Using Transcranial Direct Current Stimulation over Front-Polar Area: History
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Contributor:
Koji Ishikuro
,
Noriaki Hattori
,
Hironori Otomune
,
Kohta Furuya
,
Takeshi Nakada
,
Kenichiro Miyahara
,
Takashi Shibata
,
Kyo Noguchi
,
Satoshi Kuroda
,
Yuji Nakatsuji
,
Hisao Nishijo

Transcranial direct current stimulation (tDCS) is a noninvasive brain stimulation (NIBS) technique that applies a weak current to the scalp to modulate neuronal excitability by stimulating the cerebral cortex. The technique can produce either somatic depolarization (anodal stimulation) or somatic hyperpolarization (cathodal stimulation), based on the polarity of the current used by noninvasively stimulating the cerebral cortex with a weak current from the scalp, making it a NIBS technique that can modulate neuronal excitability. Thus, tDCS has emerged as a hopeful clinical neuro-rehabilitation treatment strategy. This method has a broad range of potential uses in rehabilitation medicine for neurodegenerative diseases, including Parkinson’s disease (PD). 

  • transcranial direct current stimulation
  • Parkinson’s disease

1. Introduction

Techniques for noninvasive brain stimulation (NIBS) have been widely used in both patients and healthy people. A more accurate description of NIBS is that it is a low-intensity transcranial stimulation to modulate cortical excitability. There are two well-known neuromodulation therapies based on this strategy: repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS). rTMS applies magnetism to modulate cortical excitability, while tDCS uses electrical stimulation instead. While rTMS can stimulate the cortex with minimal reduction in stimulation intensity from the scalp, it is essential for the patient’s head to be secured to a comfortable chair to ensure precise stimulation of the region of interest (ROI). However, clinical situations can pose a challenge for rTMS, as patients may often exhibit involuntary movements that hinder fixation of the head position. Additionally, while it is infrequent, rTMS can cause harmful effects such as seizures. Conversely, tDCS has advantages in hospital settings, such as ease of usage, fewer adverse events, and high portability. Therefore, tDCS can be used in combination with physical rehabilitation to enhance plastic changes in ongoing synapses activated during physical rehabilitation [1][2]. Furthermore, recent research has consistently demonstrated that the combination of tDCS and rehabilitation is more effective than utilizing tDCS alone in the long-term improvement of neurological disease symptoms [1][2][3][4][5][6].
tDCS can safely modulate cortical activity in both acute (immediate) and after (chronic) effects. In acute effects during stimulation, tDCS can modulate cortical neuronal activity. For example, anodal stimulation can increase cortical excitability by depolarizing the soma and basal dendrite of cortical pyramidal neurons (somatic hypothesis) [7]. On the other hand, cathodal stimulation can produce opposite effects, i.e., hyperpolarization of the basal dendrites and soma [8][9]. Consistent with the somatic hypothesis, firing rates of putative pyramidal neurons were elevated by anodal stimulation and suppressed by cathodal stimulation in monkeys [10]. However, firing rates of putative inhibitory neurons increased with both anodal and cathodal stimulation (i.e., regardless of polarity). This is likely due to network-mediated effects resulting from the modulation of other cell types [10]. In after effects, tDCS may modulate cortical and subcortical synaptic connections (synaptic plasticity) [2]. Previous studies have reported that tDCS can facilitate motor learning through synaptic plasticity. This effect is mediated through the induction of nitric oxide (NO), activation of neurotrophic tyrosine kinase receptor type 2 (TrkB), and expression of brain-derived neurotrophic factor (BDNF) to promote synaptic plasticity [11][12]. These molecular mechanisms might underlie the molecular backgrounds for long-term potentiation (LTP) and long-term depression (LTD), and modulate synaptic connections in after effects. Therefore, due to its safety, application of tDCS to modulate cortical activity has been increasing in basic and clinical research since 2000 [13][14][15].
Thus, tDCS is increasingly being applied as a therapy for the motor symptoms of diverse brain disorders such as Parkinson’s disease (PD). Recently, the front-polar area (FPA) (Brodmann area 10) has garnered increased attention in motor learning, an important factor in rehabilitation.

2. tDCS Effects of the Front-Polar Area (FPA) in Rehabilitation

2.1. A Role of the FPA in Motor Learning and Rehabilitation

Multiple lines of evidence support the notion that the FPA may represent a new therapeutic target for tDCS-based rehabilitation, aimed at motor learning. The role played by the most anterior portion of the prefrontal cortex (PFC) (i.e., FPA) in motor learning is unique in various regards. Some previous noninvasive imaging studies have demonstrated that the FPA is mainly activated when subjects acquire novel motor task(s) [16][17][18]. Recently, Kobayashi et al. (2021) examined FPA activity during the acquisition of a sequential motor task with near-infrared spectroscopy (NIRS) [19]. The study required inexperienced participants to sequentially lay the right hands on a table at a steady pace of three movements per sec, using three distinct hand postures: a fist held vertically, a palm held vertically, and a palm held horizontally [sequential motor (SM) task]. In the control motor task, the subjects repeatedly tapped the table with their right palm at the same speed. This control task could be executed without any motor learning. For both tasks, the participants completed three trials in 30 sec per trial, and performance errors were counted in each trial [19]. The results indicated that hemodynamic cortical activity (Oxy-Hb) was prominent in the PFC, including the FPA and dlPFC, in the first trial, but decreased in later trials in the SM task. No such prominent responses were observed in the control motor task. Cortical activity changes between the initial (first) and subsequent (second) trials in the sequential motor task, were positively correlated with error reduction between the initial and subsequent trials, representing performance improvement by learning. These findings support the notion that the FPA contributes significantly to motor learning, as there is a positive relation between larger hemodynamic cortical activity changes in the PFC, including the FPA, and a larger performance improvement.
These results suggest that the FPA plays a role in motor rehabilitation, where motor learning plays a crucial part. Ishikuro et al. (2014) examined the function of the FPA in motor learning in rehabilitation using NIRS [20]. Healthy participants were asked to perform a peg board task for upper-extremity functions in the simple test for evaluating hand function (STEF): they picked up a peg using their right thumb and index finger and inserted it into a hole in the STEFF board. The pegs are small pins used for this activity. In each of the eight trials, the subjects had to repeat these actions as fast as possible for 20 seconds. It is noteworthy that the subjects were required to continuously improve their performance over the eight trials, which contrasts with the study of Kobayashi et al. (2021). The results again indicated that the FPA was highly active during this task in which continuous performance improvement was required. Furthermore, both behavioral performance (peg score, i.e., the number of pegs inserted into the peg holes per trial) and cortical activity in the FPA during the peg board task increased incrementally in subsequent trials. To measure the incremental speed of these two parameters across the eight trials in each subject, both parameters were subjected to simple linear regression analysis. “Incremental speed of hemodynamic activity (Oxy-Hb gain)” was assessed by the slope of this fitted line. In the same way, “Incremental speed of behavioral performance (performance gain)” was evaluated by its slope of the fitted line. 

2.2. Modulatory Effects of the FPA on the Motor-Related Regions

Previous studies suggest that the primary motor area (M1 area) is implicated in skilled motor learning, where functional reorganization and synaptic plasticity occur [12][21]. Since the FPA projects to the M1 area indirectly by way of other cortical areas including the dlPFC [22][23][24], the FPA might reorganize synaptic connections in the M1 areas to improve motor skills. Previous tDCS studies reported that M1 tDCS reorganized not only functional connectivity within the M1 area, but also functional connectivity between the M1 and other cortical areas, and between the M1 and subcortical areas to improve motor rehabilitation [25][26][27]. Therefore, tDCS over the FPA may facilitate the FPA role to improve motor learning, partly through induction of reorganization and synaptic plasticity in the M1 area. Ota et al. (2020) investigated this possibility by activating the FPA by means of neurofeedback (NFB) training instead of tDCS [28]. In NFB training, half of the subjects were shown hemodynamic cortical activity of their own FPA on a monitor (real NFB training), while the remaining subjects were shown randomized false activity (sham NFB training). All subjects received the NFB training for 6 days, in which they performed imagery of a peg board task to increase FPA activity under the feedback of their own FPA or randomized false activity. Before and after the NFB training, the subjects received NIRS studies to assess brain hemodynamic activity during the performance of the peg board task. After the NFB training, the subjects with the real NFB training exhibited hemodynamic cortical responses in the left somatosensory and motor-related areas including the premotor area (PMA), M1 area, and primary somatosensory cortex (S1), while the subjects with the sham NFB training exhibited hemodynamic cortical responses in the supplementary motor area (SMA). Additional analyses indicated that cortical activity gain in the hand area of the M1 (lateral part of the left M (lateral Lt-M1)), which was defined as activity in the lateral Lt-M1 area before the NFB training divided by that after the NFB training, was significantly linked to performance gain, defined as peg scores before the training divided by those after the training. Furthermore, cortical activity in the left somatosensory and motor-related areas during the performance of the peg board task after the NFB training was significantly and positively linked to cortical activity in the FPA during the performance of the imagery on the last day of the NFB training. These results suggest that the FPA reorganizes synaptic connectivity patterns in the M1 area, so that reorganized activity patterns of M1 neurons in the M1 area are more suitable for the peg board task [28]. Interestingly, in the subjects with the sham NFB training, cortical activity in the SMA increased during the performance of the peg board task after the training (see above). The SMA has been proposed to function as “an action monitoring system” that provides warning signals for errors and incorrect responses [29]. In the sham NFB training, the participants were shown randomly generated feedback signals that were irrelevant to performing the peg board task, suggesting that the FPA could lead to erroneous reorganization of the synaptic connectivity patterns in the M1 area during the sham NFB training. These findings suggest the SMA activity after the sham NFB training is involved in detection of erroneous synaptic activity in the somatosensory and motor-related areas, which may promote reformation of correct (new) association between incoming sensory inputs and motor responses.

2.3. Effects of the tDCS over the FPA in Parkinson's Disease

It has been suggested that tDCS over the M1 area or dlPFC improves motor or nonmotor symptoms in PD, and that tDCS over the FPA promotes motor learning through reorganization of M1 activity in healthy people, further suggesting that tDCS over the FPA may ameliorate PD symptoms. Ishikuro et al. [30] investigated effects of tDCS (anodal, cathodal, and sham tDCS) over the FPA on motor and nonmotor symptoms in a cross-over design in PD patients [30]. They reported that anodal tDCS significantly reduced normalized scores of motor disability in the Unified PD Rating Scale (UPDRS (part III)), and significantly raised scores of motor functions in the Fugl Meyer Assessment set (FMA), while it significantly reduced time to complete a high dexterity task in STEF [30]. The same anodal tDCS also improved nonmotor function: reduction of normalized time required to complete the Trail Making Test A (TMT-A) to assess attention/executive functions. Thus, the tDCS of the FPA ameliorated not only motor, but also nonmotor symptoms in PD.

Dopamine neurons in the midbrain receive glutamate transmissions directly or indirectly from the PFC [31][32][33][34]. Additionally, dopamine neuron activity is functionally associated with PFC neuron activity [35][36], and tDCS of the PFC can substantially raise dopamine and tyrosine levels in PD model mice [37]. Therefore, it is plausible to assume that FPA stimulation, which likely sends excitatory projections to midbrain dopamine neurons or activates the dlPFC projecting to dopamine neurons, could impact dopamine cells in the midbrain of individuals with PD. Ishikuro et al. (2021) examined effects of tDCS over the FPA in one PD patient as a case report, using noninvasive imaging of neuromelanin to reveal dopamine neurons [38]. They reported that the same tDCS protocol (i.e., 2 weeks of rehabilitation with tDCS in the FPA) increased the neuromelanin-sensitive area in the substantial nigra pars compacta (SNc), where dopamine neurons are located, from 43.2 to 53.2 mm2 (increases by 18.8%), and that the patient exhibits clinically meaningful improvement of motor deficits. Since dopamine is crucial for executive functions in the PFC [39][40], these findings indicate that tDCS over the FPA, combined with physical rehabilitation, might cause plastic changes in the dopamine neurons of PD patients, resulting in an improvement of both motor and nonmotor symptoms (e.g., deficits in executive functions).

3. Conclusions

Emerging evidence suggests that tDCS can safely modulate neuronal excitability by producing either somatic depolarization (anodal stimulation) or somatic hyperpolarization (cathodal stimulation), based on the polarity of a weak current from the scalp. This technology has become increasingly popular in the field of rehabilitation medicine for treating neurodegenerative illnesses, such as PD.
Previous studies have primarily applied tDCS to the M1 region in PD patients, and have reported the usefulness of tDCS in neuro-rehabilitation. Recent neuropsychological and clinical studies have reported that tDCS of the FPA can improve motor learning and motor functions in both healthy participants and patients with PD. tDCS over the FPA may promote motor skill learning through its effects on the M1 area and/or midbrain dopamine neurons. Furthermore, recent studies have revealed additional distinctive effects of tDCS of the FPA, including impacts on persistence and motivation [41][42], which are important for rehabilitation. These results suggest that the FPA could be a new target for the application of tDCS in neuro-rehabilitation.

This entry is adapted from the peer-reviewed paper 10.3390/brainsci13111604

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