Brian P. Jacob, David C. Chen, Bruce Ramshaw, Shirin Towfigh (eds.) - The SAGES Manual of Groin Pain-Springer International Publishing (2016)

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M.J. Solnik and M.T. Siedhoff
for the indication of pelvic pain [ 4 , 5 ]. The observation that the majority
of women who have a “negative” laparoscopy will continue to experience
chronic pain suggests that more careful and systematic evaluation
before or instead of a laparoscopy might be more productive and beneficial
to the patient.
The purpose of this chapter is to provide clinicians who see female
patients with a précis and guide to allow for more effective triage of CPP
and to implement appropriate, contemporary diagnostics and therapeutic
interventions. Critical to this process is a real understanding of the
pathogenesis behind chronic pain and how this may be associated with
the spectrum of related disorders.
History and Background
The last half- century has seen significant evolution in the understanding
of chronic pelvic pain. Conceptualization was largely Cartesian
in the 1950s, where the degree of tissue damage should correlate with
the degree of pain experienced, and anything more was the result of
psychological distress. Beginning in the 1960s, Wall and Melzack began
developing the gate control theory , a concept represented by the nervous
system having both the ability to carry nociceptive input from the
periphery and the ability of central systems to temper that input with
descending modulation. The degree to which these “gates” are open or
closed relates to the amount of discomfort experienced by the patient.
Relative gate closure could thus explain how the basketball player can
play her championship game through a knee injury without thinking, but
experiences significant pain once the competition is complete. The gate
control theory is still a useful concept, but many now have grown to
accept a concept of central sensitization in understanding chronic pain.
In this paradigm, repeated noxious stimuli “ramp up” the patient’s pain
signaling over time, and coupled with a genetic predisposition or traumatic
life experience, results in a general pain hypersensitivity, regardless
of the stimulus. This helps explain the frequent finding of multiple
chronic pain syndromes comorbid in a single patient, such as dysmenorrhea
, vulvodynia , interstitial cystitis (IC) / painful bladder syndrome
(PBS), irritable bowel syndrome (IBS) , temporomandibular joint disorder
(TMJ) , migraines , and fibromyalgia [ 6 ]. These conditions are known
as “functional” pain syndromes , meaning that there is no readily identifiable
anatomic or physiologic abnormality, but rather the disease is
defined by the symptoms the patient suffers.