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e-News for Somatosensory Rehabilitation 2010, Tome 7 (Volume 4) 160 Powered by : www.orthopartner.ch PD Dr. med. Christian MAIHOEFNER Guesteditor 161 Maihöfner, Ch. Guesteditorial: :Cortical Plasticity in Complex Regional Pain Syndromes [English] 169 Ammann, J. Article : Lorsque le toucher se fait douleur [Français] 170 Della Casa, R., Coales, K., de Raemy, X. et al. Case Report : Intermittent brachial neuralgia of anterior branch of medial antebrachial cutaneous nerve with mechanical allodynia of 15 months duration [English] 182 Spicher, C.J.. Certificat en rééducation sensitive de la douleur : 1 ère volée [Français] 183 Landreau, S. Fait clinique : Névralgie dorso-intercostale incessante avec allodynie mécanique : Début de la diminution des douleurs par la rééducation sensitive [Français] 188 Desfoux, N. Fait clinique : Une diminution rapide des douleurs neuropathiques chroniques d’une névralgie fémoro-poplitée permanente par rééducation sensitive [Français] 192 Ammann, J. Article : Les géographes des nerfs [Français] 195 Mathis, F. Somatosensory Rehabilitation Sector of the EHC hospital’s Statistics [English] 197 Kafka, F. Schatten – Halbschatten: Die Baüme [Deutsch] 197 Kafka, F. Stíny a polostíny: Stromy [Česky] 198 Noël et al. Continuous Education – Weiterbildung - Formation continue [F, E, D]

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160

Powered by :

www.orthopartner.ch

PD Dr. med. Christian MAIHOEFNER Guesteditor

161 Maihöfner, Ch. Guesteditorial: :Cortical Plasticity in Complex Regional Pain Syndromes [English]

169 Ammann, J. Article : Lorsque le toucher se fait douleur [Français]

170 Della Casa, R., Coales, K., de Raemy, X. et al. Case Report : Intermittent brachial neuralgia

of anterior branch of medial antebrachial cutaneous nerve with mechanical allodynia of 15 months

duration [English]

182 Spicher, C.J.. Certificat en rééducation sensitive de la douleur : 1ère volée [Français]

183 Landreau, S. Fait clinique : Névralgie dorso-intercostale incessante avec allodynie mécanique :

Début de la diminution des douleurs par la rééducation sensitive [Français]

188 Desfoux, N. Fait clinique : Une diminution rapide des douleurs neuropathiques chroniques

d’une névralgie fémoro-poplitée permanente par rééducation sensitive [Français]

192 Ammann, J. Article : Les géographes des nerfs [Français]

195 Mathis, F. Somatosensory Rehabilitation Sector of the EHC hospital’s Statistics [English]

197 Kafka, F. Schatten – Halbschatten: Die Baüme [Deutsch]

197 Kafka, F. Stíny a polostíny: Stromy [Česky]

198 Noël et al. Continuous Education – Weiterbildung - Formation continue [F, E, D]

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C1ortical Plasticity in

Complex Regional Pain Syndromes (CRPS)

Keywords: CRPS, neuropathic pain, hyperalgesia, plasticity, reorganization

The Complex Regional Pain Syndromes (CRPS; previously called “reflex sympathetic dystrophy” or “causalgia”) belong to the remarkably large group of neuropathic pain syndromes. CRPS may develop in about 5 % of all traumas or nerve lesions in the extremities. Based on either the absence or presence of nerve lesions, CRPS is classified as CRPS 1 or 2. Clinically, these syndromes are characterized by a typical constellation of symptoms1-3: autonomic and inflammatory changes, motor symptoms and sensory disturbances (see Fig. 1).

Fig. 1: Acute CRPS: pain, swelling, reddish skin and decreased active range of motion in the left hand.

Autonomic and inflammatory symptoms include presence of distal edema, changes of the skin temperature and color, and excessive sweating. Motor symptoms in CRPS are weakness, tremor, dystonia and myoclonic jerks.4 Among the sensory symptoms spontaneous pain and stimulus-evoked pains are hallmarks. Basically, two types of stimulus- induced pains can be differentiated in CRPS. Pin- prick hyperalgesia means that a normally painful pin- prick stimulus induces an increased pain perception on the affected limb.5 Dynamic-mechanical allodynia means that non-painful gentle stroking the affected skin is perceived as painful.6 As mandatory for diagnosis, pain and hyperalgesia must not be limited to a single nerve or nerve root territory.7 Moreover, sensory abnormalities are usually distributed in a stocking or glove like manner. The reasons for these puzzling phenomena are largely unknown. However, they may be explained by changes within the CNS. In the last couple of years our group has 1 Department of Neurology, University of Erlangen-Nuremberg, Schwabachanlage 6, 91054 Erlangen & Department of Physiology and Experimental Pathophysiology, University of Erlangen-Nuremberg, Universitätsstrasse 17, D-91054 Erlangen, Germany [email protected]

To MD.      To neuroscientist To patient To therapist      

GUESTEDITORIAL PD Dr. med. Christian MAIHOEFNER1, MD, PhD

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employed functional imaging techniques and explored possible CNS pathology in CRPS.5,6,8-

10 Using functional magnetic resonance imaging (fMRI) and magnetoencephalography (MEG), we provided evidence that the pathophysiology of this syndrome is not only limited to the peripheral nervous system. Most of the complex sensory features of CRPS were found to be crucially linked to characteristic CNS changes. The aim of our first MEG study8 was to assess a possible cortical reorganization within the primary somatosensory cortex (S1) in 12 CRPS patients and correlate these changes to sensory, motor or autonomic complaints. Pneumatic tactile stimulations were used to explore the cortical representation of digits 1 (D1), 5 (D5) and the lower lip, both on the unaffected and CRPS- affected side. Projections of the respective MEG activities onto axial and coronal MRI slices demonstrated that the location of the SEF sources in the contralateral S1 cortex were arranged in a somatotopic manner, showing the cortical representation of the lower lip, D1, and D5 (Fig. 2).

Fig. 2: (A) Projection of the equivalent current dipole (ECD) localizations for D1 (filed circle) and D5 (open circle) onto individual MRI slices for one representative patient. There

was a reduction of the hand extension from 1.42 cm (unaffected side) to 0.8 cm (CRPS-affected side) during acute CRPS. After the follow up time of 62 months, the distance between D1 and D5 increased to 1.45 cm on the affected side, whereas the corresponding distance on

the unaffected side remained unchanged (1.43 cm). (B) Projection of the ECDs for the center of the hand (open squares) and the lower lip (filled

squares) onto individual MRI slices. The distance between the center of the hand and the lower lip increased from 2.05 cm to 2.92 cm following therapy on the CRPS-affected side,

whereas the respective ECD localizations for the unaffected side remained unchanged (distance hand-lip 2.92 versus 3.01 cm, before and after treatment).

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To assess changes in the somatotopic map, the center of the hand representation itself was deemed to be the mid- point between the cortical representations of D1 and D5. Surprisingly, the distance between the cortical representation of the hand and the lip was markedly decreased on the affected CRPS side compared to the unaffected side (Fig. 2). The mean distance on the unaffected side was 2.76 cm compared with 1.95 cm on the affected side (p < 0.05). Additionally, the distance between D1 and D5 was reduced on the painful affected side (1.37 versus 0.80 cm for the unaffected and affected sides; p < 0.05). However, the degree of cortical reorganization was significantly correlated to the magnitude of CRPS pain, assessed with the McGill Pain questionnaire (MPQ; r = 0.792; p < 0.05) and the area of mechanical hyperalgesia (r = 0.810; p < 0.05). The latter was found to be the best predictor, using a multiple regression model. There was no correlation with other clinical symptoms or epidemiological data. In particular, there was no correlation between the duration of CRPS, pain during movement, the impairment of hand function (active range of motion) or autonomic scores. In order to investigate whether these S1 changes are reversible and how they change after treatment, we performed a follow up study9 and traced the somatotopy within the S1 cortex of our patients employing MEG at least 1 year after therapy. Figure 2 shows a representative specimen, in which the distance between D1 and D5 increased from 0.80 cm during acute CRPS to 1.45 cm 1 year later and the distance between hand and lower lip accordingly increased from 2.05 to 2.92 cm. In contrast, the dipole locations on the unaffected side remained unchanged. For the whole group, at time of second investigation the distance between cortical representation of D1 and D5 on the CRPS side increased from 0.86 ± 0.1 cm (acute CRPS) to 1.16 ± 0.1 cm (p < 0.005). In contrast, there was no difference on the unaffected side (1.1 ± 0.1 vs 1.2 ± 0.1cm). According to hand representation, the distance between hand and lower lip increased on the CRPS side following therapy (1.6 ± 0.2 vs 2.2 ± 0.1 cm; p = 0.009). In order to determine which clinical improvement at best predicts recovery from cortical reorganization, we performed multiple regression analysis including the change of cortical reorganization (difference) between measurement one and two as dependent variable, and as independent variables the results obtained from quantitative sensory testing. The only factor that predicted the reduction of cortical reorganization was the reduction of pain, as measured by the MPQ (beta weight = 0.8; p = 0.006). Thus, reduction of neuropathic pain was directly correlated with recovery from cortical reorganization. Furthermore, symptoms associated with central nociceptive sensitization processes, in particular mechanical hyperalgesia seem to be most important for the induction of plastic CNS changes in CRPS. Therefore, in order to get more insights into the neuronal matrix involved in the central processing of stimulus- evoked pains (hyperalgesia), we performed another study5 and used fMRI to explore brain activations during pin- prick hyperalgesia in CRPS patients. Twelve patients, in whom previous quantitative sensory testing revealed the presence of hyperalgesia to punctuate mechanical stimuli (i.e. pin-prick hyperalgesia), were included in the study. Pin-prick-hyperalgesia was elicited by von-Frey filaments at the affected limb. For control, the identical stimulation was performed on the unaffected limb. The latter stimulation predominantly led to activations of contralateral S1 cortex (Fig. 3), parietal association cortex and bilateral S2 cortices. Furthermore increases of the BOLD signal were seen in the contralateral insular cortex. The identical stimulation on the affected

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side was markedly painful (i.e. pin-prick hyperalgesia) and we found the recruitment of a complex cortical network involved in the encoding for this CPRS feature (Fig. 3).

Fig. 3: Brain activations during non- painful pin- prick stimulation at the unaffected control hand and during pin- prick hyperalgesia at the CRPS- affected hand. Note the increased activations in S2, frontal cortices (in particular middle frontal cortices; MFC) and posterior part of the anterior cingulate cortex (pACC).

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Most important areas within this network were the S1 cortex (contralateral), S2 (bilateral), insula (bilateral), associative- somatosensory cortices (contralateral), frontal cortices and parts of the anterior cingulate cortex. Recently, cortical activations underlying motor dysfunction of CRPS were also investigated.11 During finger tapping of the affected extremity, CRPS patients showed a significant reorganization of central motor circuits, with an increased activation of primary motor and supplementary motor cortices (SMA). Furthermore, the ipsilateral motor cortex showed a markedly increased activation. When the individual amount of motor impairment was introduced as regressor in the fMRI analysis, it could be demonstrated that activations of the posterior parietal cortices, SMA and primary motor cortex were correlated with the extent of motor dysfunction.11 Finally, in a recent study12 we tested changes in endogenous pain modulation in CRPS patients compared to age-matched healthy controls. We applied repetitive noxious electrical stimuli (stimulation frequency 1Hz) at the dorsal aspect of affected and unaffected hands in patients and to corresponding hands in controls. As known from previous studies this protocol simultaneously activates inhibitory and facilitatory pain modulating systems. This results in (i) adaptation to the repetitive noxious stimulus, but also, simultaneously and at the same site, in (ii) development of an area of pin- prick hyperalgesia. We measured (i) pain adaptation during the course of stimulation and (ii) the provoked area of pin-prick hyperalgesia. The parameters “pain adaptation” and “area of pin-prick hyperalgesia” were used as activity measures of pain inhibitory and pain facilitatory systems. As both measures result from gross inhibitory and gross facilitatory activity in pain modulatory systems, pain adaptation reflects net pain inhibition and area of pin-prick hyperalgesia net pain facilitation. We found (i) decreased adaptation to painful electrical stimuli on both affected and unaffected hands of CRPS patients compared to healthy controls and (ii) increased areas of hyperalgesia on affected hands of CRPS patients compared to unaffected hands of CRPS patients and healthy controls. These findings imply a shift from inhibition towards facilitation of nociceptive input in CRPS patients, based on differential activation of subcomponents of the endogenous pain modulatory system. The differences were not correlated with duration of the disease, pain intensity, autonomic or motor function scores, presence or degree of evoked pain. However, significant correlation was found with the extent of adaptation and hyperalgesia on the unaffected hand. Thus, we hypothesized that differential activity in endogenous pain modulating systems may be not only a result of CRPS, but a potential risk factor for its development.12 In summary, we provide several lines of evidence that patients with CRPS have characteristic CNS changes. How does cortical reorganization and re-reorganization in response to CRPS pain modulation occur? Basically, functional or structural reorganization may underlie plastic changes within the CNS. Functional reorganization includes rapid changes in the impulse processing of synaptic circuits. Afferent input to the S1 cortex following peripheral stimulation of mechanosensitive afferent fibers has been shown to modulate intracortical inhibition in area 3b within the S1 cortex of animals.13 In fact, enhanced intracortical inhibition of motor cortex, which was accentuated in CRPS patients with hyperalgesia, has

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been recently demonstrated.14 The plastic changes demonstrated herein may therefore be explained by unmasking of preexisting, but previously latent afferent connections to S1 neurons. Alternatively, given a time frame of at least one year in our follow- up study, structural reorganization like axonal sprouting cannot be excluded. Cortical changes and altered sensorimotor processing8,15 may explain several sensory features common in CRPS. Firstly, pain and hyperalgesia spread and are not limited to peripheral innervation territories. Instead, sensory symptoms are usually distributed in a glove- or stocking like manner.2,3 Secondly, some patients with CRPS have even hemisensory deficits.16 These include decreased temperature and pin-prick sensations and hereby indicate the involvement of other cortical areas than those corresponding to the primarily affected limb. Thirdly, some patients with CRPS appear to have referred sensations following somatosensory stimulation on the affected limb.17 These referred sensations are modality specific (touch and pinprick) and perceived in the body part immediately adjacent to the S1 hand area on Penfield's cortical homunculus. Such findings could be explained by plastic S1 changes. We and others have shown that pain induces cortical reorganization, both in experimental and clinical settings.6,18 For CRPS there is evidence for facilitated neurogenic inflammation.19 A particular subtype of afferent C-fibers, the mechanoinsentitive ones, are important for neurogenic inflammation, which may explain peripheral features of CRPS.20 These mechanoinsentitive C-fibers are further essential for development and maintenance of mechanical hyperalgesia.21 Due to the fact that cortical S1 changes are correlated with mechanical hyperalgesia, at least in acute CRPS, we suggest that cortical reorganization may be induced by activation or sensitization of these particular C-fibers. The mechano-insensitive C-fibers usually are silent.20 They were “woken-up” (meaning spontaneously active or sensitized to forthcoming stimuli) by peripheral changes after trauma. Thus, these fibers appear to be the most peripheral substrates of neuronal plasticity in the nociceptive system, which finally leads to CRPS if plastic changes propagate to the CNS. If it is possible to desensitize these C-fibers by CRPS therapy, peripheral symptoms ameliorate and central changes were reversed. In chronic CRPS, however, when axonal damage and deafferentiation become more important, common peripheral therapy often is ineffective and thereby CNS changes may become irreversible and chronic. Our studies suggest that cortical reorganization in acute CRPS may be reversible following successful therapy. Therefore, strategies interfering with maladaptive plasticity may be promising new treatment approaches for this disease.22-24 Reference List 1. Maihöfner C, Seifert F, Markovic K. Complex regional pain syndromes: new

pathophysiological concepts and therapies. Eur J Neurol 2010; 17(5):649-660.

2. Veldman PH, Reynen HM, Arntz IE, Goris RJ. Signs and symptoms of reflex sympathetic dystrophy: prospective study of 829 patients. Lancet 1993; 342(8878):1012-1016.

3. Birklein F, Riedl B, Sieweke N, Weber M, Neundorfer B. Neurological findings in complex regional pain syndromes--analysis of 145 cases. Acta Neurol Scand 2000; 101(4):262-269.

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4. van Hilten JJ, van de Beek WJ, Roep BO. Multifocal or generalized tonic dystonia of complex regional pain syndrome: a distinct clinical entity associated with HLA-DR13. Ann Neurol 2000; 48(1):113-116.

5. Maihöfner C, Forster C, Birklein F, Neundorfer B, Handwerker HO. Brain processing during mechanical hyperalgesia in complex regional pain syndrome: a functional MRI study. Pain 2005; 114(1-2):93-103.

6. Maihöfner C, Neundorfer B, Stefan H, Handwerker HO. Cortical processing of brush-evoked allodynia. Neuroreport 2003; 14(6):785-789.

7. Stanton-Hicks M, Janig W, Hassenbusch S, Haddox JD, Boas R, Wilson P. Reflex sympathetic dystrophy: changing concepts and taxonomy. Pain 1995; 63(1):127-133.

8. Maihöfner C, Handwerker HO, Neundorfer B, Birklein F. Patterns of cortical reorganization in Complex Regional Pain Syndrome. Neurology 2003; 61(2):1707-1715.

9. Maihöfner C, Handwerker HO, Neundorfer B, Birklein F. Cortical reorganization during recovery from complex regional pain syndrome. Neurology 2004; 63(4):693-701.

10. Maihöfner C, Schmelz M, Forster C, Neundorfer B, Handwerker HO. Neural activation during experimental allodynia: a functional magnetic resonance imaging study. Eur J Neurosci 2004; 19(12):3211-3218.

11. Maihöfner C, Baron R, DeCol R, Binder A, Birklein F, Deuschl G et al. The motor system shows adaptive changes in complex regional pain syndrome. Brain 2007; 130(Pt 10):2671-2687.

12. Seifert F, Kiefer G, DeCol R, Schmelz M, Maihöfner C. Differential endogenous pain modulation in complex-regional pain syndrome. Brain 2009; 132(Pt 3):788-800.

13. Tommerdahl M, Delemos KA, Favorov OV, Metz CB, Vierck CJ, Jr., Whitsel BL. Response of anterior parietal cortex to different modes of same-site skin stimulation. J Neurophysiol 1998; 80(6):3272-3283.

14. Schwenkreis P, Janssen F, Rommel O, Pleger B, Volker B, Hosbach I et al. Bilateral motor cortex disinhibition in complex regional pain syndrome (CRPS) type I of the hand. Neurology 2003; 61(4):515-519.

15. Juottonen K, Gockel M, Silen T, Hurri H, Hari R, Forss N. Altered central sensorimotor processing in patients with complex regional pain syndrome. Pain 2002; 98(3):315-323.

16. Rommel O, Gehling M, Dertwinkel R, Witscher K, Zenz M, Malin JP et al. Hemisensory impairment in patients with complex regional pain syndrome. Pain 1999; 80(1-2):95-101.

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17. McCabe CS, Haigh RC, Halligan PW, Blake DR. Referred sensations in patients with complex regional pain syndrome type 1. Rheumatology (Oxford) 2003; .

18. Flor H, Elbert T, Knecht S, Wienbruch C, Pantev C, Birbaumer N et al. Phantom-limb pain as a perceptual correlate of cortical reorganization following arm amputation. Nature 1995; 375(6531):482-484.

19. Weber M, Birklein F, Neundorfer B, Schmelz M. Facilitated neurogenic inflammation in complex regional pain syndrome. Pain 2001; 91(3):251-257.

20. Schmidt R, Schmelz M, Forster C, Ringkamp M, Torebjork E, Handwerker H. Novel classes of responsive and unresponsive C nociceptors in human skin. J Neurosci 1995; 15(1 Pt 1):333-341.

21. Klede M, Handwerker HO, Schmelz M. Central origin of secondary mechanical hyperalgesia. J Neurophysiol 2003; 90(1):353-359.

22. Moseley GL. Graded motor imagery for pathologic pain: a randomized controlled trial. Neurology 2006; 67(12):2129-2134.

23. Moseley GL. Is successful rehabilitation of complex regional pain syndrome due to sustained attention to the affected limb? A randomised clinical trial. Pain 2005; 114(1-2):54-61.

24. McCabe CS, Haigh RC, Blake DR. Mirror visual feedback for the treatment of complex regional pain syndrome (type 1). Curr Pain Headache Rep 2008; 12(2):103-107.

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Quand le toucher se fait douleur SEMAINE DU CERVEAU Le thérapeute Claude Spicher évoque son rôle d’intermédiaire entre la peau, «le plus grand organe du corps humain», et le cerveau. JEAN AMMANN

2

Dans sa pratique, Claude Spicher voit passer des cas étranges: une patiente qui, en plein hiver, arrive les épaules nues; un homme qui ne supporte plus le contact de sa chemise sur son dos ou bien encore, une fille qui depuis trois ans ne pose plus le pied par terre… Et à chaque fois, il sert d’intermédiaire entre la peau, «le plus grand organe du corps humain», et le cerveau. Demain, dans le cadre de la Semaine internationale du cerveau 2010, Claude Spicher viendra parler de cette liaison complexe qui relie le cerveau à la peau: «Réveillez votre peau pour endormir vos douleurs neurogènes!», tel est le titre de sa conférence. Ergothérapeute de formation, collaborateur scientifique de l’Université de Fribourg, Claude Spicher, qui est né en 1963, a fondé en 2004 le Centre de rééducation sensitive du corps humain, à la Clinique générale Générale de Fribourg. Il est l’un des rares spécialistes de la rééducation sensitive, ou comment endormir la méfiance du système nerveux. Un court-circuit Il voit arriver des gens emmurés dans leur douleur: «Quand elle est très forte, la douleur cause des troubles du comportement, explique Claude Spicher. Un jour, j’ai reçu dans mon cabinet un patient qui souffrait d’un membre inférieur, il présentait un Sudeck: un gonflement du pied, avec une sensation de cuisson. Il se préparait à sa 27e opération. J’ai commencé à le traiter et il m’a fallu six semaines pour entendre le son de sa voix.» Ce qu’il y a de surprenant dans ces douleurs insondables, c’est la disproportion entre la cause et la réaction de l’organisme. Parfois, c’est un pied coincé dans une porte, parfois, c’est une banale entorse, et cet incident dégénère en maladie de Sudeck (ou algodystrophie), ou bien la personne

reste des années sans poser le pied par terre… «On peut trouver une explication purement physiologique à ces douleurs exacerbées: le nerf qui a été lésé par ce traumatisme repousse de manière anarchique. Il se ramifie et la douleur irradie. Il se peut aussi que le trajet nerveux soit comme court-circuité: le signal remonte vers la source.» Bilan des dégâts: «Le toucher est interprété comme une douleur», résume Claude Spicher. Le cerveau confond tout Au sommet du système nerveux, il arrive aussi que le cerveau s’emballe: c’est la tempête sous un crâne. «Quand on regarde par imagerie médicale le cerveau d’une personne qui souffre, on voit très bien les aires qui sont actives. Or, certaines aires actives ne correspondent à aucune partie blessée du corps: c’est comme si le cerveau s’emballait et si les récepteurs de la douleur s’excitaient sans facteur déclenchant». Dans ces phénomènes d’hypersensibilité, le cerveau confond tout: il ne différencie plus l’agréable du désagréable, le bienfaisant du douloureux… «Il est en stand-by permanent», dit Claude Spicher. C’est là qu’intervient la rééducation sensitive, la spécialité du thérapeute fribourgeois: «Nous allons réapprendre au patient ce qu’est un toucher agréable. Nous allons lui réapprendre à différencier les zones douloureuses de celles qui ne le sont pas. Nous allons lui réapprendre à inter- préter à leur juste mesure les mes- sages envoyés par la peau ». «Malgré vingt ans de lutte» Le spécialiste travaille avec des outils aussi surprenants qu’une peau de lapin. Au début du traitement, la caresse de cette fourrure passe pour une agression. Au fil des semaines, la douceur se démasque. Une patiente a raconté son expérience : « Alors que la souffrance semblait prendre défi-

nitivement ses quartiers, malgré 20 ans de lutte acharnée, ce fut la peau d’un autre qui me sauva, celle d’un lapin!» Le traitement est soutenu: de 4 à 8 séances par jour que le patient re- produit souvent à domicile. Il peut être long: «La réadaptation fut longue, raconte cette femme: plus d’un an d’exercices quotidiens et as- sidus. Les douleurs ne sont actuelle- ment pas encore entièrement élimi- nées (…), mais j’ai réussi à émerger de mes plus grandes souffrances.» Une solution diplomatique La douleur régresse parce que le cerveau a appris à contourner l’obs- tacle: c’est un exemple de cette for- midable plasticité cérébrale. «Quand on regarde le fonctionnement du cer- veau par imagerie médicale, on s’aperçoit qu’il y a comme des aber- rations: chez le patient, c’est la main gauche qui travaille, mais dans le cer- veau, ce n’est pas la zone correspon- dante qui s’allume.» Claude Spicher rapproche ce phénomène de l’ap- prentissage du braille chez des en- fants aveugles de naissance: «En 1996, un chercheur japonais, Sadato, a montré que lorsque des aveugles apprennent à lire en braille, ce sont les neurones de l’aire visuelle qui s’activent! Alors que si quelqu’un de- vient aveugle plus tard, quand il sait déjà lire, ce sont les neurones du tou- cher qui travaillent à l’apprentissage du braille. Notre cerveau a développé une stratégie de substitution.» «C’est l’histoire d’une cohabitation forcée, d’un rapport de force entre ma peau et moi», a écrit une pa- tiente. Toute l’astuce des thérapeutes consiste à trouver une issue diploma- tique à cette «cohabitation forcée» entre une peau et un cerveau. > Mercredi 17 mars 2010, 20h, petit auditoire de physiologie, chemin du Musée 5, Fribourg (en face de l’école d’ingénieurs): «Réveillez votre peau pour endormir vos douleurs neurogènes! », conférence de Claude Spicher (en français, commenté en allemand).

2 Journaliste à La Liberté – Quotidien romand édité à Fribourg http://www.laliberte.ch

L’article suivant a été publié dans La LIBERTE du mardi 16 mars 2010, page 29 Nous le rééditons avec la gracieuse permission de l’auteur et de l’éditeur:

http://www.laliberte.ch

To MD

To neuroscientist

To patient To therapist

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Intermittent brachial neuralgia of

anterior branch of medial antebrachial cutaneous nerve

with mechanical allodynia of

15 months duration

Della Casa3, R.

Coales4, K.

de Raemy5, X.

Spicher6, C.J.

ABSTRACT

A 15 month history of neuropathic pain was resolved using distant vibrotactile counter

stimulation (DVCS): The technique of the somatosensory rehabilitation method used to

eradicate allodynia. After 35 days of treatment, therapist and patient noted a reduction in

allodynia, initially in severity and then in overall area. Once the allodynia had disappeared, an

area of underlying hypoaesthesia was exposed. Allodynia has been termed paradoxically

painful hypo-aesthesia in previous articles because the presence of a hypoaesthetic territory

under tender skin is systematic. The underling hypoaesthesia was then treated to prevent

relapse. This case report illustrates the DVCS therapeutic management. The different stages

of treatment are discussed in details.

Keywords: Neuropathic pain, allodynia, distant vibrotactile counter stimulation,

underlying hypoaesthesia, somatosensory rehabilitation

3 OT, Somatosensory Rehabilitation Centre; General Clinic; 6, Hans-Geiler, Street, CH-1700 Friburgh, Europe. e-mail : [email protected] 4 OT, Rheumatology Departement, Royal National hospital for Rheumatic Diseases, Upper Borough Walls, Bath, BA147QU, UK.e-mail: [email protected] 5 MD, Orthopaedic and Hand surgery, co-head medical doctor of HFR, Riaz, Switzerland 6 University Scientific Collaborator, University of Fribourg, Medicine Department, Physiology Unit; Rue du Musée 5; CH - 1700 Fribourg . http://www.unifr.ch/neuro/rouiller/collaborators/spicher.php & OT, Swiss HT, Somatosensory Rehabilitation Centre; General Clinic; 6, Hans-Geiler, Street, Friburgh.

To MD.    To neuroscientist To patient To therapist      

Case Report

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INTRODUCTION Pain which is described as “radiating” and “tenderness” to touch are, in the context of

neuropathic pain, often symptoms that indicate the presence of a territory of Static

Mechanical Allodynia (SMA). The mechanisms of Allodynia, defined as “Pain due to a

stimulus which does not normally provoke pain.”(Merskey & Bogduk, 1979, 1994) have

already been widely described. Significantly, Devor proposes that SMA occurs in the

situation of central sensitization, initiated and maintained by an abnormal afferent discharge

triggered after axonal injury along C-fiber nociceptors. His most recent research implicates

“A-pain”.“Pain can be evoked by activity in low threshold A touch afferents.” (Devor,

2009).

By distant vibrotactile stimulation (DVCS) treatment, the SMA territory is supposed to

disappear, revealing a numb territory named the underlying hypoaesthesia. (Spicher et al.,

2008). In practical, how does SMA resolve when treated by DVCS ?

The aims of this case study, which has already been presented in Orlando7 by Spicher, are to

inform the reader of the appropriate DVCS working zones as treatment progresses to resolve

the SMA and to illustrate the concordance between the location of the underlying

hypoaesthesia and the allodynic territory.

PATIENT & METHODS

Patient

E. is a 17 year old female, Caucasian, au-pair, who complains of pain in the upper extremity.

This pain has been present for 15 months at the time of the first assessment.

Methods

E. was treated by three different therapists using somatosensory rehabilitation. Prior to

beginning of treatment and as permanent evaluation, she was assessed using the three

methods described below. Somatosensory rehabilitation was organized on the basis of one

weekly session, alterning between the therapists.

7 25.6.2010, Orlando, 8th Triennal Congress of IFSHT. Mechanical allodynia: Definition, Assessment & Treatment (CS-4.2 NEW TREATMENT APPROACHES and CS-5.3 [repeat] NEW TREATMENT APPROACHES) http://www.asht.org/meeting/handouts/2010/IFSHT/friday/MechanicalAllodynia_DefinitionAssessment-and-Treatment.pdf

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Somatosensory Testing

McGill Pain Questionnaire (MPQ)

The perception and evolution of the patient’s pain was assessed using the Questionnaire de la

douleur St-Antoine, (Boureau et al., 1984), the French version of the McGill Pain

Questionnaire (Melzack, 1975). This tool is helpful in enabling the patient and therapist to

define and quantify pain as it makes a useful distinction between sensory and affective pain.

The patient’s pain was assessed using the Questionnaire de la douleur St-Antoine by two

therapists; once during the first treatment session and again during the final session. It has

also been assessed several times as a permanent evaluation during the course of treatment.

Allodynography

Allodynography (Spicher, 2006; Spicher et al., 2008) is a technique which enables the

therapist to quantify and map a area of SMA on the skin. Mapping of the SMA territory

facilitates visual inspection in diagramic form of the allodynic area of skin. The assessment is

conducted by varying the application site of a 15 gram aesthesiometer across the skin surface

in order to delineate the borders of the SMA territory as defined by using a 1’cm visual

analogue scale, where 3cm is defined as a positive pain response.

Rainbow pain scale

The rainbow pain scale (Spicher, 2003, 2006, Noël et al., 2005, Spicher et al., 2008) is used

to qualifie the severity of SMA within the allodynic territory and to map the area of this most

intense pain. A range of 7 different aesthesiometers from 0.03 to 15 gram are utilised. The

therapist begins by stimulating the patient’s skin using the finest aesthesiometer, 0.03 gram

which is represented by the colour red on the scale. If this does not elicit a pain response, the

therapist then proceeds to the next, thicker, aesthesiometer 0.2 gram, which is represented by

the colour orange. The assessment continues working through the 7 aesthesiometers until a

positive pain response is provoked on skin simulation. The therapist then uses this selected

aesthesiometer to map the territory of skin which is painful on stimulation to complete the

assessment. Should a pain response be elicited by a finer aesthesiometer than the 15 gram one

used to map the full extent of the allodynic territory, then the area mapped will be smaller and

fall within the full allodynic territory. This method allows the therapist to assess the severity

of the patient’s allodynia without causing undue pain.

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Secondary Aesthesiography

The secondary aesthesiography (Spicher et al., 2008) is used to assess the area of underlying

hypoaesthesia once the SMA territory has been completely removed.

The term “aesthesiography” is used because it refers to a mapping of the hypoaesthesia, while

“secondary” is used to avoid any confusion with “aesthesiography” (Spicher & Kohut, 2001).

Which is a very sensitive assessment, used in the diagnosis of axonal lesions without

associated allodynia (Spicher, 2006).

Somatosensory Rehabilitation

The somatosensory rehabilitation received by E. was based on the somatosensory

rehabilitation method described earlier in detail (Spicher, 2006). This method can be taught to

a clinician in 56 hours. The duration of each weekly session of somatosensory rehabilitation

ranges between 30 to 75 min (average time: 45 min). The therapeutic management regime that

was chosen by the therapists was: Distant vibrotactile countersitmulation (DVCS), and then,

rehabilitation of the underlying hyposensibility.

DVCS (Spicher et al., 2009)

“This technique, initially reported in an article published in French (Spicher et al. 2006),

has been described in detail in a recent report (Spicher et al., 2008). In the case of an

allodynic territory, a tactile device is used at home and a vibratory one in therapy, allowing

the patient to perceive a non-nociceptive stimulus in a non-nociceptive manner proximal to

the SMA territory. The variable parameter of the DVCS is the location of the stimulus.

In consecutive sessions, the DVCS progressively and slowly invades the SMA territory,

transforming formerly painful zones into comfortable zones.”

The task of the somatosensory therapist is:

i) To presume which cutaneous branch is damaged. As, at this stage, the extraterritorial

pain is overlapping the cutaneous distribution of the damaged branch, it is only

possible to presume it.

ii) To define a limited zone of skin where DVCS should be done at home six times a day

for 1 minute and in the therapy once a week.

iii) To delineate a limited zone of skin that should be touched as little as possible.

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RESULTS

The following, describes the correlation between the shrinking of the allodynic territory and

the progression of DVCS recorded during the somatosensory rehabilitaton sessions. During

the initial assessment the therapist presumed which damaged cutaneous branch was damaged,

completed the allodynography and recorded the severity of the allodynia with the rainbow

pain scale.

The presumed damaged cutaneous branch was the anterior branch of the medial antebrachial

cutaneous nerve. The allodynography was positive and the severity recorded was indigo (8.7

gram increases the VAS to 3/10).

The comfortable zone to be stimulated with tactile stimulation was located low down on the

territory of the 2nd thoracic nerve. This zone was assessed by applying tactile stimulation to

the skin and, asking the patient how she perceived it. The underlying reasoning applied was:

DVCS must be carried out, as far as possible, on the proximal part of the territory of the

cutaneous distribution of the nerve assumed to be damaged. As tactile stimulation in this zone

proved to be uncomfortable to E., the therapist then assessed the skin territory of the proximal

« cousin » nerve of the medial cord of brachial plexus. Tactile stimulation of this zone also

proved to be uncomfortable. The therapist therefore determined that, DVCS could only be

undertaken on the lower segmentary level relative to the presumed damaged nerve.

The rainbow pain scale indigo was mapped during the next session (t14), 2 weeks later. The

therapist determined that E. now found tactile stimulation of the cutaneous department of the «

cousin » nerve comfortable, so was enable to progress DVCS on that area. This continued to

be the zone stimulated until disappearance of the indigo rainbow pain scale (after a total of 28

days of treatment).

On the same day, the allodynography was mapped for the second time. We observed then, that

it had also shrunk in size.

The zone to be counter stimulated had now progressed to the proximal area of the territory of

the anterior branch of the medial antebrachial cutaneous nerve.

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A:t0 A:t0 Allodynography

15.0 gram [mark : 5.18] The upper and/or lower segmentary level

B:t14 B:t14 Rainbow pain scale indigo

8.7 gram [mark :4.93] The territory of a « cousin » nerve and

not a « neighbour » nerve

C:t21 C:t21 Rainbow pain scale indigo

8.7 gram [mark :4.93] The territory of a « cousin » nerve and

not a « neighbour » nerve

D:t28 D:t28 No Rainbow pain scale indigo

8.7 gram any more [mark :4.93] The proximal part of the territory of

cutaneous distribution

Fig. 1: Legend: A: (the 29thof January 2010) [t0], the application of a force of 15.0 gram provoked a touch-evoked pain (SMA) of 3/10 cm on the VAS, supposably on the territory of

the anterior branch of medial antebrachial cutaneous nerve . On the right panel: the comfortable zone to counter stimulate through DVCS is the lower segmentary level. B: (the

12th of Februar 2010) [t14], the application of 8.7 gram provoked a touch-evoked pain (Indigo rainbow painscale) of 3/10 cm on the VAS. On the right panel: the comfortable zone to

counter stimulate is the “cousin” nerve (The medial brachial cutaneous nerve). C: (the 19th of February 2010) [t21] the surface of the indigo rainbow pain scale diminished On the right

panel: the comfortable zone to counter stimulate is the “cousin” nerve (Medial brachial cutaneous nerve). D: (the 26th of February 2010) [t28] Panel left: the indigo rainbow pain scale disappeared. On the right panel: The comfortable zone to counter stimulate through

DVCS is on the proximal part of the cutaneous territory (Anterior branch of medial antebrachial cutaneous nerve)

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Figure 2 illustrates the transition from SMA to underlying hypoaesthesia. The secondary aesthesiography was mapped 35 days after the beginning of DVCS. Rehabilitation of the underling hypoaesthesia started on that same day.

A B

Fig. 2: When the SMA territory determined by allodynography (panel A) disapppeared, the presence of an underlying hypoaesthetic territory was found, based on a secondary

aesthesiography procedure (panel B; see also Spicher et al., 2008). A: Allodynography (the 29th of January 2010 [t0], the application of a force of 15.0 gram provoked a touch-evoked

pain (SMA) of 3/10 cm on the VAS. B: Secondary aesthesiography (the 5th of March 2010 [t35], the application of a force of 0.7 gram was not detected).

This period of rehabilitation lasted until the 7th of May 2010 (Table I) the treatment lasted 108 days in total.

Sen

sory

Qualifiers 29th of January 2010 7th of May 2010

Radiating 3 0-1

Hot sensation 3 0-1

Tingling 3 0-2

Tender 2 0

Sub-total of sensory pains 17 points 6 points

Affective

Fearful 2 1

Troublesome 2 1

Sub-total of affective pains 11 points 6 points

Total

Total of pains 15 points 6 points

Table I : McGill Pain Questionnaire score: Decrease of pain between the first

session (19th of January 2011) and the last somatosensory rehabilitation

session (7th of May 2010 ). Initially using DVCS and then rehabilitation of the

underlying hyposensibility.

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E.’s neuropathic pain decreased from 15 to 6 points during treatment. She was still bothered

by pain in some activities but generally her symptoms had decreased.

DISCUSSION

The time required SMA to disappear directly correlates to the severity of the allodynia as

assessed using the Rainbow Pain Scale one (Spicher et al., 2008; Spicher, et al., 2009).

Thanks to those studies, it is possible to establish a DVCS prognosis at the end of the first

session. In this case study, the disappearance of the indigo rated allodynic territory resolved

after 35 days of DVCS treatment. This was actually accomplished in less time than the

predicted time course for disappearance as determined by Spicher. (Spicher et al., 2009) As

hypothesised, a hypoaesthetic territory of the medial antebrachial cutaneous nerve was then

revealed. This underlying hypoaesthesia was then treated in a way similar to the rehabilitation

of hyposensitivity (initial hypoaesthesia without mechanical allodynia). The specificity of that

program is that the time of stimulation increases in a progressive way.

SMA may not necessarily be restricted to the cutaneous distribution of one branch of a nerve.

It may spread over adjacent skin innervated by other cousin branches of the same nerve or by

neighbouring nerves. The phenomenon of overlapping also called extraterritorial pain was

described ten years ago (Decosterd, 2006) As a consequence, a therapist will have to look for

“comfortable skin” to stimulate in proximal zones, sometimes quite far from the original

allodynic territory, in order to establish effective DVCS.

The progression of DVCS described follows the progression originally described in French.

(Noël & Spicher, 2007)

The proximal part of the territory of cutaneous distribution

The territory of a « cousin » nerve and not a « neighbour » nerve

The upper and/or lower segmentary level

An average decrease of 30% of the McGill pain questionnaire score between beginning and

end of somatosensory rehabilitation has been published in the e-News for Somatosensory

Rehabilitation. This study was led on a cohort of 53 patients (Spicher et al. 2005) In this case,

the score decrease was of 60%.

The persistence of a tingling sensation in some particular gestures, lead us to suspect an additional Thoracic Outlet Syndrome (TOS). Therefore

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simple exercises, aimed at resolving compression on the medial cord of the brachial plexus, were added to her program during the two last weeks of somatosensory rehabilitation to address this (Barbis et al., 1990).

CONCLUSION

During a follow up phone call, one month post treatment, E. asked her therapist: “What did I

actually have?” It’s always a very positive sign when a patient uses the past tense when

talking about neuropathic pain. It is an indication that the pain is no longer a part of their day

to day life.

This case report presents a very useful illustration of the process of somatosensory

rehabilitation in the presence of an allodynic territory. It shows clearly how DVCS invades the

previously allodynic territory as this resolves with treatment.progressively.

Once the allodynic territory disappears an underlying hypoaesthetic territory of the damaged

nerve is revealed. This can then be assessed using secondary aesthesiography and rehabilitated

accordingly to prevent recurrence of painful allodynia. The knowledge of aesthesiology

(Spicher et al. 2010) guides the therapists for DVCS.

REFERENCES

1. Melzack, R. (1975). The McGill Questionnaire: Major Properties and Scoring Methods.

Pain, 1, 277-229. 2. Boureau, F., Luu, M., Gay, C. & Doubrere, J.-F. (1984). Elaboration d’un questionnaire

d’auto-évaluation de la douleur par la liste des qualificatifs. Thérapie, 39, 119-129.

3. Barbis, J. (1990) Therapist's management of thoracic outlet syndrome. In: JM Hunter, LH Schneider, E Mackin and AD Callahan, Editors, Rehabilitation of the hand, (Ed.), CVMosby, St. Louis pp. (3rd ed.) 540–562.

4. Spicher C.J., Degrange B. & Mathis F. (2005). The Vibrotactile Sense Assessment: A Path

to Relieve Chronic Neurological Pain; About 83 Axonal Lesions in the Upper Extremity. e-News for Somatosensory Rehabilitation, 2(3), 51 – 61. http://www.unifr.ch/neuro/rouiller/somesthesie/somato.enews.php

5. Noël, L., Spicher, C.J., Degrange, B. & Rouiller, E.M. (2005). Une esthésiographie

intestable signe des lésions axonales ou comment cartographier une hypoesthésie douloureuse. In M.-H. Izard, R. Nespoulous (Eds.), Expériences en ergothérapie, 18ème série, (pp. 127 -135). Montpellier, Paris: Sauramps médical.

6. Decosterd, I. (2006). Neuropathic Pain Symptoms: Toward Mechanism-based Pain

Management? e-News for Somatosensory Rehabilitation, 3(1), page 2. http://www.unifr.ch/neuro/rouiller/somesthesie/somato.enews.php#page=2

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7. Degrange, B., Noël, L., Spicher, C.J., & Rouiller, E.M. (2006). De la rééducation de

l’hyposensibilité à la contre-stimulation vibrotactile. In M.-H. Izard & R. Nespoulous (Eds.), Expériences en ergothérapie, 19ème série (pp. 207 -220). Montpellier, Paris: Sauramps médical.

8. Spicher, CJ. (2006). Handbook for Somatosensory Rehabilitation. Montpellier, Paris:

Sauramps Médical [The English translation of : Spicher, C. (2003). Manuel de rééducation sensitive du corps humain. Genève, Paris: Médecine & Hygiène]. http://www.bookofsense.com/bookofsense/HandbookEn.html

9. Noël, L. & Spicher, C.J. (2007). L’hypoesthésie douloureuse parasite souvent nos

traitements : Définitions, évaluation, rééducation. In F. Morestin & N. Sève-Ferrieu (Eds.), Actes des premières journées européennes et francophones d’ergothérapie, 1ère série, (pp. 217 -223). Paris: ADERE

10. Spicher, C.J., Mathis, F., Degrange, B., Freund, P. & Rouiller, E.M. (2008). Static

Mechanical Allodynia is a Paradoxical Painful Hypoaesthesia: Observations derived from neuropathic pain patients treated with somatosensory rehabilitation. Somatsens Mot Res, 25(1), 77-92.

11. Spicher, C.J., Freund, P., Desfoux, N. & Della Casa, R. (2009). Time Course of

Disappearance of Static Mechanical Allodynia through Somatosensory Rehabilitation: Reexamination of a Larger Cohort of Neuropathic Pain Patients. e-News for Somatosensory Rehabilitation, 6(4), 151-170. Available (17.3.2010): http://www.unifr.ch/neuro/rouiller/somesthesie/enews2009/e-News%206(4)#page=10.pdf

12. Spicher, C.J. (2008). FC35 Distant Vibrotactile Counter Stimulation (DVCS): A New

Technique to Treat Chronic Neuropathic Pain Patients (NPP) of the Upper Extremity. J Hand Surg, 33E (supplement 1), 201-202. http://jhs.sagepub.com/cgi/reprint/33/Supplement_1/181.pdf Spicher, C.J. (2008). Abstract of Distant Vibrotactile Counter Stimulation (DVCS): A New Technique to Treat Chronic Neuropathic Pain Patients (NPP) of the Upper Extremity. Eurohand: IXth Congress of the EFSHT, June 20th, 2008, Lausanne.

13. Spicher, C., Desfoux, N. & Sprumont, P. (2010). Atlas des territoires cutanés du corps

humain : Esthésiologie de 240 branches. Montpellier, Paris : Sauramps Médical http://www.bookofsense.com/bookofsense/AtlasEn.html

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www.unifr.ch/neuro/rouiller/teaching/continedu.php

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www.unifr.ch/neuro/rouiller/teaching/continedu.php

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Après 16 ans de communication (n = 215), après 10 ans de cours de 2, 4, voire 8 jours (n = 34),

la 1ère volée du Certificat CREA - Haute Ecole Libre de Bruxelles

(HELB) en rééducation sensitive de la douleur a vu le jour sous l’égide de

M. Pierre Castelein. Merci.

Cette formation compte 56 heures ou équivalents.

Lauréates et lauréats de la 1ère volée 2010 du Certificat CREA - Haute Ecole Libre de Bruxelles (HELB) en Rééducation sensitive de la douleur (par ordre alphabétique) :

- Cynthia Lathion, Montana,

- Irene Inauen, Rheinfelden,

- Murielle Macchi, Delémont,

- Nadège Desfoux, Fribourg,

- Nathalie Drezet-Munch, Genève,

- Paolo Signorino, Bruxelles,

- Pascal Latière, Genève,

- Rebekah Della Casa, Fribourg,

- Sandrine Clément-Favre, Fribourg,

- Séverine Landreau, Fouquière-les-Lens.

Expertisé par Dr Mélanie Kaeser (PhD), Research Associate, Unit of Physiology and Program in Neurosciences, Department of Medicine, University of Fribourg, CH N’hésitez pas à vous inscrire pour devenir Lauréate de la 2ème volée !!! Vous découvrez depuis cet été, e-News 7(3), leur travail final de Certificat.

To MD.    To neuroscientist To patient To therapist    

Certificat en rééducation sensitive de la douleur

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Névralgie dorso-intercostale incessante avec allodynie mécanique :

Début de la diminution des douleurs par la rééducation sensitive

RESUME

La prise en charge de la douleur est complexe et pourtant en tant que thérapeute, il est difficile

d’ignorer la douleur que nos patients expriment chaque jour. A travers le cas d’un patient

présentant une allodynie mécanique, nous allons montrer le début d’une prise en charge via la

technique de rééducation sensitive.

Mots-clés : douleur, rééducation sensitive, allodynie mécanique, contre-stimulation,

questionnaire de la douleur St-Antoine, arc-en-ciel, allodynographie

Landreau8, S. lauréate de la 1ère volée du Certificat CREA - Haute Ecole Libre de Bruxelles (HELB) en Rééducation sensitive de la douleur

Expertisé par Dr Mélanie Kaeser (PhD), Research Associate, Unit of Physiology and Program in Neurosciences, Department of Medicine, University of Fribourg, CH

INTRODUCTION

Douleur et douceur : ces deux termes ne sont pas si opposés par leur orthographe et

pourtant… : l’un désigne le toucher de la peau d’un patient, et l’autre celui de la peau d’un

lapin. Il faudra du temps pour que l’un et l’autre se rencontrent et que leur contact se fasse de

façon agréable.

C’est tout l’intérêt de la rééducation sensitive de pouvoir contrer cette douleur au toucher

autrement appelée allodynie mécanique. Cette douleur n’est autre qu’une hyposensibilité

douloureuse et est présente chez 23% des patients présentant des douleurs neuropathiques[1].

Ce travail a pour but de présenter le début d’une prise en charge tendant vers la diminution de

ce type de douleur.

8 ET, C. R. R. F. Sainte-Barbe; 4, rue d'Artois F – 62740 Fouquière-les-Lens, Nord-Pas-de-Calais e-mail : [email protected];

To MD.    To neuroscientist To patient To therapist      

Fait clinique

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PATIENT & METHODES

Patient

Mr J., 52 ans, présente des douleurs neuropathiques depuis 2001. En 2001, une pompe

intrathécale de Liorésal® est mise en place dans le cadre d’une spasticité gênante du membre

inférieur droit suite à un AVP. Elle est retirée dû à des complications et reposée 6 mois après.

En 2004, la 2ème pompe doit être de nouveau retirée pour causes de douleurs et d’inefficacité,

et une 3ème est reposée à un endroit différent. Elle est retirée en 2007 car les douleurs sont

persistantes. Depuis Mr J. présente toujours des douleurs. Un essai de mésothérapie a été

effectué le 21/04/09 mais il n’a pas réellement diminué les douleurs. Le TENS

(Transcutaneous Electrical NeuroStimulation) a été mis en place depuis 2001 et Mr J dit être

soulagé pendant 45 minutes. Il suit également un traitement médicamenteux : Rivotril®,

Lyrica 300®, Versatis 5% patch® (depuis juin 2010).

A l’interrogatoire, Mr J. décrit une « hypersensibilité au toucher » importante, et supporte

difficilement le frottement du T-shirt et la station assise prolongée.

Hypothèse de travail

Elle fait suite à nos bilans : l’allodynographie et l’arc-en-ciel de la douleur [2], [3] :

Névralgie dorso-intercostale incessante de la branche perforante antérieure du 10ème nerf

thoracique (Th10) avec allodynie mécanique (Stade IV de lésions axonales).

Méthode

En présence d’une allodynie mécanique, il ne faut surtout pas stimuler le territoire

allodynique car cela entretient voire aggrave le processus douloureux. Ainsi la rééducation va

se faire suivant le principe de contre-stimulation [4] :

- la contre-stimulation tactile : elle est effectuée 6 à 8 fois par jour par Mr J pendant 1 minute

(ou moins longtemps) avec une peau de lapin. Il s’agit de réapprendre au cerveau à percevoir

un stimulus agréable comme non-nociceptif. Elle s’effectue pour Mr J, selon la 3ème règle de

contre-stimulation, soit sur le 1er niveau segmentaire inférieur et/ou supérieur perçu comme

agréable. Ces zones de travail sont réévaluées au fur et à mesure des séances.

- la contre-stimulation vibratoire : avec le VibralgicTM. Les stimulations appliquées sont de

faible amplitude et s’effectuent pendant 1 minute sur le ganglion rachidien de la zone

inférieure et/ou supérieure de la zone de travail et sur le ganglion rachidien de Th10 quand

celui-ci sera devenu confortable (vraisemblablement dès le 30/06/10).

- la contre-stimulation médicamenteuse : étant donné le principe de base de l’allodynie

mécanique, l’application de tout patch sur la zone allodynique est déconseillée. Ainsi il s’agit

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de le poser à distance de cette zone, soit sur les zones de travail (voire sur le ganglion

rachidien de TH10 à partir du 30/06/10).

RESULTATS

Fin juillet, Mr J évoque une diminution de ses douleurs et précise qu’il supporte davantage la

station assise prolongée. L’essai de contre-stimulation médicamenteuse avec le patch sur le

ganglion rachidien de la zone « supérieure » de travail n’a pas été concluant, puisque devant

l’augmentation des douleurs, Mr J a replacé les patchs sur sa zone allodynique qui pour lui a

un effet plus anesthésiant. Il s’agit aujourd’hui de poursuivre le traitement en réexpliquant à

Mr J le principe de la contre-stimulation médicamenteuse et son importance dans la

diminution de ses douleurs.

A : t0

B : t20 C : t50

Tableau I : Evolution des zones de travail, séances après séances (A, B, C),

de lésions, a priori, de la branche perforante antérieure du 10ème nerf thoracique

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Date Questionnaire de la douleur St-Antoine

Territoire de

distribution cutanée

SPP Stade

07/06/10 55 à 58 points Allodynie Intestable IV

29/06/10 34 à 36 points Allodynie Intestable IV

29/07/10 11 à 14 points Allodynie Intestable IV

Tableau II : Evolution des douleurs

DISCUSSION

En observant une diminution progressive de la douleur chez Mr J., nous pouvons espérer

pouvoir lever l’allodynie mécanique au maximum en 186 jours (136 jours restants)[4].

Sachant qu’une allodynie mécanique recouvre toujours une peau qui « dort »[5], il s’agira

ensuite d’évaluer cette hypoesthésie sous-jacente et de rééduquer cette peau afin qu’elle se

normalise [1] et ainsi éviter que les douleurs ne reviennent.

CONCLUSION

Les résultats de ce début de prise en charge permettent d’objectiver chez ce patient une

diminution progressive des douleurs de type allodynique par un traitement médicamenteux

adapté et par la rééducation sensitive.

En plus de soulager les douleurs, comme d’autres méthodes, la rééducation sensitive permet

également d’envisager avec le patient une éventuelle « guérison ». Il est important de

souligner que le patient devient, dans ce cas, un véritable acteur dans son parcours vers la

guérison puisqu’il participe activement à son traitement.

REFERENCES BIBLIOGRAPHIQUES

[1] Degrange, B., Noël, L., Spicher, C.J., & Rouiller, E.M. (2006). De la rééducation de l’hyposensibilité cutanée tactile à la contre-stimulation vibrotactile. In M.-H. Izard & R. Nespoulous (Eds.), Expériences en ergothérapie, 19ème série, (pp. 207 -211). Montpellier, Paris : Sauramps médical.

[2] Spicher, C. (2003). Manuel de rééducation sensitive du corps humain. Genève, Paris : Médecine & Hygiène

[3] Spicher, C., Desfoux N. & Sprumont, P. (2010). Atlas des territoires cutanés du corps humain. Montpellier, Paris : Sauramps Médical

[4] Somatosensory Rehabilitation Centre’s Statistics (2010). e-News for Somatosensory Rehabilitattion, 7(1), 19-22. http://www.unifr.ch/neuro/rouiller/somato.enews.htm

[5] Spicher C.J., Ribordy F., Mathis F., Desfoux N., Schönenweid F. & Rouiller E.-M (2008). L’allodynie mécanique masque une hypoesthésie: observations topographiques de 23 patients douloureux neuropathiques chroniques. Doul. & Analg, 21, 239-251.

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Martin WINCKLER, MD Editorialiste invité

En juillet 2004 l'ébauche d'une idée prenait forme: la parution d'un journal électronique, libre d'accès, hébergé par l'unité de neurophysiologie de l'université de Fribourg, qui voulait tenter de tisser un réseau autour de la rééducation sensitive de la douleur pour les patients, les thérapeutes, les médecins et les neurosciences. Notre publication comptant plus de 30'000 lecteurs, nous avons le grand plaisir de vous annoncer la création du e-journal "Douleurs neuropathiques" : le recueil francophone du e-News for Somatosensory Rehabilitation multilingue. Depuis le 10 septembre 2010, L’Association Nationale Française d’Ergothérapie (ANFE) héberge à Paris (France) Douleurs neuropathiques, le recueil francophone du e-News for Somatosensory Rehabilitation multilingue. Le 10 novembre de chaque année vous pourrez recevoir tous les textes francophones parus dans les 4 volumes de l’e-News, dans une Tome téléchargeable sur le site : www.anfe.fr Afin de vous offrir ce nouveau service, notre équipe s’est étoffée de :

Laurence KOCH, assistante de rédaction internationale

Murielle MACCHI, assistante de marketing Bonne lecture

o

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Une diminution rapide des douleurs neuropathiques chroniques

d’une névralgie fémoro-poplitée permanente

par rééducation sensitive

RESUME

Contexte : La neurologie périphérique est le parent pauvre de la traumatologie. Il est connu que la rééducation sensitive offre une alternative efficace pour les traitements des douleurs neuropathiques chroniques, d’origine périphérique, avec 56 % de succès (diminution des douleurs de 50% ou plus) (Mathis et al., 2006).

But : Ce fait clinique a pour but d’illustrer l’efficacité de la rééducation sensitive dans le traitement des douleurs neuropathiques chroniques en démontrant la relation entre la diminution du score au questionnaire de la douleur Saint-Antoine (QDSA) et l’amélioration de la capacité de détection de la peau.

Matériel et méthodes : Une patiente, présentant une névralgie fémoro-poplitée depuis 6 ans, a été traitée par rééducation sensitive. L’efficacité du traitement a été contrôlée par les tests de discrimination de deux points statiques, du seuil de perception à la pression (SPP), du seuil de perception à la vibration et par l’évaluation des douleurs au QDSA.

Résultats : Le traitement a duré 105 jours, avec des exercices pluriquotidiens et une séance hebdomadaire en thérapie. La rééducation sensitive a permis de faire diminuer de 93 % le score au QDSA (avant le traitement : 40 points et après le traitement : 3 points). En parallèle, la sensibilité tactile cutanée s’est améliorée avec un SPP qui est passé de 39,6 grammes à 2,5 grammes et un test de discrimination de 2 points statiques qui est passé d’un échec à 105 mm à 35 mm.

Conclusion : L’efficacité de la méthode de rééducation sensitive, pour soulager les douleurs neuropathiques chroniques, s’élève à 56% de succès et peut être comparée à celle d’autres traitements notamment médicamenteux : le succès pour un traitement par gabapentine est de 26 %, pour la pregabaline 28% et pour l’oxycodone 38 %.

Keywords : Neuropathic Pain, Hypoaesthesia, Neuroplasticity, Somatosensory rehabilitation Desfoux9, N. lauréate de la 1ère volée du Certificat CREA - Haute Ecole Libre de Bruxelles (HELB) en Rééducation sensitive de la douleur

Expertisé par Dr Mélanie Kaeser (PhD), Research Associate, Unit of Physiology and Program in Neurosciences, Department of Medicine, University of Fribourg, CH

9 ET, Centre de rééducation sensitive, Clinique Générale, Rue Hans-Geiler 6, CH- 1700 Fribourg, Suisse.

To MD.    To neuroscientist To patient To therapist      

Fait clinique

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INTRODUCTION

La neurologie périphérique est le parent pauvre de la traumatologie. Il est connu que la rééducation sensitive offre une alternative efficace pour les traitements des douleurs neuropathiques chroniques, d’origine périphérique, avec 56 % de succès (diminution des douleurs de 50% ou plus) [1].

Une patiente qui présentait une névralgie fémoro-poplitée permanente du nerf cutané sural latéral, suite à l’ablation d’un lipome, qui datait de 6 ans, a obtenu un très bon résultat, au moyen de la rééducation sensitive.

Ce fait clinique a pour but d’illustrer l’efficacité de la rééducation sensitive dans le traitement des douleurs neuropathiques chroniques en démontrant le lien entre la diminution du score au questionnaire de la douleur Saint-Antoine (QDSA) et l’amélioration de la capacité de détection de la peau.

PATIENTE & METHODES

Anamnèse et clinique

Mme S., femme de 56 ans, employée de bureau dans une entreprise familiale, a été adressée au centre de rééducation sensitive par son chirurgien pour des « douleurs neuropathiques du territoire du sciatique poplité externe, distal de la jambe droite ». Mme S. avait subi une intervention chirurgicale, 5 ans auparavant, pour enlever un lipome qui se situait sur la face externe de son mollet. Des douleurs neuropathiques ont commencé à apparaître dans les semaines qui ont suivi l’opération. Mme S. était gênée dans son quotidien, notamment pour faire le repassage et la station debout prolongée augmentait les douleurs. Elle ne pouvait plus pratiquer ses loisirs, tel que le vélo ou le jardinage. Lors de l’entretien du 13 janvier 2009, avec l’aide du questionnaire de la douleur Saint-Antoine, la patiente décrivait des douleurs de type sensations de décharges électriques, irradiation et pression dans le mollet. L’hypothèse de lésions axonales est la suivante : Névralgie fémoro-poplitée permanente du nerf cutané sural latéral (Stade IV de lésions axonales).

A l’examen, l’esthésiographie [2] des téguments de la face latéral de la jambe est positive (Fig. 1).

Fig. 1 : Esthésiographie à 0,7 gramme du nerf cutané sural latéral ; testée le 13.1.2009 sur la

face latérale du mollet (esthésiomètre de Semmes-Weinstein 3.84).

L’efficacité du traitement a été contrôlée par les tests de discrimination de deux points statiques, du seuil de perception à la pression (SPP) et par l’évaluation des douleurs au QDSA. Tous ces tests ont été faits, alternativement, par deux thérapeutes travaillant au centre de rééducation sensitive. Chaque évaluation a été faite dans les mêmes conditions et au même endroit. Méthodes

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Le test de discrimination de deux points statiques L’esthésiomètre à deux points a été utilisé. Le test a été passé comme l’a décrit Dellon [3] et tel que repris par Spicher [4]. La distance minimale en millimètres pour laquelle le patient peut correctement identifier une ou deux pointes est enregistrée (au moins sept réponses justes sur dix).

Le seuil de perception à la pression [5] Le set des vingt esthésiomètres de Semmes-Weinstein a été utilisé selon la passation originale ADADAD (A=ascendant, D=descendant) ; ce qui signifie que nous avons calculé la moyenne arithmétique des six monofilaments retenus comme décrit par Semmes et al. en 1960 [6] et repris par Spicher [4].

Traitement Le traitement, comme les évaluations, a été dispensé par les mêmes thérapeutes lors des 17 séances, d’environ 45 minutes (min : 30 minutes, max : 60 minutes), échelonnées sur 15 semaines, ceci à raison d’une séance hebdomadaire. La rééducation de l’hypoesthésie a été effectuée en séances par des stimulations par vibrations mécaniques. L’amplitude des vibrations appliquées correspondait au seuil de perception à la vibration augmenté de 0,10 mm. La durée de la stimulation durait au maximum 10 minutes. Cette thérapie a été complétée à domicile, par une rééducation de l’hyposensibilité avec, dans un premier temps, la rééducation des tracés, puis, dans un second temps, la rééducation du touche-à-tout. La rééducation des tracés consiste, sans contrôle visuel, à identifier 2 stimuli différents. La rééducation du touche-à-tout consiste à comparer les sensations bizarres de la zone hypoesthésique, avec des sensations normales d’une zone saine. La rééducation de l’hyposensibilité à domicile a été faite à raison de 4 fois 5 minutes par jour.

RESULTATS

Le traitement a duré 105 jours avec des exercices pluriquotidiens et une séance hebdomadaire en thérapie. La rééducation sensitive a permis de faire diminuer de 93 % le score au QDSA (avant le traitement : 40 points et après le traitement : 3 points - Tableau I).

Date SPP Test de discrimination

de 2 points statiques

Questionnaire de la douleur St-Antoine

Stade

13.01.2009 39,6 g > 105 mm 14 à 40 pts. IV

04.02.2009 12,3 g ND ND IV

11.02.2009 9,7 g 77 mm 6 à 26 pts. III

25.02.2009 8,7 g ND ND III

11.03.2009 5,9 g ND ND III

17.03.2009 3,9 g ND ND III

24.03.2009 2,8 g 55 mm 4 à 5 pts I

28.04.2009 2,5 g 35 mm 0 à 3 pts I

Tableau I : La diminution de l’hypoesthésie covarie avec la diminution des douleurs neuropathiques chroniques

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En parrallèle, la sensibilité tactile cutanée s’est améliorée avec un SPP qui est passé de 39,6 grammes à 2,5 grammes et un test de discrimination de 2 points statiques qui est passé d’un échec à 105 mm à 35 mm. DISCUSSION

La rééducation sensitive offre une alternative efficace pour les traitements des douleurs neuropathiques chroniques [1]. Ce paradigme de la rééducation sensitive « Rechercher l’hypoesthésie car la diminution de l’hypoesthésie diminue les douleurs neuropathiques »s’est à nouveau incarné [7] dans la vie quotidienne d’une patiente ; par la diminution du seuil de perception à la pression et du test de discrimination de 2 points statiques, le score du questionnaire de la douleur a diminué. Cette récupération correspond vraisemblablement à des mécanismes de neuroplasticité des tissus sains ; en particulier des nerfs adjacents [8].

CONCLUSION

La méthode de rééducation sensitive est un moyen pour soulager les douleurs neuropathiques chroniques. L’efficacité de la méthode de rééducation sensitive, avec 56% de succès, peut être comparée à celle d’autres traitements notamment médicamenteux : le succès pour un traitement par gabapentine est de 26 %, pour la pregabaline 28% et pour l’oxycodone 38 %.

REFERENCES BIBLIOGRAPHIQUES

[1] - Mathis, F., Desfoux, N., Sprumont, P., Hecker, E., Rossier, Ph. & Spicher, C.J. (2007). Diminution des douleurs neuropathiques périphériques par la rééducation sensitive. Rev Med Suisse, 3(135), 2745-2748. http://revue.medhyg.ch/print.php3?sid=32307 (4.8.2010) [2] - Spicher, C. & Kohut, G. (2001). Jean Joseph Emile Létiévant : A review of his contributions to surgery and rehabilitation. J Reconstr Microsurg, 17(3), 169-177. [3] - Dellon, A.L. (1978). The moving two-points discrimination test: Clinical evaluation of the quickly adpating fiber/receptor system. J Hand Surg(A), 3(5), 474-481. [4] - Spicher, C. (2003). Manuel de rééducation sensitive du corps humain. Genève, Paris: Médecine & Hygiène. [5] - Spicher, C.J., Haggenjos, L., Noël, L. & Rouiller, E.M. (2004). Cartographier un territoire hypoesthésique n’est pas rechercher le seuil de perception à la pression (SPP). In M.-H. Izard & R. Nespoulous (Eds.), Expériences en ergothérapie, 17ème série, (pp. 161-166). Montpellier, Paris: Sauramps médical. [6] - Semmes, J., Weinstein, S., Ghent, L. & Teuber, H.-L. (1960). Somatosensory changes after penetrating brain wounds in man. Cambridge, MA : Harvard University Press. [7] - Desfoux, N., Mathis, F. & Spicher, C.J. (2007). Diminution rapide par rééducation sensitive de douleurs neuropathiques chroniques d’une névralgie brachiale permanente. e-News for Somatosensory Rehabilitation, 4(3), 123-133. http://www.unifr.ch/neuro/rouiller/somesthesie/enews2007/e-News%204(3).pdf (4.8.2010) [8] - Inbal, R., Rousso, M., Ashur, H., Wall, P.D. & Devor, M. (1987). Collateral sprouting in skin and sensory recovery after nerve injury. Pain, 28(2), 141-154.

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Les géographes des nerfs

JEAN AMMANN10

Il y a encore des terres inconnues, la terra incognita dont rêvent les explorateurs: c'est le corps humain. Avec Nadège Desfoux et Pierre Spru- mont, Claude Spicher a entrepris une vaste opération topographique: la cartographie des nerfs cutanés humains. Les auteurs de cet ouvrage à paraître à la mi-mai aux Editions Sauramps Médical ont plongé dans 94 atlas d'anatomie. Et là, surprise! Le corps humain varie selon les édi- tions! «Nous nous sommes rendu compte que les connaissances res- taient vagues», déclare Claude Spi- cher. En s'appuyant sur ses propres expériences cliniques et en recoupant les données des différents atlas ana- tomiques, l'équipe fribourgeoise a décrit les 240 branches des nerfs cutanés. Cet atlas est conçu pour faciliter la prise en charge des patients qui souffrent de troubles neurologiques. «Cet atlas nous

permet de devenir les géographes de la sensibilité», dit Claude Spicher, avec un sens de la métaphore. JA

10 Journaliste à La Liberté – Quotidien romand édité à Fribourg http://www.laliberte.ch

ARTICLE

To MD To neuroscientist To patient To therapist

L’article suivant a été publié dans La LIBERTE du mardi 16 mars 2010, page 29. Nous le rééditons avec la gracieuse permission :

de l’auteur et de l’éditeur : « La Liberté – Quotidien romand édité à Fribourg »

http://www.laliberte.ch

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www.saurampsmedical.com

In English, French & Latin

Topography of the cutaneous distribution of 240 branches are illustrated and named in

English, French and Latin in this atlas (n = 1528 observations). It is a book for clinicians

for the assessment of neuropathic pain patients (NPP).

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To MD.      To neuroscientist To patient To therapist      

Nouvelles de l’industrie

  La responsabilité de la rédaction n'est pas engagée dans le contenu de cette rubrique 

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From the 11st of November 2008 until the 26rd of July 2010, 100 patients with 164 axonal lesions have been assessed in the Somatosensory Rehabilitation Sector of the EHC hospital’s occupational therapist centre

Stade I with

somatosensory disorders

without pain

Stage II, III, IV & V11 with neuropathic pain syndromes

Stage II Stage III Stage IV Stage V

(CRPS II)

10 0 95 50 9

154 164 axonal lesions

Table I: 164 axonal lesions generated neuropathic pain syndromes and 10 only presented somatosensory disorders without pain.

With spontaneous ongoing pain

Without touch- evoked pain

1) CRPS with hypoaesthesia

3) Permanent neuralgia with hypoaesthesia

5) Intermittent neuralgia with hypoaesthesia

2) CRPS with SMA1

4) Permanent neuralgia with SMA

6) Intermittent neuralgia with SMA

With touch-evoked pain

Stage I

7) Single mechanical

allodynia

Without spontaneous ongoing pain

1Static Mechanical Allodynia

Table II: Neuropathic pain patients are suffering from spontaneous ongoing and/or touch-evoked pain. These two symptoms are distributed in 7 different neuropathic pain statuses.

i.e. 4) Permanent neuralgia with static mechanical allodynie (for more details see also Table III).

11 CRPS : Complex Regional Pain Syndrome

To MD.      To neuroscientist To patient To therapist      

Somatosensory Rehabilitation Sector of the EHC hospital’s Statistics

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Table III: SMA Distribution of the 4 neuropathic pain statuses with touch-evoked pain:

1. CRPS II 2. Incessant Neuralgia 3. Intermittent Neuralgia 4. Single mechanical allodynia i.e. 67 % of the CRPS II presented static mechanical allodynia

(for more details see also Table I & III).

Neuropathic Pain Syndromes

Mechanical Allodynia

Distribution

CRPS II

67 %

Incessant Neuralgia

66 %

Intermittent Neuralgia

48 %

Mean

55 %

Table IV: About 154 axonal lesions assessed, 85 axonal lesions presented a positive allodynography: 85 / 154 = 55 %. In other words in this group of patients, half of neuropathic

pain syndromes are associated with a static mechanical allodynia (touch-evoked pain)

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Die Bäume

"Denn wir sind wie Baumstämme im Schnee. Scheinbar liegen sie glatt auf, und mit kleinem

Anstoß sollte man sie wegschieben können. Nein, das kann man nicht, denn sie sind fest mit

dem Boden verbunden. Aber sieh, sogar das ist nur scheinbar."

Kafka, F. (1912) - Betrachtung. Leipzig: Ernst Rowohlt Verlag.

Stromy

"Neboť jsme jako kmeny stromů ve sněhu. Napohled tu hladce spočívají a řekl bys, že stačí

malý náraz, abys je odsunul. Nikoli, nejde to, jsou totiž pevně spojeny s půdou. Ale pohleď,

dokonce i to je jen zdánlivé."

Kafka, F. (1912)- Rozjímání. Leipzig: Erst Rowohlt Verlag.

To MD.      To neuroscientist To patient To therapist      

Schatten - Halbschatten

To MD.      To neuroscientist To patient To therapist      

Stíny a polostíny

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Continuous Education – Weiterbildung - Formation continue

Date: 7-10 March 2011

3rd Week for Somatosensory Rehabilitation

Claude Spicher, OT, swiss certified Hand Therapist

Rebekah Della Casa, OT

Place : Somatosensory Rehabilitation Centre, Fribourg, Switzerland, Europe

Info : This issue 7(4) page 180

http://www.unifr.ch/neuro/rouiller/teaching/cont.edu/3rdweekSSR.2011.pdf

http://www.unifr.ch/neuro/rouiller/teaching/continedu.php

Date: 3 - 4 février 2011

Certificat de rééducation sensitive

Diminution des douleurs neuropathiques par rééducation sensitive

Module 1 : Troubles de base I & II

Lieu : CREA-HELB, Campus ERASME, Bruxelles

Info : www.crea-helb.be / [email protected]

Ces formations peuvent être comptabilisées pour le Certificat de rééducation sensitive

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29. – Handtherapie Nervenkurs 30. Oktober 2010 Ort Handtherapie Fortbildung

8707 Uetikon am See (Schweiz) Info www.handtherapie-fortbildung.com

17–20 novembre 2010 10e Congrès annuel de la Société Française d'Etude et de Traitement de la Douleur (SFETD)

Lieu Parc Chanot, Marseille (France) Info www.congres-sfetd.fr / [email protected]

21-24 mars 2011 Le traitement des syndromes douloureux neuropathiques par la rééducation sensitive

Troubles de base I & II, Complications douloureuses I & II Lieu Institut de Formation en Ergothérapie, Montpellier, France Info http://www.ergotherapiemontpellier.com/formation.html

25-26 mars 2011 Ergothérapie tous azimuts VIIème édition Lieu Campus d’Erasme, Bruxelles, Belgique Info [email protected]

29 April – 1 May 2011 6th WIP World Pain Congress Place Seoul, South Korea Info [email protected] / www.kenes.com/wip

11-13 mai 2011 Certificat de rééducation sensitive : module 2 Complications douloureuses I, Analyse de pratique &

Anatomie clinique I Lieu CREA-HELB, Campus ERASME, Bruxelles Info www.crea-helb.be / [email protected] www.anfe.fr / [email protected]

26–28 May 2011 XVIth FESSHT Congress & Xth EFSHT Congress Place Oslo, Norway Info www.eurohand2011.com

21–24 September 2011 7th Congress of EFIC European Federation of IASP

® Chapters

Place Hamburg, Germany Info http://www2.kenes.com/efic/pages/home.aspx

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16–18 novembre 2011 Certificat de rééducation sensitive : module 3 Gestion du lien thérapeutique, Anatomie clinique II &

Complications douloureuses II Lieu CREA-HELB, Campus ERASME, Bruxelles Info www.crea-helb.be / [email protected] www.anfe.fr / [email protected]

25 November 2011 The NSF for Long-Term Conditions: Five Years On British Society of Rehabilitation Medicine Place Royal College of Physicians, London Info http://events.rcplondon.ac.uk/details.aspx?e=1758 [email protected]

2–6 October 2012 14th World Congress on Pain International Association for the Study of Pain Place Yokohama, Japan Info http://www.iasp-pain.org/Yokohama

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