Neuroimaging Advances in Stroke Rehabilitation The Role of Spasticity
Virtually none of the studies cited above addressed the issue of spasticity, although it is a major sequel of stroke, impairing recovery.94
Spasticity develops within weeks after acute brain lesions, mainly in antigravity muscles such as leg extensors and arm flexors. Spasticity affects movement in terms of velocity and the movement path of limbs. It also requires an extra effort to move the afflicted limbs. One medical treatment option is to inject botulinum toxin (BTX) locally into the motor end plate regions of antigravity muscles to partially paralyse the concerned muscles. Agonists and antagonists immobilised by spasticity prior to injection can then move more freely again. The effect of BTX lasts for about three months until the blocked motor end plates have regenerated entraining a return of spasticity. BTX has been shown to be a safe, effective treatment of upper-limb spasticity caused by stroke or traumatic brain injury.95–97
In a recent
study, cyclic ergometer training prolonged the antispastic effect of BTX injection and yielded an increased range of motion of the paretic arm. In patients with residual motor function the decrease of spasticity due to combined cyclic ergometer training and BTX injection into forearm muscles was paralleled by an increase of fMRI activity in relation to passive arm movements in the dorsomedial portion of the sensorimotor cortex in the lesioned hemisphere and in the secondary somatosensory area of the non-lesioned hemisphere (see Figure 4). In contrast, there was no training-induced increase of fMRI activity with passive arm movements in completely paralysed patients, suggesting that in these patients both the efferent motor fibres and the afferent somatosensory fibres were severely damaged.98
High-resolution structural and functional brain imaging (including DTI) and TMS as diagnostic tools to assess motor evoked potentials constitute a powerful combination to explore the normal structure
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and function of the motor system as well as alterations of motor circuits caused by a stroke. Parameters derived from these modalities of systems physiology can be used as surrogate markers of the motor system’s functional integrity. Clinicians can potentially rely on this physiological information to determine which rehabilitation strategies are most appropriate for individual patients. Further, future developments in rehabilitation may employ this physiological information for designing innovative rehabilitation approaches and for predicting the therapeutic response to such interventions. n
Rüdiger J Seitz is a Professor of Neurology and Vice Chairman of the Department of Neurology at the University Hospital Düsseldorf and Biomedical Research Centre at the Heinrich-Heine-University Düsseldorf. He is a Distinguished Fellow of the Institute of Advanced Study at LaTrobe University and National Stroke Research Institute in Melbourne and an Honorary Professor at the Florey Neuroscience Institutes.
Robert Lindenberg is an Instructor in Neurology in the Department of Neurology at Beth Israel Deaconess Medical Center, Harvard Medical School and the Department of Neurology at the University Hospital Düsseldorf. He was a Research Fellow at Beth Israel Deaconess Medical Center and Harvard Medical School, and prior to that completed a residency in neurology at the University Hospital Düsseldorf.
Gottfried Schlaug is Chief of the Division of Cerebrovascular Disorders in the Department of Neurology at the Beth Israel Deaconess Medical Center and an Associate Professor of Neurology at Harvard Medical School. His research interests include the role of neuroimaging in stroke recovery and acute stroke treatment, and the effects of instrumental music training on brain and cognitive development.
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