For those of us who are perimenopausal.

An interesting article.

http://www.medscape.com/viewarticle/755254

Oh, c*ap, I am not a member so it won't let me use it as I need to log in first - any chance of finding this article anywhere else?

Risa

Question:

What are the current recommendations for assessing and managing migraines in the perimenopausal woman? What are the latest theories of migraine management in general?

Commentary from Andrea L. Sikon, MD, FACP, NCMP

Pathophysiology
Migraines are more common in women than men and a source of great disability, with considerable resultant financial burden as well. Migraines often begin in the mid-third decade with peak prevalence in middle life.[1] Menstruation is one of the most significant triggers of migraines, as estrogen has numerous central effects.[2] Perimenopause can be a time of migraine exacerbations, likely due in part to hormonal fluctuation. Natural menopause often diminishes migraine without aura by approximately half, but does not necessarily diminish migraines with aura.[2,3]

Estrogen withdrawal during the late luteal phase preceded by several days of high estrogen priming is the fairly well-established theory behind this foremost migraine trigger. There has been conflicting evidence regarding an association between migraines and menopausal vasomotor symptoms, but the common link between both may be serotonin.[2,3] Intriguing evidence is accumulating to suggest that the predominant modulator in hormonally triggered migraines is serotonin, as estrogen affects serotonin levels and metabolism.[2] Progestogen’s role in migraines is less clear, although progesterone does influence neuronal activity.

Historically, migraines were thought to be a purely vascular phenomenon; however, growing evidence supports an etiology of disordered brain excitability. Investigators have identified three genes linked to migraines that modulate various cell types within the brain and carry a 10% to 15% greater risk for the condition.[5] These theories have considerable implications for further innovative therapies.

Assessment of migraines in the perimenopausal woman
The International Headache Society has published diagnostic criteria for migraines.[1] Common triggers include bright or flashing lights, lack of food or sleep, stress, and changes in hormones and hormonal levels (commonly menstrually related). Migraines can be further categorized into those with and those without aura (the latter being the most common subtype.)

Aura is comprised of a group of neurological symptoms that occur just before or at the onset of a migraine. Most auras include visual disturbances that appear as flashing lights, positive colored or uncolored zigzag lines, or a temporary loss of vision (scotomata) often in the peripheral visual fields. Sensory symptoms are also common (numbness of the face, arm, or leg) with or without speech symptoms. Such deficits occur gradually over 5 minutes or greater, lasting no longer than 1 hour, and include a mix of positive and negative features with complete reversibility. Several different symptoms or deficits can occur in succession.[1]

Data on migraines and the risk of stroke is complex. Migraines have been variably reported as an independent risk factor for stroke. Furthermore, women with migraines who use contraceptive doses of estrogen may have an additional risk of stroke; however, studies here too have been variable, as such risk is confounded by numerous risk factors that are likely synergistic, such as smoking, hypertension, diabetes, and hyperlipidemia, as well as the dose of estrogen.[6]

It remains important to determine the presence of aura, as most evidence suggests a small but increased risk of ischemic stroke (IS) associated with migraines with aura mainly in young women (< age 45), especially in those who smoke and/or who use oral contraceptives.[3,6] There is inconsistent evidence for an association between migraine and IS in older women and in men.[6,7] Despite this increased risk of IS in migraine sufferers, the absolute risk to any one person remains fairly low.[7,8] More study is needed to determine whether treating migraines and preventing attacks can impact IS risk.[9]

Management
A useful initial tool in the optimal management for migraines is to have the patient keep a diary of her flares to help identify any triggers and the relation of flares to her menstrual history.[1] Avoidance of behavioral or other triggers is an obvious next step.

Pharmacologic therapies for migraines are divided into acute and prophylactic categories. There are no FDA-approved agents specifically for menstrual migraines. The agents used for acute abortive therapy in perimenopause are the same agents used for nonhormonal migraines, mainly triptans and nonsteroidal anti-inflammatory drugs (NSAIDs).

Preventive medications for migraines in perimenopause can be further classified into short term and long term, and whether or not they are hormonally related. A consideration for women with menstrual migraines is use of preventive medication during part of the month, only related to the menstrual cycle, instead of daily dosing. Medications studied but not FDA approved for use in this way are magnesium, NSAIDs, triptans, ergots, and hormone therapy (HT).[10] This requires, though, that menstrual cycles are regular and predictable, and thus may not be a feasible option for those in perimenopause, who often have a higher likelihood of irregular bleeding.

HT affects each woman differently. Some benefit by a reduction in their migraines, while others may have exacerbated symptoms.[3] Often, contraceptive doses of combined HT can also address concomitant needs during the menopause transition: the need for contraception, control of menorrhagia, and relief from early vasomotor symptoms. Almost 70% of women with migraines report an association with their menstrual cycles due to the associated drop in estrogen levels during menses—many find relief with HT that eliminates such fluctuations.[4]

Because perimenopausal women are starting with a background of fluctuating endogenous estrogen levels, attempts to deliver a more constant serum concentration and reduce any additional variability may result in improvement of migraine without aura. This delivery might include nonoral route and consistent dosing routes, with either extended-cycle monophasic estrogen-progestin types when prescribing contraceptive doses, estrogen supplementation during the placebo week or during menses, or by using noncyclical/continous types when prescribing postmenopausal HT.[3,4] Also, as transdermal ET has less effect on coagulation factors than the oral formulations, they may impart fewer potential thrombotic triggers and may be preferred, although this is not definitive.[3]

Contraceptive estrogen doses (20-50 mcg estradiol) should be avoided in women with migraines with aura, due to an increased risk of IS in such women, according to international studies; however, no US studies have clearly shown this risk. The World Health Organization recommends that women of any age with migraines with aura, as well as women age 35 and older with migraine without aura, avoid using oral contraceptives.[11] Similarly, the American College of Obstetricians and Gynecologists recommends that these women avoid contraceptive doses of HT, as should migraine sufferers who smoke, have significant comorbidities for stroke, or are over age 35.[12] A similar contraindication has not been identified for those with migraine with aura who need menopausal HT doses.[3,6,13]

For menstrual migraines during perimenopause, use of low-dose estrogen may be an acceptable alternative on days surrounding menses to counter the premenstrual drop in estrogen. This can be achieved with a transdermal estradiol patch or gel (0.1-mg patch/d or 1.5 mg gel/day). This may be challenging if menses are unpredictable, as is common in perimenopause.[3]

HT is not necessarily contraindicated in postmenopausal women with migraine with aura, as the Women’s Health Study did not show a statistically significant increase in IS risk in this group.[3,6,13] Stroke risk proportionally increases with the dose of estrogen in studies of women using menopausal HT. Some evidence suggests that there may be threshold levels of estrogen beyond which aura is triggered, which might also explain the significant variability of response to estrogen between patients and for each patient over time, as well as why lowering the estrogen dose and altering the delivery route can influence improvement.[3]

Other than HT to relieve migraines, the same prophylactic medications used for migraines in general are recommended for women with migraines in perimenopause and younger women with hormonal migraines (including beta-blockers, calcium channel blockers, antiseizure medications, and selective serotonin reuptake inhibitors.) Some studies have shown benefit to boosting doses of these conventional medications during the menstrual period if migraines seem to flare at those times.[10]

Newer interventions for migraines are showing some promise, such as greater occipital nerve blocks and acupuncture.[14,15]

From the NAMS Menopause e-Consult-newsletter released October 2011
For more, please visit http://www.menopause.org/Members/eConsulteNewsletter.aspx

Thank you so much, Kim!!!!

Because perimenopausal women are starting with a background of fluctuating endogenous estrogen levels, attempts to deliver a more constant serum concentration and reduce any additional variability may result in improvement of migraine without aura. This delivery might include nonoral route and consistent dosing routes, with either extended-cycle monophasic estrogen-progestin types when prescribing contraceptive doses, estrogen supplementation during the placebo week or during menses, or by using noncyclical/continous types when prescribing postmenopausal HT.[3,4] Also, as transdermal ET has less effect on coagulation factors than the oral formulations, they may impart fewer potential thrombotic triggers and may be preferred, although this is not definitive.


I had trans-dermal estrogen patch first (I am in menopause now, as my last period was in February) but unfortunately
these are expensive and not covered by our Pharmacare program.
So I had to switch to an oral form of estrogen, but thankfully it doesn't affect my migraines in any significant way- yet
and

It was a huge help in reducing the infernal hot flashes. I was going bonkers from these!!!
Interesting article, thank you so much, guys!



Risa