Generalities, so useless. Damn it all, THE WHOLE FUCKING POINT OF STROKE RESEARCH IS PROTOCOLS LEADING TO 100% RECOVERY, not this pablum.
Non-invasive brain stimulation in neurorehabilitation: local and distant effects for motor recovery
MARCO SANDRINI1,2 AND LEONARDO G. COHEN1* 1Human Cortical Physiology and Stroke Neurorehabilitation Section, National Institutes of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA 2Center for Neuroscience and Regenerative Medicine at the Uniformed Services University of Health Science, Bethesda, MD, USA
INTRODUCTION
Stroke is the major cause of long-term disability worldwide (Kolominsky-Rabas et al., 2001) and recovery of motor function is often incomplete (Roger et al., 2011). Six months after the ictal event, two-thirds of stroke survivors are unable to carry out independently activities of daily living with their paretic hand to the extent they could before (Kolominsky-Rabas et al., 2001), and only a few are able to return to their previous job (Lai et al., 2002). Patients with motor deficits resulting from stroke must confront the need to generate compensatory strategies or to relearn the motor programs utilized to accomplish a particular goal before the lesion (Frey et al., 2011; Pomeroy et al., 2011; Sathian et al., 2011). From a behavioral point of view, there are different ways to accomplish the same goal in neurorehabilitation (e.g., grasp a glass of water). One possibility is to implement a motor strategy different from that utilized before the stroke (i.e., compensation) (Levin et al., 2009). An alternative way is to relearn to perform the task in the same way it was done before the lesion. Clearly, both processes are likely to involve fundamentally different pathophysiological mechanisms, even when the goals and outcomes are the same. Different motor training strategies have been tested in neurorehabilitation of motor function. Examples include constraint-induced movement therapy, bilateral arm training, mirror therapy, randomized training schedules, robotic-based approaches, virtual reality, electromyogram-triggered stimulation, action observation, motor imagery, and brain–computer interfaces between others (Cauraugh and Kim, 2003; Wittenberg
et al., 2003; Bolton et al., 2004; Deutsch et al., 2004; Luft et al., 2004; Krakauer, 2006; Sharma et al., 2006; Birbaumer and Cohen, 2007; Ertelt et al., 2007; Page et al., 2007; Buch et al., 2008, 2012; Celnik et al., 2008; Cramer, 2008b; Cheeran et al., 2009a; Lo et al., 2009; Dimyan and Cohen, 2011). Noninvasive somatosensory (Conforto et al., 2007, 2010), transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS) (Hallett, 2000; Kaelin-Lang et al., 2002; Nitsche et al., 2008; Wassermann et al., 2008; Sandrini et al., 2011; Tanaka et al., 2011; Brunoni et al., 2012) have been proposed as adjuvant ways to improve the beneficial effects of training protocols on functional recovery. In this chapter, we discuss the use of noninvasive brain stimulation (NIBS) in the setting of stroke rehabilitation. Interest in NIBS developed after the observation of long-term effects on cortical excitability that occur after repeated stimulation (Huang et al., 2005; Fitzgerald et al., 2006; Nitsche et al., 2008). Depending on the stimulation parameters, motor cortical excitability can be reduced (inhibition) by means of low-frequency repetitive TMS (rTMS), continuous theta-burst stimulation(cTBS),andcathodaltDCS,orenhanced(facilitation) by means of high-frequency rTMS, intermittent thetaburst stimulation (iTBS), and anodal stimulation. There isevidencethatlinkstheeffectsoftheseNIBStechniques to long-term potentiation (LTP)-like and long-term depression (LTD)-like mechanisms (Cooke and Bliss, 2006; Thickbroom, 2007; Wagner et al., 2007; Ziemann et al., 2008; Fritsch et al., 2010). After stroke, NIBS has been studied as a tool to modulate cortical excitability in the affected and intact hemispheres, predominantly
*Correspondenceto:LeonardoG.Cohen,HumanCorticalPhysiologyandStrokeNeurorehabilitationSection,NationalInstitute of Neurological Disorders and Stroke, National Institutes of Health, 10 Center Drive Bethesda, Maryland 20892-1430, USA. E-mail: cohenl@ninds.nih.gov
Handbook of Clinical Neurology, Vol. 116 (3rd series) Brain Stimulation A.M. Lozano and M. Hallett, Editors 2013 Published by Elsevier B.V.
with the goal of correcting hypothesized imbalances in interhemispheric interactions (Kinsbourne, 1974; Hummel and Cohen, 2006).
INTRODUCTION
Stroke is the major cause of long-term disability worldwide (Kolominsky-Rabas et al., 2001) and recovery of motor function is often incomplete (Roger et al., 2011). Six months after the ictal event, two-thirds of stroke survivors are unable to carry out independently activities of daily living with their paretic hand to the extent they could before (Kolominsky-Rabas et al., 2001), and only a few are able to return to their previous job (Lai et al., 2002). Patients with motor deficits resulting from stroke must confront the need to generate compensatory strategies or to relearn the motor programs utilized to accomplish a particular goal before the lesion (Frey et al., 2011; Pomeroy et al., 2011; Sathian et al., 2011). From a behavioral point of view, there are different ways to accomplish the same goal in neurorehabilitation (e.g., grasp a glass of water). One possibility is to implement a motor strategy different from that utilized before the stroke (i.e., compensation) (Levin et al., 2009). An alternative way is to relearn to perform the task in the same way it was done before the lesion. Clearly, both processes are likely to involve fundamentally different pathophysiological mechanisms, even when the goals and outcomes are the same. Different motor training strategies have been tested in neurorehabilitation of motor function. Examples include constraint-induced movement therapy, bilateral arm training, mirror therapy, randomized training schedules, robotic-based approaches, virtual reality, electromyogram-triggered stimulation, action observation, motor imagery, and brain–computer interfaces between others (Cauraugh and Kim, 2003; Wittenberg
et al., 2003; Bolton et al., 2004; Deutsch et al., 2004; Luft et al., 2004; Krakauer, 2006; Sharma et al., 2006; Birbaumer and Cohen, 2007; Ertelt et al., 2007; Page et al., 2007; Buch et al., 2008, 2012; Celnik et al., 2008; Cramer, 2008b; Cheeran et al., 2009a; Lo et al., 2009; Dimyan and Cohen, 2011). Noninvasive somatosensory (Conforto et al., 2007, 2010), transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS) (Hallett, 2000; Kaelin-Lang et al., 2002; Nitsche et al., 2008; Wassermann et al., 2008; Sandrini et al., 2011; Tanaka et al., 2011; Brunoni et al., 2012) have been proposed as adjuvant ways to improve the beneficial effects of training protocols on functional recovery. In this chapter, we discuss the use of noninvasive brain stimulation (NIBS) in the setting of stroke rehabilitation. Interest in NIBS developed after the observation of long-term effects on cortical excitability that occur after repeated stimulation (Huang et al., 2005; Fitzgerald et al., 2006; Nitsche et al., 2008). Depending on the stimulation parameters, motor cortical excitability can be reduced (inhibition) by means of low-frequency repetitive TMS (rTMS), continuous theta-burst stimulation(cTBS),andcathodaltDCS,orenhanced(facilitation) by means of high-frequency rTMS, intermittent thetaburst stimulation (iTBS), and anodal stimulation. There isevidencethatlinkstheeffectsoftheseNIBStechniques to long-term potentiation (LTP)-like and long-term depression (LTD)-like mechanisms (Cooke and Bliss, 2006; Thickbroom, 2007; Wagner et al., 2007; Ziemann et al., 2008; Fritsch et al., 2010). After stroke, NIBS has been studied as a tool to modulate cortical excitability in the affected and intact hemispheres, predominantly
*Correspondenceto:LeonardoG.Cohen,HumanCorticalPhysiologyandStrokeNeurorehabilitationSection,NationalInstitute of Neurological Disorders and Stroke, National Institutes of Health, 10 Center Drive Bethesda, Maryland 20892-1430, USA. E-mail: cohenl@ninds.nih.gov
Handbook of Clinical Neurology, Vol. 116 (3rd series) Brain Stimulation A.M. Lozano and M. Hallett, Editors 2013 Published by Elsevier B.V.
with the goal of correcting hypothesized imbalances in interhemispheric interactions (Kinsbourne, 1974; Hummel and Cohen, 2006).
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