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)