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Dolore pelvico cronico: epidemiologia ed eziopatogenesi
F. Cappellano
Neurourology Dept “Pain Team” Coordinator
Policlinico Multimedica IRCCSSesto San Giovanni ( Milano)
DEFINITIONACUTE vs CHRONIC PAIN
ACUTE PAIN occurs in conjunction with autonomic reflex responses and associated with signs of
inflammation and infectionsymptom of underlying tissue injury and
diseaseit is a protective mechanism.
CHRONIC PAINin contrast doesn’t have such physiologic role it is itself not a symptom, but a disease
lasting 6 months or longeris characterized by psychological, affective
and behavioral responses that differ from acute pain.
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 !
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
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
Pudendal neuropathy
Integrated pathophysiology of CPP
Stress, nerve damage, tissue injury, inflammation
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).
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
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 )
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
Central sensitization sustains pain
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)
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
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
Pudendal nerve anatomy
Pudendal nerve anatomy
Mahakkanukrauh, 2005, Clinical Anatomy 18:200-205
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
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
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
Diagnosis
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.
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.
Pudendal nerve block
Pudendal nerve block
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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)