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Women and Chronic Pain

Insights into the physiologic adaptations that predispose women to more frequent, sustained pain events and increased likelihood of chronic pain.
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Neuromuscular problems (neck, back, and head pain) are the second most common pain next to viral- and bacterial-induced pain. Pain in the cervical masticatory muscles (head pain) is one of the most common problems for females.1 In double-blind, randomized studies, the female-to-male ratio is 3-to-1 for chronic pain in most of the major head and neck pathologies. However, the actual number of women seeking care is closer to 10-to-1, or even as high as 15-to-1 for some chronic pain clinics. In 2001, the ratio of females-to-males requesting examination at Raleigh Facial Pain Services was 84% and in 2002 it was 80%. The exact reasons for this predisposition are difficult to research due to its multiple causes—hormonal influences, central sensitization (rewiring), and sympathetic system changes.

Increasingly, research is linking chronic pain to gender. The study of chronic muscle syndromes, such as myofascial pain, jaw joint pathologies,2 dysfunction,3 atypical odontalgia,4 Meniere’s disease,5 Lupus,6 burning mouth,7 and cervical dysfunction,8 all reveal a strong female pre-disposition. Some 86% of female chronic pain sufferers in a Swedish study were found to clench or grind their teeth.9 Tension headache also has a female predominance with 46% of females having frequent tension headache compare to males at 38%.10 Nearly all the chronic pain syndromes, such as chronic fatigue syndrome, fibromyalgia,11 and certain malignancies, have a female predominance.12 Migraines affect 18% of females while only 6% of males. Menstrual migraine is reportedly associated with estrogen fluxes with many of these migraines but typically resolves at menopause.14

There are currently three theories for women’s predisposition to pain:

  1. hormonal differences
  2. rewiring of the nervous system
  3. sympathetic issues

Hormonal Reasons for Pain

For many years, it has been found that hormone replacement therapy exacerbates migraines.15 Oral contraceptives change the character and frequency of migraines.14 In the presence of estrogen, there is a heightened response to neural injury.16 Mechanical sensitivity of masticatory muscles increases with ovarian hormone fluctuations.2 In 60% of migraine sufferers, the headache worsens around the premenstrual phase of the menstrual cycle.18 Fourteen percent of women with migraine experience headache only with the menses.18 Most women see changes in their headache frequency at puberty and menopause.19 These numbers provide an obvious relationship between estrogen and chronic pain. Only recently have these pieces of the puzzle about the pathophysiology of women’s hormones and headache relationship begun to make sense.

One of the most fascinating research findings in recent years is the estrogen receptor on the female’s mast cell. This receptor — genetically coded to provide the female with an inflammation enhancement — is absent in men. The mast cell is a storage tanker for many neurogenic chemicals and is the predominant cell in the inflammation process. When the estrogen levels flux and blood levels of estrogen increase, estrogen couples with the mast cell receptor making it more sensitive to an inflammation stimulus and the dumping of its load of neurogenic chemicals.20 As it does so, neurogenic chemicals are released more quickly, and with greater numbers of mast cells responding. One of the substances released by the mast cell is NGF (nerve growth factor)21 which stimulates production of substance P and VIP (vasoactive intestinal polypeptide)3 — the main messenger molecules (neurotransmitters) of the pain system. As a result, a female will get more chemicals, more inflammation, more pain, and more swelling from the same stimulus than will a male. This monthly bombardment of neurogenic chemicals takes its toll on the female body. The estrogen-enhanced mast cell inflammation chemical release explains some of the female predominance in the migraine population.

The migraine headache is now thought to be a neurogenic chemical overload that reaches toxic levels in the blood stream going to the brain. The neurogenic chemicals come from a variety of head and neck structures such as muscle and joint over use, sinus infections, ear infections, eye contact with environment, mouth bacterial invasion, and allergies. The main source of this inflammation stimulus is the use of jaw and neck muscles for bad posture, clenching, chewing gum, damaged joints, bad bite, or tension in the muscles. When blood levels of neurogenic inflammation chemicals reach a level that the brain perceives as toxic and threatening to brain safety, the migraine receptor is stimulated to cause vasodilation of blood vessels. This serves to flush toxins away from the brain. The pain from a migraine is mostly from the receptors in the blood vessels that are aggravated due to the stretching caused by this sudden enlargement of the blood vessel. Each person’s migraine generator threshold is set at different levels by genetics. It is believed that certain females have a lower setting than others. The neurotransmitter, serotonin, which has long been associated with the migraine headache, varies with the plasma levels of estrogen.22 The number of serotonin receptors available, it’s binding capacities, and its functional status are all associated with estrogen levels.23 Imitrex is a serotonin mimicking drug used to abort (stop) migraines once they are in full swing.

Further complicating the migraine experience of women is that females exhibit greater sensitivity to laboratory pain as compared to males. Gender differences in pain sensitivity are not site specific, and they seem more noticeable in deep sustained pain sensations similar to the pain of back, neck, and head.24 Not only are migraines more prevalent in this population but the ensuing pain is felt more intensely.

Estrogen and progesterone also induce increased secretions of prostaglandin, which inhibits central norepinephrine release (a nerve messenger in the pain inhibitory system), antagonizes morphine analgesia (rendering pain pills not as effective), sensitizes pain receptors (more pain receptors react to same stimulus), and increases neurogenic inflammation.25 This increase in inflammation and pain in the female sets the stage for central nervous system involvement in chronic pain. An increase in stimulus causes an increase in reactivity of the pain system occurring each month. PMS is thought to be nothing more than the side effects of neurogenic chemicals in blood stream.

Last updated on: January 6, 2012
First published on: July 1, 2004