Understanding
Physiology
of
Dysmenorrhea
Edward M. Lichten, M.D., F.A.C.S.
Fellow American College of
Obstetricians and Gynecologists
Senior Attending, Hutzel Hospital
540 Henrietta Street
Birmingham, Michigan 48009
http://www.usdoctor.com
Email: drlichtren@yahoo.com
Cara Glavin, M.S.
Wayne State, College of Medicine
Abstract:
Although the prevailing hypothesis concerning dysmenorrhea is focused on excessive
prostaglandin production initiating uterine contractions, this hypothesis fails to include or
explain the 100 years of successful surgical treatments of dysmenorrhea with procedures
that interrupt nerves to the pelvis. The author proposes and provides support for a new
hypothesis that includes the known treatments of dysmenorrhea, following the four steps
outlined in the Scientific Method. He proposes that “the origin of primary dysmenorrhea
is the physiological obstruction of the cervix and that the associated pain is a result of the
increase in uterine pressure caused by the contraction of the uterine musculature against
the constricted cervical os.” The author reviews the data from the literature and adds
uterine and cervical pressure tracings during a dysmenorrheic menstruation to support
this hypothesis. Furthermore, he proposes the unification of the prostaglandin and the
hypertonic cervix hypotheses by explaining that the prostaglandins may trigger the
cervical contractions by directly exciting efferent nerves or by interfering with downregulatory nerves to the cervix. In either case, the result is the obstruction of the cervical
egress of menstrual debris.
Introduction:
The prevailing theory of dysmenorrhea is that excessive prostaglandin production causes
abnormal uterine contractions and pain. However, this hypothesis fails to consider more
than 100 years of successful treatment of dysmenorrhea with various surgical procedures.
Ruggi1 in 1898 performed a sympathectomy on 12 women, successfully curing their pain.
Cotte2 in 1929 popularized the presacral neurectomy, which was the mainstay of
treatment until Doyle3 in 1955 described similar results with vaginal transection of the
uterosacral nerves. Lichten4 in 1987 described the laparoscopic transection of the
uterosacral nerve (L.U.N.A.) and Perez5 in 1991 described the laparoscopic presacral
neurectomy. In each case, surgical treatment proved successful in approximately 70- 80
percent of patients at follow up. Both L.U.N.A. and presacral neurectomy continue to be
used by gynecologic surgeons today.
Background:
The author performed his initial Laparoscopic Uterine Nerve Ablation (L.U.N.A.) in
August 1982 on Jodi, a 23 year-old and nulliparous Caucasian female. She had
experienced 7 days of incapacitating menstrual pain every month since age 13. She had
seen more than 30 health professionals including gynecologists, surgeons, internists,
psychiatrists and alternative healers. She had had two negative laparoscopies and
necessitated prescription Demerol and Codeine for pain control prior to the author’s
initial evaluation and treatment. The author performed Jodi’s third laparoscopy in 1981
and found no disease. Having exhausted all other treatments and medications, he
performed a paracervical block in the office on her first day of dysmenorrhea in July
1982. Surprisingly, her pain abated for that entire cycle. Since laparoscopic biopsies
were being performed to identify herpes virus in the uterosacral nerves, the author
reasoned that he could cauterize these very nerves and execute a more permanent
laparoscopic paracervical block.
The successful experience with Jodi in August, 1982 led the author to evaluate the
effectiveness of this procedure on other consenting patients with pelvic pain. L.U.N.A.
failed to work for chronic pelvic pain, adenomyosis, degenerating or enlarged
leiomyomata, and all non-midline pelvic pain. It was observed to be generally a
successful surgical option for women in whom non-steroidal anti-inflammatory drugs
failed to alleviate the pain of primary dysmenorrhea and pain associated with midline
endometriosis.
Method
Having observed that L.U.N.A. offered relief of primary dysmenorrhea to women
without evidence of disease, Milton Goldrath, Department Chairmen of Gynecology at
Sinai Hospital, Detroit, Michigan designed a double-blind study to determine,
objectively, if L.U.N.A. was superior to placebo (no treatment). The study was
specifically limited to only these individuals without evidence of pathology. The
evidence-based double-blind study was published in the Journal of Reproductive
Medicine in 19874 and did show strong statistical significance. The observation was that
LUNA offered significant pain relief compared to placebo at 6 months and less so at one
year.
But any evidence-based study was just the first step toward a scientific conclusion. The
standard for medicine decision-making was and remains the Scientific Method. The
methodology consists of four steps: 5
1. Defining a problem: in this case, primary dysmenorrhea.
2. Gathering data. Original data of L.U.N.A. article.4
3. Drafting the hypothesis.
4. Empirically testing the hypothesis to explain all relevant observations.
The original hypothesis put forth in the referenced Journal of Reproductive Medicine
article4 was that L.U.N.A. offered pain relief to those individuals with primary
dysmenorrhea because it interrupted afferent sensory fibers of pain from the uterus. This
conclusion was a reiteration of the hypothesis put forth by J. Doyle in 19553 (who
described vaginal transection of uterosacral nerves) and Cotte in 19312 (who described
abdominal transection of superior hypogastric plexus; i.e. presacral neurectomy).
However, the author’s (EML) continued observations failed to support the accepted
hypothesis of Cotte, Doyle, Lichten and Perez. These L.U.N.A. women who had relief
from dysmenorrhea still had pain in labor, pain with spontaneous abortion and pain when
undergoing an office dilatation and curettage. Meigs6 in 1949 clearly delineated that the
uterus had sensory innervations from two different spinal areas: sympathetic from T10L1 to the fundus of the uterus and parasympathetic innervations from S2-S4 to the cervix.
He noted that the uterus and cervix were phylogenetically of different origins.
Interruption of the sympathetic T10-L1 nerves eliminated only the pain of uterine
curettage. The author (EML) questioned, “if L.U.N.A. interrupted the afferent sensory
fibers of the sympathetic plexus from T10-L1, then why did these patients have pain from
curettage and why the paracervical block just as effective?”
Review of the Literature
The technique of scientific measurements of uterine pressure was reviewed in the medical
literature dating back to 1934. Cibil7, Hendricks8 and Woodbury9 had used scientific
instrumentation to report that the uterine pressures in women with dysmenorrhea were
abnormally elevated as seen in Woodbury’s figures 1 and 2. A comprehensive review of
this subject also appeared in Chronic Pelvic Pain in Women by Marcel Renaer M.D.,
Ph.D.10 In an effort to better understand the physiology of dysmenorrhea, the effect of
paracervical block and the surgical treatments for dysmenorrhea, a research project was
designed to use Swan-Ganz instrumentation for measuring intrauterine and intracervical
pressure before and after the treatment. These catheters are constructed with pressure
sensors in the tips and avoid the distortion and effects of the balloon technology used by
previous authors. Observations were to be made of a nulliparous woman during
menstruation with dysmenorrhea and laparoscopic confirmed absence of secondary
causes of dysmenorrhea.
Results
The author aligned two Swan-Ganz catheters with sterile hemorrhoid bands. One catheter
was aligned 1.5cm longer than the other. [figure 3] The hemorrhoid bands were placed
at 1.5cm below the shorter catheter. Therefore, when the bands were at the cervical os,
the shorter catheter was in the cervix and the longer catheter was in the uterine cavity.
Using a dual pressure recording system,[figure 4] the author recorded the uterine
pressure tracings on her first day of menstruation. The baseline pressures and amplitude
spikes were records and appear below in figure 5. Note the very high baseline pressure in
both the uterus and cervix. The pressure in the uterus spiked over 250 mm Hg. The
pressure in the cervix was likewise abnormally elevated with frequent spikes to 50 mm of
Hg.. After recording the tracing for more than 30 minutes, the author performed a
paracervical block injecting 5cc of 1% lidocaine into the cervix at 4 and 8 o’clock
position. Within 30 seconds, the pressure tracing in the cervix changed. The amplitude
dropped and the frequency of cervical contractions became clearing identified in figure 6.
Furthermore, the change in pressure in the uterus reverted to “normal” amplitude with a
low baseline. The changes in the uterus followed the normalization of pressure in the
cervix and the patient reported clinical relief of pain.
Discussion
It was observed that the cause of dysmenorrhea in this individual was the increased
baseline pressure and amplitude spikes from uterine contractions, not unlike those
observed during labor and delivery. It was also observed that the increased cervical
pressure caused the physiological obstruction to the normal menstrual egress through the
cervix. The result of the paracervical block was the drop in cervical baseline pressure
and contraction frequency. Subsequently, the uterine contraction amplitude, baseline
pressure and frequency began to decrease until reaching a normal pattern. But how could
the cervix generate such pressure? The answer may come from the anatomic dissections
of Leppert11 . Leppert showed that in the cervix are elastic fibers parallel to the
endocervical canal. The muscle fibers in the cervix are similarly oriented. Could the
muscle fibers oriented parallel to the cervical isthmus generate a low pressure over the
length of the canal to obstruct any flow?
To explain these new observations, a second hypothesis was devised. The author
presented this new hypothesis to the attendants at the annual meeting of the American
Association of Gynecologic Laparoscopists in Las Vegas on October 23, 1991.12
The new hypothesis stated that:
“The origin of primary dysmenorrhea is the physiological obstruction of the cervix and
that the associated pain is a result of the increase in uterine pressure caused by the
contraction of the uterine musculature against the constricted cervical isthmus.”
Anatomically, the author defended this new hypothesis by explaining that the physiology
for the successful cases of L.U.N.A. could be explained by surgery interrupting the
efferent nerve fibers that cause this circular, sphincter-like muscles to relax. Likewise,
any surgical procedure that interrupted the nerves to this muscle, or dilated or overstretched the cervix, would also prevent the cervical sphincter from obstructing menstrual
flow.
As noted in the last step of the Scientific Method, this hypothesis explains many of the
often ignored observations from the medical literature. Clinically, there were reports of
relief from primary dysmenorrhea with (1) relaxing incisions to weakening the cervix
(circa 1910), (2) cervical pessaries (1940’s) and (3) repeated vaginal delivery. The
author’s hypothesis was not without precedence: theories of obstruction of the cervix
were proposed by Sims in 1868 and practiced by Hippocrates in 425 B.C. who treated
dysmenorrhea by dilating the cervix with increasing diameter dilators made from willow
bark.
There was also strong support in the previously published pressure recordings of Cibil,
Hendricks and Woodbury. In figure 1, Woodbury9 demonstrated that the elevated
pressure in the cervix had prevented egress of blood through the cervical os. In figure 2,
Woodbury called this a “contraction ring.”9 Barberi13 constructed a model that
demonstrated that narrowing of the cervical os contributed to retrograde menstruation
through the fallopian tubes. Youseef in 1958 had clearly identified that a sphincter
activity of the uterine isthmus existed.14, 15 Yousef injected 2-3 ml of iodized oil
(Lipiodol) directly into the uterine cavity through the posterior vaginal cul-de-sac to
perform a “direct” hysterography, showing that in normal women the tone of the isthmus
was highest during the secretory phase and lowest during the proliferative phase.
When the [injection] examination took place one or two days before the period,
however, it was found that, shortly after the Lipiodol was injected into the uterine
cavity, the patient started to complain of severe colicky pains. The uterus did not
empty itself as rapidly as it normally does at that particular time and some
Lipiodol remained inside the uterus two or three hours after injection; but finally
it passed, as it did in normal cases, through the isthmus and cervix and not
through the tubes. The isthmus appeared, however, much less relaxed than it was
in normal cases in the immediate premenstrual phase. (in Renear, p. 50).
These publications support this author’s observations that dysmenorrheic individuals
have:
(1) elevated uterine baseline and amplitude pressures,
(2) abnormal uterine-cervical pressure gradients, and
(3) abnormal cervical contraction patterns.
It appeared that the second hypothesis, strictly limited to primary dysmenorrhea, was
compatible with 100 years of scientific obstetrical and surgical observations. However,
the author questioned whether we could unify our hypothesis with the observations that
cautery, excision, and L.U.N.A. relieved dysmenorrhea in specific cases of
endometriosis? And how could this hypothesis explain relief of dysmenorrhea with nonsteroidal anti-inflammatory drugs?
Moghissi16, Acherlund17, Ylikorkala and Dawood18 had each confirmed the 4-fold
increase in prostaglandin F-2-alpha in human endometrium on the first day of
menstruation in dysmenorrheic individuals. “The high prostaglandin content of the
endometrium of the 1st day of the period seems to determine the contractility patterns
associated with most cases of primary dysmenorrhea…..this may be the result of a
disturbed outflow of menstrual blood through the cervix.”10 (Moghissi, Acherlung)
Dawood19 and others have found an increase in prostaglandins in peritoneal washing in
individuals with endometriosis, dysmenorrhea and infertility.
Ultimately, the authors proposed to modify this hypothesis to include the concept that a
chemical compound existed that triggers the physiological cervical obstruction, the
increased uterine pressure and the pain associated with menstruation. Although it has
yet to be completely proven, others have already observed that prostaglandins from
endometriosis can trigger the increased cervical and uterine contractility.20, 21 The author
proposed that these chemical compound could directly cause an irritation of the efferent
nerve fibers, thereafter, precipitating the constriction of the cervical isthmus, the
increased intrauterine pressure, and clinical presentation of dysmenorrhea. Whether the
surgeon excised endometriosis, performed a surgical nerve interruption, or chemically
reduced the release and actions of prostaglandins, leucotrienes, or some other noxious
compound, relief from dysmenorrhea could occur. The medical therapy could include
NSAIDs (non-steroidal anti-inflammatory drugs: ibuprofen, naproxen sodium,
mefenamic acid, ketoprofen, etc.) or a suppressor of estrogen release (luprolide acetate,
danazol, megesterol acetate, medroxy-progesterone acetate or even testosterone
injections).
Physiology
Mechanical modeling was used by Barberi to explain the retrograde egress of menstrual
debris in cases of cervical obstruction. The authors created an anatomical model of the
cervix based on the standard measurements in Textbook of Gynecology.38 The
conditions for the cervical model were the following:
1. Firm, exterior surface of the cervix. Assumption, relatively inflexible.
2. Orientation of muscle fibers parallel to cervical isthmus interspersed with elastic
fibers.
3. Internal cervical os measurements: internal cervical os (isthmus) 5mm
4. Maximal muscle contraction under normal physiological conditions is
approximately 22 percent.39
Therefore, under these stated conditions, contraction of muscle fibers in the longitudinal
axis have the potential to narrow the internal os by 4.5 mm. The shortening of the
longitudinal fibers result in a “fattening” in its mid-portion which “bulges” into the
cervical isthmus.
This model adds support to the observations and recordings of the many authors who
support the obstructive hypothesis of primary dysmenorrhea. The cervical ring of
Hendricks and the cervical obstruction of Yousef can be explained as a physiological
narrowing at the internal os and isthmus where the maximum concentration of cervical
muscle fibers are found. Just as in the urethra (another cloacal structure), low pressure
over an extended distance can prevent egress of fluid. This hypothesis further explains
why the pressures we recorded in the cervix were significantly less than one-fourth of the
pressure measured simultaneously within the uterus.
Conclusion
In the medical climate on the early 1980’s, women with dysmenorrhea were classified as
histrionic (hysterical). As the public became more aware of the effectiveness of the
NSAIDs medications in lay books (publicized by Penny Budoff, M.D.22 in No More
Menstrual Cramps and Other Good News) and the support of a national endometriosis
organization (Mary Lou Balweg, RN),23 in Overcoming Endometriosis), the surgical
treatments of dysmenorrhea were ignored. The knowledge of the physiology of
obstructive dysmenorrhea gathered over sixty years was ignored. Today, many physicians
and most lay individuals remain ignorant of this information. Yet, they have come to
realize that minimal endometriosis can cause severe pain and that women with primary
dysmenorrhea have a physiological not a psychosomatic basis for their complaints.
Many gynecologists now recognize that primary dysmenorrhea is most likely due to
microscopic endometriosis. Whichever modality is used as treatment, whether NSAIDs,
hormonal suppression, or surgical procedures of excision with or without nerve
transection, relief is expected in 65-80 percent, significantly better than placebo.
Laparoscopic evaluation remains the appropriate step after NSAIDs and oral
contraceptives have failed to relieve dysmenorrhea. Laparoscopy remains necessary to
document the extent and presence of disease. At the time of laparoscopy, many
gynecologists incorporate L.U.N.A. or laparoscopic presacral neurectomy as an adjunct
surgery to the excision and cautery of endometriosis because of the many published
studies that observe their benefits as stand-alone procedures24-33, albeit the rare
complication and naysayer.33-36 Clearly, the author37 never considers L.U.N.A. or
presacral neurectomy as a cure-all for pelvic pain, rather as a surgical alternative in cases
in which NSAIDs could not offer pain relief for some women with dysmenorrhea,
dyspareunia and endometriosis. With Jodi still pain free after almost 24 years, the
authors consider their original observations of L.U.N.A. as just the first steps in a lifetime
of study that leads to a clearer understanding of the physiology of menstrual pain.
References:
1. Ruggi J. Crosen HS (editors): Gynecology. St. Louis, CV Mosby, 1915
5. Lichten E, Bombard J. Surgical treatment of primary dysmenorrhea with Laparoscopic
Uterine Nerve Ablation (LUNA). Journal of Reproductive Medicine. 1987; 32(1): 37-41.
4. The Lexicon Webster Dictionary. The English-Language Institute of America,Inc.1979
3. Doyle JB: Paracervical uterine denervation by transection of the cervical plexus for the
relief of dysmenorrhea. American Journal of Obstetrics and Gynecology 1955; 70:11
2. Cotte G, Dechaume J (1931) Les plexalgies hypogastrigues. Documents
histopatholoques. Presse Medice 1931; 373-376
6. Ingersoll FM, Meigs JV: Presacral neurectomy for dysmenorrhea New England
Journal of Medicine 1948; 238:357-12.
7. Csapo I: A rationale for the treatment of dysmenorrhea. Journal of Reproductive
Medicine. 1980; 25:213
8.Hendricks C. Inherent motility patterns and response characteristics in the nonpregnant human uterus. American Journal of Obstetrics and Gynecology. 1966; 96:824843.
9. Woodbury RA, Torpin RA, Child GP, Watson M, Jarboe M. Myometrial physiology
and its relation to pelvic pain. Journal of the American Medical Association. 1947; 134:
1081-1085
10.Renear M.Chronic Pelvic Pain in Women.Springer-Verlag, New York, 1981.pp 47-65.
11, Leppert PC, Cerreta JM, Mandl I. Orientation of elastic Fibers in the human cervix.
Am J of Ob Gyn 1986;155:219-224.
12. Lichten E. Controversies in Gynecology: L.U.N.A. American Association of
Gynecologic Laparoscopists Annual Meeting. October 23, 1991. Las Vegas, Nevada.
1991
13. Barbieri RL, Callery M, Perez SE. Directionality of menstrual flow: cervical os
diameter as a determinant of retrograde menstruation. Fertil Steril 1992;57(4):727-30
14.Youseef AE. The uterine isthmus and its sphincter mechanism. I. The uterine isthmus
under normal conditions. American Journal of Obstetrics Gynecology.1958,75:13051319
15. Ibid. The uterine isthmus and its sphincter mechanism. II. The uterine isthmus under
normal conditions. American Journal of Obstetrics and Gynecology. 1958, 75:1320-1332
16. Moghissi KS. Prostaglandins in reproduction. Obstetrics and Gynecology Annuals
1972; 1: 297
17. Ackerlund M. Pathophysiology of dysmenorrhea. Acta Obstetrics and Gynecology.
Scand. 1979; 87 [Suppl]: 27-32
18.Ylikorkala O, Dawood YM: New concepts in dysmenorrhea. American Journal of
Obstetrics and Gynecology 1978; 130:833.
19. Dawood YM: Premenstrual Syndrome and Dysmenorrhea. Baltimore, Urban &
Schwarzenberg, 1985, p. 99
20. Lundstrom V, Green K. Endogenous levels of prostaglandin F2-alpha and its main
metabolites in plasma and endometrium of normal and dysmenorrheic women. American
Journal of Obstetrics and Gynecology 1978; 130: 640-646.
21. Lumsden MA, Kelly RW, Baird DT: Is prostaglandin-F2 involved in the increased
myometrial contractility of primary dysmenorrhea? Prostaglandins 1983; 25:683
22. Benedetto C. Eicosanoids in primary dysmenorrhea, endometriosis and menstrual
migraine. Gynecol Endocrinol 1989;3(1):71-94
23. Budoff P. No More Menstrual Cramps and Other Good News. Penguin Press. 1981.
24. Balweg ML. Overcoming Endometriosis. 1987. New York City.
25. Carter JE. Surgical Treatment for chronic pelvic pain. J Soc Laparoendosc Surg
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neurectomy and laparoscopic uterine nerve ablation for primary dysmenorrhea. J Reprod
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27. Daniell JF, Lalonde CJ. Advanced laparoscopic procedures for pelvic pain and
dysmenorrhea. Baillieres Clin Obstet Gynaecol 1995;9(4):795-808
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Assoc Gynecol Laparosc 1995;2(3):255-62
29. Sutton CJ, Ewen SP, Whitelaw N, Haines P. Prospective, randomized, double-blind,
controlled trial of laser laparoscopy in the treatment of pelvic pain associated with
minimal, mild, and moderate endometriosis. Fertil Steril 1994;62(4):696-700
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laser uterine nerve ablation and tubal surgery. Baillieres Clin Obstet Gynecol
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airborne trainees. A report of three cases. Journal of Reproductive Medicine
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transection. A case report. Journal of Reproductive Medicine 1992;37(12):995-6
37. Lichten, E.M. "Three Years Experience with L.U.N.A.: Outpatient Surgical
Treatment of Dysmenorrhea." American Fertility Society. Program Supp., Sept 27, 1986,
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38.
Copeland, L.J. Textbook of Gynecology. W.B. Saunders Co., Philadelphia. 1993.
39.
chapter in skeletal muscle textbook…..
Figure 1: from Woodbury RA et al. Myometrial physiology and its relation to pelvic pain.
Journal of the American Medical Association. 1947; 134: 1084. Reproduced with
permission.
Figure 2: from Woodbury RA et al. Myometrial physiology and its relation to pelvic pain.
Journal of the American Medical Association. 1947; 134: 1084. Reproduced with
permission.
Dual Catheters
Figure 3:
Dual Swan-Ganz
catheters of unequal
length.
The longer is placed in
the uterus, the shorter
one, in the cervical
isthmus.
The upper band is placed
at the external cervical
os.
Figure 4: Dual recording devices for Swan-Ganz catheters.
Figure 5: Primary dysmenorrhea. Uterine tracings shown above, cervical tracings below
from Swan-Ganz pressure catheters. Tracings recorded at 5mm/min. Y-axis recorded
pressure in mm of Mercury. Amplitude of uterine contractions exceeded 250mm Hg
scale while cervical contraction spike exceeded 150 mm Hg. Note elevated baseline
pressures from both recorders as compared to Figure 2.
Figure 6: Same patient. Ten minutes after paracervical block with 10cc of 1% lidocaine.
X-axis is recorded at 25mm/ minute to allow for closer scrutiny of uterine and cervical
contraction patterns. Note the absence of the uterine pressure spikes, the maximum
pressure of just over 100mg Hg and the decrease in uterine baseline pressure. The lower
graph shows the independent cervical contraction pattern with maximum contraction
amplitude of 30 mm Hg over baseline pressure.
Textbook of Gynecology. Editor: Copeland, Larry J. WB Saunders & Co. Philadelphia.
1993. pp. 736-737
The urethra has both smooth muscle and skeletal muscle compartments. The inner
longitudinal smooth muscle is continuous with the bladder’s; the outer circular urethra
musculature is both smooth, with fibers throughout the urethra, and striated, with
decussating fibers of the surrounding muscles. More bundles of smooth muscle are
present anteriorly than laterally or inferiorly. The striated fibers cross laterally and
superiorly and encompass both the urethra and the vagina in the lower third of the urethra
but surrond the urethra only in the middle third, where they are more prominent on the
superior (anterior) surface.
Delaney’s work (1986) ushered in a modern era of more complete understanding of
preiurethra anatomy. The urethra is now divided into fifths instead of thirds, and each
part has significant relationships to preiurethra structures. The first part (0-20%), being
intramural, and the 15-20% is the area of urethra support afforded by the superior
attachment of the vagina to the elevator any musculature, allowing voluntary control of
upward and downward motion of the urethra superior to the argental diaphragm. The
next tow first (20-40%), is the mid urethra. Here is the areas of greatest striated urethral
sphincter muscle mass. The vaginal levator attachments (23-60%) form both muscular
and fascial connections of the uretha to the levator musculature. Fibers in the areas of the
urogenital diaphragm (60 to 8 %) encircle both the vagina and the urethra (urethrovaginal sphincter) while other fibers pass laterally to insert in to the pubic rami (the
compressor urethra). The distal fifth, surrounded by nonconnnectin bulbocavernosus
muscles, lacks skeletal and smooth muscle and is a low-pressure, fibrous conduit.
…
In the 60-80% (urogenital diaphragm area) is the greatest voluntary increase in intraurethral pressure, where (56%) urine flow stops as a woman contracts the pelvic floor.
The urethra enters the urogenital diaphragm at just this point, and the urethra becomes
relatively “fixed,” losing the mobility present proximally. This is also areas of greatest
pressure “transmission.” Sudden increases in Intra-abdominal (thus intravesical)
pressures are remitted in continent women to the uretha. In fact, the pressures here in the
urethra raise more, and precede, the intra-abdominal rise by 0.25 seconds, suggesting
reflex muscle contractions rather than simple ”transmission.” (Costantinou, 1982.)
Constatinntou CE. Spatial distribution and timing of transmitted and relaxation generated
pressure in healthy women. J Urol 1092; 127:964.
Copeland. Page 77.
The portion of the cervix that protrudes into the vaginal lumen and generally rests against
the posterior wall of the vagina is termed the portio vaginalis. The superficial tissue of
the portio vaginalis, which is readily viewed on speculum examination, is termed the
ectocervix. The lumen or the external cervical os, usually 0.5 to 0.75 cm in diameter,
opens into the wider cervical canal, narrows again at the isthmus to form the internal
cervcial os, and then adjoins the endometrial cavity.
DeLancy JOL. Correlative study of preiurethra anatomy. Obsteric Gynecol 1986:68:1:91.
Westby M, Rasmussen M, Olmsted U. Location of maximal intraurethra in the female
subject as studied by simultaneous tenuous ururethracystomettry and voiding
urethrocystography. Am J Obstetrics and Gynecol 1982; 244:408?