Scholarly article on topic 'Post-stroke hemiplegia rehabilitation: Evolution of the concepts'

Post-stroke hemiplegia rehabilitation: Evolution of the concepts Academic research paper on "Clinical medicine"

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Abstract of research paper on Clinical medicine, author of scientific article — P. Marque, D. Gasq, E. Castel-Lacanal, X. De Boissezon, I. Loubinoux

Abstract Stroke rehabilitation has undergone a revolution over the last three decades. Cohort studies have consistently reinforced the importance of post-stroke rehabilitation to stimulate recovery, but the concepts of empirical methods originally proposed by therapists to rehabilitate these patients have not withstood clinical analysis. Functional neuroimaging and animal models have unveiled the mechanisms underlying functional recovery and helped teams understand its limitations and improvement modalities. These neuroscience discoveries constitute the grounds needed to understand the emergence of new technologies: robotics and virtual reality. The objective of this review of the literature was to select key works in this field to better understand current therapeutic possibilities.

Academic research paper on topic "Post-stroke hemiplegia rehabilitation: Evolution of the concepts"

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Annals of Physical and Rehabilitation Medicine xxx (2014) xxx-xxx

Literature review / Revue de la litterature

Post-stroke hemiplegia rehabilitation: Evolution of the concepts

Rééducation de l'hémiplégie vasculaire : évolution des concepts

qi P. Marque a*b, D. Gasqb, E. Castel-Lacanal a,b, X. De Boissezonab, I. Loubinoux

a Service de médecine physique et réadaptation, CHU Rangueil, 1, avenue Poulhes, 31059 Toulouse cedex 9, France Unité 825 Inserm, CHU Purpan, 1, place Baylac, 31059 Toulouse cedex 9, France

Received 6 August 2014; accepted 6 August 2014

Abstract

Stroke rehabilitation has undergone a revolution over the last three decades. Cohort studies have consistently reinforced the importance of post-stroke rehabilitation to stimulate recovery, but the concepts of empirical methods originally proposed by therapists to rehabilitate these patients have not withstood clinical analysis. Functional neuroimaging and animal models have unveiled the mechanisms underlying functional recovery and helped teams understand its limitations and improvement modalities. These neuroscience discoveries constitute the grounds needed to understand the emergence of new technologies: robotics and virtual reality. The objective of this review of the literature was to select key works in this field to better understand current therapeutic possibilities. © 2014 Published by Elsevier Masson SAS.

Keywords: Stroke; Rehabilitation; Neuroimaging; Hemiplegic; Plasticity Résumé

La readaptation des patients victimes d'AVC a connu une veritable revolution au cours des 3 dernieres decennies. Les etudes de cohortes ont toujours souligne; l'intérêt de la readaptation après un AVC pour stimuler la recuperation, mais les concepts des methodes empiriques initialement proposees par les therapeutes pour réeduquer ces patients n'ont pas résisté a l'analyse clinique critique. Parallelement, les travaux de neuroimagerie fonctionnelle et les modeles animaux ont permis tout d'abord d'objectiver les mecanismes de la récuperation fonctionnelle, puis d'en comprendre les limites ainsi que les modalités d'amtîlioration. Ces decouvertes des neurosciences sont les bases sans lesquelles on ne peut pas comprendre l'apparition des nouvelles technologies : robotique et realite virtuelle. Cette revue de la litterature se propose de faire une selection de ces travaux ctés qui permettent de mieux comprendre les propositions actuelles. © 2014 Publie par Elsevier Masson SAS.

Mots clés : AVC ; Reeducation ; Imagerie fonctionnelle ; Hemiplegique ; Plasticite

1. English version

1.1. Introduction

Recovery is a spontaneous phenomenon observed even in the absence of rehabilitation, and has been known to physicians

* Corresponding author. Service de meidecine physique et readaptation, CHU Rangueil, 1, avenue Poulhes, 31059 Toulouse cedex 9, France.

E-mail address: marque.ph@chu-toulouse.fr, philippe.marque@gmail.com (P. Marque).

http://dx.doi.org/10.1016/j.rehab.2014.08.004 1877-0657/© 2014 Published by Elsevier Masson SAS.

for a long time. In the 19th century, Broca defined vascular syndrome as the onset of a sudden focal deficit improving over time, thus enclosing in the definition of stroke itself the notion of recovery [1].

In the eighties, cohort studies validated the improvement of impairments and autonomy in the weeks following a stroke. The Copenhagen study [2,3] published in the Annals of Physical Medicine and Rehabilitation (AMPR) in the nineties is one of these studies. Because of its prospective and exhaustive nature in the relatively homogenous Danish health care system, especially in the rehabilitation field, it became a flagship study.

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This clinical study evaluated motor impairments and autonomy post-stroke, from the admission into the neurology unit up to the discharge from the PM&R center. Results from this study validated the existence of motor recovery affecting, contrarily to the notions too readily widespread later on, all categories of hemiplegic patients, including the most severe ones: 40% of patients with severe motor impairments during the acute phase end up with mild or moderate impairments after the recovery process [3].

The second relevance of this study was its valuable analysis of the recovery time course: for motor impairments, most improvements occur during the first 15 weeks, regardless of the severity of the initial motor deficit [2]. This was a very original result at a time when it was the norm to speak of recovery over the span of several years. Furthermore, this rather quick timeline suggests, by analogy with the child's development, the notion, still debated today, of critical period. Several other studies validated this motor recovery kinetic and it is now commonly used to define residual motor impairments as stable and chronic after six months post-stroke [4].

1.2. Rehabilitation improves motor recovery

In parallel, since the eighties the number of publications on the impact of rehabilitation or physiotherapy on this recovery process has continued to increase. One of the first systematic reviews of the literature on this topic was published by Ottenbacher and Jannell in 1993 [5]. Since then, several metaanalyses have been devoted to this theme [4-17]. Along the years, the conclusions of these reviews have been constant. First of all these different studies continuously backed-up the evidence of the effectiveness of rehabilitation on post-stroke motor recovery: today 467 controlled studies on this topic have been identified amounting to 25,373 patients [12]. Rehabilitation care can improve the recovery of lower limb [9,16,17] and upper limb [6,9] impairments, gait [13] and balance [16,17], as well as autonomy in activities of daily living [4,5,11,14].

For the past 30 years, various publications have reported the same factors promoting effective post-stroke rehabilitation.

Early management is a factor affecting the effectiveness of post-stroke rehabilitation [4,10,18,19]. The issue of harmful effects of exercise during the initial phase in the intensive care unit remains, even if the results of two recent clinical studies are rather reassuring [20,21]. However, beyond that first week, all studies agree that rehabilitation care should be initiated.

Rehabilitation care intensity is also a factor promoting effective stroke rehabilitation [8,9]. In this case again, the optimal dose has not been clearly determined, but 30 minutes of daily physiotherapy have been validated as more effective than 30 minutes three times a week and this duration seems to be the minimum amount recommended to observe positive effects on gait and autonomy [5,8,9]. In the framework of constraint-induced movement therapy (CIMT), the daily duration of rehabilitation therapy was sometimes increased up to six hours per day [4,6].

Finally, the medical team effect is an element frequently encountered [4,11,18]. Rehabilitation care in multidisciplinary

units specialized in neuro-rehabilitation seems more effective than the one proposed by a non-specialized or non-coordinated rehabilitation unit.

However, these studies do not highlight a stroke-specific physiotherapy technique. This was an essential result in the context of the nineties. In fact at the time, post-stroke physiotherapy was made up of different empirical techniques often identified by the names of their creator: Bobath, Brunstrom, Vojda, Kabat, Perfetti... Sixteen controlled studies have compared these different techniques especially the ones most often used at the time: Bobath and Brunstrom [5,7,17].

These comparisons might seem dated today, yet on a fundamental level they remain relatively interesting and at the time, these two techniques did seem dramatically opposed.

The first one, the Bobath method, proposes techniques based on spasticity and the inhibition of automatic reactions, and recommends avoiding any type of strength training exercises, which are suspected of increasing these spastic phenomena considered archaic and noxious for motor recovery. The second one, the Brunstrom method, uses techniques based on repetitive training of the automatic reflexes, including resistance training, which are both strictly prohibited in the Bobath method. However, no comparative study has evidenced the superiority of one of these techniques over the other [7,17].

At the same time, several studies reported conclusions that were not in favor of the concepts underlying the Bobath method. Thilmann et al. [22] highlighted that in spastic subjects, the gain in stretch reflexes was more altered than the onset threshold of stretch reflexes. The authors did not find stretch reflexes below 357s., where under that threshold difficulties were more related to the paralysis than the spasticity itself. Furthermore, additional studies showed that physical exercise, especially strength training, which is banned in the Bobath method, did not increase spasticity in a chronic manner [23,24].

In fact, physiotherapy appeared to be an effective treatment to promote motor recovery post-stroke, yet the precise modalities of an effective therapy were not properly defined in the nineties. However, at the time, it seemed quite clear that these modalities did not rely on acquiring specific, empirical techniques difficult to master for most physiotherapists.

1.3. Uncovering brain plasticity after a stroke

Brain plasticity is defined as all the mechanisms allowing the brain to adapt its own function to a new situation. The evidence of lasting clinical improvements post-stroke did in fact brought to light this type of adaptation. In the eighties already, some authors [25] after having drawn conclusions from animal studies in dissimilar contexts explained post-stroke functional recovery by mechanisms that unveiled redundant neuronal networks, alterations in synaptic effectiveness or dendritic sprouting phenomena.

The appearance of brain functional neuroimaging validated these mechanisms of motor recovery. These imaging techniques

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164 219

165 can measure the local blood flow, either by using a radiotracer as post-stroke, we can observe a lateral reorganization of these 220

166 in PET scans, or using the paramagnetic properties of activations on the contralateral side [31,32]. These activations 221

167 oxyhemoglobin in fMRI. These methods assume that in the remain significantly greater than in the control group. One year 222

168 brain this blood flow is directly correlated to neuronal activation. later, the authors did not find any differences compared to the 223

169 Since the differences in blood flow between two tasks are quite control group [31,32]. 224

170 modest, they need task repetition and a statistical analysis of the In parallel, Murase et al. in 2004 [33] reported the noxious 225

171 differences observed to evidence these differences. In fact, role of interhemispheric inhibition post-stroke. This author 226

172 results are presented as a mapping of the statistical differences showed that in the 20 milliseconds before a unilateral hand 227

173 obtained between two situations: movement and rest for movement, there was a marked reduction in interhemispheric 228

174 example. PET study of brain activation in case controls who inhibition mechanisms normally observed in healthy subjects at 229

175 recovered in a satisfactory manner from a subcortical lacunar rest [34]. This decrease is always limited and in all cases less 230

176 infarct (LACI) showed a reorganization of the somatotopic important on the hemiplegic side vs. the healthy side for stroke 231

177 arrangements of the primary motor areas for these patients when patients but also compared to a population of healthy subjects. 232

178 they performed opposite movement of the thumb and the other Murase et al. developed the concept of maladaptive brain 233

179 fingers. Chollet et al. [26] found an activation affecting both plasticity [33]. The lesion triggers a decreased interhemispheric 234

180 hemispheres when moving the paretic hand. However, Weiller inhibition from the injured hemisphere towards the healthy one. 235

181 et al. [27] did not observe in similar patients the same activation, This reduction leads to an overactivation of the ipsilateral motor 236

182 but rather a displacement of the hand-related cortical activation networks, which in turn trigger an increased inhibition of the 237

183 towards the facial motor areas. Beyond their interpretation which injured hemisphere. This imbalance mechanism affecting the 238

184 remains quite complicated, these results validate for the first time interhemispheric inhibition equilibrium might, at least initially, 239

185 the existence of brain plasticity in stroke patients. worsen the impairments and explain the activations observed by 240

186 Brain imaging has validated some mechanisms involved in Loubinoux et al. 15 days post-stroke [31,32]. Brain plasticity 241

187 these brain plasticity phenomena. Diaschisis [28] was the first could represent a negative factor in some circumstances. 242

188 of these mechanisms to be uncovered. The definition of

189 diaschisis corresponds to a depression of blood flow in certain 1.5. Brain plasticity is limited

190 areas of the brain not directly injured but functionally 243

191 connected to the necrotic area. In other words, part of the Certainly, neuroimaging studies might present several 244

192 impairment-related symptoms observed in patients with sources of bias: small cohort, over-representation of sub- 245

193 neurovascular lesions is correlated to the phenomenon of cortical lesions and moderate impairments. However, they were 246

194 deafferentation of brain areas that are not impaired but which able to propose a hierarchical ranking in the recovery process 247

195 receive projections from the injured area. Crossed cerebellar and set the limits of spontaneous brain plasticity. When the 248

196 diaschisis (CCD) was the first mechanism to be highlighted and supplementing network is anatomically and functionally close 249

197 could explain the highly ataxic nature of some types of motor to the initial injured network (redundancy) the deficit is less 250

198 impairments observed after lesions of the middle cerebral artery severe and the recovery will be better [35-41]. Conversely, 251

199 (MCA) territory. The second mechanism evidenced was the when the compensation network is located at a distance from 252

200 discovery of a pre-existing, yet inactive, network able to the initial network the impairment will be more severe and the 253

201 substitute itself to the deficient function, When this network is recovery will be partial or of poor quality [26,42-44]. In adults 254

202 located in the same functional area the term "redundant" [29] with hemiplegia, the use of a compensation network 255

203 is commonly used, when this substitution relies on networks contralateral to the lesion and thus ipsilateral to the movements 256

204 located farther away in areas normally used by other functions, of the paretic hand, translates into a poor quality recovery and 257

205 the term "vicarious" is preferably used [30]. In all cases, in the persistence of severe impairments. To model this principle, 258

206 order for all these networks to become functional, long term some authors proposed a lateralization index [45-47]. This 259

207 potentiation or long term depression (LTP) or LTD synaptic index calculates the ratio between the volumes of activated 260

208 changes are required. pixels in the motor areas contralateral to the movement and for 261

all the ipsilateral or contralateral motor areas. This index varies 262

1.4. Brain plasticity: is it always a positive phenomenon? between 0 and 1. An index score close to 1 supports proper 263

209 brain plasticity and points to a good recovery. This index is now 264

210 Nevertheless, more than a decade was necessary to used in neuroimaging studies as an intermediate criterion to 265

211 understand the real meaning of these changes. First of all, evaluate the impact of some rehabilitation or pharmacological 266

212 Loubinoux et al. [31,32] described the time course of these interventions on recovery [48,49]. 267

213 changes in patients who recovered in a satisfactory manner.

214 They showed that the interpretation of these results was not 1.6. Animal models in rehabilitation studies

215 univocal. In fact, 15 days post-stroke the increase in the 268

216 activations observed were rather evidenced on the ipsilateral It is also in the eighties that the first animal models appeared. 269

217 side of the solicited hand with a decreased cortex activation in The first of them was the enriched environment model and 270

218 the injured side. These images appeared to be quite similar to concerned the rat [50]. This model was initially used to study 271 the ones described by Chollet 10 years earlier [26]. Four months developmental brain plasticity in newborns. This model was

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adapted to post-lesions plasticity. The enriched environment is Conforto et al. [63] reported that two hours of TENS in the 328

represented by a larger cage, with a diversity of architectural median territory enabled the improvement of hand grip function 329

settings and accessories, with several animals in it. This in chronic hemiplegic patients. 330

environment stimulates the relationships between the animals The effects of passive mobilization are probably limited if 331

and implicitly offers to the rats a greater range of motor activity they are not integrated within a finalized movement and an 332

than in an individual cage. Rats placed after a vascular lesion of associative learning process. In fact, coupled stimulation 333

the MCA, in cages with an enriched environment presented, techniques associating peripheral electrical stimulation and 334

after a few weeks, a better quality motor recovery on the clinical central stimulation via TMS done in healthy [64-66] and 335

tests than rats in individual cages [50]. Furthermore, on a hemiplegic [67] patients, showed that sensory stimulations are 336

histological level, the density of dendrites per neurons was often more effective when coupled to an associative learning 337

greater in rats placed in the enriched environment underlining a conditioning training. 338

more important sprouting [50]. Afterwards, robotics and virtual reality techniques appeared 339

Similarly, a rehabilitation model was developed in monkeys. as interesting techniques since these tools can provide repeated 340

Precise and reproducible brain mapping is possible thanks to and finalized movement even in severely impaired patients. 341 cortical micro-stimulation techniques. Nudo et al. studied the

reorganization of brain topography after a vascular lesion in the 1.8. Post-lesion brain plasticity and critical period

hand territory in adult squirrel monkeys [51]. He first noted that 342

in the hours following the lesion, areas peripheral to the lesion Finally, studies conducted in rats, underline the notion of 343

appeared and responded by contractions of the wrist and critical period similar to the framework of developmental 344

fingers. These results underline a rapid plasticity, probably by plasticity. The positive effects of the enriched environments are 345

the unveiling of inactive networks. But after a few weeks, Nudo no longer perceived if the animal is placed in this type of 346

et al. observed a disappearance of these stimulation sites environment beyond week 4 post-stroke [68,69]. These results 347

answering to the wrist and fingers in favor of other areas obtained in animal models are similar to other results reported 348

answering to the elbow and shoulder [51]. Conversely, in in human subjects. The recovery timeline post-stroke described 349

monkeys where the healthy upper limb was immobilized, thus in a cohort study promotes these mechanisms [2]. A 350

making it mandatory to use the impaired limb, the number of longitudinal study of coupled stimulation in stroke patients 351

areas and the cortical surface, when stimulated, led to an with hemiplegia showed that brain plasticity capacities were 352

increased response in the hand, wrist and finger muscles greater three months after the stroke than at 1-year post-stroke 353

[52,53]. This study underlined a use-dependent plasticity as [67]. This notion of critical period does not imply the absence 354

well as competition phenomena between cortical representa- of brain plasticity on the long term, but rather that in the weeks 355

tions. Similar use-dependent cortical representation competi- following the lesion, facilitation mechanisms and brain 356

tion phenomena or dependent or sensory afferents were plasticity are predominant compared to mechanisms regulating 357

highlighted in humans: in upper-limb amputees [54] or right brain plasticity inhibition [69]. These results underline the 358

after having placed a tourniquet [55]. A catch phrase was then relevance of intensive daily rehabilitation care during the first 359

proposed as a rehabilitation motto: "use it or lose it''. few weeks post-stroke. 360

Neuroscience and clinical studies from the end of the 20th 361

1.7. Sensory stimulation, constraint-induced therapy century have completely altered the way we approach stroke 362

rehabilitation. We went from rehabilitation care based on 363

Constraint-induced therapy of the healthy upper limb is also empirical methods that were quite analytic, to rehabilitation 364

a technique that has showed its effectiveness in humans, on a care focused on tasks and repetition: use or lose the function. 365

clinical level in studies with a good methodology [56], as well The principles of stroke rehabilitation for patients with 366

as on intermediate criteria in functional neuroimaging trials hemiplegia are now quite similar to the ones for motor 367

[40] or TMS cortical mapping studies [57]. learning (Fig. 1). Q2 368

Yet constraint-therapy is a technique only concerning a

small portion of paretic patients. It is not meant for patients who Disclosure of interest

are too severely impaired or during the first stages of 369

rehabilitation training. The authors have not supplied their declaration of conflict of 370

Passive mobilization is involved in the effectiveness of interest. Q3 371 rehabilitation during the initial stages and in patients who are

completely paralyzed. In fact, PET [58] or EEG/fMRI [59] 2. Version française

neuroimaging studies showed that passive mobilization allowed 372

the activation of motor networks. Furthermore, passive 2.1. Introduction

rehabilitation training is able to durably alter brain activation 373

as evidenced by fMRI in healthy [60] and hemiplegic subjects La recuperation est un phenomene spontane qui est observe 374

[61] alike. These results are in accordance with clinical studies meme en l'absence de readaptation et qui est connu des 375

that showed the positive effect of transcutaneous electrical cliniciens depuis longtemps. Broca au 19e siecle definissait le 376

nerve stimulation (TENS) on motor recovery [62]. Finally, syndrome vasculaire comme l'apparition d'un deficit brutal,

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Fig. 1. Principles of new rehabilitation techniques post-stroke. Neuroimaging [31,32] and electrophysiology [33] studies showed an imbalance of the interhemispheric equilibrium, responsible for an overactivation of the healthy hemisphere and under-activation of the injured hemisphere. The objective of these new rehabilitation techniques is to restore the interhemispheric balance by stimulating the injured hemisphere and/or inhibiting the healthy hemisphere (CIT: constraint-induced therapy; NIBS: non-invasive brain stimulation-rTMS, tDCS). Adapted from Loubinoux et al. [31].

focal et qui s'améliore avec le temps, incluant donc dans la définition meme de l'AVC la notion de recuperation [1].

Dans les annees 1980, les etudes de cohortes ont permis de verifier cette amelioration des deficiences et de l'autonomie dans les semaines qui suivent un AVC. La cohorte de Copenhague [2,3] publiee dans les APMR dans les annees 1990 est une de ces etudes. Son caractere prospectif, exhaustif, dans un systeme de sante danois relativement homogene en particulier dans le domaine de la readaptation, en font une etude emblematique. Cette etude clinique a evalue les deficiences motrices et l'autonomie après AVC, de l'admission en unite de neurologie jusqu'a la sortie du centre de readaptation. Ses résultats confirment l'existence d'une recuperation motrice touchant, contrairement aux notions trop souvent répandues par la suite, toutes les categories de patients hemiplegiques, y compris les plus severement atteints initialement : 40 % des patients présentant un deficit moteur très severe a la phase aigue ont un deficit leger ou moyen a l'issue du processus de recuperation [3].

Le second interèt de cette etude est d'avoir etudie le decours temporel de cette recuperation : l'essentiel des progrès en termes de deficiences motrices est effectue au cours des 15 premieres semaines quelle que soit l'importance du deficit moteur initial [2]. Il s'agit la d'un résultat tout a fait original a une epoque où il etait de coutume de parler de recuperation sur des periodes de l'ordre de plusieurs annees. Par ailleurs, ce decours temporel relativement rapide suggere par analogie avec le developpement de l'enfant, la notion encore discutee de nos jours, de periode critique. Plusieurs autres etudes ont confirme cette cinetique de la recuperation motrice et il est classique maintenant de definir le deficit moteur sequellaire comme stable et chronique a partir du 6e mois [4].

2.2. La réadaptation améliore la récupération

Parallèlement, le nombre de publications concernant l'influence de la readaptation ou de la kinesitherapie sur ces processus de recuperation n'a cesse d'augmenter depuis les annees 80. Une des premieres revues systematiques sur ce sujet est publiee par Ottenbacher et Jannell en 1993 [5]. Depuis de nombreuses meta-analyses ont ete consacrées a ce sujet [4-17]. Les conclusions de ces revues restent constantes au fil du temps. Tout d'abord ces différents travaux n'ont cesse de renforcer l'evidence de l'efficacite de la reeducation sur la recuperation motrice après AVC : actuellement 467 essais contrôles peuvent etre identifies sur cette question représentant 25 373 patients [12]. La prise en charge de readaptation permet d'ameliorer la recuperation du deficit moteur du membre inférieur [9,16,17] et du membre superieur [6,9], de la marche [13] et de l'equilibre [16,17], de l'autonomie dans les activites de la vie quotidienne [4,5,11,14].

Les facteurs d'efficacité de la readaptation après AVC restent les memes de publications en publications depuis maintenant 30 ans.

La précocité de la prise en charge en readaptation est un facteur de l'efficacite de la readaptation [4,10,18,19]. Il existe certes des interrogations sur le caractere deletére de l'exercice au decours de la phase initiale en soins intensifs, meme si les résultats de deux essais récents sont plutot rassurants [20,21]. Mais au-dela de cette premiere semaine, toutes les etudes montrent que la readaptation doit etre debutée.

L'intensite de la prise en charge est aussi un facteur essentiel de l'efficacite de la readaptation [8,9]. Ici encore la dose optimale n'est pas clairement determine, mais 30 min de kinesitherapie quotidienne sont plus efficaces que 30 min trois

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440 495

441 fois par semaine et semblent être le minimum recommandé fonctionnement à une situation nouvelle. La mise en évidence 496

442 pour observer une efficacite de la prise en charge sur la marche d'une amelioration clinique durable après une lesion cerébrale 497

443 et l'autonomie [5,8,9]. Dans le cadre des protocoles de therapie vasculaire est en soit deja la mise en evidence de ce type 498

444 contrainte, la duree quotidienne de readaptation a pu etre portee d'adaptation. Deja dans les annees 1980, par deduction des 499

445 jusqu'a 6 h par jour [4,6]. résultats d'etudes réalisees chez l'animal dans des contextes 500

446 Enfin l'effet equipe est un element régulierement retrouve pourtant souvent eloignes, certains auteurs [25] proposaient 501

447 [4,11,18]. La prise en charge dans des unites pluridisciplinaires, pour expliquer la récuperation fonctionnelle après lesion 502

448 specialisees en neurorèadaptation semble plus efficace que cerébrale chez l'adulte, des mecanismes de demasquage de 503

449 celle propose par une unite de readaptation non specialisee ou reseaux neuronaux redondants, des modifications d'efficacite 504

450 non coordonnee. synaptiques ou des phenomenes de bourgeonnements den- 505

451 Par contre, ces etudes ne permettent pas d'identifier une dritiques. 506

452 technique de kinesitherapie specifique a l'hemiplegique L'arrivee de l'imagerie fonctionnelle cerébrale a permis 507

453 vasculaire. Il s'agit d'un résultat essentiel dans le contexte d'objectiver ces mecanismes de la récuperation de la motricite. 508

454 des annees 1990. En effet, la kinesitherapie après AVC a cette Ces techniques d'imagerie permettent de mesurer le debit 509

455 epoque est constituee de differentes techniques empiriques le sanguin cerébral local soit par l'utilisation d'un radio-isotope 510

456 plus souvent identifiees par le nom de leur créateur : Bobath, dans le cas du TEP, soit par l'utilisation des proprietes 511

457 Brunstrom, Vojda, Kabat, Perfetti... 16 essais contrôles ont paramagnetique de l'oxyhemoglobine dans l'IRMf. Ces 512

458 compare ces differentes techniques et plus particulierement les methodes font l'hypothese qu'au niveau cerébral ce debit 513

459 deux plus utilises acetteepoque : Bobath et Brunstrom [5,7,17]. sanguin est lineairement corréle a l'activation neuronale. Les 514

460 Si ces comparaisons peuvent apparaître desuetes aujourd'- differences de debit entre deux taches etant modestes, elles 515

461 hui, elles restent sur le plan fondamental, relativement necessitent pour etre mises en evidence la répetition des taches 516

462 interessantes. En effet sous leurs formes de l'epoque, ces deux et une analyse statistiques des differences observees. Les 517

463 techniques peuvent apparaître comme radicalement opposees. résultats sont donc présentes sous forme de cartographie des 518

464 L'une, la methode Bobath, propose des techniques d'inhibition differences statistiques obtenues entre deux situations : 519

465 de la spasticite et des reactions automatiques, elle recommande mouvement et repos par exemple. L'étude en TEP de 520

466 d'eviter tout exercice en force suspect d'augmenter ces l'activation cerébrale réalisee chez des cas temoins ayant bien 521

467 phenomenes spastiques considerés comme archaïques et récuperé d'un AVC lacunaire sous-cortical montre qu'il existe 522

468 peéjoratifs pour la reécupeération. L'autre, la meéthode Brunstrom, une reéorganisation de la somatotopie des aires motrices 523

469 utilise des techniques de renforcement des reactions réflexes primaires chez ces patients lors de la réalisation de mouvements 524

470 automatiques, y compris contre résistance, qui sont rigoureu- d'opposition du pouce et des autres doigts. Chollet et al. [26] 525

471 sement prohibees par la methode Bobath. Pourtant aucun essai retrouvent une activation interessant les deux hemispheres, lors 526

472 comparatif n'a permis de mettre en evidence de superiorite d'un mouvement de la main parétique. De son cote, Weiller 527

473 d'une de ses techniques sur l'autre [7,17]. et al. [27] observent chez un patient similaire, non pas une 528

474 Parallelement plusieurs travaux ont propose des conclusions activation bilaterale, mais un deplacement de l'activation 529

475 qui n'etaient pas favorables aux concepts sous-tendant la corticale correspondant a la main, vers les aires de la face. Au- 530

476 methode Bobath. Thilmann et al. [22] montrent que le gain du dela de leur interprétation qui reste complique, ces résultats 531

477 réflexe d'etirement est plus modifie que le seuil d'apparition du objectivent pour la premiere fois l'existence d'une plasticite 532

478 réflexe chez le sujet spastique. Il ne retrouve pas de réflexe cerébrale après lesion cerébrale chez l'adulte. 533

479 d'etirement en dessous de 357s. En dessous de ces vitesses les L'imagerie cerébrale a permis aussi de valider certains 534

480 difficultes sont donc plus en rapport avec la paralysie qu'avec la mecanismes mis en jeu au cours de ces phenomenes de 535

481 spasticite. De meme, d'autres travaux ont montre que l'exercice plasticite cerébrale. Le diaschisis [28] fut le premier de ces 536

482 physique et en particulier, le renforcement musculaire qui etait mecanismes. Le diaschisis correspond a la baisse de debit 537

483 penalise dans la methode Bobath, n'augmentait pas de facon sanguin cerébral dans certaines zones cerébrales non lesees 538

484 chronique la spasticiteé [23,24]. mais relieées fonctionnellement avec la zone neécroseée. En 539

485 La kinesitherapie apparaît donc comme un traitement d'autre terme, une partie des symptômes deficitaires observes 540

486 efficace pour favoriser la récuperation motrice après AVC, chez les patients victimes de lesions neurovasculaires est en 541

487 mais les modalites précises de cette efficacite restent encore a relation avec un phenomene de deafferentation d'aires 542

488 definir dans les annees 1990. Il semble pourtant deja clair que cerébrales non lesees mais recevant des projections issues de 543

489 celles-ci ne passent pas par l'acquisition de techniques la zone lesee. Le diaschisis cerébelleux fut un de premiers a etre 544

490 specifiques, empiriques difficiles a maîtriser pour la plupart mis en evidence et pourrait expliquer le caractere très ataxique 545

491 des kinesitherapeutes. de certaines formes de deficits moteurs observes après lesion du 546

territoire de l'ACM. 547

492 2.3. Mise en évidence de la plasticité cérébrale après Le demasquage d'un reseau préexistant mais quiescent 548 lésion vasculaire capable de suppleer la fonction deficitaire fut le second 549

493 mecanisme mis evidence. Lorsque ce reseau ce situe dans le 550

494 La plasticite cerébrale est definie comme l'ensemble meme territoire fonctionnel le terme de redondance [29] est 551 des mecanismes qui permettent au cerveau d'adapter son habituellement utilise, lorsque cette suppleance fait appel a des

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réseaux plus lointains situés dans des territoires initialement utilisés par d'autres fonctions, le terme de vicariance est préféré [30]. Dans tous les cas, pour que ces réseaux deviennent fonctionnels des modifications de l'efficacité synaptique de type LTP ou LTD sont necessaires.

2.4. La plasticité cérébrale : un phénomene toujours positif ?

Neanmoins, il a fallu plus d'une decennie pour comprendre le sens exact de ces modifications. Tout d'abord, Loubinoux et al. [31,32] ont decrit le decours temporel de ces changements chez des patients ayant bien recupere. Elle montre que l'interprétation de ses résultats n'est pas univoque. En effet 15 j après l'AVC l'augmentation des activations observees sont plutôt ipsilaterales a la main mobilisee avec une diminution d'activation dans le cortex du cote lese. Ces images apparaissaient en definitive relativement proches de celle observee par Chollet 10 ans plus tot [26]. Quatre mois après l'AVC on assiste a une relatéralisation des activations du coté contralateral [31,32]. Ces activations restent significativement plus importantes que dans la population témoin. Un an plus tard ces auteurs ne retrouvent plus de differences avec le groupe de témoin [31,32].

Parallelement Murase et al. en 2004 [33] mettaient en evidence le role deletère de l'inhibition interhemispherique après lesion cerebrale. En effet cet auteur a montre qu'il existe dans les 20 ms qui precedent un mouvement unilateral de la main, une levee des mecanismes d'inhibition interhemispherique normalement observee chez le sujet sain au repos [34]. Cette diminution est toujours limitée et dans tous les cas beaucoup moins importante du cote hemiptégique aussi bien par comparaison au cote sain qu'a une population de sujet sain. Murase et al. developpent le concept de plasticité cerebrale inadaptée [33]. La lesion declenche une diminution de l'inhibition interhemispherique de l'hemisphere lese vers le sain. Cette diminution conduit a une hyperactivation des réseaux moteurs ipsilatéraux qui en retour vont augmenter l'inhibition de l'hemisphere lese. Ce mecanisme de desequilibre de la balance inhibitrice interhemispherique, pourrait au moins initialement, majorer le deficit et expliquer les activations observees par Loubinoux et al. 15 jours après l'AVC [31,32]. La plasticité cerebrale pouvait etre un facteur negatif dans certaine circonstance.

2.5. La plasticitéé cerebrale est limitee

Les etudes de neuroimageries présentent certainement plusieurs sources de biais : petite population, sur-représentation des lesions sous-corticales et des deficits moderes. Elles ont permis pourtant de proposer une htérarchie dans les processus de recuperation et de fixer les limites de la plasticité cerebrale spontanee. Plus le réseau de supptéance est proche anatomi-quement et fonctionnellement du réseau initial lese (redondance) plus le deficit est leger et meilleure sera la recuperation [35-41]. A l'oppose plus le réseau de compensation se situe a distance du réseau initial plus le deficit sera lourd et la

récupération partielle ou de mauvaise qualité [26,42-44]. L'utilisation d'un reseau de compensation controlatéral a la lesion et donc ipsilatéral aux mouvements la main lese se traduit chez l'adulte hemiptégique, par une récuperation de mauvaise qualité et par la persistance d'un deficit important. Pour modeliser ce principe, un indice de latéralisation a ete propose par certains auteurs [45-47]. Cet indice fait le ratio entre les volumes de pixels actives dans les aires motrices controlatérales au mouvement et dans l'ensemble des aires motrices ipsi- ou controlatérales. Cet indice varie entre 0 et 1. Un indice proche de 1 signe une plasticité cerebrale favorable et est en faveur d'une bonne récuperation. Cet indice est maintenant utilise dans les etudes en neuroimagerie comme critère intermediaire pour evaluer l'influence sur la récuperation de certaines interventions reeducatives ou medicamenteuses [48,49].

2.6. Les modèles animaux de rééducation

C'est dans les annees 1980 que sont aussi apparus les modeles animaux. Le premier de ces modeles est celui de l'environnement enrichi et concerne le rat [50]. Il s'agit d'un modele initialement utilise pour etudier la plasticité develop-pementale chez le nouveau-ne. Ce modele a ete adapte a la plasticité postlesionnelle. Le milieu enrichi est représenté par une cage de taille plus importante, avec une diversité architecturale et d'accessoire, où plusieurs individus sont présents. Il s'agit donc d'un environnement qui stimule les relations inter-individus et qui implicitement impose aux individus une activité motrice plus importante que dans une cage individuelle. Les rats places après une lesion cerebrale vasculaire de l'artère cerebrale moyenne, dans des cages avec environnement enrichi présentaient au bout de quelques semaines, une récuperation motrice de meilleure qualité sur les epreuves cliniques que ceux places dans des cages individuelles [50]. De plus sur le plan histologique la densité de dendrites par neurones etait plus grande pour les rats places en milieu enrichis témoignant d'un bourgeonnement synaptique plus important [50].

De meme un modele de réeducation a ete developpe chez le singe. Les techniques de microstimulations corticales permettent de réaliser des cartographies cerebrales précises et reproductibles. Nudo et al. ont etudie la reorganisation de ses cartographies après la réalisation d'une lesion vasculaire dans le territoire de la main chez des singes macaques [51]. Il note tout d'abord que dans les heures qui suivent la lesion, des sites situes en peripherie de la lesion repondant par des contractions du poignet et des doigts, apparaissent. Ces résultats témoignent d'une plasticité rapide, probablement par demasquage de reseaux redondants quiescents. Mais Nudo et al. observent au bout de quelques semaines une disparition de ces sites de stimulation repondant pour le poignet et les doigts, au profit de sites repondant pour le coude et ltépaule [51]. A l'opposer, les singes chez lesquels on immobilise le membre superieur sain, contraignant ainsi l'usage du membre deficitaire, voient le nombre de sites et la surface corticale dont la stimulation entraîne une réponse au niveau des muscles de la main, du poignet et des doigts, augmenter [52,53]. Cette etude met en

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661 évidence une plasticité dépendante de l'usage ainsi que des

662 phenomenes de competition entre les representations cortica-

663 les. Des phenomenes similaires de competitions des repré-

664 sentations corticales, dependantes de l'usage ou des afferences

665 sensitives ont ete mis en evidence chez l'homme : chez

666 l'ampute du membre superieur [54] ou dans les minutes qui

667 suivent la mise en place d'un garrot [55]. Un veritable slogan est

668 alors propose comme base de la reeducation : « utilises le

669 ou perds le ».

670 2.7. Stimulations sensitives, thérapie induite par la contrainte

672 La therapie induite par la contrainte du membre superieur

673 sain est une technique qui a aussi demontré son efficacite

674 l'homme aussi bien sur le plan clinique dans des etudes avec

675 une methodologie de bon niveau [56], que sur des criteres

676 intermediates dans des essais de neuroimagerie fonctionnelle

677 [40] ou des cartographies corticales réalisees par TMS [57].

678 Mais la therapie contrainte est une technique qui s'adresse a

679 une petite fraction des malades paretiques. Elle reste

680 inapplicable chez les patients trop deficitaires ou pendant les

681 premieres etapes de la réadaptation.

682 La mobilisation passive participe de l'efficacite de la

683 réadaptation au cours des premieres etapes et chez les patients

684 totalement plegiques. En effet, les travaux de neuroimagerie en

685 TEP [58] ou EEG/IRMf [59] ont montre que la mobilisation

686 passive permettait d'activer les réseaux moteurs. De meme la

687 realisation d'un entraînement passif est capable de modifier

688 durablement l'activation cerébrale en IRMf chez le sujet sain

689 [60] comme chez le sujet hemiplegique [61]. Ces résultats sont

690 concordants avec des etudes cliniques qui montraient l'effet

691 favorable des TENS sur la recuperation motrice [62]. Enfin

P. Marque et al./Annals of Physical and Rehabilitation Medicine xxx (2014) xxx-xxx

Conforto et al. [63] ont montreé que la reéalisation de 2 h de 692

TENS dans le territoire du median permettait d'ameliorer le 693

hand grip de patient hemiplegique chronique. 694

Les effets des mobilisations passives sont probablement 695

limites s'ils ne s'integrent pas dans un mouvement finalise et 696

dans une forme d'apprentissage de type associatif. En effet les 697

techniques de stimulations coupleées associant une stimulation 698

electrique peripherique et une stimulation centrale par TMS et 699

qui ont ete réalisees chez le sujet sain [64-66] et l'hemiplegique 700

[67], montrent que les stimulations sensitives sont plus 701

efficaces lorsqu'elles s'integrent dans une forme de condi- 702

tionnement associatif de ce type. 703

C'est dans ce sens que les techniques de robotiques et de 704

reéaliteé virtuelle sont apparues comme des techniques inteér- 705

essantes car ce sont des outils qui permettent de repondre a ces 706

objectifs de mouvements reépeéteés et finaliseés y compris chez des 707

malades très deficitaires. 708

2.8. Plasticité cérébrale postlésionnelle et période critique

Enfin les eétudes reéaliseées chez le rat font eémerger la notion 710

de peériode critique comme dans le cadre de la plasticiteé 711

deéveloppementale. Les effets positifs de l'environnement 712

enrichi ne sont plus perçus si l'animal est place dans ce type 713

d'environnement au-dela de la 4e semaine après l'ictus [68,69]. 714

Ces reésultats obtenus chez l'animal sont concordants avec 715

d'autres résultats obtenus chez l'homme. Le decours temporel 716

de la récuperation après AVC decrit par les etudes de cohortes 717

est en faveur de ce type de mecanismes [2]. L'étude 718

longitudinale des stimulations coupleées chez l'heémipleégique 719

montre des capacites de plasticite beaucoup plus importante a 720

trois mois qu'a un an après l'AVC [67]. Cette notion de periode 721

critique ne signifie pas qu'il n'y a plus de plasticite cerébrale a 722

Fig. 1. Principes des nouvelles techniques de rêêducation apres AVC. Les travaux de nêuroimagêriê [31,32] et d'êlêctrophysiologiê [33] ont montre qu'il existait un dêsêquilibrê de la balance intêrhêmisphêriquê, responsable d'une hyperc^^at^ de l'hêmisphêrê sain et d'une hypoactivation de l'hêmisphêrê lese. L'objectif des nouvelles techniques de réadaptation est de restaurer cette balance intêrhêmisphêriquê en stimulant l'hêmipshêrê lese et/ou en inhibant l'hêmisphêrê sain. (CIT : therapie induite par la contrainte ; NIBS : stimulations cêrêbralês non invasivês-rTMS, tDCS). Adapté de Loubinoux et al. [31].

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P. Marque et al./Annals of Physical and Rehabilitation Medicine xxx (2014) xxx-xxx

long terme, mais que dans les semaines qui suivent une lésion les mecanismes de facilitation de la plasticite cerebrale est predominante sur les mecanismes régulateurs d'inhibition de la plasticite cerebrale [69]. Ces résultats soulignent l'intérêt d'une prise en charge quotidienne intensive durant les premieres semaines.

Les travaux de neurosciences et des etudes cliniques de la fin du 20e siecle modifient totalement l'approche de la readaptation après un AVC. Nous sommes passes d'une prise en charge basee sur des methodes empiriques globales relativement analytiques a une readaptation orientée vers la tache et la répetition : utiliser ou perdre la fonction. Les principes de la readaptation de l'hemiplegique vasculaire se rapprochent maintenant beaucoup plus de celles de l'apprentissage moteur (Fig. 1).

Déclaration d'intérêts

Les auteurs n'ont pas transmis de declaration de conflits d'intérêts.

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