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10.1576/toag.12.3.149.27596 http://onlinetog.org

2010;12:149154

Review

Review Dysmenorrhoea
Authors Suzanne Wallace / Amy Keightley / Clive Gie

Key content:
Dysmenorrhoea is a common condition of women in their reproductive years.
Local factors and the centralised response to pain are thought to be involved
in the pathophysiology.
The majority of women will respond to medical treatments.
The role of surgical treatments is small.
More evidence is now available on the use of complementary therapies to treat
dysmenorrhoea.

Learning objectives:
To understand the theories regarding the aetiology of dysmenorrhoea.
To update knowledge of evidenced-based treatments for dysmenorrhoea.

Ethical issues:
Is there a role for surgical treatments to interrupt nerve pathways in the
treatment of dysmenorrhoea?
Would women who fail to respond to medical treatments for dysmenorrhoea be
best treated by chronic pain teams?
Keywords combined oral contraceptive pill / menstruation / nonsteroidal
anti-inflammatory drugs / presacral neurectomy / prostaglandins /
uterosacral nerve ablation
Please cite this article as: Wallace S, Keightley A, Gie C. Dysmenorrhoea. The Obstetrician & Gynaecologist 2010;12:149154.

Author details
Suzanne Wallace MA MRCOG
Specialist Registrar
Nottingham University Hospitals NHS Trust,
Derby Road, Nottingham NG7 2UH, UK

Amy Keightley BM BS BMedSci

Specialty Trainee Year 2
Derby Hospitals NHS Foundation Trust,
Royal Derby Hospital, Uttoxeter Road,
Derby DE22 3NE, UK

2010 Royal College of Obstetricians and Gynaecologists

Clive Gie FRCOG FCOG (SA) DCH (SA)

Consultant Gynaecologist
Department of Obstetrics and Gynaecology,
Sherwood Forest Hospitals NHS Foundation
Trust, Sutton-in-Ashfield, UK
Email: clivegie@btinternet.com
(corresponding author)

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Introduction
Dysmenorrhoea is one of the most common
gynaecological conditions that affect the quality
of life of many women in their reproductive
years. This article explores current ideas on the
management of dysmenorrhoea and considers
causes, appropriate investigations and treatments.
In particular, it looks at the trend away from
therapies solely targeted at the pelvis towards a
more holistic approach to pain management.

Definition
The term dysmenorrhoea is derived from the
Greek words dys, meaning difficult/painful/
abnormal; meno, month; and rrhea, to flow.
Dysmenorrhoea can occur a few days prior to
menstruation as well as during menstruation
but normally subsides as menstruation finishes.
Primary dysmenorrhoea occurs in the absence
of any underlying uterine condition whereas
secondary dysmenorrhoea occurs where pelvic
pathology is present.

Epidemiology
Prevalence rates of dysmenorrhoea are thought
to be high, although estimates vary widely in the
literature. A systematic review1 of dysmenorrhoea
in the UK population more than 10 years ago
found prevalence rates of 4197%, with 1114%
of cases described as severe. However, the studies
identified by that review were generally small and
study populations differed widely in age and
baseline characteristics.
A Swedish cross-sectional study2 of nearly
600 women aged 19 years reported
dysmenorrhoea in 72%, of whom 15% had
dysmenorrhoea that was not responsive to
analgesics and which limited their activities.
This study further identified that more than
50% of these women had been absent from
work or school on at least one occasion due to
dysmenorrhoea and that 7.9% were absent every
menstruation for at least half a day. At 5-year
follow-up, rates of dysmenorrhoea had fallen to
67% with 10% having dysmenorrhoea that was
not responsive to analgesics and which limited
their activities.3 This was a significant fall but
still shows that many women continue to suffer
with dysmenorrhoea beyond their teenage
years.
Risk factors for dysmenorrhoea include early
menarche, nulliparity and family history. 2,3
Women with a longer duration of menstruation
and heavier menstrual flow were significantly
more likely to have dysmenorrhoea but there
was no association with cycle length. The
majority of studies have shown cigarette
smoking to be positively correlated with
dysmenorrhoea.3,4
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Pathophysiology of primary
dysmenorrhoea
This appears to be multifactorial. Towards the end
of the menstrual cycle, progesterone withdrawal
upregulates various inflammatory cytokines,
prostaglandins, vascular endothelial growth factor
and several matrix metalloproteinases (MMPs).
These MMPs act to degrade, leading to loss of
integrity of blood vessels, destruction of
endometrial interstitial matrix and the resultant
bleeding characteristic of menstruation. Theories
of the aetiology of dysmenorrhoea look at how
these normal pathways have the potential to cause
pain. There are several theories and it is likely that
an individual may have varying contributions
from a combination of these mechanisms. These
can be split into three main categories: uterine
contraction and vasoconstriction; modulation
and stimulation of pain fibres; and behavioural
and psychological factors.
Uterine contraction and vasoconstriction
The uterine contraction and vasoconstriction
theory currently has the strongest scientific basis.
Disintegrating endometrial cells release
prostaglandin F2, a myometrial stimulant and
vasoconstrictor. This mediates prolonged uterine
contractions and reduced blood flow, which is
postulated to cause pain.5 Women experiencing
primary dysmenorrhoea have an abnormal pattern
of contraction with a higher basal resting tone.
Peak uterine work correlates with the greatest
amount of pain.6 Elevated prostaglandin levels are
found in the endometrial fluid of women with
dysmenorrhoea and correlate with the degree of
pain.7 Other factors implicated in the aetiology of
dysmenorrhoea include leukotrienes, vasopressin
and a reduction in prostacyclin levels. Leukotrienes
increase myometrial stimulation and
vasoconstriction; women who fail to respond to
prostaglandin inhibitors have been shown to
have elevated levels of leukotrienes.8 Vasopressin
appears either to have a direct influence on
myometrial blood flow and myometrial
hypersensitivity, or to exert actions via
prostaglandin release.9 Prostacyclin is a potent
vasodilator and myometrial relaxant in vivo, thus
reduced levels may lead to hypoxia, ischaemia and
pain.10
Modulation and stimulation of pain fibres
The stimulation of pain fibres in the uterus
causes activation of the afferent pain pathways
transmitted up to the central nervous system.
In addition, there is some evidence of a direct
effect on the pain fibres themselves in cases of
dysmenorrhoea. This theory is based on the
potential effect of ischaemia on pain fibres.
Vasoconstriction leads to ischaemia and it is
thought that type C pain neurons are stimulated
by the anaerobic metabolites generated by an
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ischaemic endometrium.11 It has also been

suggested that leukotrienes can increase the
sensitivity of pain fibres.12
The multimodal response to pain
The impact of psychological and behavioural
modification on dysmenorrhoea is yet to be fully
understood.
Pain is defined by the International Association
for the Study of Pain as an unpleasant sensory and
emotional experience associated with actual or
potential tissue damage.13 Understanding the
impact of pain must, therefore, acknowledge both
the stimulation of sensory receptors by a harmful
stimulus and other factors acting centrally and
contributing to pain perception.
There is a general consensus that primary
dysmenorrhoea often coexists with other pain
conditions, such as dyspareunia, irritable bowel
syndrome and fibromyalgia. Research is being
undertaken to investigate the degree of this
overlap. It may be partly due to the difficulty in
objective assessment of the symptoms and the
challenge in diagnosing some of the chronic pain
conditions, as many of these conditions are
diagnoses of exclusion.14
Primary dysmenorrhoea, as with chronic pelvic
pain, seems to be more prevalent in those with a
history of sexual abuse.15,16 However, compared
with other pelvic pain syndromes, there is limited
research into the impact of psychosocial factors on
dysmenorrhoea.

Pathophysiology of secondary
dysmenorrhoea
There are a number of clinical conditions with
underlying pelvic pathology which can lead to
secondary dysmenorrhoea (see Box 1). Many of the
ways in which each specific pathology causes pain
overlap with the mechanisms found in primary
dysmenorrhoea. This may explain why they
respond, in part, to treatment strategies used
in primary dysmenorrhoea.
The most common cause of secondary
dysmenorrhoea is endometriosis. Many trials
have failed to show a correlation between disease
severity and the severity of pain; the exact
mechanism as to how ectopic endometrial tissue
causes pain has not been established. However,
some studies have suggested increased levels of
prostaglandin (including prostaglandin F2)
in women with endometriosis.17
Another common cause of secondary
dysmenorrhoea is chronic pelvic inflammatory
disease. Pain may be caused by the release of
inflammatory mediators, prostaglandins, scar
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Common

Less common

Endometriosis

Allen-Masters syndrome

Chronic pelvic
inflammatory disease

Congenital uterine
abnormalities

Adenomyosis

Cervical stenosis

Intrauterine polyps

Asherman syndrome

Submucosal fibroids

Uterine retroversion

Intrauterine contraceptive
devices

Pelvic congestion
syndrome

Review

Box 1

Causes of secondary
dysmenorrhoea

Ovarian cysts

tissue formation and abnormal uterine

contraction.
Adenomyosis is thought to cause secondary
dysmenorrhoea by causing tonic uterine
contractions through endometrial gland
destruction. Intrauterine polyps, submucosal
fibroids and intrauterine contraceptive devices
can also cause dysmenorrhoea by abnormal
uterine contraction in the attempt to expel them.
Less common causes of secondary dysmenorrhoea
include Allen-Masters syndrome (scarring
secondary to laceration of the broad ligaments,
usually during childbirth), congenital uterine
abnormalities, cervical stenosis, Asherman
syndrome, uterine retroversion and pelvic
congestion syndrome. Theories of pain causation
in all of these conditions relate to the production
of abnormal uterine contractions.
Ovarian cysts and tumours are associated with
dysmenorrhoea but the mechanism by which this
occurs is not clear.

Clinical presentation
Primary dysmenorrhoea typically presents
612 months after menarche. Pain is usually
cramping in nature and occurs in the lower
abdomen or pelvis but may radiate to the back or
down the thighs. It may commence before the onset
of bleeding and usually lasts 872 hours. Associated
symptoms include nausea and vomiting, fatigue
and headache.
By contrast, secondary dysmenorrhoea usually
occurs a number of years after the menarche and
pain may occur throughout the luteal phase of the
menstrual cycle as well as during menstruation.
Deep dyspareunia may also be present.
Symptoms of bowel disturbance should be
sought to identify cases of irritable bowel
syndrome and enquiry should be made as to
the coexistence of other pain conditions.
Examination findings are usually normal in
cases of primary dysmenorrhoea, whereas in
secondary dysmenorrhoea examination findings
may be abnormal, reflecting the underlying
disease.
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Investigations
Where the history and examination findings are
suggestive of primary dysmenorrhoea, further
investigations are rarely warranted. However,
if there are atypical symptoms, abnormal
examination findings, or if a trial of therapy in
suspected primary dysmenorrhoea is unsuccessful,
then pelvic ultrasound and laparoscopy should be
considered. The role of laparoscopy is still debated;
one study reported that 35% of laparoscopies for
pelvic pain or suspected secondary
dysmenorrhoea were negative.18

Treatment
Treatments for primary dysmenorrhoea (see Box 2)
are predominantly based on the three main theories
of aetiology. In secondary dysmenorrhoea, any
treatment strategy should be based on treatment
of the underlying disease, although some of the
treatment strategies employed for primary
dysmenorrhoea may also have some benefit
even with organic pathology.
A preferred approach is to individualise therapy
based on a womans concomitant symptoms
(for example, menorrhagia), age and need for
contraception.
Targeting uterine contraction and
vasoconstriction
The mainstays of treatment for dysmenorrhoea
have been nonsteroidal anti-inflammatory drugs
(NSAIDs) and the combined oral contraceptive
pill. Nonsteroidal anti-inflammatory drugs act
by blocking prostaglandin production and
so potentially may target the high levels
of prostaglandins found in women with
dysmenorrhoea. A Cochrane review19 found that
NSAIDs were significantly more effective for pain
relief than placebo (OR 7.91; 95% CI 5.6511.09)
but with a significant risk of adverse effects, in
particular gastric reflux. There is no evidence to
suggest a greater benefit of any specific NSAID.

Box 2

Treatments for primary

dysmenorrhoea

The oral contraceptive pill has long been held to

be a successful treatment for dysmenorrhoea,
based on epidemiological studies showing lower
rates of dysmenorrhoea in women on the
combined oral contraceptive pill.2,3 The presumed
mode of action is a combination of ovulation
inhibition and reduced prostaglandin production
by endometrial glands. However, a recent
Cochrane review20 concluded that there is limited
evidence for improvement in symptoms of
dysmenorrhoea with the oral contraceptive pill
mainly because of a lack of well-conducted
studies. Nevertheless, there was some evidence
that low and medium-dose estrogen pills may be
more effective than placebo. There were no
randomised controlled trials comparing the oral
contraceptive pill with NSAIDs. The oral
contraceptive pill has the added benefit of
contraception if required, although the adverse
effects, from weight gain through to venous
thromboembolism and cardiovascular effects, are
well described.
The levonorgestrel-releasing intrauterine system
is increasingly being used for both contraception
and as a treatment for menstrual disorders. It
achieves a contraceptive effect through a variety
of mechanisms but effects on menstruation are
thought to be due to resultant atrophy of
endometrial glands. Whilst there are no goodquality studies looking specifically at the effect
of the intrauterine system on dysmenorrhoea,
reductions in dysmenorrhoea have been reported
as secondary outcomes in other trials.21 It has also
been shown to be effective in the treatment of
secondary dysmenorrhoea associated with
endometriosis and adenomyosis.21,22 The
intrauterine system can be used in women in
whom estrogen is contraindicated and is well
tolerated.21
Other medical treatments that have been suggested
to reduce uterine contractility through their effects
on relaxing the myometrium include calcium
channel blockers and glyceryl trinitrate, but these
are still under evaluation.8

Medical
Nonsteroidal anti-inflammatory drugs
Combined oral contraceptive pill
Levonorgestrel-releasing intrauterine system
Surgical
Uterosacral nerve ablation (can be carried out
laparoscopically)
Presacral neurectomy (can be carried out laparoscopically)
Complementary therapies
High frequency transcutaneous electrical nerve stimulation
(TENS)
Dietary therapy; for example, vitamin B1 and magnesium
Acupuncture
Chinese herbal medicine
Behavioural therapies, including relaxation training, biofeedback
techniques and pain management sessions

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Although many women do respond to medical

therapy there is an overall failure rate of 2025%.23
Targeting pain pathways
The persistence of dysmenorrhoea despite
medical management has led to increased interest
in surgical interruption of visceral pain pathways
in women for whom medical therapy has failed.
Two main surgical techniques have been described:
uterosacral nerve ablation and presacral
neurectomy. In the former, the uterosacral
ligaments are transected, causing interruption to
the visceral afferent nerves from the pelvis; in the
latter the presacral plexus of visceral nerves is
removed. Both procedures can be carried out
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laparoscopically. Presacral neurectomy in

particular requires a high level of laparoscopic
skill. A Cochrane review23 found only limited
evidence to support this approach, concluding that
uterosacral nerve ablation was not associated with
any improvement of pain in the short term,
although there was some evidence of improvement
in pain in the long term (more than 12 months
post-procedure). The results were slightly
improved with presacral neurectomy but this was
at the expense of more frequent adverse effects,
including constipation, urinary urgency and
painless labour.
A recent large UK randomised controlled trial of
laparoscopic uterosacral nerve ablation (LUNA)
in women with chronic pelvic pain including
dysmenorrhoea showed no significant difference
in pain scores when denervation was carried out.
Follow-up reached 5 years in 72% of
participants.24 Given these findings, it appears that
there is no longer a role for LUNA in the
management of dysmenorrhoea.
The multimodal approach to pain management
Interest in managing dysmenorrhoea is now
turning towards a more holistic approach, in line
with other chronic pain conditions. High
frequency transcutaneous electrical nerve
stimulation (TENS) has been used in other pain
conditions and has been shown to be effective in
treating dysmenorrhoea in a small number of
trials, with 4260% of women having at least
moderate relief.25 There is also some evidence that
dietary therapy may be of benefit, in particular
vitamin B1 (taken at a dose of 100 mg daily) and
magnesium.26 There is some evidence for the use
of acupuncture and Chinese herbal medicine but
trials are often small.25,27 A recent Cochrane
review28 looked at behavioural therapies, including
relaxation training, biofeedback techniques and
pain management sessions, with some evidence of
efficacy, although, again, trials were small and of
variable methodological quality. However, not all
complementary therapies evaluated have shown
effectiveness; for example, meta-analysis has
shown no evidence for the role of spinal
manipulation in treating dysmenorrhoea.29
Other therapies
Historically, surgical treatments for
dysmenorrhoea have included cervical dilatation
and ventrosuspension; however, their role in
management has been discredited and they are
now rarely used.30 Hysterectomy continues to be
used occasionally as a treatment for refractory
dysmenorrhoea. The evidence base for this is
limited, although in our experience hysterectomy
may be warranted in women with severe
symptoms where other therapies have failed, who
have coexisting symptoms such as menorrhagia,
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Review

who have completed their family, and who are fully

counselled about the short and long-term risks of
the procedure.

Conclusion
Dysmenorrhoea is a common condition affecting
young women. As with other pain conditions, the
aetiology appears to be multifactorial and involves
inflammatory mediators, pain pathways and a
centralised response. Many women will obtain
relief from a combined individualised approach to
treatment, reflecting the likely multiple underlying
mechanisms.
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