dolore pelvico cronico

1. Dolore pelvico cronico:
epidemiologia ed
eziopatogenesi
F. Cappellano
Neurourology Dept
“Pain Team” Coordinator
Policlinico Multimedica IRCCS
Sesto San Giovanni ( Milano)

2. DEFINITION
ACUTE vs CHRONIC PAIN
ACUTE PAIN
occurs in conjunction with autonomic reflex
responses and associated with signs of
inflammation and infection
symptom of underlying tissue injury and disease
it is a protective mechanism.
CHRONIC PAIN
in contrast doesn’t have such physiologic role
it is itself not a symptom, but a disease
lasting 6 months or longer
is characterized by psychological, affective and
behavioral responses that differ from acute pain.

3. Chronic pelvic pain
 Chronic pelvic pain is defined as a chronic or
persistent pain, continuous or recurrent for at least 6
months, perceived in structures related to the pelvis
or lower abdomen (Guidelines on Chronic Pelvic Pain – EAU,
2012)
 Real incidence not known (about 4-15% of women),
 Female to male ratio 9:1 ,
 10% of gynecology referrals,
 12% of hysterectomies, 40% of diagnostic
laparoscopies,
 High impact on quality of life,
 In 30% of cases no apparent cause is determined.
 Consider :
pudendal neuralgia and neurogenic inflammation !

4. EPIDEMIOLOGY
• Follow up study  1 to 6 years (mean follow-up period 3.4y)
• From April 1998 to November 2002
• age >18 year-old
• 72/139 women (60%)
• Life Chart interview
• Demographic and clinical variables
• MPQ-DLV to assess self-reported pain + McGill VAS
• SCL-90 to assess psychological distress
Pain 132 (2007) S117–S123

5. EPIDEMIOLOGY
• After 6 years of follow up 75% women had not reach recovery
• No women reported malignancy or any newly diagnosed physical illness
• 25% recovery (improvement gain scores)89% clinical improvement
50% after 2 years
25% after 3 years
11 % no pain
• Recovery was not associated with any demographic, clinical or pain related
variable measures at baseline
Pain 132 (2007) S117–S123

6. Pudendal neuropathy

7. Integrated pathophysiology of CPP
Stress, nerve damage, tissue injury, inflammation

8. Neural mechanisms of pain
 Elbadawi and Light proposed
neurogenic inflammation as a
trigger taking place in this disease
 When activated by noxious events
such as nociception, C-fibers not
only do they convey information to
the CNS (afferent function), but
they also can release substance P,
CGRP, tachykinins, somatostatin,
nitric oxide and other factors into
the local environment (efferent
function).

9. Neurogenic inflammation
 NI is not necessarily a mechanism leading
to a disease but it’s part of the tissue
response to injury
 It seems to be an adaptive response,
activating cells for local defence but
sometimes it can become maladaptive
 Recently the involvement of NI has also
been suggested in the development of IC
Elbadawi, Steers, 1997

10. Neural mechanisms of pain
 Once activated, C-fibers can
become sensitized, meaning
that they no longer remain
silent even after inflammation
resolves (Gebhart, 1999)
 Efferent actions increase
local vascular permeability
and inflammation, a process
called ‘neurogenic
inflammation’ (Holzer, 1998 )

11. Wind–up phenomenon
 Wind-up is a form of short-
term plasticity in spinal dorsal
horn that can be observed
during electrical stimulation of
C-fibers
 The action potential firing of
some wide dynamic range
(WDR) neurons in deep dorsal
horn increases progressively.
 Wind-up may facilitate
induction of LTP at C-fiber
synapses, as a progressive
postsynaptic depolarization
 Central sensitization is
triggered by impulses in
nociceptive C-fibers.
3 Hz

12. Central sensitization sustains pain

13. Neurogenic inflammation and estrogen
 Women have a higher incidence of inflammatory
disorders than men and also appear to perceive painful
stimuli differently
 Estrogen have the capacity to modulate neurogenic
inflammation through interaction with a variety of
mediators of inflammation
 Estrogen receptors may play a role in determining the
intensity of the response to neurogenic inflammation .
(Bjorling 2001)

14. Estradiol’s influence on CNS
function
 The CNS can retain a
‘memory’ of central
neuronal changes
induced by neuronal
input that can be
‘recalled’ by estradiol
action on activity of
CNS neurons

15. Pudendal neuropathy
 Pudendal neuralgia by a mechanical
and/or inflammatory damage to the
nerve may be the underlying condition of
CPP once other causes for the
symptoms may be excluded.
 Usually a pudendal nerve entrapment
(PNE) is believed to be the cause of
pudendal neuralgia, but a neurogenic
inflammation can often sustain this
condition

16. Pudendal nerve anatomy

17. Pudendal nerve anatomy
Mahakkanukrauh, 2005, Clinical Anatomy 18:200-205

18. Neurogenic inflammation
 NI is not necessarily a mechanism leading
to a disease but it’s part of the tissue
response to injury
 It seems to be an adaptive response,
activating cells for local defence but
sometimes it can become maladaptive
 Recently the involvement of NI has also
been suggested in the development of IC
Elbadawi, Steers, 1997

19. NI and organs cross talk
 In visceral pain
conditions NI not only
plays a role in pain and
inflammation at the site
of viscus, but also
appears to be an
important mechanism in
referred pain.
Malykhina 2007, Neuroscience

20. Diagnosis
 Clinical examination is necessary
 Sensory loss on perineum or genitals is suggestive of
sacral nerve root lesion, without pain but associated
with sphincters motor disorders
 Unilateral pain elicited by compression of the area
near the ischial spine during rectal or vaginal
examination
 CT scan, MRI and other radiological procedures are
not useful for diagnosis
 Neurophysiology tests may serve as complementary
diagnostic measures
 Psycological evaluation for depression is mandatory

21. Diagnosis

22. Pudendal nerve block
 Guided pudendal nerve blocks are the first
line of conservative treatment for pudendal
neuralgia, usually associated to oral drugs
and physical therapy.
 They are performed for making a diagnosis
of pudendal neuralgia, for its prognostic
value and mainly for the therapeutic effect.

23. Pudendal nerve block
 Responders have a complete relief of pain
for about 36-48 hours , a mild flare up of
pain for 2 to 3 days and then a relief up to
complete wellness for about 15 days.
 The subsequent blocks are made at 3
weeks interval, after a clinical reassessment
of the patient and an evaluation of the VAS,
until a complete recovery or stabilization of
the pain at an acceptable level is obtained.

24. Pudendal nerve block

25. Pudendal nerve block

26. 26
NERVE BLOCK EFFICACY
Successful result  decrease in VAS scale > 50%
(N=110)
PAIN ASSESSMENT
Pain before nerve block (VAS) 10 (3,5 – 10)
Pain after nerve block (VAS) 4 (0 – 10)
Success rate (after blocks cycle) 69/110 (63%)
Relapse 6/69 (9%)
Success rate ( 11.5 months f.u.) 63/110 (57%)
Data are reported as median (range) or absolute value and percentage (n = 110)