular (AV) block
Change in heart rate
Shortness of breath
Increased levels in liver enzymes
Flushing and fluid in the lungs
Avoid Verapamil if they have severe heart abnormalities, low blood pressure, poor heart function, certain heart rhythm problems, certain types of blockages in the heart called second or third degree Atrioventricular (AV) block, rapid heart rate or any allergic reaction to Verapamil.
Anti-seizure drug appear to control migraine symptoms by targeting one or more sites in the brain - altering transmission of neurologic electrical signals through their effects on ion channels, neurotransmitter receptors, and neurotransmitter metabolism. Not all anti-epileptics have equal effectiveness.
Some examples are:
Divalproex sodium (Depakote)
Valproic acid (Depakene)/sodium valproate (Epilim)
Tingling in the hands or feet is common but will pass with continued use of Topiramate
Change in taste, particularly with carbonated drinks
Nausea, vomiting, diarrhea, cramps
Fatigue and sleepiness
Topiramate can reduce the efficacy of the contraceptive pill
Valproate and Divalproex can cause serious side effects of inflammation of the pancreas (pancreatitis) and damage to the liver. Monitor liver function and platelets.
Studies show that migraine sufferers have lower brain and blood levels of micronutrients (riboflavin, magnesium and coenzyme Q10) than nonmigraineurs (Hershey, 1999; Hershey, 2007; Mauskop, 1998).
A deficit of these nutrients could play a role in how well nerves can function. The common effect of these micronutrients on mitochondrial dysfunction may explain why they are ineffective for some people who likely do not suffer from this etiology of their migraine disease and only partially reduce symptoms in other people in this complex disease.
Magnesium - Needed in various biological processes that occur with migraine (vasoconstriction, platelet inhibition, secretion of serotonin). Magnesium is also needed as a co-factor for proper functioning of the ATP-synthase, which produces ATP. Furthermore, magnesium is the physiological antagonist at the NMDA-channel which is involved in the regulation of neuronal excitability.
Riboflavin - A precursor for flavin-mononucleotide (FMN) and flavin-adenine-dinucleotide (FAD). Both are essential components of complex I and complex II responsible for electron-transport in the mitochondrial membrane. Like CoQ10, it also works as an antioxidant by mopping up the damaging free radicals.
Memantine - May reduce migraine symptoms by blocking a glutamate receptor in the brain (glutamate N-methyl-D-aspartate receptor antagonist). Like serotonin, glutamate is a chemical that helps to send messages between nerve cells.
Melatonin - Linked to a variety of mechanisms related to the pathophysiology of headaches such as its anti-inflammatory effects, toxic free radical scavenging, reduction of pro-inflammatory cytokine up-regulation, inhibition of nitric oxide synthase activity and dopamine release, GABA and opioid analgesia potentiation, glutamate neurotoxicity protection, neurovascular regulation, and serotonin modulation. Melatonin’s chemical structure is also very similar to indomethacin, a common NSAID. (Peres, 2005)
Coenzyme Q10 - A vitamin-like compound that can be synthesized by the body from phenylalanine and tyrosine. Coenzyme Q10 is needed for all cellular processes requiring energy. Coenzyme Q10 is an electron-carrier, transferring electrons from complex I/complex II to cytochrome C.
Feverfew - A study of 17 migraine patients, those on feverfew had half as many headaches. (Johnson, 1985) In a second study of 72 patients those who took feverfew had a 24% reduction in the mean number and severity of attacks although the duration of the individual attacks was unaltered. (Murphy, 1988)
Butterbur (Petasites hybridus) 50 or 75 mg - This herbal remedy has been used for migraine and other uses for centuries. More recently, two studies (Diener, 2004; Lipton, 2002) demonstrated efficiency and safety of butterbur in adults. Another study (Lipton, 2004) showed that patients who used 75 mg butterbur twice daily for 4 months enjoyed 58% migraine attack reduction versus 28% in placebo group.
Risk of side effect increases with higher doses. If any of these symptoms were to occur, a lower dose may still be well tolerated and effective.
Diarrhea (remember Milk of Magnesium)
Minimal because the absorption of oral riboflavin is limited.
At high doses it will produce:
A harmless yellow discoloration of urine.
Excess melatonin can cause
Short-term feelings of depression
Hypothermia (reduced body temperature)
Stimulate overproduction of the hormone prolactin, which can cause hormonal problems and even kidney and liver issues in men
Nausea and/or vomiting
Heartburn and stomach pain
Loss of appetite
Itching or rash
The butterbur plant also contains liver-toxic pyrrolizidine alkaloids and potential cancer causing chemicals, which are removed by a special patented treatment and only marketed under the name Petadolex®. No part of the Petasites plant should be ingested other than the commercial products.
The United Kingdom Medicines and Healthcare products Regulatory Agency (MHRA) announced in 2012 that Butterbur products are linked with liver toxicity and should be removed from the market.
Studies have reported safety and good tolerability of commercially available butterbur products that are free of potentially carcinogenic pyrrolizidine alkaloid constituents, when used short-term, orally and in recommended doses.
Four major types of antidepressants are available:
Tricyclic antidepressants (TCAs)
Selective serotonin re-uptake inhibitors (SSRIs)
Monoamine oxidase inhibitors (MAOIs)
Serotonin norepinephrine re-uptake inhibitors (SNRIs)
All have been used for prevention of migraine, although they occasionally cause headaches to worsen. They are useful in patients with co-existing depression, anxiety, tension-type headache or primary stabbing headache. The most commonly used antidepressants are TCAs and SSRIs.
Amitriptyline inhibits the uptake of both norepinephrine and serotonin (5-HT), allowing them to be more effective. Amitriptyline may inhibit the formation of sodium channels within neurons, enhance GABA’s suppression of migraines, potentiate endogenous opioids, and inhibit the transmission of pain signals in the midbrain (the descending monoamine system). Serotonin receptors are found throughout the vestibular and cochlear cells of the inner ear, as well as the trigeminal system.
Possible side effects
Weight gain (affects 20% of users and those who have weight gain, add only 7 pounds on average)
Dry mouth or eyes
Sleepiness (People who sleep poorly often benefit from these medicines)
These medicines are also antidepressants, but they can act as pain relievers. Not usually as effective as amitriptyline or nortriptyline. There is very limited evidence to support the use of SNRIs in migraine.
Antidepressants take 3-10 days to be effective. Taper off this medication after 6 months.
Slight increase in BP slightly
Problems with vision
Worse head pain
Drowsiness, dizziness, feeling nervous
Changes in appetite or weight
Mild nausea, constipation
Decreased sex drive, impotence, or difficulty having an orgasm
The Sphenopalatine Ganglion (SPG) is a group of nerve cells located just beneath the mucosa high in the nasal cavity, above the deep tail of the middle turbinate. It carries pain and pressure signals from the nose, sinuses and face. It also is linked to the autonomic nervous system that produces a runny, stuffy nose.
One of the most common blocking techniques involves applying or injecting an anesthetic (a numbing medicine) in the SPG. Lidocaine and the longer lasting Marcaine (bupivacaine) are the two commonly used anesthetics. The use of Marcaine by topical administration is outside the FDA approved routes of administration at this time. There are different techniques for delivering the anesthetics.
Application of numbing medicine on cotton swabs in the nose
Application of numbing medicine via catheters (thin plastic tubes) into the nose. Three devices have been FDA approved for performing SPG blocks: Sphenocath®, Allevio®, and Tx360®. They are claimed to be more effective than cotton swabs but do not require any needles.
Injection the SPG through an area in the cheek or mouth. Some specialists use an x-ray machine to correctly place the injection.
Repeated use of an anesthetic nasal spray. Example, a compounding pharmacy can mix a 2% lidocaine spray.
A burning sensation or numbness in the nose or in and around the eyes
Numbness in the throat (This can be a strange change in sensation that makes it feel as if you are gagging but it will return to normal in 1-2 hours). Avoid eating and drinking until your throat feels normal again since you do not want food or drink to mistakenly go into your lungs and cause an infection.
Drop in blood pressure
Allergic reaction to Marcaine and other local anesthetic agents
Repeated anesthetic application to the nasal mucosa may hurt that tissue. It is not yet clear how to many SPG blocks is too much
Botulinum toxin type A is a neurotoxin that causes a temporary cessation of nerve activity. It lasts 2-4 months. FDA-approved for prevention of chronic migraine only.
The appropriate use for botulinum toxin type A is a person with chronic migraine headache symptoms (more than 15 headache days per month of which at least 8 are migrainous, for more than 3 months) and there has been adequate management of medication overuse.
It is recommended that a chronic migraineur try at least three migraine preventative medicines at effective dosages for 6 weeks or more.
Discomfort at injection site: 12%
Temple hollowing: 23%
Neck weakness: 27%
Eyelid droop: 10%
Erythema and/or bleeding at injection site
Infection at an injection site
Rare hypersensitivity reactions include anaphylaxis, urticaria, soft-tissue edema, and dyspnea
Rare reports of adverse events involving the cardiovascular system
Chiropractic, physical therapy and massage are all modalities that have been shown to have similar effectiveness in controlling the intensity of pain for migraineurs (Chaihi, 2011). Studies have shown that they might be comparable to the effectiveness of some preventive medications, but often the studies are not of the most rigorous quality. They may be most effective when combined with other therapies.
Examples of external manipulations are:
Cefaly is a headband designed to deliver electrical impulses to nerves that transmit migraine pain and thereby theoretically suppress this trigger mechanism. In 2014 the device became the first transcutaneous electrical nerve stimulation (TENS) system to win FDA approval for migraine prevention.
The device consists of a battery-operated electrical pulse generator and a self-adhesive electrode. The patient applies the electrode to the middle of the forehead and lowers a headband containing the electrical pulse generator over the forehead to engage a pin located on the electrode. Pressing a button on the band generates a pulsed electric current that stimulates the upper branches of the trigeminal nerve.
Peripheral nerve stimulation (PNS) of the occipital nerves is a potentially promising therapy for chronic migraine patients. The concept is to implant a neurostimulator near the occipital nerves, near the back of the neck.
Recently Plastic surgeons have advertised nerve decompression surgery as an innovative new treatment of migraine headaches.
The Surgical Migraine Procedure is the removal of the corrugator muscles (small muscles associated with the eyebrows). They are responsible for the frown lines above the nose. The theory is that with the removal of the muscles, there is a reduction of migraine-generating electrical signals to the brain along the trigeminal nerve. Muscles in the temples, inside the nose, and back of the neck can also be removed for the same reason.
This procedure may not be effective for all migraine sufferers and each patient should undergo a botulinum toxin (Botox) test. Only those who have a 50% reduction of headaches with Botox should try migraine trigger point decompression.
The relationship between migraine and the symptoms of acute, recurring and chronic sinusitis has not yet been fully worked out, but there is a significant body of information to argue that our sensory nervous system can either enhance or closely simulate the symptoms of a sinus infection.
While it might seem to be an odd decision to operate on patients complaining of facial pressure and other sinus symptoms, but also meet the diagnostic criteria of chronic migraine disease, a study of 229 patients with medically refractory chronic rhinosinusitis were evaluated at 6,12 and 18 months after sinus surgery with quality-of-life questionnaires. All patients with and without migraine had a statistically similar QOL improvement.