Donate Help Contact The AHA Sign In Home
American Heart Association
Stroke
Search: search_blue_button Advanced Search
« Previous Article | Table of Contents | Next Article »
Stroke. 2006;37:314-316
Published online before print January 12, 2006, doi: 10.1161/01.STR.0000200454.98176.04
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
37/2/314    most recent
01.STR.0000200454.98176.04v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Heiss, W.-D.
Right arrow Articles by Teasel, R. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Heiss, W.-D.
Right arrow Articles by Teasel, R. W.
Right arrowPubmed/NCBI databases
Medline Plus Health Information
*Stroke
Related Collections
Right arrow Exercise/exercise testing/rehabilitation

(Stroke. 2006;37:314.)
© 2006 American Heart Association, Inc.

Advances in Stroke 2005

Brain Recovery and Rehabilitation

Wolf-Dieter Heiss, MD Robert W. Teasel

From the Max-Planck-Institut für Neurologische Forschung and Department of Neurology der Universitat zu Köln (W.-D.H.), and the University of Western Ontario and St Joseph’s Health Care, London (R.T.)

Correspondence to Wolf-Dieter Heiss, der Universitat zu Köln Joseph-Stelzmann-Str. 9, D-50931 Köln, Germany. E-mail wdh{at}nf.mpg.de


Key Words: brain recovery • rehabilitation

Rehabilitation after a stroke is undergoing a renaissance of sorts, with growing evidence of rehabilitation’s impact extending from cortical reorganization to its effect on health-related quality of life.

Functional Neuroimaging

Functional recovery after focal brain lesions is dependent on the adaptive plasticity of the cerebral cortex and of the nonaffected elements of the functional network.1 For the motor system, it has been convincingly demonstrated that after cortical injury the adjacent spared cortical tissue as well as more remote cortical areas are altered resulting in a functionally modified network.2–4 Small lesions in the somatosensory cortex lead to changes of excitability attributable to down-regulation of GABAA-receptors and up-regulation of NMDA-receptors5 in remote brain areas, and these changes in both excitatory and inhibitory neurotransmission may be part of an adaptive process involved in functional reorganization.6 As a consequence, newly learned movements after focal cortical injury are represented over larger cortical territories,3,4,7,8 an effect which is dependent on the intensity of rehabilitative training.9 Along with these changes in excitatory and inhibitory neurotransmitter systems, widespread structural changes with dendritic sprouting and synapse formation take place in spared regions of the damaged hemisphere, but also in the sensorimotor cortex of the hemisphere contralateral to the injury.10,11 One could speculate that the change in excitability in adjacent and contralateral homotopic regions of a cortical lesion is a consequence of reduced collateral and transcallosal inhibition.

It was also convincingly demonstrated that specialized areas inhibit neighboring regions and (even contralateral) brain regions connected by fiber pathways.12–18 Recent repetitive transcranial magnetic stimulation (rTMS) studies gave evidence that unilateral stroke lesions indeed reduce transcallosal inhibition19 and that the unaffected hemisphere actually inhibits the generation of a voluntary movement by the paretic hand.20,21

Increases in relative cerebral blood volume in contralateral regions during speech in aphasia patients22 indicated overactivation of right language homologues, which may represent a maladaptive strategy. This "paradoxical functional facilitation"23 can be interpreted as a result of decreased transcallosal inhibition attributable to damage of the specialized and lateralized speech areas. As a consequence, suppression of the (paradoxical) activation in these right hemispheric language homologue areas by slow rTMS improved naming in chronic, nonfluent aphasia patient.24

Changes in the interaction within the functional network of language are important for the recovery from aphasia after stroke. In particular, studies of changes in the activation patterns during speech tasks have demonstrated that patients with favorable recovery predominantly activate structures in the ipsilateral hemisphere,25–28 but some activation was also seen in the right hemisphere. Despite such responses in the right superior temporal gyrus29,30 and in the inferior frontal gyrus,31 efficient restoration of language is usually achieved only if left temporal areas are preserved and can be reintegrated into the functional network.32 It was also suggested33 that the increased activation within the right hemisphere may be a marker of failed or faulty recovery attempts in the sense of maladaptive plasticity or the breakdown of normal interhemispheric control within the distributed neural network.

The role of activation in the right hemisphere for residual language performance can be investigated by combining rTMS with functional imaging (eg, positron emission tomography).34 Such an approach was used in 11 patients with aphasia 2 weeks after left sided middle cerebral artery infarction.35 rTMS stimulation sites were selected according to maximum flow activation within left and right inferior frontal gyrus (IFG). Of these patients 3 activated the left and 8 activated the bilateral IFG. rTMS resulted in increased reaction time latency or error rate in the semantic task in 5 patients with right IFG activation, indicating essential language function. In a verbal fluency task, these patients had a lower performance than patients with effects of rTMS only over the left IFG, suggesting a less effective compensatory potential of right sided network areas.

The concept of the different efficacy of intra- and interhemispheric compensation, attributable to collateral and transcallosal disinhibition, may be even taken 1 step further: stimulation of the motor cortex improves ipsilateral finger movements and performance in Purdue Pegboard test by functional facilitation of the unstimulated counterpart cortex because of suppression of transcallosal inhibition.36,37 This result suggests an interhemispheric rivalry and explains an abnormally high inhibitory drive from the motor area of the intact hemisphere to that of the lesioned side.20 The blockade of the contralateral intact area by rTMS, therefore, can be used to modulate these inhibitory interactions, to influence motor disability, to improve attention to ipsilateral targets and to reduce hemispatial neglect.38–41 In a preliminary study in patients with nonfluent aphasia 5 to 11 years after left hemisphere-stroke, Naeser et al40 observed significant and persistent improvement in naming pictures after rTMS application to the pars triangularis of the right inferior frontal gyrus (homologue to Broca’s area). The authors postulated that rTMS decreased excitation in right BA 45, which in turn modulated activity in the distributed, bihemispheric language network. This result suggests the paradoxic effect of contralateral facilitation attributable to transcallosal disinhibition and supports the inferior capability of interhemispheric compensation for language recovery. The clinical and long-term efficacy of this novel complementary treatment for aphasia, however, must be proven in larger clinical trials.

Clinical Rehabilitation Strategies

Despite the excitement generated by early thrombolysis in acute stroke care, the greatest advancement in stroke care continues to be the stroke unit. Although stroke units are often thought to represent organized specialized stroke care, there is now overwhelming evidence of the effectiveness of interdisciplinary stroke rehabilitation units, but less clear evidence of effectiveness of organized stroke care during the acute phase. Gilligan et al,42 based on the community-based NorthEast Melbourne Stroke Incidence Study, estimated that if different treatment strategies available for stroke patients were maximized, stroke units would reduce death and dependency of 46 of every 1000 stroke patients, a number over 4-fold greater than that of tissue plasminogen activator (assuming 10% of all stroke patients receive tissue plasminogen activator).

Although it is well recognized that stroke patients who receive organized in-patient stroke unit care are more likely to survive, be discharged to home, and achieve independence again, there remains uncertainty as to what elements of the "stroke units" are contributing to this improvement. The Stroke Units Trialists Collaboration43 in a systematic review of 29 clinical trials used a direct and indirect comparative analysis against conventional care on a general ward, using death and dependency as the critical outcomes. They found that acute-subacute combined stroke units, subacute rehabilitation units, and mixed rehabilitation units all resulted in significant reductions in death and dependency, while results were trending toward a benefit in the acute semi-intensive stroke units. Clinical outcomes appear to be better in stroke units because of greater adherence to processes of care.44,45 Moreover, it is becoming increasingly apparent that it is the interdisciplinary stroke rehabilitation therapeutic environment that appears to account for much of the success of "stroke units". The success of stroke units appears to be more a consequence of stroke rehabilitation therapies than acute intensive medical monitoring although more research is needed.

Comprehensive stroke rehabilitation units are expensive, but mobile stroke teams do not confer the same benefit46 and have no major impact on death, dependency, or the need for institutional care when compared with care in general wards47 Along these lines, Kalra et al48 compared the outcomes between stroke patients managed on a stroke unit, on general wards with stroke team support, or at home by a specialist homecare team. Stroke units were discovered to be more effective than a specialist stroke team or specialist homecare in reducing mortality, institutionalization, and dependence following stroke. Stroke unit care was a more cost-effective intervention than either stroke team or stroke homecare. Meta-analysis of research on early supported discharge shows benefits for coordinated multidisciplinary early supportive discharge teams in stroke patients with only mild to moderate disability.49

One concept which is becoming increasingly recognized is that not only is the brain capable of reorganization poststroke as we have stated earlier but that the brain is primed to recover early after a stroke and that delays in rehabilitation will reduce the opportunity for maximal neurological recovery.50 Hence, the statement "time is brain recovery" appears to hold true for rehabilitation. There is also a greater appreciation from the animal data of the benefits of keeping stroke patients active in a stimulating environment, which presents a real challenge where rehabilitation resources are limited. Moreover, Yagura et al51 were able to demonstrate that patients with severe strokes, where cortical reorganization is less of an issue, nevertheless appear to benefit the most with an interdisciplinary team approach in that a greater number of them are able to return home at the time of discharge, pointing out the importance of discharge planning to the success of stroke rehabilitation units for severe strokes. Finally, Paul et al52 found 20% of first-ever strokes assessed 5 years poststroke onset were found to be suffering from a very low health-related quality of life. Having established the efficacy of stroke rehabilitation in improving poststroke survival, functional outcomes, and improved discharge destination, future emphasis in stroke rehabilitation will be on improving health-related quality of life.

Received December 2, 2005; accepted December 8, 2005.

References

  1. Ward NS. Plasticity and the functional reorganization of the human brain. Int J Psychophysiol. 2005; 58: 158–161.[CrossRef][Medline] [Order article via Infotrieve]
  2. Nudo RJ. Recovery after damage to motor cortical areas. Curr Opin Neurobiol. 1999; 9: 740–747.[CrossRef][Medline] [Order article via Infotrieve]
  3. Jang SH, Ahn SH, Yang DS, Lee DK, Kim DK, Son SM. Cortical reorganization of hand motor function to primary sensory cortex in hemiparetic patients with a primary motor cortex infarct. Arch Phys Med Rehabil. 2005; 86: 1706–1708.[CrossRef][Medline] [Order article via Infotrieve]
  4. Carey LM, Abbott DF, Egan GF, Bernhardt J, Donnan GA. Motor impairment and recovery in the upper limb after stroke: behavioral and neuroanatomical correlates. Stroke. 2005; 36: 625–629.[Abstract/Free Full Text]
  5. Qü M, Mittmann T, Luhmann HJ, Schleicher A, Zilles K. Long-term changes of ionotropic glutamate and GABA receptors after unilateral permanent focal cerebral ischemia in the mouse brain. Neuroscience. 1998; 85: 29–43.[CrossRef][Medline] [Order article via Infotrieve]
  6. Witte OW, Buchkremer-Ratzmann I, Schiene K, Neumann-Haefelin T, Hagemann G, Kraemer M, Zilles K, Freund HJ. Lesion-induced network plasticity in remote brain areas. Trends Neurosci. 1997; 20: 348–349.[Medline] [Order article via Infotrieve]
  7. Nudo RJ, Milliken GW. Reorganization of movement representations in primary motor cortex following focal ischemic infarcts in adult squirrel monkeys. J Neurophysiol. 1996; 75: 2144–2149.[Abstract/Free Full Text]
  8. Fridman EA, Hanakawa T, Chung M, Hummel F, Leiguarda RC, Cohen LG. Reorganization of the human ipsilesional premotor cortex after stroke. Brain. 2004; 127: 747–758.[Abstract/Free Full Text]
  9. Nudo RJ, Wise BM, SiFuentes F, Milliken GW. Neural substrates for the effects of rehabilitative training on motor recovery after ischemic infarct. Science. 1996; 272: 1791–1794.[Abstract]
  10. Kozlowski DA, Schallert T. Relationship between dendritic pruning and behavioral recovery following sensorimotor cortex lesions. Behav Brain Res. 1998; 97: 89–98.[CrossRef][Medline] [Order article via Infotrieve]
  11. Stroemer RP, Kent TA, Hulsebosch CE. Neocortical neural sprouting, synaptogenesis, and behavioral recovery after neocortical infarction in rats. Stroke. 1995; 26: 2135–2144.[Abstract/Free Full Text]
  12. Ferbert A, Priori A, Rothwell JC, Day BL, Colebatch JG, Marsden CD. Interhemispheric inhibition of the human motor cortex. J Physiol. 1992; 453: 525–546.[Abstract/Free Full Text]
  13. Innocenti GM. Some new trends in the study of the corpus callosum. Behav Brain Res. 1994; 64: 1–8.[CrossRef][Medline] [Order article via Infotrieve]
  14. Netz J, Ziemann U, Homberg V. Hemispheric asymmetry of transcallosal inhibition in man. Exp Brain Res. 1995; 104: 527–533.[Medline] [Order article via Infotrieve]
  15. Chen R, Yung D, Li JY. Organization of ipsilateral excitatory and inhibitory pathways in the human motor cortex. J Neurophysiol. 2003; 89: 1256–1264.[Abstract/Free Full Text]
  16. Gilio F, Rizzo V, Siebner HR, Rothwell JC. Effects on the right motor hand area excibility produced by low-frequency rTMS over the contralateral homologous cortex. J Physiol. 2003; 551: 563–573.[Abstract/Free Full Text]
  17. Lang N, Nitsche MA, Paulus W, Rothwell JC, Lemon RN. Effects of transcranial direct current stimulation over the human motor cortex on corticospinal and transcallosal excitability. Exp Brain Res. 2004; 156: 439–443.[CrossRef][Medline] [Order article via Infotrieve]
  18. Trompetto C, Bove M, Marinelli L, Avanzino L, Buccolieri A, Abbruzzese G. Suppression of the transcallosal motor output: a transcranial magnetic stimulation study in healthy subjects. Exp Brain Res. 2004; 158: 133–140.[Medline] [Order article via Infotrieve]
  19. Shimizu T, Hosaki A, Hino T, Sato M, Komori T, Hirai S, Rossini PM. Motor cortical disinhibition in the unaffected hemisphere after unilateral cortical stroke. Brain. 2002; 125: 1896–1907.[Abstract/Free Full Text]
  20. Murase N, Duque J, Mazzocchio R, Cohen LG. Influence of interhemispheric interactions on motor function in chronic stroke. Ann Neurol. 2004; 55: 400–409.[CrossRef][Medline] [Order article via Infotrieve]
  21. Duque J, Hummel F, Celnik P, Murase N, Mazzocchio R, Cohen LG. Transcallosal inhibition in chronic subcortical stroke. Neuroimage. 2005; 28: 940–946.[CrossRef][Medline] [Order article via Infotrieve]
  22. Naeser MA, Martin PI, Baker EH, Hodge SM, Sczerzenie SE, Nicholas M, Palumbo CL, Goodglass H, Wingfield A, Samaraweera R, Harris G, Baird A, Renshaw P, Yurgelun-Todd D. Overt propositional speech in chronic nonfluent aphasia studied with the dynamic susceptibility contrast fMRI method. Neuroimage. 2004; 22: 29–41.[CrossRef][Medline] [Order article via Infotrieve]
  23. Kapur N. Paradoxical functional facilitation in brain-behaviour research. A critical review. Brain. 1996; 119 (Pt 5): 1775–1790.[Abstract/Free Full Text]
  24. Martin PI, Naeser MA, Theoret H, Tormos JM, Nicholas M, Kurland J, Fregni F, Seekins H, Doron K, Pascual-Leone A. Transcranial magnetic stimulation as a complementary treatment for aphasia. Semin Speech Lang. 2004; 25: 181–191.[CrossRef][Medline] [Order article via Infotrieve]
  25. Warburton E, Price CJ, Swinburn K, Wise RJS. Mechanisms of recovery from aphasia: evidence from positron emission tomography studies. J Neurol Neurosurg Psychiatry. 1999; 66: 155–161.[Abstract/Free Full Text]
  26. Miura K, Nakamura Y, Miura F, Yamada I, Takahashi M, Yoshikawa A, Mizobata T. Functional magnetic resonance imaging to word generation task in a patient with Broca’s aphasia. J Neurol. 1999; 246: 939–942.[CrossRef][Medline] [Order article via Infotrieve]
  27. Heiss W-D, Kessler J, Karbe H, Fink GR, Pawlik G. Cerebral glucose metabolism as a predictor of recovery from aphasia in ischemic stroke. Arch Neurol. 1993; 50: 958–964.[Abstract]
  28. Price CJ, Crinion J. The latest on functional imaging studies of aphasic stroke. Curr Opin Neurol. 2005; 18: 429–434.[Medline] [Order article via Infotrieve]
  29. Weiller C, Isensee C, Rijntjes M, Huber W, Müller S, Bier D, Dutschka K, Woods RP, Noth J, Diener HC. Recovery from Wernicke’s aphasia: a positron emission tomographic study. Ann Neurol. 1995; 37: 723–732.[CrossRef][Medline] [Order article via Infotrieve]
  30. Musso M, Weiller C, Kiebel S, Müller SP, Bülau P, Rijntjes M. Training-induced brain plasticity in aphasia. Brain. 1999; 122 (Pt 9): 1781–1790.[Abstract/Free Full Text]
  31. Ohyama M, Senda M, Kitamura S, Ishii K, Mishina M, Terashi A. Role of the nondominant hemisphere and undamaged area during word repetition in poststroke aphasics—a PET activation study. Stroke. 1996; 27: 897–903.[Abstract/Free Full Text]
  32. Gainotti G. The riddle of the right hemisphere’s contribution to the recovery of language. Eur J Disord Commun. 1993; 28: 227–246.[Medline] [Order article via Infotrieve]
  33. Belin P, van Eeckhout P, Zilbovicius M, Remy P, Francois C, Guillaume S, Chain F, Rancurel G, Samson Y. Recovery from nonfluent aphasia after melodic intonation therapy: a PET study. Neurology. 1996; 47: 1504–1511.[Abstract/Free Full Text]
  34. Siebner HR, Takano B, Peinemann A, Schwaiger M, Conrad B, Drzezga A. Continuous transcranial magnetic stimulation during positron emission tomography: a suitable tool for imaging regional excitability of the human cortex. Neuroimage. 2001; 14: 883–890.[CrossRef][Medline] [Order article via Infotrieve]
  35. Winhuisen L, Thiel A, Schumacher B, Kessler J, Rudolf J, Haupt WF, Heiss WD. Role of the contralateral inferior frontal gyrus in recovery of language function in poststroke aphasia: a combined repetitive transcranial magnetic stimulation and positron emission tomography study. Stroke. 2005; 36: 1759–1763.[Abstract/Free Full Text]
  36. Kobayashi M, Hutchinson S, Theoret H, Schlaug G, Pascual-Leone A. Repetitive TMS of the motor cortex improves ipsilateral sequential simple finger movements. Neurology. 2004; 62: 91–98.[Abstract/Free Full Text]
  37. Mansur CG, Fregni F, Boggio PS, Riberto M, Gallucci-Neto J, Santos CM, Wagner T, Rigonatti SP, Marcolin MA, Pascual-Leone A. A sham stimulation-controlled trial of rTMS of the unaffected hemisphere in stroke patients. Neurology. 2005; 64: 1802–1804.[Abstract/Free Full Text]
  38. Oliveri M, Rossini PM, Traversa R, Cicinelli P, Filippi MM, Pasqualetti P, Tomaiuolo F, Caltagirone C. Left frontal transcranial magnetic stimulation reduces contralesional extinction in patients with unilateral right brain damage. Brain. 1999; 122 (Pt 9): 1731–1739.[Abstract/Free Full Text]
  39. Hilgetag CC, Theoret H, Pascual-Leone A. Enhanced visual spatial attention ipsilateral to rTMS-induced ‘virtual lesions’ of human parietal cortex. Nat Neurosci. 2001; 4: 953–957.[CrossRef][Medline] [Order article via Infotrieve]
  40. Naeser MA, Martin PI, Nicholas M, Baker EH, Seekins H, Kobayashi M, Theoret H, Fregni F, Maria-Tormos J, Kurland J, Doron KW, Pascual-Leone A. Improved picture naming in chronic aphasia after TMS to part of right Broca’s area: an open-protocol study. Brain Lang. 2005; 93: 95–105.[CrossRef][Medline] [Order article via Infotrieve]
  41. Brighina F, Bisiach E, Oliveri M, Piazza A, La Bua V, Daniele O, Fierro B. 1 Hz repetitive transcranial magnetic stimulation of the unaffected hemisphere ameliorates contralesional visuospatial neglect in humans. Neurosci Lett. 2003; 336: 131–133.[CrossRef][Medline] [Order article via Infotrieve]
  42. Gilligan AK, Thrift AG, Sturm JW, Dewey HM, MacDonell RA, Donnan GA. Stroke units, tissue plasminogen activator, aspirin and neuroprotection: which stroke intervention could provide the greatest community benefit? Cerebrovasc Dis. 2005; 20: 239–244.[CrossRef][Medline] [Order article via Infotrieve]
  43. Stroke Unit Trialists’ Collaboration. The effect of different types of organized in-patient (stroke unit) care: an updated systematic review and meta-analysis. 14th European Stroke Conference, Bologna, Italy. May 26, 2005.
  44. Cadilhac DA, Ibrahim J, Pearce DC, Ogden KJ, McNeill J, Davis SM, Donnan GA; SCOPES Study Group. Multicenter comparison of processes of care between Stroke Units and conventional care wards in Australia. Stroke. 2004; 35: 1035–1040.[Abstract/Free Full Text]
  45. Irwin P, Hoffman A, Lowe D, Pearson M, Rudd AG. Improving clinical practice in stroke through audit: results of three rounds of National Stroke Audit. J Eval Clin Pract. 2005; 11: 306–314.[CrossRef][Medline] [Order article via Infotrieve]
  46. Dey P, Woodman M, Gibbs A, Steele R, Stocks SJ, Wagstaff S, Khanna V, Chaudhuri MD. Early assessment by a mobile stroke team: a randomised controlled trial. Age Ageing. 2005; 34: 331–338.[Abstract/Free Full Text]
  47. Langhorne P, Dey P, Woodman M, Kalra L, Wood-Dauphinee S, Patel N, Hamrin E. Is stroke unit care portable? A systematic review of the clinical trials. Age Ageing. 2005; 34: 324–330.[Abstract/Free Full Text]
  48. Kalra L, Evans A, Perez I, Knapp M, Swift C, Donaldson N. A randomised controlled comparison of alternative strategies in stroke care. Health Technol Assess. 2005; 9: 1–94.[Medline] [Order article via Infotrieve]
  49. Langhorne P, Taylor G, Murray G, Dennis M, Anderson C, Bautz-Holter E, Dey P, Indredavik B, Mayo N, Power M, Rodgers H, Ronning OM, Rudd A, Suwanwela N, Widen-Holmqvist L, Wolfe C. Early supported discharge services for stroke patients: a meta-analysis of individual patients’ data. Lancet. 2005; 365: 501–506.[Medline] [Order article via Infotrieve]
  50. Biernaskie J, Chernenko G, Corbett D. Efficacy of rehabilitative experience declines with time after focal ischemic brain injury. J Neurosci. 2004; 24: 1245–1254.[Abstract/Free Full Text]
  51. Yagura H, Miyai I, Suzuki T, Yanagihara T. Patients with severe stroke benefit most by interdisciplinary rehabilitation team approach. Cerebrovasc Dis. 2005; 20: 258–263.[CrossRef][Medline] [Order article via Infotrieve]
  52. Paul SL, Sturm JW, Dewey HM, Donnan GA, MacDonell RA, Thrift AG. Long-term outcome in the North East Melbourne Stroke Incidence Study: predictors of quality of life at 5 years after stroke. Stroke. 2005; 36: 2082–2086.[Abstract/Free Full Text]




This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
37/2/314    most recent
01.STR.0000200454.98176.04v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Heiss, W.-D.
Right arrow Articles by Teasel, R. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Heiss, W.-D.
Right arrow Articles by Teasel, R. W.
Right arrowPubmed/NCBI databases
Medline Plus Health Information
*Stroke
Related Collections
Right arrow Exercise/exercise testing/rehabilitation

Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search
Copyright © 2006 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.