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Neuropatie periferiche meccaniche in clinica della riabilitazione 21 Corso di Aggiornamento

Neuropatie periferiche meccaniche in clinica della riabilitazione 21 Corso di Aggiornamento Riccione 10-13 Maggio 2010. Dolore neuropatico e dolore da deafferentazione. Roberto Casale Fondazione Salvatore Maugeri, I.R.C.C.S. Istituto di Riabilitazione di Montescano

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Neuropatie periferiche meccaniche in clinica della riabilitazione 21 Corso di Aggiornamento

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  1. Neuropatie periferiche meccaniche in clinica della riabilitazione 21 Corso di Aggiornamento Riccione 10-13 Maggio 2010

  2. Dolore neuropatico e dolore da deafferentazione Roberto Casale Fondazione Salvatore Maugeri, I.R.C.C.S. Istituto di Riabilitazione di Montescano Divisione di Riabilitazione Neuromotoria III , Servizio di Neurofisiopatologia & Unità di Riabilitazione del Dolore

  3. Classificazione clinica del dolore neuropatico (DN) Dolore Neuropatico DN definito DN possibile DN improbabile • Dolore in un'area neurologica definita • Disturbo sensitivo nell'area dolorosa • Malattia che causa lesione del nervo • Lesione neurogena molto definita • Dolore in un'area neurologica definita • Disturbo sensitivo nell'area dolorosa • Eziologia ignota • Malattia causadi dolore nocicettivo • Dolore in areanon riferibile ad alcun tipo di innervazione • Malattia causadi dolore nocicettivo • Nessun disturbo sensitivo

  4. Dolore neuropatico e dolore da deafferentazione • Non tutti i dolori con caratteristiche cliniche “neuropatiche” sottintendono una lesione nervosa • Non tutte le lesioni nervose esitano in un disturbo “positivo” della sensibilità • Cosi come non tutte le deafferentazioni esitano in un dolore, ovvero in un disturbo “positivo” della sensibilità • Anche nelle lesioni del plesso brachiale il dolore non è una regola assoluta

  5. Radicolopatia C5 + C6 ? Dolore da compressione del mediano al polso? Dolore osteo-mioarticolare della spalla ?

  6. DN improbabile DN possibile DN definito Classificazione del dolore neuropaticoTermini descrittivi 0,30 *p=0,005 0,25 0,20 * Frequenza relativa 0,15 0,10 0,05 0,00 Bruciante Pungente Tenebrante Sordo Acuto Nessuno Lancinante Pulsante A strappo Tagliente Opprimente

  7. Allodinia tattile evocata Allodinia a stimoli freddi 55 0,16 p=0,015 p=0,675 50 0,14 45 0,12 40 35 0,10 30 Frequenza relativa Frequenza relativa 0,08 25 0,06 20 15 0,04 10 0,02 5 0 0,00 DN improbabile DN possibile DN definito DN improbabile DN possibile DN definito Intensità del dolore evocato (96 pazienti con allodinia tattile) Intensità del dolore evocato (26 pazienti con allodinia a stimoli freddi) 100 100 p=0,064 p=0,94 80 80 60 60 VAS VAS 40 40 20 20 0 0 DN improbabile DN possibile DN definito DN improbabile DN possibile DN definito Classificazione del dolore neuropaticoAllodinia Svendsen et al. 2003

  8. ? + + + + - - + + + - - - - - - + - + - + - + + + - - + - - - - + + - - + + - - + + - + - + - + - - + - + - + - - - + - + Dolore e lesione: un legame incerto OUCH! Casale R. 1995

  9. Dolore e lesione: un legame incerto • Lesione senza dolore • Insensibilità congenita al dolore • Analgesia episodica (Jom Kippur) • Dolore senza lesione • Dolore psicogeno • Back pain (apparente) • Dolore sproporzionato alla gravità della lesione • Algodistrofie • Colica renale • Dolore dopo la guarigione clinica • Dolore neurogeno

  10. NEUROPATIE EREDITARIE SENSITIVE & AUTONOMICHEDyck et al., 1983 HSAN tipo I HSAN tipo II HSAN tipo III HSAN tipo IV INSENSIBILITA’ CONGENITA AL DOLORE Thrush, 1973 HSAN tipo V

  11. l primo caso documentato di insensibilità congenita al dolore (Van Ness Dearborn, 1932) sia quello di un tal E.G. Gibson, immigrato boemo di Praga che affetto da insensibilità congenita al dolore, • Passò alla storia come “The human pin-cushion”: l’uomo portaspilli, esibendosi per alcuni anni, in uno spettacolo di vaudeville.

  12. Nolano M,et al.. Absent innervation of skin and sweat glands in congenital insensitivity to pain with anhidrosis Clin. Neurophysiol. 2000 Sep;111(9):1596-601.

  13. Lesione senza doloreL’analgesia episodica • Molti soldati feriti in battaglia durante la II guerra mondiale hanno negato di aver avuto dolore (Beecher,1959). • Soldati israeliani hanno descritto l’amputazione traumatica di un arto come un “bang” “thump” “blow” (Carlen et al.,1978)

  14. Dolore senza lesione apparente • Vi rientrano i cosi detti dolori psicogeni (patologia rara e termine comunque abusato) ma anche tutta una serie di situazioni cliniche molto comuni quali il back pain

  15. Dolore sproporzionato alla gravità della lesione • Una lesione triviale (in questo caso una distorsione alla TT SX) può generare una risposta algica sproporzionata. Le algodistrofie spesso vedono come fattore eziologico traumi minori. • Il banale passaggio di un sassolino nell’ uretere è causa di dolori viscerali insopportabili

  16. Dolore che permane dopo la guarigioneclinica • Molto spesso la guarigione clinica della lesione traumatica non fa scomparire anche il dolore. Uno dei casi più drammatici è quello del dolore da avulsione del plesso brachiale ed in genere nel dolore neurogeno

  17. No evidence of chronic pain behaviour or neuropathic syndromes, Pain is reported normally to external stimuli in unaffected regions. Anand & Birch Restoration of sensory function and lack of long-term chronic pain syndromes after brachial plexus injury in human neonates Brain,125, 1, 113-122, 2002 Bisinella & Birc hObstetric Brachial Plexus Lesions: A Study of 74 Children Registered with the British Paediatric Surveillance Unit (March 1998-March 1999)J Hand Surg Eur; 28(1): 40 - 45., 2003

  18. The brachial plexus is a network of nerves that conducts signals from the spine to the shoulder, arm, and hand. Brachial plexus injuries are caused by damage to those nerves.

  19. The nerve may be stretched (Neuropraxia).  Stretched nerves usually heal, to varying degrees of success, over time. This is the “best case” scenario and the degree of injury is typically good. There may a neuroma.  This is when scar tissue builds up around the injured part of the nerve as it tries to repair itself.  This disrupts the nerve’s signal to its respective muscle group. The nerve may be ruptured.  This is when the nerve is torn somewhere along its path to the muscles, but not where it attaches to the spine.  Primary surgery involving nerve grafts or transfers is often recommended in these cases. The nerve may be avulsed.  This is when the nerve root is torn from the spinal cord.  Primary surgery is strongly recommended.  This is the most serious type of nerve injury.

  20. Clinical patterns of Brachial Plexus Injuries

  21. Epidemiology of BPIs in the adult Flores LP. Arq Neuropsiquiatr 2006;64(1):88-94 • Most of the lesions are supraclavicular (62%). • traction (60%), • gun shot wound (25%), • compression (8.5%) • perf o r a t i o n / l a c e r a t i o n (5.7%). • Motorcycle accidents were the cause of trauma in 54% of patients. • root avulsion (76%). • Partial spontaneous neurological re c o v e ry in 43% • Neuropathic pain occurs in (71%) cases, • Pain is controlled by the use of some oral intake drugs (as amitriptiline • or carbamazepine) in 64% . • The rate of incidence to the local populationis 1.75/100000/year.

  22. Upper (C5-6) and middle (C7) root injuries • The consequences of injury at this level depend on severity of the inciting event, whether mechanical, neoplastic or inflammatory. • Loss of function of the shoulder and biceps due to a complete C5-6 injury renders the limb severely disabled, but capable of some useful function since the hand is intact.

  23. Upper (C5-6) and middle (C7) root injuries • Serial clinical examination tends to be the best method to indicate surgery versus conservative management. • Reconstructive surgery should be considered if there is no evidence of motor recovery by 4 to 6 months after injury. • Passed the 1-year deadline for primary reconstruction, terminal muscle atrophy is present and provision of a nerve supply cannot result in function.

  24. Lower root (C8-T1) • In lower root lesion, due to the time and distance constraints of nerve regeneration, severe injuries to the lower roots usually result in difficult reconstructive situations. • Best solution: staged combination of nerve transfer to restore innervation, followed several months later by free muscle transfer to replace atrophic muscle for hand function. Chammas M., et al. Glenohumeral arthrodesis in upper and total brachial plexus palsy. A comparison of functional results. J Bone Joint Surg Br. 2004 Jul;86(5):692-5.

  25. Complete (C5-T1) injury • In complete injuries to all 5 roots, there are few ipsilateral sources for nerve restoration, but intercostals nerves can serve as partial donors.The contralateral C7 provides a source of motor as well as sensory nerve. • Once the intercostals and contralateral C7 have been transferred, then multiple free muscle transfers are needed to restore elbow flexion and finger function. • Shoulder movement is restored by glenohumeral fusion (although fusion seems intuitively to prevent movement, this fusion links the paralysed humerus to the still-active scapula, thus allowing arm movement through shrugging and other scapular movements that will still be present).  Chammas M., et al. Glenohumeral arthrodesis in upper and total brachial plexus palsy. A comparison of functional results. J Bone Joint Surg Br. 2004 Jul;86(5):692-5.

  26.  There is a rare syndrome called Parsonage-Turner Syndrome, or brachial plexitis, which causes inflammation of the brachial plexus without any obvious shoulder injury.  This syndrome can begin with severe shoulder or arm pain followed by weakness and numbness. (winging of the scapula) • The suprascapular nerve was almost invariably involved (in 97% of shoulders) in patients with PTS. Axillary nerve involvement also was commonly observed (in 50% of shoulders). Subscapular nerve involvement was uncommon (in 3% of shoulders).

  27. An EMG can give useful information about injury patterns and the presence of avulsion but is not very specific as to lesser degrees of injury: a neuropraxic injury may mimic a complete rupture *. For this reason also for EMG, serial examinations are mandatory for a correct diagnosis in term of pattern and severity of the lesion. *Smith SGM Electrodiagnosis. In Surgical disorders of peripheral nerves. Birch, Bonney Winn Parry Eds.London Churchill Livingstone, 1998, 467-490

  28. Brachial plexus is usually injured at very proximal levels. Location factors render: • lower root injuries (physically farther from their motor targets than the upper roots) devastating in most cases. • Upper root injuries less devastating and even if may be severe,usually reconstructable.  Kim DH et al. Outcomes of surgery in 1019 brachial plexus lesions treated at Louisiana State University Health Sciences Center. J Neurosurg. 2003 ;98(5):1005-16 Nath RK et al. Physiological and clinical advantages of median nerve fascicle transfer to the musculocutaneous nerve following brachial plexus root avulsion injury. J Neurosurg. 2006 ;105(6):830-4

  29. A peripheral lesion induces important modifications within the central nervous system: Plasticity

  30. Hypometabolic (Fig 1) and hypermetabolic (Fig 2) areas in the patients with spontaneous pain due to BPA compared with the healthy subjects. These findings suggest that the brain areas involved in emotion, attention and internal modulation of pain may be related to the chronic spontaneous pain due to BPA.  (CHEN Fu-yong, et al.CMJ,2008) 1 2

  31. DREZ operation for Brachial plexus avulsion pain (229 patients)

  32. Mechanisms that can contribute to neuropathic pain: role of the periphery • Primary intact afferent nociceptors in a partially damaged nerves become spontaneously active • Ectopic impulses may be generated at sites distant to the lesion (dorsal ganglia) • Neuromas at the site of lesion are more sensitive to chemical, mechanical and electrical stimuli (Tinel signs) • Increased sensitivity of nociceptors to normal sympathetic activity • Inflammatory component surrounding the nerve stump (nervi nervorum)

  33. Mechanisms that can contribute to neuropathic pain: role of the CNS • Continuous primary afferent nociceptors activity induces allodynia and hyperpatia (central sensitization – NMDA receptors activity) • Dorsal horn cells become spontaneously active after rizotomy or severe peripheral nerve lesions) (denervation supersensitivity) • Loss of activity from unmyelinated fibers induce a sprouting of myeliated non-nociceptive fibers in the dorsal horn (reorganization of primary afferent in the dorsal horn) • Lack of activity from myelinated afferents releases inhibition on unmyelinated pain-related fibers (loss of inhibition) • Somatosensory related areas are site of functional changes ( plastic changes)

  34. 3 main factors direct possible recovery: • speed of nerve regeneration (about 1 mm per day; 1 inch per month) • time beyond which motor recovery is impossible (about 1 year from date of injury). • distance from the nerve root beyond which motor recovery is unlikely in severe injuries: 30 cm (12 inches).  Shin AY, et a.. Adult traumatic brachial plexus injuries. J Am Acad Orthop Surg. 2005 t;13(6):382-96 Nath RK , Mackinnon SENerve transfers in the upper extremity. Hand Clin. 2000 ;16(1):131-9

  35. Some brachial plexus injuries may heal without treatment. Many children who are injured during birth improve or recover by 3 to 4 months of age. Treatment for brachial plexus injuries includes physical therapy and, in some cases, surgery. • The site and type of brachial plexus injury determines the prognosis. For avulsion and rupture injuries, there is no potential for recovery unless surgical reconnection is made in a timely manner. The potential for recovery varies for neuroma and neuropraxia injuries. Most individuals with neuropraxia injuries recover spontaneously with a 90-100% return of function.

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