Why Are Menstrual Migraines So Bad? Where Do They Hurt? Treatment Chart

menstrual migraine
Menstrual migraines involve a drop in estrogen levels before your period and an altered pain perception, which results in excruciating headache pain.

Menstrual migraines occur about the time of menses (or two to three days before the onset of menses) in women.

The cause for these migraines is multifaceted, involving the effect of low estrogen levels on the gray matter of the brain, the blood vessels in the central nervous system, the central pain pathways (mid-brain), and the altered pain perception. Therefore, the headaches are excruciating and may not respond to over-the-counter nonsteroidal anti-inflammatory drugs, which tackle only one pain mechanism (the prostaglandin pathway).

5 mechanisms of menstrual migraine

  1. Role of estrogen: The fall in estrogen levels just before the menses begin has been known to trigger abnormal nerve signals in the gray matter via complex mechanisms, which are still being studied.
  2. Activation of central pain pathways: Studies confirm the origin of abnormal neural impulses in the midbrain (brain stem) due to estrogen deficit. These abnormal impulses stimulate the trigeminal nerve (supplies the structures of the face and neck and innervates the blood vessels of the brain). The migraine pain is due to disturbed physiology of the trigeminal nerve and hence responds poorly to many nonsteroidal anti-inflammatory drugs.
  3. Inflammatory chemicals: The abnormal neuronal firing in the midbrain causes a massive release of vascular inflammatory substances, such as calcitonin gene-related peptide (CGRP), cytokines, and prostaglandins, in the body. This causes hyperalgesia (increased sensitivity to painful stimuli) and allodynia (pain produced by normally non-noxious stimulation) at the level of pain receptors in the body.
  4. Sensitization: Over time, the trigeminal nerve becomes increasingly sensitive to the estrogen level fluctuations and inflammatory markers. Hence, even a little change in the milieu around the nerve causes the migraine attack to recur. This sensitization is responsible for many of the clinical symptoms of migraine, such as throbbing pain, the way the pain worsens on increased pressure during coughing, bending, or sudden head movements, and migraine aura.
  5. Altered neurotransmitter levels: Estrogen affects the serotonin and dopamine levels in the brain, which are responsible for mood and pain perception. The drop in estrogen triggers depressed mood, minute changes in blood vessel caliber, and an increase in sensitivity to nociceptive responses (related to pain perception) to the peripheral and central stimuli. Low estrogen lowers your pain threshold.

Where do migraines hurt?

Once triggered, the migraine pain is enough to incapacitate a person for the next 48 hours. 

The migraine is often experienced at the following sites:

  • A one-sided throbbing headache, rarely headache on both sides
  • Stabbing pains that start around either eye or even ears
  • Frontal (involving the forehead or front part of the head) pain that worsens on movement, loud noise, or bright light
  • Tingling and numbness around face and neck region
  • Pain that originates deep within the head and is experienced around cheeks, nape of the neck, and shoulders
  • Tenderness over the scalp

Why do only some people get menstrual migraines?

Though estrogen triggers bio-physiological changes in migraines, not every woman suffers from menstrual migraine.

Functional brain imaging has identified cell structure changes in the ascending and descending pain pathways (brain circuits) of patients with migraine during and in between attacks. Those who are susceptible to migraine attacks often have more discernible alterations in the blood flow to the midbrain regions that control pain pathways (the dorsal pons and anterior cingulate cortex) than others.

The susceptibility of the visual cortex and auditory association cortex cells to altered blood flow at a cellular level may be the reason for the migraine aura (tingling, numbness over the face, increased sensitivity to light, nausea, vomiting, temporary blindness, or paralysis).

Latest Migraine News

Trending on MedicineNet

Migraine Treatments:
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Can patients with migraine use estrogen-containing contraceptives?

Individuals with menstrual migraines must not use estrogen-containing contraceptives for the following reasons:

  • Estrogen in oral contraceptive pills (OCP) can trigger migraine attacks
  • OCP use in those with migraine is associated with an increased stroke risk
  • Those on OCP, who have migraine, and those who smoke are at the highest risk of getting blood clots anywhere in the body

On the contrary, menopause brings more stable hormone levels, resulting in a reduced intensity and frequency of migraine attacks. In many women who experience perimenopausal migraines, hormone replacement therapy with estrogen and progesterone relieves migraine pain, hot flashes, and other distressing symptoms. This could be initiated after a thorough evaluation of risk and benefits.

How to treat menstrual migraine

Along with nonsteroidal anti-inflammatory drugs, such as acetaminophen, ibuprofen, and naproxen, which may help in some cases, menstrual migraines are treated with prophylactic therapy. This aims to prevent attacks and cure an active migraine attack.

Here is a list of drugs that may prove effective:

Table 1. Treatment for active migraine attacks Drug class Drug name Route Triptans

Imitrex, Tosymra (sumatriptan), and Maxalt, Maxalt-MLT (rizatriptan)

  • Pills
  • Shots
  • Nasal sprays
Lasmiditan

Reyvow
Oral

Calcitonin gene-related peptide receptor (CGPR) antagonist
  • Ubrelvy (ubrogepant)
  • Nurtec ODT (imegepant)

Oral

Opioid medications


Oral

Table 2. Migraine prevention Botox injections

Botox (onabotulinum toxin A) about every 12 weeks help prevent migraines in some adults
Injection

CGPR monoclonal antibodies
  • Aimovig (erenumab-aooe) 
  • Ajovy (Fremanezumab-vfrm)
  • Emgality (Galcanezumab-gnlm)
  • Vyepti (Eptinezumab-jjmr)

Monthly or quarterly by injection

Tricyclic antidepressant

Amitriptyline, fluoxetine
Oral

Antiseizure drugs

Topamax, Qudexy XR (valproate and topiramate)
Oral

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Why Are Menstrual Migraines So Bad? Where Do They Hurt? Treatment Chart

menstrual migraine
Menstrual migraines involve a drop in estrogen levels before your period and an altered pain perception, which results in excruciating headache pain.

Menstrual migraines occur about the time of menses (or two to three days before the onset of menses) in women.

The cause for these migraines is multifaceted, involving the effect of low estrogen levels on the gray matter of the brain, the blood vessels in the central nervous system, the central pain pathways (mid-brain), and the altered pain perception. Therefore, the headaches are excruciating and may not respond to over-the-counter nonsteroidal anti-inflammatory drugs, which tackle only one pain mechanism (the prostaglandin pathway).

5 mechanisms of menstrual migraine

  1. Role of estrogen: The fall in estrogen levels just before the menses begin has been known to trigger abnormal nerve signals in the gray matter via complex mechanisms, which are still being studied.
  2. Activation of central pain pathways: Studies confirm the origin of abnormal neural impulses in the midbrain (brain stem) due to estrogen deficit. These abnormal impulses stimulate the trigeminal nerve (supplies the structures of the face and neck and innervates the blood vessels of the brain). The migraine pain is due to disturbed physiology of the trigeminal nerve and hence responds poorly to many nonsteroidal anti-inflammatory drugs.
  3. Inflammatory chemicals: The abnormal neuronal firing in the midbrain causes a massive release of vascular inflammatory substances, such as calcitonin gene-related peptide (CGRP), cytokines, and prostaglandins, in the body. This causes hyperalgesia (increased sensitivity to painful stimuli) and allodynia (pain produced by normally non-noxious stimulation) at the level of pain receptors in the body.
  4. Sensitization: Over time, the trigeminal nerve becomes increasingly sensitive to the estrogen level fluctuations and inflammatory markers. Hence, even a little change in the milieu around the nerve causes the migraine attack to recur. This sensitization is responsible for many of the clinical symptoms of migraine, such as throbbing pain, the way the pain worsens on increased pressure during coughing, bending, or sudden head movements, and migraine aura.
  5. Altered neurotransmitter levels: Estrogen affects the serotonin and dopamine levels in the brain, which are responsible for mood and pain perception. The drop in estrogen triggers depressed mood, minute changes in blood vessel caliber, and an increase in sensitivity to nociceptive responses (related to pain perception) to the peripheral and central stimuli. Low estrogen lowers your pain threshold.

Where do migraines hurt?

Once triggered, the migraine pain is enough to incapacitate a person for the next 48 hours. 

The migraine is often experienced at the following sites:

  • A one-sided throbbing headache, rarely headache on both sides
  • Stabbing pains that start around either eye or even ears
  • Frontal (involving the forehead or front part of the head) pain that worsens on movement, loud noise, or bright light
  • Tingling and numbness around face and neck region
  • Pain that originates deep within the head and is experienced around cheeks, nape of the neck, and shoulders
  • Tenderness over the scalp

Why do only some people get menstrual migraines?

Though estrogen triggers bio-physiological changes in migraines, not every woman suffers from menstrual migraine.

Functional brain imaging has identified cell structure changes in the ascending and descending pain pathways (brain circuits) of patients with migraine during and in between attacks. Those who are susceptible to migraine attacks often have more discernible alterations in the blood flow to the midbrain regions that control pain pathways (the dorsal pons and anterior cingulate cortex) than others.

The susceptibility of the visual cortex and auditory association cortex cells to altered blood flow at a cellular level may be the reason for the migraine aura (tingling, numbness over the face, increased sensitivity to light, nausea, vomiting, temporary blindness, or paralysis).

Latest Migraine News

Trending on MedicineNet

Migraine Treatments:
What are your other options?

Learn More on

Can patients with migraine use estrogen-containing contraceptives?

Individuals with menstrual migraines must not use estrogen-containing contraceptives for the following reasons:

  • Estrogen in oral contraceptive pills (OCP) can trigger migraine attacks
  • OCP use in those with migraine is associated with an increased stroke risk
  • Those on OCP, who have migraine, and those who smoke are at the highest risk of getting blood clots anywhere in the body

On the contrary, menopause brings more stable hormone levels, resulting in a reduced intensity and frequency of migraine attacks. In many women who experience perimenopausal migraines, hormone replacement therapy with estrogen and progesterone relieves migraine pain, hot flashes, and other distressing symptoms. This could be initiated after a thorough evaluation of risk and benefits.

How to treat menstrual migraine

Along with nonsteroidal anti-inflammatory drugs, such as acetaminophen, ibuprofen, and naproxen, which may help in some cases, menstrual migraines are treated with prophylactic therapy. This aims to prevent attacks and cure an active migraine attack.

Here is a list of drugs that may prove effective:

Table 1. Treatment for active migraine attacks Drug class Drug name Route Triptans

Imitrex, Tosymra (sumatriptan), and Maxalt, Maxalt-MLT (rizatriptan)

  • Pills
  • Shots
  • Nasal sprays
Lasmiditan

Reyvow
Oral

Calcitonin gene-related peptide receptor (CGPR) antagonist
  • Ubrelvy (ubrogepant)
  • Nurtec ODT (imegepant)

Oral

Opioid medications


Oral

Table 2. Migraine prevention Botox injections

Botox (onabotulinum toxin A) about every 12 weeks help prevent migraines in some adults
Injection

CGPR monoclonal antibodies
  • Aimovig (erenumab-aooe) 
  • Ajovy (Fremanezumab-vfrm)
  • Emgality (Galcanezumab-gnlm)
  • Vyepti (Eptinezumab-jjmr)

Monthly or quarterly by injection

Tricyclic antidepressant

Amitriptyline, fluoxetine
Oral

Antiseizure drugs

Topamax, Qudexy XR (valproate and topiramate)
Oral

Check Also

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