| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Stroke. 2000;31:223.)
© 2000 American Heart Association, Inc.
Special Report |
Presented as the Willis Lecture at the 24th American Heart Association International Conference on Stroke and Cerebral Circulation, Nashville, Tenn, February 4, 1999. The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.
From the Division for Experimental Neurology, Wallenberg Neuroscience Center, University Hospital, Lund, Sweden.
Correspondence to Barbro B. Johansson, MD, PhD, Division for Experimental Neurology, Wallenberg Neuroscience Center, University Hospital, S-221 85 Lund, Sweden. E-mail Barbro.Johansson{at}neurol.lu.se
| Abstract |
|---|
Key Words: neuronal plasticity recovery rehabilitation stroke
| Introduction |
|---|
The above words were written in 1973 by Alf Brodal, a Norwegian neuroanatomist, based on his own experience after a stroke. To what extent has his assumption been shown to be correct? In this review I will present current concepts on brain plasticity in intact and lesioned brain, and evidence that postischemic interventions can alter molecular events and influence functional recovery after brain lesions.
| Current Concepts on Brain Plasticity |
|---|
Another aspect of brain plasticity, first and most extensively
demonstrated by Merzenich and coworkers, is that cortical
representation areas, cortical maps, can be modified by sensory
input, experience, and learning (Figure 1
), as well as in response to brain
lesions.17 18 19 20 21 22 23 24 25 26 27 28 29 30 The potential relevance for stroke
rehabilitation of those data was proposed more than a decade
ago.19 Transient alterations of cortical
representation areas may be common in everyday life, as
indicated by transcranial magnetic stimulation studies
during learning tasks in human volunteers.31 If we
regularly have to perform a very skilled motor task, the
cortical representation for the muscles involved will remain
enlarged, as seen for the fingers of the left but not the right hand in
string players.32 Similarly, the sensorimotor cortical
representation of the reading finger is expanded in blind
Braille readers33 and, furthermore, fluctuates with the
reading activity pattern.34
|
| Possible Mechanisms Behind Brain Plasticity |
|---|
-Aminobutyric acid (GABA)-A
receptor antagonists can facilitate LTP induction in
neocortical synaptic systems, and the induction can be blocked by
GABA-A receptor agonists.40 Transmitters released by the
diffuse neuromodulatory systems originating in locus coeruleus
(noradrenalin), nucleus basalis (acetylcholine), lateral
tegmentum (dopamine), and raphe nuclei (serotonin) may
modify the process.44 45 Nitric oxide is another candidate
for dynamic modulation of cerebral cortex synaptic
function.46 There is evidence that mechanisms involved in
synaptic plasticity varies between cortical regions.35 47
Local neurotrophin actions, transmitter release, and synaptic protein
synthesis are thought to promote synaptic remodeling and changes in
receptor expression or activation.12 As illustrated in
Figure 2
|
There is increasing evidence that astrocytes take an active part in synaptic plasticity.49 50 Rapid astrocytic changes in cortex and ultrastructural evidence for increased contact between astrocytes and synapses in rats reared in a complex environment suggest a close relationship between astrocytic plasticity and experience-induced synaptic plasticity.51 52 Nonsynaptic transmission may also play a role in plasticity processes.53 Plastic changes occur not only in the cortex but have also been demonstrated in subcortical regions, including thalamus and brain stem.54 55
| Spontaneous Events and Training Effects |
|---|
Cortical mapping by intracellular recordings in primates has demonstrated that the tissue surrounding a small lesion in the hand-representation area of primary motor cortex in adult monkeys undergoes a further territorial loss in the functional representation of the affected body part, perhaps through nonuse or disruption of local intrinsic cortical circuitry.28 This further tissue loss could be prevented and functional reorganization in the undamaged surrounding motor cortex stimulated by retraining of hand use, starting 5 days after induction of the lesion.29 Similarly, reorganization of primary somatosensory cortex occurs in parallel with sensorimotor skill recovery in monkeys after restricted lesions. No significant changes were recorded in the hand representation area in somatosensory cortex in the opposite intact (untrained) hemisphere.30
Morphologic studies in the rat indicate that cortical lesions can induce an increase of dendritic branching in the contralateral hemisphere, with a maximum 2 to 3 weeks after the lesion.57 If the rats were prevented from using the intact forelimb, both the morphologic changes and functional recovery were inhibited.58 Although some studies with other techniques could not verify those findings,59 60 a detailed electromicroscopic longitudinal study61 has confirmed the development of time-dependent morphologic changes with a significant increase in dendritic volume in cortical layer of the contralateral motor cortex 18 days after the lesion, and in the number of synapses per neuron 30 days after the lesion.
After a focal brain infarct, an increased density and distribution of GAP 43 immunoreactivity has been observed in the ipsilateral cortex 3 to 14 days after the vascular occlusion and of synaptophysin immunoreactivity in the same areas at postoperative days 14 to 60. A larger distribution of synaptophysin immunoreactivity was also noted in the contralateral hemisphere.62 An increased neuronal labeling of MAP-2, GAP-43, and cyclin D1 immunoreactivity from day 2 and up to 28 days has been found in the penumbra zone.63
| Enriched Environment and Neurotrophic Factors |
|---|
We hypothesized that the beneficial effect of enriched environment might be caused by increased synthesis of neurotrophic factors. Neurotrophic factors are polypeptides capable of promoting neuronal survival. Local neurotrophin action may promote synaptic remodeling and changes in receptor expression.12 Ischemia is a strong inducer of gene expression in the brain.69 70 71 More than 90 different genes have been shown to be acutely induced, generally with an early peak within minutes or hours of onset of ischemia and a rapid return to normal or subnormal levels. Whether the early transient increase in gene expression during the initial postischemic hours is related to outcome is not known. There is some evidence that trophic factors can rescue neurons in the acute stage. In addition to reducing infarct size even when given hours after the ischemic insult, basic fibroblast growth factor (bFGF) may attenuate the thalamic degeneration following cortical infarction.72 73 74 Nerve growth factor (NGF) has been reported to improve memory and motor functions and reduce dendritic atrophy in the remaining pyramidal neurons.75 As reviewed elsewhere,76 several other growth factors, including brain-derived growth factor (BDNF), insulin growth factor-1, transforming growth factor ß1, and glial cell linederived neurotrophic factor, have been reported to be beneficial in the early ischemic period. Whether some of these trophic factors can be beneficial in the rehabilitation phase has not yet been evaluated. Because of the poor penetration of many growth factors into the brain, an interesting approach is to use substances that induce endogenous growth factor synthesis in the brain after peripheral administration. A ß2-adrenoceptor agonist as been shown to reduce infarct volume and induce an earlier and more pronounced increase in mRNA of nerve growth factor (NGF), bFGF, and transforming growth factor-ß1 (TGF-ß1) than was seen in untreated rats after permanent focal ischemia.77 Cholecystokinin-8 increases both NGF protein and NGF mRNA in mouse cortex and hippocampus when injected intraperitoneally at physiological doses and may thus represent a potential experimental model for investigating the effects of endogenous NGF upregulation after brain lesions.78
Based on data on the role of BDNF for plasticity in the intact brain,79 80 we have studied the late postischemic gene expression for this protein in rats killed 2 to 30 days after the ischemic event. Moreover, intraventricular BDNF has been shown to rescue neurons in acute ischemia.81 Unexpectedly, a secondary increase in BDNF gene expression observed in control rats did not occur in rats housed in an enriched environment, who had significantly lower BDNF expression in ipsilateral and contralateral cortex than rats in a standard environment 2 to 12 days after the insult.82 Similar results were obtained for expression of NGFI-A mRNA,83 a gene that earlier had been shown to be activated in an enriched environment in intact rats.10 However, a late increase of NGFI-A mRNA expression was observed at 30 days after the lesion, which suggested that it might be important for later postischemic events.83
The reason for the early dampening of the postischemic increase seen in control animals for BDNF is not clear. BDNF is related to synaptic activity. Cortical networks adjacent to a focal brain ischemia are hyperexcitable because of an imbalance between excitatory and inhibitory synaptic function.84 85 86 Hyperexcitability has been recorded not only around the infarct but also in the contralateral hemisphere measured 1 week after the ischemic event.87 88 89 Both a detrimental role (impaired processing of incoming information) and a beneficial role (adaptation and favorable recovery) of this hyperexcitability have been proposed.87 Could it be that rats in an enriched environment have a better balance between inhibitory and excitatory transmission and that depression of hyperexcitability might be beneficial in the early stage? Clearly, more studies are needed before any conclusions can be drawn. The relationship between growth inhibitory and growth promotor factors are likely to be important, and it should be noted also that growth inhibitory factor mRNA is increased during the postischemic period after focal ischemia in the rat.90 The recent reports on increased corticofugal plasticity after neutralization of a myelin-associated neurite growth inhibitor is a reminder that inhibitors of brain plasticity may be just as important as stimulating factors for postischemic functional outcome.91 92
| Pharmacological Interventions |
|---|
-adrenergic
stimulating drugs can enhance motor performance after
unilateral ablation of sensorimotor cortex95 99 and have
also been shown to enhance the immunoreactivity to synaptic proteins
after focal brain ischemia.100 However,
amphetamine had no additional effect on outcome in rats housed in an
enriched environment after focal brain
ischemia,101 perhaps due to enhanced
noradrenergic release under such housing
conditions. | What Is the Possible Role of Neurogenesis? |
|---|
The aspects of neurogenesis that are relevant for this review are the following: (1) Does neurogenesis increase in response to brain lesions? (2) If so, is neurogenesis related to outcome? (3) Can those events be influenced by postlesion interventions? and (4) Can stem cells or progenitor cells be used for transplantation after stroke? The first question can be answered affirmatively. It has been shown to occur in excitotoxic and mechanical lesions in the dentate gyrus (hippocampus) in the adult rat112 and after transient global ischemia in gerbils.113 The second and third questions remain to be answered, and the fourth question will be discussed in the transplantation section below.
| Transplantation |
|---|
Immortalized embryonic neuronal cells lines or cultured neural multipotent progenitor cells (the transition from stem cell to progenitor cell is not sharp) implanted into a lesioned brain have shown promising results in other experimental models. When implanted into the neocortex of adult mice undergoing targeted apoptosis of neocortical pyramidal neurons, they migrate long distances into the regions of cell death, where they differentiate and make appropriate long-distance projections.117 118 119 The results indicate the presence of environmental signals that promote differentiation of the implanted cells. Furthermore, adult mature astrocytes in the host brain have been shown to retain the capacity to transform into developmental radial glia that may help the active migration of transplanted neural precursors.120 Whether transplantation of neuronal precursor cells to neocortical infarct cavities would be a good substitute for the currently used fetal neocortical tissue block techniques remains to be demonstrated.
| Clinical Evidence for Reorganization of Cortical Networks |
|---|
| Stroke Units and Early Training |
|---|
Clinical data are thus strongly in favor of early mobilization and training. On the other hand, there are some disturbing animal data indicating that overtraining of the lesioned forelimb induced by immobilization of the intact forelimb can expand cortical lesions.139 140 Referring to those studies, Nudo et al29 started training monkeys 5 days after the lesion. Housing animals in an enriched environment with the opportunity to perform various activities but no specific training significantly improves functional outcome without increasing tissue loss. However, if combined with more specific training from 24 hours after the insult, an increased tissue loss was observed.141 Despite the larger tissue loss in the early training group, the rats improved more than standard rats, confirming earlier data of poor correlation between infarct volume and functional outcome in rats housed in an enriched environment. The better outcome in the early training group than in standard rats may be related to compensatory adaptation in the contralateral hemisphere, subcortical region, or cerebellum.
Even if the increased tissue loss did not correspond to unfavorable outcome, it is clearly an unwanted effect, one which might make the brain more vulnerable to additional insults or aging. What could be the course of this vulnerable early postischemic period? Motor activity stimulates the release of glutamate and catecholamines.142 One possible explanation for the increased tissue loss might be that hyperexcitability of the surrounding tissue in the early postischemic period makes the surrounding neurons vulnerable to excitation. As discussed above in the section on enriched environment and neurotrophic factors, cortical networks adjacent to a focal brain ischemia are hyperexcitable because of an imbalance between excitatory and inhibitory synaptic function with increased NMDA receptor-mediated excitation and decreased efficacy of GABAergic inhibition.84 85 86 In the presence of excitatory and toxic substances from the ischemic tissue, an additional release of excitatory substances induced by motor activity may be harmful in the early postischemic stage. Consistent with this hypothesis is the observation that the NMDA receptor antagonist MK-801can prevent secondary cortical damage in rats forced to use their impaired limb after a lesion in the sensorimotor cortex.143
It is important to define the window for a possible increased vulnerability and additional peri-infarct neuronal loss. However, I do not think these animal data should make us change the policy of early mobilization of stroke patients. Housing animals in an enriched environment, which may correspond to early mobilization, has no aggravating effects. The most important tasks in the early stage are to prevent complications and train the patient to regain balance and body symmetry. In addition, cortical and lacunar infarcts may differ.
| Age and Plasticity |
|---|
| Concluding Remarks |
|---|
| Acknowledgments |
|---|
| References |
|---|
2. Hebb DO. The effects of early experience on problem solving at maturity. Am Psychol. 1947;2:737745.
3. Hebbs DG. The Organization of Behavior. New York, NY: John Wiley & Sons Inc; 1949.
4.
Bennett EL, Diamond MC, Krech D, Rosenzweig
MR. Chemical and anatomical plasticity of brain. Science. 1964;146:610619.
5. Rosenzweig MR. Environmental complexity, cerebral change, and behavior. Am Psychol. 1966;21:321332.[Medline] [Order article via Infotrieve]
6. Holloway RL. Dendritic branching: some preliminary results of training and complexity in rat visual cortex. Brain Res. 1966;2:393396.[Medline] [Order article via Infotrieve]
7.
Volkmar FR, Greenough WT. Rearing complexity
affects branching of dendrites in the visual cortex of the rat.
Science. 1972;176:14451447.
8. Turner AM, Greenough WT. Differential rearing effect on rat visual cortex synapses, I: synaptic and neuronal density and synapses per neuron. Brain Res. 1985;329:195203.[Medline] [Order article via Infotrieve]
9. Torasdotter M, Metsis M, Henriksson BF, Winblad B, Mohammet AH, Donaldson LF. Environmental enrichment results in higher levels of nerve growth factor mRNA in the rat visual cortex and hippocampus. Behav Brain Res. 1992;51:179183.[Medline] [Order article via Infotrieve]
10. Olsson T, Mohammet AH, Donaldson LF, Henriksson BF, Seckl JR. Glucocorticoid receptor and NGFI-A gene expression are induced in the hippocampus after environmental enrichment in adult rats. Molec Brain Res. 1994;23:349353.[Medline] [Order article via Infotrieve]
11. Kolb B. Brain Plasticity and Behaviour. Hillsdale, NJ: Lawrence Erlboum; 1995.
12. Klintsova AY, Greenough WT. Synaptic plasticity in cortical systems. Curr Opin Neurobiol. 1999;9:203208.[Medline] [Order article via Infotrieve]
13. Greenough WT, Larson JR, Withers GS. Effect of unilateral and bilateral training in a reaching task on dendritic branching of neurons in the rat motor-sensory forelimb cortex. Behav Neurol Biol. 1985;44:301314.[Medline] [Order article via Infotrieve]
14. Van Reemts J, Dikova M, Werbrouck L, Clincke G, Borgers M. Synaptic plasticity in rat hipppocampus associated with learning. Behav Brain Res. 1992;51:179183.
15. Neeper SA, Gomez-Pinilla F. Choi J, Cotman C. Exercise and brain neurotrophins. Nature. 1995;373:109. Letter.[Medline] [Order article via Infotrieve]
16.
Kleim JA, Lussnig E, Schwarz ER, Comery TA,
GreenoughWT. Synaptogenesis and Fos expession in the motor cortex of
the adult rat after motor skill learning. J Neurosci. 1996;16:45294535.
17. Merzenich MM, Kaas JH, Wall JT, Nelson RJ, Sur M, Felleman D. Topographic reorganization of somatosensory cortical areas 3b and 1 in adult monkeys following restricted deafferentation. Neuroscience. 1983;8:3355.[Medline] [Order article via Infotrieve]
18. Merzenich MM, Nelson RJ, Stryker MP, Cynader MS, Schoppmann A, Zook JM. Somatosensory cortical map changes following digit amputation in adult monkeys. J Comp Neurol. 1984;224:591605.[Medline] [Order article via Infotrieve]
19. Jenkins WM, Merzenich MM. Reorganization of neocortical representations after brain injury: a neurophysiological model of the bases of recovery from stroke. Progr Brain Res. 1987;71:249266.[Medline] [Order article via Infotrieve]
20.
Pons TP, Garraghty PE, Mishkin M.
Lesion-induced plasticity in the somatosensory cortex of adult
macaques. Proc Nat Acad Sci U S A. 1988;85:52795281.
21. Jenkins WM, Merzenich MM, Ochs MT, Allard R, Guic-Robles E. Functional reorganization of primary somatosensory cortex in adult owl monkeys after behaviorally controlled tactile stimulation. J Neurophysiol. 1990;68:82104.
22. Kaas JH. Plasticity of sensory and motor maps in adult mammals. Ann Rev Neurosci. 1991;14:137167.[Medline] [Order article via Infotrieve]
23. Liepert J, Tegenthoff M, Malin JP. Changes of cortical motor area size during immobilization. Electroencephalogr Clin Neurophysiol. 1995;97:382386.[Medline] [Order article via Infotrieve]
24. Seitz RJ, Huang Y, Knorr U, Tellmann L, Herzog H, Freund HJ. Large-scale plasticity of the human motor cortex. Neuroreport. 1995;6:742744.[Medline] [Order article via Infotrieve]
25. Schieber MH. Physiological basis for functional recovery. J Neurol Rehabil. 1995;9:6571.
26.
Florence SL, Taub HB, Kaas JH. Large-scale
sprouting of cortical connections after peripheral injury
in adult macaque monkeys. Science. 1998;282:11171121.
27.
Hallett M. Plasticity in the human motor
system. Neuroscientist.. 1999;5:324332.
28.
Nudo RJ, Milliken GW. Reorganization of
movement representations in primary motor cortex following
focal ischemic infarcts in adult squirrel monkeys. J
Neurophysiol. 1996;75:21442149.
29. Nudo RJ, Wise BM, SiFuentes F, Milliken GW. Neural substrates for the effects of rehabilitative training on motor recovery after ischemic infarct. Science. 1996;272:17911794.[Abstract]
30.
Xerri C, Merzenich MM, Peterson BE, Jenkins W.
Plasticity of primary somatosensory cortex paralleling sensorimotor
skill recovery from stroke in adult monkeys. J
Neurophysiol. 1998;79:21192148.
31.
Pascual-Leone A, Grafman J, Hallett M.
Modulation of cortical motor output maps during development of implicit
and explicit knowledge. Science. 1994;263:12871289.
32.
Elbert T, Pantev C, Wienbruch C, Rockstroh B,
Taub E. Increased cortical representation of the fingers of the
left hand in string players. Science. 1995;270:305307.
33.
Pascual-Leone A, Torres F. Plasticity of the
sensorimotor cortex representation of the reading finger in
Braille readers. Brain. 1993;116:3952.
34. Pascual-Leone A, Wassermann EM, Sadato N, Hallett M. The role of reading activity on the modulation of motor cortical outputs to the reading hand in Braille readers. Ann Neurol. 1995;38:910915.[Medline] [Order article via Infotrieve]
35. Shaw CA, Lanius RA, van den Doel K. The origin of synaptic neuroplasticity: crucial molecules or a dynamic cascade? Brain Res Rev. 1994;19:241263.[Medline] [Order article via Infotrieve]
36. Bear MF, Malenka RC. Synaptic plasticity: LTP and LTD. Curr Opin Neurobiol. 1994;4:389399.[Medline] [Order article via Infotrieve]
37. Buonomano DV, Merzenich MM. Cortical plasticity: from synapses to maps. Annu Rev Neurosci. 1998;21:149186.[Medline] [Order article via Infotrieve]
38.
Hess G, Donoghue JP. Long-term potentiation of
horizontal connections provides a mechanism to reorganize cortical
motor maps. J Neurophysiol. 1994;71:25432547.
39. Das A, Gilbert CD. Long-range horizontal connections and their role in cortical reorganization revealed by optical recording of cat primary visual cortex. Nature. 1995;375:780784.[Medline] [Order article via Infotrieve]
40.
Hess G, Aizenman CD, Donoghue JP. Conditions
for the induction of long-term potentiation in Layer II/III horizontal
connections of the rat motor cortex. J Neurophysiol.. 1996;75:17651777.
41. Kano M, Lino K, Kano M. Functional reorganization of adult cat somatosensory cortex is dependent on NMDA receptors. Neuroreport. 1991;2:7780.[Medline] [Order article via Infotrieve]
42. Hess G, Jacobs KM, Donoghue JP. N-Methyl-D-aspartate receptor mediated component of field potentials evoked in horizontal pathways of rat motor cortex. Neuroscience. 1994;61:225235.[Medline] [Order article via Infotrieve]
43. Garraghty PE, Muja N. NMDA receptors and plasticity in adult primate somatosensory cortex. J Comp Neurol. 1996;367:319326.[Medline] [Order article via Infotrieve]
44.
Kilgard MP, Merzenich MM. Cortical map
reorganization enabled by nucleus basalis activity. Science. 1998;279:17141718.
45.
Kirkwood A, Rozas C, Kirkwood J, Perez F, Bear
MF. Modulation of long-term synaptic depression in visual cortex by
acetylcholine and norepinephrine. J
Neurosci. 1999;19:15991609.
46. Kara P, Friedlander MJ. Dynamic modulation of cerebral cortex synaptic function by nitric oxide. Prog Brain Res. 1998;118:183198.[Medline] [Order article via Infotrieve]
47. Castro-Alamancos MA, Donoghue JP, Connors BW. Different forms of synaptic plasticity in somatosensory and motor areas of the neocortex. J Neurosci. 1995;15:53245333.[Abstract]
48. Fischer M, Kaech S, Knutti D, Matus A. Rapid actin-based plasticity in dendritic spines. Neuron. 1998;20:847854.[Medline] [Order article via Infotrieve]
49. Vernadakis A. Glia-neuron intercommunications and synaptic plasticity. Prog Neurobiol. 1996;49:185214.[Medline] [Order article via Infotrieve]
50. Pfrieger FW, Barres BA. New views on synapse-glia interactions. Curr Opin Neurobiol. 1996;6:615621.[Medline] [Order article via Infotrieve]
51. Jones TA, Hawrylak N, Greenough WT. Rapid laminal-dependent changes in GFAP immunoreactive astrocytes in the visual cortex of rats reared in a complex environment. Psychoneuroendocrinology. 1996;21:189201.[Medline] [Order article via Infotrieve]
52. Jones TA, Greenough WT. Ultrastructural evidence for increased contact between astrocytes and synapses in rats reared in a complex environment. Neurobiol Learn Mem. 1996;65:4856.[Medline] [Order article via Infotrieve]
53. Bach-y-Rita P. Nonsynaptic diffusion neurotransmission (NDN) in the brain. Neurochem Int. 1993;23:297318.[Medline] [Order article via Infotrieve]
54. Nicolelis MAL. Dynamic and distributed somatosensory representations as the substance for cortical and subcortical plasticity. Semin Neurosci. 1997;9:2433.
55.
Jones EG, Pons TP. Thalamic and brain stem
contributions to large-scale plasticity of primate somatosensory
cortex. Science. 1998;282:11211125.
56.
Jacobs KM, Donoghue JP. Reshaping the cortical
motor map by unmasking latent intracortical connections.
Science. 1991;251:944947.
57. Jones TA, Schallert T. Overgrowth and pruning of dendrites in adult rats recovering from neocortical damage. Brain Res. 1992;581:156160.[Medline] [Order article via Infotrieve]
58. Jones TA, Schallert T. Use-dependent growth of pyramidal neurons after neocortical damage. J Neurosci. 1994;14:21402152.[Abstract]
59. Forgie ML, Gibb R, Kolb B. Unilateral lesions of the forelimb area of rat motor cortex: lack of evidence for use-dependent neural growth in the undamaged hemisphere. Brain Res. 1996;710:249259.[Medline] [Order article via Infotrieve]
60. Prusky G, Whishaw IQ. Morphology of identified corticospinal cells in the rat following motor cortex injury: absence of use-dependent change. Brain Res. 1996;714:18.[Medline] [Order article via Infotrieve]
61. Jones TA, Kleim JA, Greenough WT. Synaptogenesis and dendritic growth in the cortex opposite unilateral sensorimotor cortex damage in adult rats: a quantitative electron microscopic examination. Brain Res. 1996;733:142148.[Medline] [Order article via Infotrieve]
62.
Stroemer RP, Kent TA, Hulsebosch CR.
Neocortical neural sprouting, synaptogenesis, and behavioral recovery
after neocortical infarction in rats. Stroke. 1995;26:21352144.
63.
Li Y, Jiang N, Powers C, Chopp M. Neuronal
damage and plasticity identified by microtubule-associated protein 2,
growth-associated protein 43, and cyclin D1 immunoreactivity after
focal cerebral ischemia in rats. Stroke. 1998;29:19721981.
64. Will B, Kelche C. Environmental approaches to recovery of function from brain damage: a review of animal studies (19811991). In: Rose FD, Johnson DA, eds. Recovery From Brain Damage. New York, NY: Plenum Publishing Corp; 1992:79103.
65. Held JM, Gordon J, Gentile AM. Environmental influences on locomotor recovery following cortical lesions in rats. Behav Neurosci. 1985;99:678690.[Medline] [Order article via Infotrieve]
66.
Ohlsson A-L, Johansson BB. Environment
influences functional outcome of cerebral infarction in rats.
Stroke. 1995;26:644649.
67.
Johansson BB. Functional outcome in rats
transferred to an enriched environment 15 days after focal brain
ischemia. Stroke. 1996;27:324326.
68. Johansson BB, Ohlsson A-L. Environment, social interaction, and physical activity as determinants of functional outcome after cerebral infarction in the rat. Exp Neurol. 1996;139:322327.[Medline] [Order article via Infotrieve]
69. Kinouchi H, Sharp FR, Chan PH, Koistinaho J, Sagar SM, Yoshimoto T. Induction of c-fos, junB, c-jun, and hsp70 mRNA in cortex, thalamus, basal ganglia, and hippocampus following middle cerebral artery occlusion. J Cereb Blood Flow Metab. 1994;14:808817.[Medline] [Order article via Infotrieve]
70.
Akins PT, Liu PK, Hsu CY. Immediate early gene
expression in response to cerebral ischemia: friend or foe?
Stroke. 1996;27:16821687.
71. Koistinaho J, Hökfelt T. Altered gene expression in brain ischemia. Neuroreport.. 1997;8:i-viii.
72. Yamada K, Kinoshita A, Kohmura E, Sakaguchi T, Taguchi J, Kataoka K. Basic fibroblast growth factor prevents thalamic degeneration after cortical infarction. J Cereb Blood Flow Metab. 1991;11:472478.[Medline] [Order article via Infotrieve]
73.
Lin DA, Finklestein SP. Basic fibroblast growth
factor: a treatment for stroke? Neuroscientist. 1997;3:247250.
74.
Kawamata T, Dietrich WD, Schallert T, Gotts JE,
Cocke RR, Beowitz LI, Finkelstein SP. Intracisternal basic fibroblast
growth factor enhanced functional recovery and upregulates the
expression of a molecular marker of neuronal sprouting following focal
cerebral infarction. Proc Natl Acad Sci U S A. 1997;94:81798184.
75. Kolb B, Cote S, Ribeiro da Silva A, Cuello AC. Nerve growth factor treatment prevents dendritic atrophy and promotes recovery of function after cortical injury. Neuroscience. 1997;76:11391151.[Medline] [Order article via Infotrieve]
76. Johansson BB. Neurotrophic factors and transplants. In: Goldstein LB, ed. Restorative Neurology: Advances in Pharmacotherapy for Recovery After Stroke. Armonk, NY: Futura Publishing Co; 1998:141166.
77. Culmsee C, Stumm RK, Schafer MK, Weihe E, Krieglstein J. Clenbuterol induces growth factor mRNA, activates astrocytes, and protects rat brain tissue against ischemic damage. Eur J Pharmacol. 1999;379:3345.[Medline] [Order article via Infotrieve]
78.
Tirassa P, Aloe L, Stenfors C, Turrini P,
Lundeberg T. Cholecystokinin-8 protects central cholinergic neurons
against fimbria-fornix lesions through the upregulation of nerve growth
factor synthesis. Proc Natl Acad Sci U S A. 1999;96:64736477.
79.
Castrén E, Zafra F, Thoenen H, Lindholm
D. Light regulated expression of brain-derived neurotrophic factor mRNA
in rat visual cortex. Proc Natl Acad Sci U S A. 1992;89:94449448.
80.
Rocamora N, Welker E, Pascual M, Soriano E.
Upregulation of BDNF mRNA expression in the barrel cortex of adult mice
after sensory stimulation. J Neurosci. 1996;16:44114419.
81. Schäbitz W-R, Schwab S, Spranger M, Hacke W. Intraventricular brain derived neurotrophic factor reduces infarct size after focal cerebral ischemia in rats. J Cereb Blood Flow Metab. 1997;17:500506.[Medline] [Order article via Infotrieve]
82. Johansson BB, Zhao L-R, Mattsson B. Environmental influence on neurotrophic gene expression after experimental brain infarction in the rat. In: Ito U, Fieschi C, Orzi F, Kuroiwa T, Klatzo I, eds. Maturation Phenomenon in Cerebral Ischemia III. Berlin, Germany: Springer-Verlag; 1999:261266.
83. Dahlqvist P, Zhao L, Johansson I-M, Mattsson B, Johansson BB, Seckl JR, Olsson T. Environmental enrichment alters NGFI-A and glucocorticoid receptor mRNA expression after MCA occlusion in rats. Neuroscience. 1999;93:527535.[Medline] [Order article via Infotrieve]
84. Schiene K, Bruehl C, Zilles K, Qü MS, Hagemann G, Kraemer M, Witte OW. Neuronal hyperexcitability and reduction of GABAA-receptor expression in the surround of cerebral photothrombosis. J Cereb Blood Flow Metab. 1996;16:906914.[Medline] [Order article via Infotrieve]
85. Mittmann T, Qu M, Zilles K, Luhmann HJ. Long-term cellular dysfunction after focal cerebral ischemia: in vitro analyses. Neuroscience. 1998;85:1527.[Medline] [Order article via Infotrieve]
86. Qu M, Mittmann T, Luhmann HJ, Schleicher A. Long-term changes of ionotropic glutamate and GABA receptors after unilateral permanent focal cerebral ischemia in the mouse brain. Neuroscience. 1998;85:2943.[Medline] [Order article via Infotrieve]
87.
Buchkremer-Ratzmann I, August M, Hagemann G,
Witte OW. Electrophysiological transcortical
diaschisis after cortical photothrombosis in rat brain.
Stroke. 1996;27:1051111.
88. Reinecke S, Lutzenburg M, Hagemann G, Bruehl C, Neumann-Haefelin T, Witte OW. Electrophysiological transcortical diaschisis after middle cerebral artery occlusion (MCAO) in rats. Neurosci Lett. 1999;261:8588.[Medline] [Order article via Infotrieve]
89. Qu M, Buchkremer-Ratzmann I, Schiene K, Schroeter M, Witte OW, Zilles K. Bihemispheric reduction of GABAA receptor binding following focal cortical photothrombotic lesions in the rat brain. Brain Res. 1998;813:374380.[Medline] [Order article via Infotrieve]
90. Yuguchi T, Kohmura E, Sakaki T, Nonaka M, Yamada K, Yaahita T, Yamashita T, Kishiguchi T, Sakaguchi T, Hayakawa T. Expression of growth inhibitory factor mRNA after focal ischemia in rat brain. J Cereb Blood Flow Metab. 1997;17:745752.[Medline] [Order article via Infotrieve]
91. Kartje GL, Schultz MK, Lopez-Yunez A, Schnell L, Schwab ME. Corticostriatal plasticity is restricted by myelin-associated neurite growth inhibitors in the adult rat. Ann Neurol. 1999;45:77886.[Medline] [Order article via Infotrieve]
92. Wenk CA, Thallmair M, Kartje GL, Schwab ME. Increased corticofugal plasticity after unilateral cortical lesions combined with neutralization of the IN-1 antigen in adult rats. J Comp Neurol. 1999;410:143157.[Medline] [Order article via Infotrieve]
93. Goldstein LB. Basic and clinical studies on pharmacologic effects on recovery from brain injury. J Neurol Transplant Plast. 1993;4:175192.
94.
Goldstein LB. Potential effects of common drugs
on stroke recovery. Arch Neurol. 1998;55:454456.
95. Feeney DM. Mechanisms of noradrenergic modulation of physical therapy: effects on functional recovery after cortical injury. In: Goldstein LB, ed. Restorative Neurology: Advances in Pharmacotherapy for Recovery After Stroke. Armonk, NY: Futura Publishing Co; 1998:3578.
96. Saponjic RM, Hoane MR, Barth TM. Acetylcholine and recovery of function following brain injury. In: Goldstein LB, ed. Restorative Neurology: Advances in Pharmacotherapy for Recovery After Stroke. Armonk, NY: Futura Publishing Co; 1998:7989.
97. Schallert T, Hernandez TD. GABAergic drugs and neuroplasticity after brain injury: impact on functional recovery. In: Goldstein LB, ed. Restorative Neurology: Advances in Pharmacotherapy for Recovery After Stroke. Armonk, NY: Futura Publishing Co; 1998:91120.
98. Barth TM, Hoane MR, Barbay S. Effect of glutamate antagonists on the recovery and maintenance of behavioral functions afterbrain injury. In: Goldstein LB, ed. Restorative Neurology: Advances in Pharmacotherapy for Recovery After Stroke. Armonk, NY: Futura Publishing Co; 1998:91120.
99.
Feeney DM, Gonzalez A, Law WA. Amphetamine,
haloperidol and experience interact to affect the rate of recovery
after motor cortex injuries. Science. 1982;217:855857.
100.
Stroemer RP, Kent TA, Hulsebosch CR. Enhanced
neocortical neural sprouting, synaptogenesis, and behavioral recovery
with d-amphetamine therapy after neocortical infarction in rats.
Stroke. 1998;29:23812395.
101. Johansson BB, Mattsson B, Ohlsson A-L. Functional outcome after brain infarction: effect of enriched environment and amphetamine. In: Ito U, Kirino T, Kuroiwa T, Klatzo I, eds. Maturation Phenomenon in Cerebral Ischemia II. Berlin, Germany: Springer-Verlag; 1997:159167.
102. Altman J, Das GD. Autoradiographic and histological evidence of postnatal hippocampal neurogenesis in rats. J Comp Neurol. 1965;124:319335.[Medline] [Order article via Infotrieve]
103. Altman J, Das GD. Postnatal neurogenesis in the guinea-pig. Nature. 1967;214:10981101.[Medline] [Order article via Infotrieve]
104.
McKay R. Stem cells in the central nervus
system. Science. 1997;276:6671.
105. Snyder EY. Neural stem-like cells: developmental lessons with therapeutic potential. The Neuroscientist. 1998;4:408425.
106.
Palmer TD, Markakis EA, Willhoite AR, Safar F,
Gage FH. Fibroblast growth factor-2 activates a latent
neurogenic program in neural stem cells from diverse regions of the
adult CNS. J Neurosci. 1999;19:84878497.
107. Kirschenbaum B. Nedergaard M, Preuss A, Barami I, Fraser RA, Goldman SA. In vitro neuronal production and differentiation by precursor cells derived from the adult human forebrain. Cereb Cortex. 1994;6:576589.
108. Eriksson PS, Perfilieva E, Björk-Eriksson T, Alborn A-M, Nordborg C, Peterson DA, Gage FH. Neurogenesis in the adult human hippocampus. Nat Med. 1998;4:13131317.[Medline] [Order article via Infotrieve]
109. Kempermann G, Kuhn HG, Gage FH. More hippocampal neurons in adult mice living in an enriched environment. Nature. 1997;386:493495.[Medline] [Order article via Infotrieve]
110.
Kempermann G, Kuhn HG, Gage FH.
Experience-dependent neurogenesis in the senescent dentate gyrus.
J Neurosci. 1998;18:32063212.
111. Nilsson M, Perfilieva E, Johansson U, Orwar O, Eriksson PS. Enriched environment increases neurogenesis in the adult rat dentate gyrus and improves spatial memory. J Neurobiol. 1999;39:569578.[Medline] [Order article via Infotrieve]
112. Gould E, Tanapat P. Lesion-induced proliferation of neuronal progenitors in the dentate gyrus of the adult rat. Neuroscience. 1997;80:427436.[Medline] [Order article via Infotrieve]
113.
Liu J, Solway K, Messing RO, Sharp FR. Increased
neurogenesis in the dentate gyrus after transient global
ischemia in gerbils. J Neurosci. 1998;18:77687778.
114. Grabowski M, Brundin P, Johansson BB. Functional integration of cortical grafts placed in brain infarcts of rats. Ann Neurol. 1993;34:362368.[Medline] [Order article via Infotrieve]
115. Grabowski M, Sørensen JC, Mattsson B, Zimmer J, Johansson BB. Influence of an enriched environment and cortical grafting in functional outcome in brain infarcts of adult rats. Exp Neurol. 1995;133:96102.[Medline] [Order article via Infotrieve]
116.
Mattsson B, Sørensen JC, Zimmer J, Johansson
BB. Neural grafting to experimental neocortical infarcts improves
behavioral outcome and reduces thalamic atrophy in rats housed in
enriched but not in standard environments. Stroke. 1997;28:12251232.
117. Macklis JD. Transplanted neocortical neurons migrate selectively into regions of neuronal degeneration produced by chromophore-targeted laser photolysis. J Neurosci. 1993;13:38483863.[Abstract]
118. Hernit-Grant CS, Macklis JD. Embryonic neurons transplanted to regions of targeted photolytic cell death in adult mouse somatosensory cortex re-form specific callosal projections. Exp Neurol. 1996;139:131142.[Medline] [Order article via Infotrieve]
119.
Snyder EY, Yoon C, Flax JD, Macklis JD.
Multipotent neural progenetors can differentiate toward replacement of
neurons undergoing targeted apoptotic degeneration in adult
mouse neocortex. Proc Natl Acad Sci U S A. 1997;94:1164511650.
120. Leavitt BR, Hernit-Grant CS, Macklis JD. Mature astrocytes transform into transitional radial glia within adult mouse neocortex that supports directed migration of transplanted immature neurons. Exp Neurol. 1999;157:4357.[Medline] [Order article via Infotrieve]
121. Weiller C, Chollet KJ, Friston KJ, Wise RJS, Frackowiak RSJ. Functional reorganization of the brain in recovery from striatocapsular infarction in man. Ann Neurol. 1992;31:463472.[Medline] [Order article via Infotrieve]
122. Weiller C, Ramsay SC, Wise RJS, Friston KJ, Frackowiak RSJ. Individual patterns of functional reorganization in the human cerebral cortex after capsular infarction. Ann Neurol. 1993;33:181189.[Medline] [Order article via Infotrieve]
123. Weiller C. Imaging recovery from stroke. Exp Brain Res. 1998;123:131718.[Medline] [Order article via Infotrieve]
124.
Cramer SC, Nelles G, Benson RR, Kaplan JD,
Parker RA, Kwong KK, Kennedy DN, Finklestein SP, Rosen BR. A functional
MRI study of subjects recovered from hemiparetic stroke.
Stroke. 1997;28:25182527.
125. Rossini PM, Tecchio F, Pizzella V, Lupoi D, Cassetta E, Pasqualetti P, Romani GL, Orlacchio A. On the reorganization of sensory hand areas after mono-hemispheric lesion: a functional(MEG)/anatomical (MRI) integrative study. Brain Res. 1998;782:153166.[Medline] [Order article via Infotrieve]
126. Pizzamiglio L, Perani D, Cappa SF, Vallar G, Paolucci S, Grassi F, Paulesu E, Fazio F. Recovery of neglect after right hemispheric damage. Arch Neurol. 1999;55:561568.
127.
Warburton E, Price CJ, Swinburn K, Wise RJS.
Mechanisms of recovery from aphasia: evidence from positron emission
tomography studies. J Neurol Neurosurg Psychiatry. 1999;66:155161.
128. Small SL, Flores DK, Noll DC. Different neural circuits subserve reading before and after therapy for acquired dyslexia. Brain Lang. 1998;62:298308.[Medline] [Order article via Infotrieve]
129. Heiss WD, Kessler J, Thiel A, Ghaemi M, Karbe H. Differential capacity of left and right hemispheric areas for compensation of poststroke aphasia. Ann Neurol. 1999;45:430438.[Medline] [Order article via Infotrieve]
130.
Musso M, Weiller C, Kiebel S, Muller SP, Bulau
P, Rinjtjes M. Training-induced brain plasticity. Brain. 1999;122:17811790.
131. Kopp B, Kunkel A, Muhlnickel W, Villringer K, Taub E, Flow H. Plasticity in the motor system related to therapy-induced improvement of movement after stroke. Neuroreport. 1999;10:807810.[Medline] [Order article via Infotrieve]
132. Pulvermüller F, Mohr B. The concept of transcortical cell assemblies: a key to the understanding of cortical lateralization and interhemispheric interaction. Neurosci Biobehav Rev. 1996;20:557566.[Medline] [Order article via Infotrieve]
133.
Stroke Unit Trialists Collaboration.
Collaborative systematic review of the randomised trials of organised
in-patient (stroke unit) care after stroke. BMJ. 1997;314:11511159.
134.
Indredavik B, Slørdahl SA, Bakke F, Rokseth R,
Håheim LL. Stroke unit treatment: long-term effects.
Stroke. 1997;28:18611866.
135.
Stroke Unit Trialists Collaboration. How do
stroke units improve patient outcomes? A collaborative systematic
review of the randomized trials. Stroke. 1997;28:21392144.
136. Wolf SL, Lecraw DE, Barton LA, Jann BB. Forced use of hemiplegic upper extremities to reverse the effect of learned nonuse among chronic stroke and head-injured patients. Exp Neurol. 1989;104:125132.[Medline] [Order article via Infotrieve]
137. Taub E, Miller NE, Novack TA, Cool EW, Fleming WC, Nepomuceno CS, Connell JS, Crago JE. Technique to improve chronic motor deficit after stroke. Arch Phys Med Rehabil. 1993;74:347354.[Medline] [Order article via Infotrieve]
138. Kunkel A, Kopp B, Muller G, Villringer K, Villringer A, Taub E, Flor H. Constraint-induced movement therapy for motor recovery in chronic stroke patients. Arch Phys Med Rehabil. 1999;80:624628.[Medline] [Order article via Infotrieve]
139.
Kozlowski DA, James DC, Schallert T.
Use-dependent exaggeration of neuronal injury after unilateral
sensorimotor cortex lesions. J Neurosci. 1996;16:47764786.
140. Humm JL, Kozlowski DA, James DC, Gotts JE, Schallert T. Use-dependent exacerbation of brain damage occurs during an early post-lesion vulnerable period. Brain Res. 1998;783:286292.[Medline] [Order article via Infotrieve]
141. Risedal A, Zeng J, Johansson BB. Early training may exacerbate brain damage after focal brain ischemia in the rat. J Cereb Blood Flow Metab. 1999;19:9971003.[Medline] [Order article via Infotrieve]
142. Vanderwolf CH, Cain DP. The behavioral neurobiology of learning and memory: a conceptual reorientation. Brain Res Brain Res Rev. 1994;19:264297.[Medline] [Order article via Infotrieve]
143. Humm JL, Kozlowski DA, Bland ST, James DC, Schallert T. Use-dependent exaggeration of brain injury: is glutamate involved? Exp Neurol. 1999;157:349358.[Medline] [Order article via Infotrieve]
144.
Futrell N, Garcia JH, Peterson E, Millikan C.
Embolic stroke in aged rats. Stroke. 1991;22:15821591.
145.
Davis M, Mendelow AD, Perry RH, Chambers IR,
James OF. Experimental stroke and neuroprotection in the aging rat
brain. Stroke. 1995;26:10721078.
146.
Sutherland GR, Dix GA, Auer RN. Effect of age in
rodent models of focal and forebrain ischemia.
Stroke. 1996;27:16631668.
147. Popa-Wagner A, Schroder E, Schmoll H, Walker LC, Kessler C. Upregulation of MAP1B and MAP2 in the rat brain after middle cerebral artery occlusion: effect of age. J Cereb Blood Flow Metab. 1999;19:425434.[Medline] [Order article via Infotrieve]
148. Saito S, Kobayashi S, Ohashi Y, Igarashi M, Komiya Y, Ando S. Decreased synaptic density in aged brains and its prevention by rearing under enriched environment as revealed by synpatophysin contents. J Neurosci Res. 1994;39:5762.[Medline] [Order article via Infotrieve]
149. Buell SJ, Coleman PD. Quantitative evidence for selective dendritic growth in normal human aging but not in senile dementia. Brain Res. 1981;214:2341.[Medline] [Order article via Infotrieve]
150. Wilson RS, Bennett DA, Beckett LA, Morris MC, Gilley DW, Bienias JL, Scherr PA, Evans DA. Cognitive activity in older persons from a geographically defined population. J Gerontol B Psychol Sci Soc Sci. 1999;54:P155P160.
151. Corkin S. Penetrating head injury in young adulthood exacerbates cognitive decline in later years. J Neurosci. 1989;9:38763883.[Abstract]
152.
Ulrich R. View through a window may influence
recovery from surgery. Science. 1984;224:420421.
This article has been cited by other articles:
![]() |
Y. Takatsuru, D. Fukumoto, M. Yoshitomo, T. Nemoto, H. Tsukada, and J. Nabekura Neuronal Circuit Remodeling in the Contralateral Cortical Hemisphere during Functional Recovery from Cerebral Infarction J. Neurosci., August 12, 2009; 29(32): 10081 - 10086. [Abstract] [Full Text] [PDF] |
||||
![]() |
A Meyer-Heim, C Ammann-Reiffer, A Schmartz, J Schafer, F H Sennhauser, F Heinen, B Knecht, E Dabrowski, and I Borggraefe Improvement of walking abilities after robotic-assisted locomotion training in children with cerebral palsy Arch. Dis. Child., August 1, 2009; 94(8): 615 - 620. [Abstract] [Full Text] [PDF] |
||||
![]() |
L.-R. Zhao, S. Singhal, W.-M. Duan, J. Mehta, and J. A. Kessler Brain Repair by Hematopoietic Growth Factors in a Rat Model of Stroke Stroke, September 1, 2007; 38(9): 2584 - 2591. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. G. Lindberg, C. Schmitz, M. Engardt, H. Forssberg, and J. Borg Use-Dependent Up- and Down-Regulation of Sensorimotor Brain Circuits in Stroke Patients Neurorehabil Neural Repair, July 1, 2007; 21(4): 315 - 326. [Abstract] [PDF] |
||||
![]() |
L. A Boyd, E. D Vidoni, and J. J Daly Answering the Call: The Influence of Neuroimaging and Electrophysiological Evidence on Rehabilitation Physical Therapy, June 1, 2007; 87(6): 684 - 703. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. F. Johnston, C. Yang, K.-K. Hui, B. Xiao, X. Li, and A. Rusiewicz Acupuncture for Chemotherapy-Associated Cognitive Dysfunction: A Hypothesis-Generating Literature Review to Inform Clinical Advice Integr Cancer Ther, March 1, 2007; 6(1): 36 - 41. [Abstract] [PDF] |
||||
![]() |
J.-C. Chen, C.-C. Liang, and F.-Z. Shaw Facilitation of Sensory and Motor Recovery by Thermal Intervention for the Hemiplegic Upper Limb in Acute Stroke Patients: A Single-Blind Randomized Clinical Trial Stroke, December 1, 2005; 36(12): 2665 - 2669. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Jaillard, C. D. Martin, K. Garambois, J. F. Lebas, and M. Hommel Vicarious function within the human primary motor cortex?: A longitudinal fMRI stroke study Brain, May 1, 2005; 128(5): 1122 - 1138. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. N. Alexander, S. Cen, K. J. Sullivan, G. Bhavnani, X. Ma, S. P. Azen, and ASAP Study Group Effects of Acupuncture Treatment on Poststroke Motor Recovery and Physical Function: A Pilot Study Neurorehabil Neural Repair, December 1, 2004; 18(4): 259 - 267. [Abstract] [PDF] |
||||
![]() |
F Alarcon, J C M Zijlmans, G Duenas, and N Cevallos Post-stroke movement disorders: report of 56 patients J. Neurol. Neurosurg. Psychiatry, November 1, 2004; 75(11): 1568 - 1574. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. R. Dinse Sound Case for Enrichment. Focus on "Environmental Enrichment Improves Response Strength, Threshold, Selectivity, and Latency of Auditory Cortex Neurons" J Neurophysiol, July 1, 2004; 92(1): 36 - 37. [Full Text] [PDF] |
||||
![]() |
J. Bernhardt, H. Dewey, A. Thrift, and G. Donnan Inactive and Alone: Physical Activity Within the First 14 Days of Acute Stroke Unit Care Stroke, April 1, 2004; 35(4): 1005 - 1009. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. H Crosbie, S. M McDonough, D. H Gilmore, and M I. Wiggam The adjunctive role of mental practice in the rehabilitation of the upper limb after hemiplegic stroke: a pilot studya Clinical Rehabilitation, January 1, 2004; 18(1): 60 - 68. [Abstract] [PDF] |
||||
![]() |
N. Byl, J. Roderick, O. Mohamed, M. Hanny, J. Kotler, A. Smith, M. Tang, and G. Abrams Effectiveness of Sensory and Motor Rehabilitation of the Upper Limb Following the Principles of Neuroplasticity: Patients Stable Poststroke Neurorehabil Neural Repair, September 1, 2003; 17(3): 176 - 191. [Abstract] [PDF] |
||||
![]() |
T Ago, T Kitazono, H Ooboshi, J Takada, T Yoshiura, F Mihara, S Ibayashi, and M Iida Deterioration of pre-existing hemiparesis brought about by subsequent ipsilateral lacunar infarction J. Neurol. Neurosurg. Psychiatry, August 1, 2003; 74(8): 1152 - 1153. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. M. Dijkhuizen, A. B. Singhal, J. B. Mandeville, O. Wu, E. F. Halpern, S. P. Finklestein, B. R. Rosen, and E. H. Lo Correlation between Brain Reorganization, Ischemic Damage, and Neurologic Status after Transient Focal Cerebral Ischemia in Rats: A Functional Magnetic Resonance Imaging Study J. Neurosci., January 15, 2003; 23(2): 510 - 517. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. J. Gladstone, S. E. Black, and A. M. Hakim Toward Wisdom From Failure: Lessons From Neuroprotective Stroke Trials and New Therapeutic Directions Stroke, August 1, 2002; 33(8): 2123 - 2136. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. L. Small, P. Hlustik, D. C. Noll, C. Genovese, and A. Solodkin Cerebellar hemispheric activation ipsilateral to the paretic hand correlates with functional recovery after stroke Brain, July 1, 2002; 125(7): 1544 - 1557. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. H. Cauraugh and S. Kim Two Coupled Motor Recovery Protocols Are Better Than One: Electromyogram-Triggered Neuromuscular Stimulation and Bilateral Movements Stroke, June 1, 2002; 33(6): 1589 - 1594. [Abstract] [Full Text] [PDF] |
||||
![]() |
V. Hachinski Stroke: The Next 30 Years Stroke, January 1, 2002; 33(1): 1 - 4. [Full Text] [PDF] |
||||
![]() |
R. M. Dijkhuizen, J. Ren, J. B. Mandeville, O. Wu, F. M. Ozdag, M. A. Moskowitz, B. R. Rosen, and S. P. Finklestein Functional magnetic resonance imaging of reorganization in rat brain after stroke PNAS, October 12, 2001; (2001) 231235598. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Nilsson, J. Carlsson, A. Danielsson, A. Fugl-Meyer, K. Hellstrom, L. Kristensen, B. Sjolund, K. S. Sunnerhagen, and G. Grimby Walking training of patients with hemiparesis at an early stage after stroke: a comparison of walking training on a treadmill with body weight support and walking training on the ground Clinical Rehabilitation, May 1, 2001; 15(5): 515 - 527. [Abstract] [PDF] |
||||
![]() |
B. B. Johansson, E. Haker, M. von Arbin, M. Britton, G. Langstrom, A. Terent, D. Ursing, and K. Asplund Acupuncture and Transcutaneous Nerve Stimulation in Stroke Rehabilitation : A Randomized, Controlled Trial Stroke, March 1, 2001; 32(3): 707 - 713. [Abstract] [Full Text] [PDF] |
||||
![]() |
F. J. Seil and R. Drake-Baumann TrkB Receptor Ligands Promote Activity-Dependent Inhibitory Synaptogenesis J. Neurosci., July 15, 2000; 20(14): 5367 - 5373. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. M. Dijkhuizen, J. Ren, J. B. Mandeville, O. Wu, F. M. Ozdag, M. A. Moskowitz, B. R. Rosen, and S. P. Finklestein Functional magnetic resonance imaging of reorganization in rat brain after stroke PNAS, October 23, 2001; 98(22): 12766 - 12771. [Abstract] [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2000 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |