COMPLEX REGIONAL PELVIC PAIN SYNDROME. TIME FOR A NEW PARADIGM

COMPLEX REGIONAL PELVIC PAIN SYNDROME…. TIME FOR A NEW PARADIGM Alain Watier md, md, LMCC, FRCP Professor of Gastroenterology Pelvic Floor Unit CHUS,...
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COMPLEX REGIONAL PELVIC PAIN SYNDROME…. TIME FOR A NEW PARADIGM

Alain Watier md, md, LMCC, FRCP Professor of Gastroenterology Pelvic Floor Unit CHUS, Qué Québec, Canada

PELVI-PERINEAL PAIN

BLADDER PAIN SYNDROME ENDOMETRIOSIS TESTICULAR PAIN VESTIBULITIS

VULVODYNIA URETHRAL SYNDROME DYSMENORRHEA

PROCTALGIA FUGAX

IBS

LEVATOR ANI SYNDROME

CRONIC PELVIC PAIN IN MAN

PUDENDAL NEURALGIA CLUNEAL NEUROPATHY

As specialists in pelvi-perineal pain what can we learn from… PELVIC ORGAN CROSS SENSITIZATION NEUROPATHIC PAIN COMPLEX REGIONAL PAIN SYNDROME FIBROMYALGIA POST TRAUMATIC STRESS SYNDROME IBS TMD CFS !!!! ENDOMETRIOSIS !!!!!

Vestibulitis/CPP/urethral obstruction/IBS /constipation CPP/dyspareunia/urological problems/IBS IBS/Dyspareunia/Urethral problems/CPP Urethral syndrome/dyspareunia/IBS/ abdominal pain CPP/unexplained genital pain/bladder outlet obstruction/prostatodynia

Fibromyalgia/IBS/vestibulitis Penismus/anismus/IBS IC/headache/FM/IBS/depression/vulvodynia

PELVIC ORGAN CROSS-SENSITIZATION

PELVIC PAIN ASSESSMENT FORM

Information about pain Pain maps Surgical history Medications Obstetrical history Family history Medical history Health habit (Sleep habit) Menstrual history (dysmenorrhea, endometriosis) GI / Eating / Rome III criteria IBS Urinary symptoms (IC) (Kidney stones) Sexual / Physical abuse history Pelvic varicosity pain syndrome Fibromyalgia Impact of pain on sexual activities Coping mecanisms Short Form McGill questionnaire

Posture, gait, back, abdomen, lower extremities Sacroiliac joints Changes of skin sensation, numbness, tenderness Changes in temperature, colour Fibromyalgia External genitalia Q tip test Vagina Unimanual examination Muscle tenderness Trigger points Bimanual examination Adnexal examination Speculum examination Rectovaginal examination Abdominal examination Rectoscopy Pelvic floor exam by a trained PT

NEUROPATHIC PAIN

PATHOPHYSIOLOGY OF NEUROPATHIC PAIN CUTANEOUS NOCICEPTIVE HYPERSENSITIVITY PERIPHERAL SENSITIZATION CENTRAL SENSITIZATION ACTIVATION OF DESCENDING FACILITATION ALTERED INTRACELLULAR SIGNALING ALTERED ION CHANNEL EXPRESSION

ABNORMAL FIRING OR AFFERENT AND EFFERENT PAIN PATHWAYS ALTERED PHENOTYPE OF LARGE NERVE FIBERS AUGMENTED INLAMMATORY RESPONSE IMMUNE SYSTEM INVOLMENT (MICROGLIA) GENETIC VARIATION

ALLODYNIA DYSESTHESIA HYPERALGESIA HYPERPATHY PARESTHESIA CAUSALGIA

SPECIFIC NEUROPATHIC PAIN QUESTIONNAIRES Bouhassira

QUANTITATIVE SENSORY TESTING (QST)

Gives a phenotypic mapping and may define patients that are more prone to respond to certain therapeutic agents.

QUANTITATIVE SENSORY TESTING (QST)

Sensory thresholds for pain, touch, vibration, heat, cold. A-delta fibers: cold + cold pain thresholds C-fibers: heat + heat pain detection thresholds A-beta fibers: vibration detection thresholds Permits to define different somatosensory phenotypes Does it help the pain clinician ??

NSAIDs Inhibition of serotonin and NE uptake (TCAs, Tramadol, Duloxetine, Venlafaxine)

Blockage of voltage dependant Na channels (TCAs, Lamotrigine, Carbamazepine, oxcarbazepine)

Modulation of NMDA receptors and/or glutamate release (TCAs, Lamotrigine) Blockage of voltage gated Ca channel subunit (TCAs, Gabapentin, Pregabalin)

Modulation of opioids receptors (opioids)

CANNABINOIDS

Inhibition of voltage gated Na channels Local anesthesics (Lidocaine, lidocaine 5% gel and patch) Inhibition of Ca channel function + reduction in membrane excitability Tetrazole Modulation of alpha-2 adrenoreceptor Clonidine (cream / transdermal patch) Blocage of adenosine uptake TCAs (amitrityline 2% + kétamine 1%) (Doxepin 3%) TRPV1 receptor agonist (Capsaicin 0.025%-0.075%) (gel / cream ) Capsaicin dermal patch 8%)

Amitriptyline 2-7 % Clonidine 0,05-0,2 % Gabapentine 4-6 % Baclofène 2-5 % Ibuprofène 2,5-10% Cyclobenzaprine 1% Lidocaine gel 2 % Lidocaine onguent 5 % Lidocaïne 10%/kétamine 1% (autres [ ] selon condition)

Nitroglycérine 0,2-0,8 % + Lidocaine 10 % ou Morphine 0,2-0,5 % Kétamine 1 à 10% (+ Morphine 0,2-0,5%) (+ Hydromorphone 0,04-0,1%) Diltiazem 2% Nabilone topique (Cannabinoïdes) Misoprostol 0,0024%- 0,015%

FIBROMYALGIA

CENTRAL SENSITIZATION

FIBROMYALGIE

CRPS

IBS

VULVODYNIA PTSD

THE DESCENDING PAIN CONTROL SYSTEM SHOULD BE ACCESSIBLE BY BOTH BEHAVIORAL AND PHARMACOLOGICAL TREATMENTS CAN DESCENDING PAIN CONTROL IMPROVE WITH PRACTICE ? PREDICTIVE OF POST-OP PAIN ??? POST-HYSTERECTOMY ?

What about the descending pain control system in women with a history of physical / sexual abuse ???

SLEEP DISORDERS

FM IBS CRPS QUESTIONNAIRE

PHYSICAL/SEXUAL ABUSES AND PELVI-PERINEAL PAIN

Sexual abuse history: Prevalence, Health effects, Mediators, and Psychological treatment. Jane Lesserman Psychomatic Medicine 67: 906906-915 (2005) (2005)

Long-term effects of childhood abuse on the quality of life and health of older people: Results from the depression and early prevention of suicide in general practive project. Brian Draper et al. Geriatr Soc 56: 262262-271, 2008

Sexual abuse and lifetime diagnosis of somatic disorders A systematic review and meta-analysis Molly L. Paras Jama August 5, 20092009-Vol 302 # 5

A comparaison of chronic pain patients and controls on traumatic events in childhood. Richard T. Goldbgerg et al. Disability and rehabilitation,2000: rehabilitation,2000: Vol 22 No. 17, 756756-763

Childhood sexual abuse is associated with physical illness burden and functioning in psychiatric patients 50 years of age and older. Nancy L talbot et al. Psychosom Med 2009 May; 71(4): 417417-422

Childhood trauma, attachment, and abuse by multiple partners. Pamela C. Alexander Psychological Trauma: Therapy, Therapy, research and policy. policy. 2009. Vol 1 # 1, 7878-88

Chronic pain syndromes and their relation to childhood abuse and stressful life events. Astrid Lampe et al Journal of Paychosomatic Research 54 (2003) 361361-367

WE MUST STOP TO PRETEND

THE PHENOMENA DOES EXIST

Pharmacological approach Therapeutic targets Multiple types of medication Topical creams INTERVENTION THÉRAPEUTIQUE

Pelvic floor reeducation

Évaluation complète musculo-squelettique Mobilisation des tissus mous interne (vaginal-rectal) et externe Relâchement myofascial Manipulation articulaire Traitement des trigger points Stimulation électrique Exercices thérapeutiques Entraînement de la musculature pelvi-périnéale Ultra-son thérapeutique TENS Dilatation vaginale EMG de surface Biofeedback Michel Guérineau Elizabeth Rummer / Stéphanie Prendergast (San Francisco) « Headache in the pelvis » Stimulation du nerf tibial postérieur

INFILTRATIONS

DECOMPRESSION CHIRURGICALE

BOTOX

PUDENDAL NEURALGIA

STATE OF THE ART 2009

NEUROMODULATION PUDENDALE

Those who do not respond to conventional therapies usually have a severe history of sexual abuse

PTSD COMPLEX

PSYCHO-NEURO-IMMUNOLOGY

NE

AUTONOMOUS NERVOUS SYSTEM CRF

STRESS LOCUS CERULEUS

HYPOTHALAMUS

ALLOSTATIC LOAD

The price the body pays for wear of tear on its systems, secondary to chronic psychological stress. Physiological arousal and the persistent release of stress hormones or «mediators», sleep deprivation, poor diet, and other health-damaging behaviors can result from feeling «stressed out» with resultant psysiological changes. It is possible that stress induced disturbances of endocrine and neurological systems underlie the ultimate expression of disease

CAN WE HELP THEM

Eugene Gendlin

Permits awareness of emotions. Transform a vague internal sensation into a physical sensation

FOCUSING

ERICKSONIAN HYPNOSE SUGGESTIONS METAPHORES

A new way of treating informations Permits the spontaneous emergence of new associations, new emotions, awareness

ART THERAPY

PSYCHOBIOLOGIC TRANSDUCTION Hypnose EMDR Brief therapy

A. B. C. D.

Weitzenhoffer M.H Erickson F. Shapiro E.L.Rossi

COMPLEX REGIONAL PAIN SYNDROME

A NEUROPATHIC (?) PAIN DISORDER ASSOCIATED WITH SIGNIFICANT AUTONOMIC INVOLVEMENT

A complete functional loss of cutaneous sympathetic vasoconstrictor activity in an early stage, with recovery. This autonomic dysfunction originates in the CNS A spinal component to microcirculatory abnomalities which appeared to manifest itself through a neural antidromic mechanism A positive feedback circuit, consisting of primary afferent neuron, spinal cord neurons, sympathetic neurons, and a pathologic synpathetic coupling SNS and vascular abnormalities Exagerated regional inflammation response Impairment of high-energy phosphate metabolism Abnormal oxidative stress After a partial nerve lesion, excessive antidromic activation of undamaged afferent C fibers and neuropeptide release, leading to acute vasodilatation within the innervation territory of the affected nerve has been demonstrated Frequent presence of human lymphocyte antigen-DQ1

Autoimmune disease Cortical changes Ongoing pain alters somatosensory processing Cortical hyperexcitability Cortical reorganization

Coupling between the sympathetic and afferent neurons

*****

BRADYKININ

NA

SUBSTANCE P

SKIN TEMPERATURE SUDOMOTOR FUNCTION TESTING ELECTRODIAGNOSTIC STUDIES QUANTITATIVE SENSORY TESTING LASER DOPPLER IMAGING (Test skin autonomic reflexes)

Should we test some of our patients with pain an autonomic manifestations

CRPS OF THE PELVIC FLOOR In some cases pelvi-perineal pain seems to be out of proportion to identifiable causes of pain. (Allodynia, hyperpathy) Variations in skin color and temperature and abnormal sweating has also been described

GANGLION IMPAR BLOCK

Sympathetic bloc at the level of L2 IC Perineal pain IBS

DESENSITIZATION Theoretically based on the ability of body’s tissues to adapt in response to demand Sufficient intensity and duration to provide adequate input to change the abnormal CNS activity

SELF-REGULATION Innate ability to learn to modify and modulate «autonomic» response to reach a healthier homeostatic state Technonology assisted self-modulation: Neuromotor + other learning with BFB

Try to reduce the perception of pain via modification of the autonomic components Heart beat Skin temperature Respiratory rate Sweat response Type of breathing Vasospasm Blood pressure Vasodilatation Brain wave patterns Muscular spasms Electro-dermal response

REFLECTIONS, IMAGERY, AND ILLUSIONS: THE PAST, PRESENT AND FUTURE OF TRAINING THE BRAIN IN COMPLEX REGIONAL PAIN SYNDROME Dr G. Lorimer Moseley GRADED MOTOR IMAGERY (MIRROR THERAPY) Inducing the illusion that the affected limb is smaller than it really is reduces the pain and swelling caused by movement of the limb IMPLICATIONS IN PELVI-PERINEAL PAIN !!!!!

« AUTONOMIC NERVOUS SYSTEM DYSFUNCTION »

Wilfrid Jänig

THE SYNPATHETIC NERVOUS SYSTEM AND BODY PROTECTION, INFLAMMATION, PAIN, AND HYPERALGESIA

IBS & AUTONOMIC NERVOUS SYSTEM

PSYCHOLOGY AND CHRONIC PAIN

PAIN ACCEPTANCE

RESILIENCE

HYPERVIGILENCE

CATASTROPHYSING

THE EFFECT OF PERSONNALITY ON CENTRAL PAIN PROCESSING

Traumatic life events screening questionnaire Trauma scale of Davidson Resilience scale Chronic pain acceptance questionnaire Fear avoidance beliefs questionnaire Pain and catastrophysing scale Pain vigilance and awareness questionnaire Hospital anxiety and depression scale Pain intensity questionnaire The impairment and functionning inventory Disability and functioning inventory

AND WHAT ABOUT THE

SUFFERING OF THESE PATIENTS

WHAT ABOUT…..

MOTIVATIONAL ENHANCEMENT THERAPY OPTIMISM INTERVENTION

SOMATOSENSORY LANGUAGE Where is the pain ? How is the sensation perceived ? What can I do to make the pain stop ? LIMBIC LANGUAGE What pain means to me ? How is the pain changing the life I had before the pain ? What can I do to recover my life ?

IN CONCLUSION

Overlap of patient and healthy populations…. How do you become a chronic patients….. Viscero-somatic sensitivity Peripheral and central sensitization Limbic system responsiveness Autonomic nervous system activity

Neurocognitive factors Selective attention to bodily sensations Catastrophysing Symptoms related worries Illness behavior Psychological stressors

Greater prevalence in women History of adverse early life events and stress sensitivity Comorbidity with disorders of mood and affect Response to centrally acting therapies (Duloxetine Milnacipran, TCa, SSRI)

Evidence for altered pain perception and processing Hypersensitivity to experimental stimuli Compromised diffuse noxious inhibitory control ( DNIC) (FM, IBS, Vulvodynia, CRPS) Evidence from brain imaging studies of altered pain processing and modulation

Evidence of structural brain abnormalities (Changes in grey matter density or cortical thickness in FM, IBS, headache)

Evidence of altered neurocognitive function (FM, low back pain, IBS,PTSD)

Evidence of increased activity in central arousal circuits and sympathetic nervous system activity (Enhance stress responsiveness) ( FM, IBS, TMJD, PTSD)

Evidence of common genetic susceptibility (Pain amplification and psychological distress)

WHERE ARE WE STANDING NOW !!!!!

Functional pain syndromes should not be individualized We should stop treating just the «organ» (end-organ-specific syndrome) BUT we must integrate the pain syndrome Peripheral «organic» etiology of symptoms are possible but a more integrated psychosocio-neurobiologic approach is mandatory

• • • • •

Alain Watier md, LMCC, FRCP Professor of Gastroenterology Director of Pelvic Floor Unit Pelvic Floor reeducation (Lyon) Faculté de médecine et des Sciences de la Santé de l’Université de Sherbrooke • CHUS-Hôtel-Dieu • 580 Bowen Sud Sherbrooke Québec Canada J1G2E8 • 819-346-1110 [email protected]