by admin | Jul 1, 2013 | Comorbidity
Stroke and Women
Women under the age of 45 who have migraine without aura may be at a slightly increased risk for stroke; women who have migraine with aura have more than twice the risk of heart attack or stroke than do women without aura or without migraine. This risk is further magnified if you smoke, have high blood pressure, or if you take oral contraceptives.
The relationship between migraine with aura and ischemic stroke before age 45 is well established, and there is also a relationship with TIA (transient ischemic attack) and subclinical lesions in the brain. The authors of the GEM study (Genetic Epidemiology of Migraine Study) noted: “There has been substantial literature confirming an association between migraine with aura and ischemic stroke before the age of 45. The question of whether there is a similar association with CHD before the age of 45 has not yet been definitively answered.”
It has been speculated that cortical spreading depression (CSD), which is presumed to be the basis of aura, could also predispose the brain to lesions, and possibly even stroke. Some researchers in the field think it possible that repeated episodes of CSD resulting in aura could be responsible for an increased risk of stroke.
The Reykjavik Study found that stroke occurrence was increased in men and women with migraine with aura, but that death due to stroke was only increased for men with migraine.
Meta-analyses of of studies of stroke in women with aura have determined that migraine confers a higher overall risk of both ischemic and hemorrhagic stroke. Migraine with aura in women confers an overall stroke risk of 4.3/1000, higher than either diabetes or obesity, and contributes as much risk as smoking or hypertension.
The CAMERA II study has shown that infarct size in stroke is 3.24 times larger in women with migraine with aura.
This underscores the necessity for women who have migraine with aura to control stroke risk factors as much as possible.
References:
1. Scher AI, Terwindt GM, Picavet HSJ, et al. Cardiovascular risk factors and migraine: the GEM population-based study. Neurology. 2005;64(4):614-620.
2. Schurks M, Rist PM, Bigal ME, et al. Migraine and cardiovascular disease: systematic review and meta-analysis. BMJ. 2009;339(oct27 1):b3914
3. Gudmundsson LS, Scher AI, Aspelund T, et al. Migraine with aura and risk of cardiovascular and all cause mortality in men and women: prospective cohort study. BMJ. 2010;341(aug24 1):c3966
4. Bigal ME, Kurth T, Hu H, Santanello N, Lipton RB. Migraine and cardiovascular disease. Neurology. 2009;72(21):1864 -1871.
5. Bigal ME, Kurth T, Santanello N, et al. Migraine and cardiovascular disease. Neurology. 2010;74(8):628 -635.
6. Eikermann-Haerter K, Lee JH, Yuzawa I, et al. Migraine Mutations Increase Stroke Vulnerability by Facilitating Ischemic Depolarizations. Circulation. 2012;125(2):335–345.
7. Palm-Meinders IH, Koppen H, Terwindt GM, et al. Structural Brain Changes in Migraine. JAMA. 2012;308(18):1889–1897.
by Christina Peterson, M.D.
updated 7-1-13
by admin | Jun 7, 2013 | Migraine
Do you ever delay treating your migraines?
It’s a fairly common thing to do. You think to yourself, this one won’t be all that bad. I’ll: eat lunch, have a cup of coffee, lie down for half an hour, drink a glass of water or diet soda—whatever thing you think might work that’s never really worked before. But you have hope. You have hope that this time you can beat this thing, this space alien invading your brain.
Why do we do this? I’ve done it myself. It never works. And yet, there is that hope that we can be in control, and not the migraine. I have a colleague who believes that this mistaken belief is part of the migraine itself, that there is cognitive confusion altering good decision-making because of the early stages of the migraine process. If we were thinking clearly, we’d just take our medication. I’m not so sure it’s that clear-cut, although that may be the case for some people. There are also issues of weighing out the risk-to-benefit ratios of whether the adverse effects of medication are worth the severity of this headache. There is also the issue of whether you have enough medication to last all month, and if this headache is “medication-worthy” in light of that.
“Masking the Pain”
I have also had patients tell me they did not want to treat their migraines because they did not want to mask the pain. Now, frankly, this does not make sense. About the only situation I can think of in which this might make sense would be a disaster setting in which one had sustained a head injury and needed to be monitored without benefit of a CT, MRI, or an ICU. Morphine would be withheld so that mental status could be monitored until you could be evaluated in a hospital setting.
However, there is no medical rationale for not taking migraine medication. It will not mask any damage being done to the brain unless your headache is due to something other than a migraine, and something serious at that, in which case you need to be in the emergency department anyway. So, unless you have the red flags that indicate a serious underlying problem, go ahead and take your migraine medication. You do not get points for suffering!
There is also evidence to suggest that early treatment of migraine not only ends an attack sooner, but prevents the pain from becoming fully established.
Red Flags in Headache
Red flags that indicate something serious other than a migraine might be occurring are:
- Significant fever with a headache (more than 99.5)
- Stiff-as-a-board kind of stiff neck
- Severe all-over muscle pains
- Headache that comes on like a thunderclap
- Worst headache of life
- Significant change in headache (not just it used to be on the right, and now it’s on the left – that’s actually okay)
- Any neurologic symptoms that are not part of your usual aura
If you have any of these, see your doctor or go to the emergency department for evaluation. It might not be anything serious, but better safe than sorry. And otherwise, treat your headaches. Unless you enjoy pain?
by admin | May 17, 2013 | Medication
Safety of Over-the-counter Medications
We all tend to think of over-the-counter medications as being safe. After all, regulatory agencies have allowed them to be over the counter. So, they couldn’t really be all that bad, could they?
Well, it turns out that they can—if you don’t take them properly. Some people have a tendency to think that they are safe, and that therefore, it is ok to take a few more painkillers than are recommended on the label. Some people have never actually read the label. (Have you?) And some people don’t realize that they are, in effect, getting a double dose of some medications, because one of the over-the- counter analgesics they are taking may also be a component of one of the prescription medications they are taking.
It’s important to read all labels and to avoid taking excessive amounts of over-the-counter medications. Follow the recommended amounts on the label unless your physician has specifically recommended something different. Too much anti-inflammatory medication, such as aspirin, naproxen sodium, or ibuprofen, can result in stomach irritation like gastritis, cause an ulcer, or promote gastrointestinal bleeding.
Be especially careful not to take too much acetaminophen (paracetamol). Doing so can be damaging to the liver. This damage can be magnified if you drink alcohol, even moderately. Liver damage can occur even in only 24 hours if 8 extra-strength acetaminophen caplets are combined with alcohol. At this time, more than half of all liver transplants are necessary because of the medical use of acetaminophen. Alcohol also increases the risk of gastrointestinal bleeding if combined with anti-inflammatory medications. Long-term overuse of some of these medications can also contribute to kidney damage.
Be safe—read the label, and don’t take medication in excess of the recommended amounts. Don’t combine acetaminophen, paracetamol, naproxen sodium, ibuprofen, ketoprofen or other anti- inflammatory medications with alcohol. Do remember that using over-the-counter medications more than three days a week can lead to medication overuse headache. And be aware that many prescription medications contain acetaminophen (paracetamol).
If your headaches are not responding to over-the- counter pain medication, see a doctor—more specific headache management will not only help your head, it may protect your liver, stomach and kidneys as well.
by admin | May 10, 2013 | Comorbidity
What is Rosacea?
Rosacea is a skin disorder causing redness, irritation, and sometimes, bumpy skin and acne-like breakouts.
Rosacea usually shows up between the ages of 30 and 50 or so. It occurs more commonly in women than in men, although affected men are more likely to experience more severe rosacea. Rosacea is also more common in the fair-skinned, especially those with Celtic or Scandinavian heritage.
The cause of rosacea is not known, but it is suspected to be due to a combination of genetics and environmental factors. In one study, 52% of rosacea sufferers had a family history of at least one family member with rosacea. People with rosacea are more likely to be infected with H. pylori (the bacteria causing ulcers). Those with the acne rosacea form of the disorder have been found to be more likely to react to Bacillus oleronius, which in turn causes overreaction of the immune system.
The Migraine-Rosacea Connection
A connection between migraine and rosacea was noted in 1976 by Tan and Cunliffe. In their study of 137 patients and 161 controls, 44% of the rosacea patients had suffered from migraine, as compared to 13% of the control group. Another Swedish study in 1996 with 809 subjects with rosacea found an overall rate of migraine of 14% as compared to 13% in the control group. However, they found a 27% rate of migraine in rosacea patients between the ages of 50 and 60, and proposed the possibility that hormonal changes were affecting both conditions.
Types of Rosacea
According to the American Academy of Dermatology, there are four types of rosacea:
- Erythematotelangiectatic rosacea – with symptoms of redness, flushing, and visible blood vessels
- Papulopustular rosacea, or rosacea acne – with symptoms of redness, swelling, and acne-like breakouts.
- Phymatous – with symptoms of skin thickness and a bumpy skin tecture.
- Ocular rosacea – with symptoms of red and irritated eyes, swollen eyelids, redness at base of eyelashes.
About half of rosacea sufferers indicate that their symptoms come and go.
Rosacea Triggers
Like migraine, rosacea has a variety of triggers. Some of the triggers between the two conditions overlap, although they are not identical. And also like migraine, not everyone has the same triggers.
The following are typical rosacea triggers:
- Hot beverages
- Alcohol
- Spicy foods
- A hot bath
- Stress
- Sun exposure – especially UVA
- Exposure to cold or humid weather
- Exposure to heat
- Exercise
- Topical creams or make-up
Treatment of Rosacea
The first step in the treatment of rosacea is trigger identification and lifestyle modification. In many cases, this is not sufficient, although it can be helpful. Skincare should include sunscreen, moisturizer, especially in cold weather, and avoidance of sunlight during midday. Many skin products or treatments can aggravate rosacea.
Medical treatment of rosacea can involve topical medications, short courses of antibiotics, and laser treatment.
It is important to see a dermatologist if you think you have rosacea, as the treatment will vary based on the rosacea type.
If you think you might have rosacea, here is a helpful rosacea quiz:
References:
1. Berg M, Liden S: Postmenopausal female rosacea patients are more disposed to react with migraine. Dermatology. 1996;193:73-74.
2. Tan SG, Cunliffe WJ. Rosacea and migraine. Br Med J. 1976;1(6000):21-21.
3. Wilkin JK. Flushing reactions: consequences and mechanisms. Ann. Intern. Med. 1981;95(4):468-476.
4. Spoendlin, Julia, Johannes J. Voegel, Susan S. Jick, and Christoph R. Meier.
Migraine, Triptans, and the Risk of Developing Rosacea: A Population-based Study Within the United Kingdom. Journal of the American Academy of Dermatology. http://www.jaad.org/article/S0190-9622(13)00308-3/abstract, accessed May 10, 2013.
Updated 5/10/2013
by admin | May 8, 2013 | Miscellaneous
What on earth is TRPV1? TRPV1 is an ion channel brain receptor – the long name is transient receptor potential vanilloid 1 (for you biology geeks). It is also known as the capsaicin receptor.
TRPV1 is activated by chemical irritants, inflammatory mediators, and physical mediators of tissue damage, like high temperatures and acid pH. The TRPV1 receptors are located in skin, tissues of the airways, gastrointestinal linings, and the outer coverings of the eye (cornea and conjunctiva). It has also been identified in various areas of the brain. It is thought to have a central role in neurogenic inflammation.
Although the functions of TRPV1 are still being identified, its role in central nervous system inflammation has made it a target for migraine research, as it may possibly play a role in causing hyperalgesia and allodynia. TRPV1 is thought to affect craniofacial pain via the trigeminal nerve system, in addition to other painful conditions. TRPV1 antagonists have been a target for drug development for various painful conditions, including migraine.
However, we already have an existing drug for migraine that has TRPV1 activity. Sumatriptan (Imitrex®, Imigran®, Sumavel®, Alsuma®) has been found to block the effects of capsaicin (the substance that makes chili peppers hot) on the trigeminal neurons in the brainstem. This confirms the role of TRPV1 receptors in the migraine process, and helps our understanding of migraine pathways. It may lead us to new therapies.
References:
1. Evans MS, Cheng X, Jeffry JA, Disney KE, Premkumar LS. Sumatriptan Inhibits TRPV1 Channels in Trigeminal Neurons. Headache: The Journal of Head and Face Pain. 2012;52(5):773–784.
2. Menigoz A, Boudes M. The Expression Pattern of TRPV1 in Brain. J. Neurosci. 2011;31(37):13025–13027.
3. Veronesi B, Oortgiesen M. The TRPV1 Receptor: Target of Toxicants and Therapeutics. Toxicol. Sci. 2006;89(1):1–3.
4. Meents JE, Neeb L, Reuter U. TRPV1 in migraine pathophysiology. Trends Mol Med. 2010;16(4):153–159.
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