اندازه گیری و القاء شکل پذیری مغز در زبان پریشی مزمن

Brain plasticity associated with anomia recovery in aphasia is poorly understood. Here, I review four recent studies from my lab that focused on brain modulation associated with long-term anomia outcome, its behavioral treatment, and the use of transcranial brain stimulation to enhance anomia treatment success in individuals with chronic aphasia caused by left hemisphere stroke. In a study that included 15 participants with aphasia who were compared to a group of 10 normal control subjects, we found that improved naming ability was associated with increased left hemisphere activity. A separate study (N = 26) revealed similar results in that improved anomia treatment outcome was associated with increased left hemisphere recruitment. Taken together, these two studies suggest that improved naming in chronic aphasia relies on the damaged left hemisphere. Based on these findings, we conducted two studies to appreciate the effect of using low current transcranial electrical stimulation as an adjuvant to behavioral anomia treatment. Both studies yielded positive findings in that anomia treatment outcome was improved when it was coupled with real brain stimulation as compared with a placebo (sham) condition. Overall, these four studies support the notion that the intact cortex in the lesioned left hemisphere supports anomia recovery in aphasia. Learning outcomes: Readers will (a) be able to appreciate the possible influence of animal research upon the understanding of brain plasticity induced by aphasia treatment, (b) understand where functional changes associated with anomia treatment occur in the brain, (c) understand the basic principles of transcranial direct current stimulation, and (d) understand how brain stimulation coupled with aphasia treatment may potentially improve treatment outcome. Highlights ► Greater left hemisphere activity is associated with better naming ability in chronic stroke. ► Positive anomia treatment outcomes are associated with left hemisphere recruitment. ► Anodal transcranial direct current stimulation (A-tDCS) enhances the effectiveness of anomia treatment in chronic aphasia. ► New developments may allow perilesional areas to be specifically targeted by tDCS.

Improved understanding of plasticity in the adult brain suggests that the human cortex is quite amenable to both functional and structural change (e.g., Butefisch, 2004, Heiss and Thiel, 2006, Meinzer et al., 2008, Nudo, 2003, Nudo, 2007, Pascual-Leone et al., 2005, Saur et al., 2006 and Thompson and den Ouden, 2008). Currently, there is no evidence suggesting that plasticity is absent or even reduced following brain damage. In fact, neural sprouting has been shown to be enhanced in the brain regions surrounding the frank cortical lesion (Nudo, 1999 and Stroemer et al., 1995). For the most part, aphasia treatment research has taken only limited advantage of the recently improved understanding of brain plasticity. Although several reasons may underlie this development, or lack thereof, it is undoubtedly important that much of the recent advances in understanding brain plasticity have been revealed in animal models of motor impairment. For example, utilizing a rat model, Jones and colleagues (as reviewed in the current issue) have shown how early training of the spared forelimb following induced motor cortex damage negatively affects later function of the affected forelimb. Related to language impairment and its rehabilitation, it is not clear how these findings by Jones’ group can be applied. More generally, it is uncertain how improved understanding of brain plasticity in animal models of motor impairment may relate to aphasia. Nevertheless, it is crucial to emphasize that principles of brain plasticity in animal models probably relate to human recovery of communication abilities. At the very least, improved understanding between training in brain lesioned animals and outcome may fuel research questions that can be applied to recovery from aphasia. For example, is it possible that early treatment that targets relatively spared communication abilities may negatively affect later recovery of less spared language functions? Although the application of animal models to the understanding of brain plasticity associated with aphasia recovery is not so straightforward, neuroimaging studies in humans have so far provided some insight into brain plasticity associated with aphasia treatment (for a brief review see Crinion and Leff, 2007 and Fridriksson, 2010). As importantly, studies have revealed, albeit indirectly, that external brain stimulation can enhance brain plasticity associated with aphasia treatment. In the following paragraphs, I will review recent studies conducted in my lab that have focused on functional brain changes associated with aphasia treatment as well as the use of low current transcranial brain stimulation to enhance aphasia treatment outcome. My aim is to demonstrate how studies of treatment-related brain plasticity (as measured with functional magnetic resonance imaging: fMRI) in persons with aphasia can motivate research that seeks to combine behavioral stimulation with transcranial brain stimulation to enhance treatment outcome and, presumably, brain plasticity.

Our studies of functional brain changes associated with improved naming in aphasia suggest that, in general, the left hemisphere is recruited for better outcome. Importantly, this does not necessarily mean that the right hemisphere does not contribute to anomia recovery in some patients. Rather, those individuals that benefit the most from treatment primarily recruit the left hemisphere to support naming improvement. Our studies also suggest that A-tDCS targeting the left hemisphere can improve anomia treatment outcome. In a series of elegant studies, Naeser and colleagues have found that low frequency transcranial magnetic stimulation (TMS) over the right hemisphere homologue of Broca's area may decrease activity in this region and, as a result, improve naming by persons with nonfluent aphasia (Martin et al., 2009, Naeser et al., 2005a, Naeser et al., 2005b and Naeser et al., 2010). It is possible that the use of cathodal tDCS (C-tDCS), a method that has been suggested to decrease cortical excitability, to target the right hemisphere homologue of Broca's treatment during anomia treatment can yield similar effects as that demonstrated by Naeser's group. Perhaps future studies can examine the combined effects of targeting maladaptive brain activation with C-tDCS while using A-tDCS to increase activity in cortical regions whose increased activation is thought to improve treatment outcome. Currently, no studies of this nature have been presented.