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      The Ipsilesional Upper Limb Can Be Affected following Stroke

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          Abstract

          Objective. Neurological dysfunction commonly occurs in the upper limb contralateral to the hemisphere of the brain in which stroke occurs; however, the impact of stroke on function of the ipsilesional upper limb is not well understood. This study aims to systematically review the literature relating to the function of the ipsilesional upper limb following stroke and answer the following research question: Is the ipsilesional upper limb affected by stroke? Data Source. A systematic review was carried out in Medline, Embase, and PubMed. Review Methods. All studies investigating the ipsilesional upper limb following stroke were included and analysed for important characteristics. Outcomes were extracted and summarised. Results. This review captured 27 articles that met the inclusion criteria. All studies provided evidence that the ipsilesional upper limb can be affected following stroke. Conclusion. These findings demonstrate that clinicians should consider ipsilesional upper limb deficits in rehabilitation and address this reduced functional capacity. Furthermore, the ipsilesional upper limb should not be used as a “control” measure of recovery for the contralateral upper limb.

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          Most cited references39

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          Reorganization of cerebral networks after stroke: new insights from neuroimaging with connectivity approaches

          The motor system comprises a network of cortical and subcortical areas interacting via excitatory and inhibitory circuits, thereby governing motor behaviour. The balance within the motor network may be critically disturbed after stroke when the lesion either directly affects any of these areas or damages-related white matter tracts. A growing body of evidence suggests that abnormal interactions among cortical regions remote from the ischaemic lesion might also contribute to the motor impairment after stroke. Here, we review recent studies employing models of functional and effective connectivity on neuroimaging data to investigate how stroke influences the interaction between motor areas and how changes in connectivity relate to impaired motor behaviour and functional recovery. Based on such data, we suggest that pathological intra- and inter-hemispheric interactions among key motor regions constitute an important pathophysiological aspect of motor impairment after subcortical stroke. We also demonstrate that therapeutic interventions, such as repetitive transcranial magnetic stimulation, which aims to interfere with abnormal cortical activity, may correct pathological connectivity not only at the stimulation site but also among distant brain regions. In summary, analyses of connectivity further our understanding of the pathophysiology underlying motor symptoms after stroke, and may thus help to design hypothesis-driven treatment strategies to promote recovery of motor function in patients.
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            Mechanisms underlying recovery of motor function after stroke.

            Stroke is the leading cause of long-term disability worldwide and a condition for which there is no universally accepted treatment. The development of new effective therapeutic strategies relies on a better understanding of the mechanisms underlying recovery of function. Noninvasive techniques to study brain function, including functional magnetic resonance imaging, positron emission tomography, transcranial magnetic stimulation, electroencephalography, and magnetoencephalography, led to recent studies that identified some of these operating mechanisms, resulting in the formulation of novel approaches to motor rehabilitation.
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              Motor cortical disinhibition in the unaffected hemisphere after unilateral cortical stroke.

              Following a hemispheric stroke, various degrees of neuronal reorganization around the lesion occur immediately after disease onset and thereafter up to several months. These include transcallosal excitability, changes of the intact motor cortex and ipsilateral motor responses after transcranial magnetic stimulation (TMS) on the intact hemisphere. To elucidate the relationship between lesion localization and motor cortex excitability (intracortical inhibition; ICI) in the intact hemisphere, we applied a paired conditioning-test TMS paradigm in 12 patients with unilateral cortical stroke (cortical group) and nine patients with subcortical stroke caudal to the corpus callosum (subcortical group), with interstimulus intervals varying from 1 to 10 ms. All patients exhibited unilateral complete hand palsy. ICI was significantly less in the cortical group than in age-matched healthy control subjects. It was especially more marked in the cortical group patients with a disease duration of less than 4 months after onset. Patients in the cortical group with a duration longer than 4 months showed a tendency for ICI to be normalized, and there was a significant correlation between ICI and disease duration. Patients in the subcortical group showed normal excitability curves. All patients in the cortical group showed no transcallosal inhibition (TCI) in the active unaffected hand muscle after TMS of the affected motor cortex, whereas all the subcortical patients showed some TCI. No ipsilateral motor responses were elicited in the paretic hand in any of the patients. The reduced ICI in the cortical group might have been a result of disruption of TCI. The normalization of ICI in the patients with longer disease duration and the normal ICI in the subcortical group patients do not support the functional significance of motor cortex hyperexcitability in the unaffected hemisphere, at least in a patient population with poor motor recovery.
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                Author and article information

                Journal
                ScientificWorldJournal
                ScientificWorldJournal
                TSWJ
                The Scientific World Journal
                Hindawi Publishing Corporation
                1537-744X
                2013
                26 November 2013
                : 2013
                : 684860
                Affiliations
                1Stroke Research, Neurology Department, John Hunter Hospital, Hunter New England Local Health District, Locked Bag 1, Hunter Regional Mail Centre, NSW 2310, Australia
                2School of Medicine and Public Health, University of Newcastle, Callaghan, NSW 2308, Australia
                3Hunter Brain Injury Service, Hunter New England Local Health District, Bar Beach, NSW 2300, Australia
                Author notes

                Academic Editors: A. Biegon and F. Gonzalez-Lima

                Article
                10.1155/2013/684860
                3860125
                24379748
                edaf76d1-c047-4465-965d-85835f967347
                Copyright © 2013 Gemma H. Kitsos et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 20 August 2013
                : 17 September 2013
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                Review Article

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