Principles Of Acute Migraine Treatment

There is no one-size-fits-all approach. Patients and physicians should keep in mind the following:

1. Early treatment of the attack should be a goal for most patients, as medications, especially triptans, are much more effective if taken early, before the attack is fully established.

2. The response of an individual patient to an acute medication cannot be predicted with certainty. Patients must understand that if the first drug is not effective, there are many other options, and followup is critical for a successful outcome.

3. Some patients have attacks of migraine of differing severity and may need more than one acute treatment option for best results.

4. Medications should be chosen based on the characteristics of the migraine attack. For example, if there is no nausea, oral medications such as triptans are a good choice. Injectable sumatriptan is the most effective but also has the highest rate of side effects. Oral disintegrating triptan tablets (Maxalt and Zomig) may be helpful for patients with mild nausea or whose nausea is worsened by taking fluids, and further, they allow for early treatment even if water is not available. They do not, however, have faster action, as they are not absorbed through the mouth but are rather swallowed and absorbed through the stomach. If nausea is more severe, triptan nasal sprays (Imitrex, Zomig) can be useful. For migraine attacks that build rapidly, are associated with early vomiting or are fully developed upon awakening (morning migraine), injectable sumatriptan has the best chance of providing relief. For attacks that build rapidly but are less severe and are not associated with vomiting, Cambia (a rapidly dissolving NSAID), effervescent aspirin, and the fast-dissolving sumatriptan tablet (Imitrex brand) are preferred.

5. If necessary, two or more acute medications can be combined. Treximet is a combined formulation of sumatriptan and naproxen and is more effective than either drug alone. Metoclopramide (Reglan) could be added to any triptan or NSAID. Caffeine enhances the effectiveness of analgesics, and the combination pill with the brand being Excedrin can work but poses risk of interference with sleep and caffeine withdrawal headache.

6. Avoid acute medication overuse. Only migraine patients get medication-overuse headaches. A study with rheumatoid arthritis patients using opioids showed that there was not an increase of medication-overuse headaches if they did not simultaneously have migraine. Medication overuse is defined by Tylenol or NSAIDs 15 or more days a month, butalbital-containing drugs, opioids, ergotamines, or triptans 10 or more days a month. NSAIDs are least likely to cause medication-overuse headaches. Especially butalbital and opioids should be avoided.

Learn more about migraine symptoms and treatments at www.headachegenius.com

Neutraceuticals For Migraine?

The most widely used are butterbur, riboflavin, CoQ10, magnesium and melatonin.

Riboflavin helps the mitochondrial energy system, which is needed for cell survival, and this is found to be reduced in migraine. It is also called vitamin B2. Most studies used 400 mg a day. The American Academy of Neurology has concluded that it is probably effective for the preventative treatment of migraine in adults though not recommended for use in children. Possible side effects are diarrhea and increased frequency of urination as well as bright yellow urine.

Coenzyme Q10 is also important in mitochondrial energy. The usual dose is 100 mg 3 times a day for a 3-month trial. Results of studies are mixed. The medication is considered possibly effective.

Magnesium has been found to be low in patients with migraine. A deficiency of this increases glutamate, a transmitter that causes hyperexcitability in neurons, and migraine patients have increased hyperexcitability in their brains. Studies show conflicting results. Recommended dose is 400 to 600 mg a day for at least 3 months. Possible side effects are diarrhea and flushing.

Butterbur is made from a shrub called Petasites. It inhibits calcium channels, which is its probable mechanism of action in migraine. It was patented in Germany in 1988. It seems helpful for adults and children, with the adult dose 150 mg a day for a 3-month trial as a preventative. It was previously considered safe, with burping being the only side effect. However, there are recent reports of liver damage. In the UK, 9 cases were reported of acute hepatitis, and 2 of the 9 cases resulted in liver failure, requiring liver transplantation. Children and pregnant women should certainly not take butterbur. Adults can do so if they are aware of the risks and liver function blood tests are monitored.

Feverfew is derived from a chrysanthemum. Its mechanism of action is unknown. It may be effective. Long-term safety data are lacking, though it appears well tolerated.

Melatonin is widely available over-the-counter, often used for insomnia, and has been tested extensively as a preventative for cluster headache and to some degree for migraine. Most studies have shown negative results.

The take-home message is that butterbur should not be used, that melatonin is not effective, that other nutraceuticals may or may not be effective but seem safe. A combination product is available over-the-counter, containing feverfew 100 mg, magnesium 300 mg, and riboflavin 400 mg and may be a reasonable choice. Another product is sublingual (under the tongue) and contains feverfew and ginger. This seemed effective in small trials.

Behavioral approaches are a safe and probably equally or more effective alternative to nutraceuticals. They include relaxation training, thermal biofeedback, EMG biofeedback, and especially cognitive behavioral therapy. They have been shown to reduce pain catastrophizing, increase the number of positive coping strategies, and reduce migraine-related disability. They are especially appropriate in women who are planning pregnancy or who are pregnant or breastfeeding. Aerobic exercise combined with behavioral management may improve outcomes.

Jack Florin, MD
Neurologist

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Look Out! The Antibodies Are Coming

The story begins at the end of the 19th century when Paul Ehrlich, a German physician, postulated that the immune system protected the body against attack from antigens, which are potentially harmful substances, by deploying what he called antibodies. Each antibody was able to locate and bind with an antigen. This lock-and-key concept proved to be true, leading to man-made antibodies, which, like magic bullets, could kill off disease-producing cells and spare healthy cells.

In 1984, two scientists, César Milstein and Georges Köhler, were awardes the Nobel Prize for discovering a way to produce monoclonal antibodies, which were identical antibodies made from cloned cells that could target specific antigens and destroy them. Their impact on healthcare has been profound, and there are now more than 30 monoclonal antibodies on the market. These include cancer treatments, such as Avastin, Herceptin, and Rituxan. There are many more to come.

Monoclonal antibodies are not as sexy as genetic engineering and stem cells are. Widespread use was delayed because the first-generation monoclonal antibodies were derived from the cells of mice or rats. This provoked severe immune reactions in the human body. Gregory Winter, a scientist at Cambridge, UK, was able to develop humanized and later fully human antibodies that overcame this problem. His laboratory did the early work which led to Humira, the world’s best-selling drug, an antibody-based treatment for rheumatoid arthritis.

The journey from laboratory to clinic was more than 30 years for Campath. It was approved as a treatment for leukemia and recently for multiple sclerosis. The drug was renamed Lemtrada, and in 2014, it was approved by the Food and Drug Administration as a treatment for multiple sclerosis. The approval came after an initial rejection by the FDA. Tysabri is another antibody that has been used since 2006 for multiple sclerosis. Rituxan is also used “off-label.” Look for the approval of ocrelizumab this year, and it likely will be available to treat multiple sclerosis in 2016.

For more information, see “The Lock and Key of Medicine: Monoclonal Antibodies and the Transformation of Healthcare” by Lara Marks, published by Yale University Press.

Jack Florin, MD
Neurologist

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LGBT Health In Neurology

I found an article in JAMA Neurology, August 2015, by Nicole Rosendal, MD, compelling. Its target audience is neurologists, but I think everyone can learn from it.

It is estimated that 9 million Americans, or 3.5% of the adult population, identify as lesion, gay, bisexual, or transgender (LGBT). An additional 19 million (8.2%) report having had same-sex sexual behavior, and 26 million (11%) acknowledged same-sex attraction.

Over 50% of lesion, gay, and bisexual individuals and 70% of transgender people in a survey in 2009 reported believing they were discriminated in the healthcare setting. Examples were being refused needed care, being blamed for their health status, having healthcare professionals refuse to touch them, have professionals use extensive precautions such as wearing masks and gloves, use abusive or harsh language, or act physically rough or abusive. Many LGBT patients are reluctant to share their sexual orientation with their physician.

The rates of neurological diseases are higher in the LGBT community. Lesbians are more likely to be obese, a difference that begins as early as adolescence. Smoking prevalence and substance abuse disorders are higher.

In order to treat patients effectively, physicians must develop trust. New levels of awareness and acceptance can improve trust. Examples include asking for the patient’s preferred name, and using terms like partner or significant other rather than boyfriend / husband / girlfriend / wife. These are nonjudgmental behaviors that help to establish trust.

Dr Rosendal correctly concludes that if physicians believe they should advocate for true equitable health for all patients, the LGBT community remains an underserved population.

Jack Florin, MD
Neurologist

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How Do We Explain Risk Factors For Multiple Sclerosis?

The cause of Multiple Sclerosis (MS) is thought to be a genetic predisposition, modified by environmental factors. These are termed risk factors, and some can be modified. Most have been shown to increase the risk of developing MS and the clinical course. They include high salt intake, high-fat diet, smoking, vitamin D deficiency, and exposure to the Epstein-Barr virus.

High sodium and high fat diets have been shown to promote development of certain lymphocytes termed Th17 cells, which produce a damaging chemical (cytokine) which affects myelin.

Regarding smoking, nicotine is not the culprit. In fact, nicotine actually may have a neuroprotective effect in Parkinson’s. Cigarette smoke has 6000 other components.

Vitamin D has been long recognized to reduce risk of developing MS, relapses, and disease progression. It is not just a vitamin but rather has important effects in the immune system. These include preventing the activated T-cells that enter the brain and do damage from in fact being attracted to the brain.

Infection with the Epstein-Barr virus seems to enhance susceptibility to MS by activating the immune system. The virus is able to change the behavior of B-cells, which serve to activate T-cells, which then enter the brain and damage myelin.

Jack Florin, MD
Neurologist

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Does Alcohol Trigger Migraine?

The problem of identifying “triggers” for migraine is that triggers are not always triggers. Patients’ perception of triggers often change when they keep headache diaries. Studies are conflicting regarding alcohol and headache. Generally, the consumption of alcohol is less among people who report headaches. A possible explanation is that migraineurs avoid alcohol to reduce the risk of triggering migraine. An interesting study involved high school students who were given questionnaires. Those who experienced headache were asked to identify what they believed triggered headache. Only a few believed that alcohol triggered their headache, while statistical analysis showed that alcohol was a trigger in more than half. These students were probably not yet taught to expect a headache when consuming alcohol. This is called a “societal bias.” In some studies, alcohol is considered a migraine trigger in about a third of people; iIn others, only about 5%.

Cluster headache patients, as opposed to migraine patients, more consistently report alcohol as a trigger during a cluster period but not between these periods.

Similarly, studies about wine as a trigger are inconsistent. Some claim white wine is the stronger trigger, whereas others red wine. Beer seems to be an important trigger for cluster headache in the US but not in other countries.

Alcohol in itself does not seem to be the main migraine trigger. Some people who have migraine after drinking red wine can drink the same amount of alcohol in spirits without a headache. Other compounds in wine, such as histamine, sulfites, and tannins, can be factors, but most studies show that they are not able alone to trigger headache.

Hangover headache has also been studied. Alcohol flushing is caused by a compound termed alcohol dehydrogenase 2. People with alcohol flushing are more prone to get alcohol hangover headache. Hangover symptoms occur in people with and without migraine, but migraineurs seem to have more migraine-like hangovers.

Jack Florin, MD
Neurologist

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Do Stimulants Worsen Tics?

About half of patients with tics also have attention deficit-hyperactivity disorder, and conversely, about 20% of ADHD patients have tic disorders. The use of stimulants, especially amphetamines (Adderall) and methylphenidate, is controversial because of Food and Drug Administration warnings against it. These warnings, however, are based on limited evidence. ADHD symptoms often cause worse cognitive and social impairment than tics. A new meta-analysis of 2385 patients in 22 research studies has shown that there is no support for this warning, as there was no worsening of tics in patients on stimulants. It is likely that case reports to the FDA represented the natural history of waxing and waning of tic disorders.

See Journal of the American Academy of Child and Adolescent Psychiatry, June 30, 2015, with lead author Cohen, CS.

Jack Florin, MD
Neurologist

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Can The Course Of Parkinson’s Disease Be Predicted?

We are making progress. Standard teaching is that patients with mainly tremor, so-called tremor-dominant Parkinson’s, and younger age of onset do better. Patients with older age of onset and initial symptoms of stiffness and slowness of movement and walking do worse. Newer studies show that this distinction is too simplistic.

In fact, there are 3 symptoms that when present at the initial visit are the defining features leading to a “malignant” subgroup. These are:

1. Orthostatic hypotension (OH), meaning a fall of systolic blood pressure of 10 points from sitting to standing which may or may not cause lightheadedness.

2. Mild cognitive impairment (MCI).

3. Rapid dreams movement sleep behavior disorder (RBD). These patients “act out” dream and often yell, kick, punch during sleep and may in fact fall out of bed and have serious injuries.

The patients in the “malignant” group usually have OH, MCI, RBD but also have severe motor symptoms, including impaired gait and frequent falls.

The group with the best prognosis may have prominent tremor, but they do not have OH, less frequently have RBD, and moderately have MCI. The intermediate group does not have cognitive impairment but may have OH and RBD. It is also possible that each of the 3 subtypes may only represent a stage in the evolution of the disease.

Being able to offer prognosis with some degree of confidence is obviously important in counseling patients and families. It is also important in that when patients enter clinical trials, they may be “stratified,” and this increases the validity of the results.

Jack Florin, MD
Neurologist

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