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Review
, 5 (6), 759-68

Transcranial Direct Current Stimulation: A Noninvasive Tool to Facilitate Stroke Recovery

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Review

Transcranial Direct Current Stimulation: A Noninvasive Tool to Facilitate Stroke Recovery

Gottfried Schlaug et al. Expert Rev Med Devices.

Abstract

Electrical brain stimulation, a technique developed many decades ago and then largely forgotten, has re-emerged recently as a promising tool for experimental neuroscientists, clinical neurologists and psychiatrists in their quest to causally probe cortical representations of sensorimotor and cognitive functions and to facilitate the treatment of various neuropsychiatric disorders. In this regard, a better understanding of adaptive and maladaptive plasticity in natural stroke recovery over the last decade and the idea that brain polarization may modulate neuroplasticity has led to the use of transcranial direct current stimulation (tDCS) as a potential enhancer of natural stroke recovery. We will review tDCS's successful utilization in pilot and proof-of-principle stroke recovery studies, the different modes of tDCS currently in use, and the potential mechanisms underlying the neural effects of tDCS.

Figures

Figure 1
Figure 1. Transcranial direct current stimulation set-up
This figure shows a mobile, battery-operated direct current stimulator connected with two electrodes. One electrode (active) is positioned over C3 (corresponding to the precentral gyrus) and the reference electrode is positioned over the contralateral supraorbital region. If current flows from C3 to the supraorbital region, then the tissue underlying C3 is subjected to anodal (increase in excitability) stimulation. If current is reversed, then the tissue underlying C3 is subjected to cathodal (decrease in excitability) stimulation.
Figure 2
Figure 2. Functional MRI (fMRI) activation pattern in stroke recovery
fMRI studies in patients recovering from a stroke have shown that the ipsilateral (to the moving hand) sensorimotor cortex can become active when a patient performs a movement with their recovering hand. The patient in (A) had a stroke in the right hemisphere and was asked to move his left wrist, which is the recovering wrist; fMRI shows activation of the contralateral (to the moving hand) motor cortex as well as the ipsilateral motor cortex. (B) Applying cathodal stimulation to the nonlesional motor cortex (the motor cortex that activated when the recovering wrist was moving) significantly decreased the activation on the ipsilateral site and was associated with an improvement in this patient’s functional motor status.
Figure 3
Figure 3. Brain model of abnormal interhemispheric inhibition and the therapeutic options to ameliorate this imbalance
(A) The balance of interhemispheric inhibition becomes disrupted after a stroke. This leaves the healthy hemisphere in a position that it could exert too much of an unopposed influence onto the lesional hemisphere and possibly interfere in the recovery process. There are two possible ways to ameliorate this process: either (B) the excitability in the affected (lesional) hemisphere is upregulated or (C) the excitability in the unaffected (normal) hemisphere is downregulated.
Figure 4
Figure 4. Diffusion tensor imaging in stroke recovery
This picture shows two patients with their representative pyramidal tract fibers that originate from the white matter underlying the precentral gyrus and travel through the internal capsule into the brainstem. The lesional hemispheres show a difference between both patients. (A) One patient shows a reduced number of fibers that descend and go through the internal capsule into the brainstem while (B) the other patient does not have fibers that originate from the hand/arm region of the precentral gyrus, although some fibers seem to descend through the internal capsule. The stroke lesion in this patient has disrupted the pyramidal fiber bundle. The improvement after transcranial direct current stimulation in combination with occupational therapy was pronounced in the patient with intact pyramidal tract but only minimal in the patient with the disrupted pyramidal tract.

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