Transcranial electrotherapy in the treatment of mental diseases

A Physiological Marriage Made in Heaven: Treating and Measuring the Brain Through Stimulation.

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INTRODUCTION Psychiatric disorders are common after stroke and traumatic brain injury (TBI) both in the short term and long term. They can be caused by regional disruption of neuronal network, impairment of regional cerebral blood flow, impaired cerebral metabolism, axonal injury, and pressure effect of intracranial bleed. Around 16 million people each year experience first ever stroke. Of these patients, 5 million become disabled and 5.7 million dies.[1] Traumatic brain injuries are also common and pose an enormous burden on families and caregivers because of the associated neuropsychiatric complications.[2] However, these neuropsychiatric complications are often remained unaddressed or not adequately treated because of the treating doctor's preoccupation with other severe physical disabilities, whereas treating these neuropsychiatric complications can improve the overall outcome of the patients to a considerable extent. In this clinical practice guideline (CPG), the assessment of psychiatric disorders following stroke and TBI is discussed together, while the management of psychiatric disorders following stroke and TBI is discussed separately under the two broad subheadings. This CPG mostly focused on the most common neuropsychiatric consequences of stroke and TBI, namely depression, psychosis, anxiety, posttraumatic stress disorders (PTSD), mania, emotional lability, fatigue, apathy, and personality changes. There is substantial overlap between neuropsychiatric disorders following stroke and TBI and repetitions will be avoided. This CPG does not include the cognitive consequences of stroke and TBI. We included researches both on ischemic stroke and intracerebral hemorrhage. However, we did not include dementia. CATEGORIES OF EVIDENCE AND STRENGTH OF RECOMMENDATIONS While writing this CPG, we ensured compliance with AGREE II instrument. We marked available evidences from Ia to IV and strengths of recommendations from A to D as per the prevailing norms.[3] Categories of evidence Ia: Evidence from meta-analysis of randomized controlled trials (RCTs) Ib: Evidence from at least one RCT IIa: Evidence from at least one controlled study without randomization IIb: Evidence from at least one quasi-experimental study III: Evidence from nonexperimental descriptive studies, such as correlation studies comparative studies, and case − control studies IV: Evidence from opinions and/or clinical experience of respected authorities or expert committee reports. Strength of recommendations A: Directly based on Category I evidence B: Directly based on Category II evidence or extrapolated recommendation from Category I evidence C: Directly based on Category III evidence or extrapolated recommendation from category I or II evidence D: Directly based on Category IV evidence or extrapolated recommendation from Category I, II or III evidence S: Standard of care. GENERAL ASSESSMENT OF PSYCHIATRIC DISORDERS FOLLOWING STROKE AND TRAUMATIC BRAIN INJURY As a referral physician, psychiatrists have the role to make thorough assessment of a patient following stroke and TBI to rule in/out the presence of any psychiatric disorders in a busy emergency room or inpatient department or intensive care unit (ICU). To assess the consciousness level of the patient, Glasgow Come Scale still remains the gold standard. It is usually very difficult to conduct a psychiatric assessment on a semi-comatose patient or a patient who is uncooperative. In that case, one can use Kirby's pro forma for examining uncooperative patients. The attending psychiatrist should examine the patient in a calm environment with not too many people around. However, the presence of primary caregiver can be allowed if the patient cannot give reliable and valid information which is more often the case. The demeanor of the treating doctor should be nonthreatening. He should talk in a clear voice with every word being uttered with due stress to reach the patient who usually have some or the other sensory impairment. If in delirium, psychiatrist should revisit the patient at a later date and time. Psychiatrist should also take the pain to bring forth the history of substance use disorders which are commonly associated with road traffic accidents and resultant TBI [Box 1].Box 1: Checklist for treating psychiatrist while evaluating post stoke and posttraumatic brain injury psychiatric disordersThe treating psychiatrist should go through the clinical records very carefully and if needed should corroborate the clinical history from the primary caregiver or the eye witnesses. Patient's past psychiatric history is of immense importance as it has some correlation with development of poststroke depression (PSD) and other psychiatric disorders. Psychiatrist should also go through the laboratory reports carefully and look for underlying infection, blood loss, electrolyte disturbances, endocrine dysfunction, and other systemic comorbid conditions which are reflected in complete blood count, urine culture and sensitivity, cerebrospinal fluid study, hemoglobin level, serum sodium, serum potassium, serum chloride, serum thyroid-stimulating hormone, serum parathyroid hormone, fasting blood sugar, liver function test, serum creatinine, etc. If needed and when in doubt, the referral psychiatrist should order for more biochemical investigation to rule out organic condition. The psychiatrist should also pay attention to the neuroimaging reports (computed tomography scan, magnetic resonance imaging, etc.,) to decipher a possible connection between the neurological insult and psychiatric disorder. Electroencephalography should be ordered to rule out subconvulsive status epilepticus which can mimic a psychiatric disorder. A detailed scrutiny of the medications already received should be done to rule out any iatrogenic psychiatric disorder. If needed, the psychiatrist should talk to treating neurologist or the neurosurgeon regarding stoppage of medicine, replacing the offending drug, or possible dose adjustment. A detailed mental status examination should be done with particular focus on obtaining an adequate speech sample, looking for the predominant affect, presence of any delusion or hallucination, and assessment of cognitive function, particularly judgment, abstract thinking, and lobar functions. There are provisions to diagnose various psychiatric disorders following stroke, transient ischemic attack (TIA), and brain injury in DSM 5 and ICD10. The diagnosis of poststroke and post-TBI psychiatric disorders depends on structured clinical interview and using of a screening instrument. There is no universally accepted screening instrument for diagnosing psychiatric disorders following stroke or TBI. For the diagnosis of PSD, Beck Depression Inventory, Hamilton Depression Rating Scale, Nine-item Patient Health Questionnaire-9, Hospital Anxiety Depression Scale, Geriatric Depression Scale, and the Center for Epidemiological Studies Depression (CES-D) Scale have been used. Anxiety disorders can be screened by Hospital Anxiety and Depression Scale-Anxiety Subscale and Hamilton Anxiety Scale. For screening of PTSD, psychiatrist can use clinician administered PTSD Scale, PTSD checklist for a stressor, TIA or stroke as stressor; Post-Traumatic Stress Diagnostic Scale; Impact of Events Scale-Revised. Brief Psychiatric Rating Scale can be used for screening of psychosis and Young's Mania Rating Scale can be used for screening of mania. For the assessment of personality disorders or personality changes, a detailed psychological evaluation with Eysenck's Personality Questionnaire, Minnesota Multiphasic Personality Inventory, International Personality Disorder Examination, or Iowa Personality Disorder Screen may be needed [Table 1].Table 1: Screening tools and management of various psychiatric disorders following stroke/traumatic brain injuryMANAGEMENT OF POSTSTROKE PSYCHIATRIC DISORDERS Poststroke depression PSD is the one of the most commonly reported neuropsychiatric conditions following stroke. Often undiagnosed, PSD is a treatable condition. PSD can occur within 1–18 months following stroke and its prevalence vary considerably over time (reported prevalence at 1, 3, 6, 12, and 18 months were 24.5%, 27.1%, 28.3%, 19.8%, and 26.3%, respectively).[4] PSD is believed to be associated with worse functional outcome following stroke. A meta-analysis showed that, PSD had a adverse impact on survival rates following stroke and it affected short-term mortality more than long-term mortality.[5] Various meta-analysis and systematic review have looked into the role of prophylactic antidepressant treatment to reduce the chance of developing PSD.[6789] Many of them found that, selective serotonin reuptake inhibitors (SSRIs), cognitive behavioral therapy (CBT), and physical exercise improved mood symptoms in PSD. A Cochrane review which included 63 RCTs and over 9000 participants and specifically looked into the role of SSRIs in PSD found that, SSRIs should not be used routinely to promote recovery after stroke as they do not improve recovery after stroke (A).[10] In the Effect of fluoxetine on functional outcomes after acute stroke trial, eligible patients with stroke were recruited and randomly given fluoxetine (20 mg daily) or placebo for 6 months, starting after 2 − 15 days of stroke. After 12 months of follow-up, fluoxetine was found to improve the neuropsychological scale score but not other variables. Therefore, it did not support the routine use of prophylactic fluoxetine in PSD (A).[11] Similar was the finding from the efficacy of citalopram treatment in acute stroke (TALOS study) (A).[12] The efficacy of CBT on PSD remains undetermined due to low quality of the studies and high degree of heterogeneity among them as found by one meta-analysis (A).[13] Neuromodulation techniques such as transcranial direct current stimulation and transcranial magnetic stimulation can offer some benefit, but there are the lack of high quality RCTs (B).[14] SSRIs and SNRIs are often used in conjunction with anti-platelet medication such as clopidogrel in PSD. Fluoxetine and fluvoxamine (CYP2C19 inhibiters) can reduce the efficacy of clopidogrel and can increase the risk of ischemic disease.[15] There have been concerns regarding intracranial bleed following the use of SSRIs also. Studies have suggested that, if given before stroke, SSRIs were associated with severity and mortality in patients with hemorrhagic stroke.[16] However, one recent review pointed out the lack of evidence in support of SSRIs alone increasing the risk of spontaneous intracranial bleed. Therefore, it can be concluded that, SSRIs should not be prescribed prophylactically in all poststroke patients. Rather, they should be screened for PSD and if diagnosed, then only SSRIs and SNRIs can be prescribed as needed (S) with some sort psychological intervention (CBT) (B). Both neurologists and psychiatrists need to be aware of drug-drug interaction which can be potentially life threatening in such group of patients (S). Poststroke psychosis The symptoms of PSP include delusions, hallucinations, psychomotor agitation, irrelevant and incoherent speech, catatonic symptoms, and sleep cycle disturbances. These symptoms usually manifest within a week following stroke but may manifest several weeks later also. Studies form the early 90s indicated that PSP is relatively rare and after 9 years' follow-up only 5 patients developed PSP.[17] A recent meta-analysis found the prevalence of PSP to be around 4.86%.[18] Literature on the management of PSP is sparse compared to PSD or poststroke anxiety (PSA). RCTs on the management of PSP are lacking. The treatment usually follows same principles which are followed for the management and treatment of primary psychotic disorders. Secondgenerationantipsychotics(SGAs), for example, quetiapine, risperidone, andolanzapinearemostcommonlyusedtotreatPSP (D). However, their safety in patients with stroke is highly debatable. Olanzapine can have deleterious effect of plasma glucose and lipids which are not welcome in patients with stroke. Quetiapine can cause postural hypotension, whereas risperidone can cause extra-pyramidal side effects. The concern of anti-psychotics being associated with high incidences stroke has been refuted by a large case − control study.[192021] TheusualpracticeistostartlowandgoslowincaseoftreatmentofPSP(S). However, incertaincases(agitatedandviolentpatients)injectablesmightberequiredandinthatcaseinjectableolanzapineorinjectablehaloperidolcanbeused(D). Asinpatientswithprimarypsychoticdisorders, CBTforhallucinationordelusioncanbebeneficialinPSP(S).[22] Poststroke anxiety disorders PSA is common and only second to PSD in terms of prevalence. All kind of anxiety disorders can be seen following stroke but the core symptoms remain the same – palpitation, psychic and physical restlessness, excessive worry and fear, feeling of nervousness, pseudo neurological symptoms, for example, dizziness, blurring of vision, tingling and numbness of hands and feet, fine tremors, etc. Sensory impairment, ICU admission, painful physical conditions, communication difficulties, and sleep disturbance can lead to the development of PSA. A meta-analysis found the prevalence of PSA to vary between 20% to 24% depending on the time elapsed following stroke.[23] SSRIs, SNRIs, Tri-CyclicAntidepressants(TCAs), Mirtazapine, Buspirone, Benzodiazepines, and Z-drugsallhavebeenusedinthetreatmentofPSAintheabsenceofanydefiniteguideline(D).[24] Meta-analyses conducted by Chun etal. reported beneficial effect of pharmacotherapy (paroxetine, imipramine, and buspirone) and psychotherapy compared to control. However, the studies were of low quality and highly heterogeneous, and therefore, the positive conclusion could be due to bias.[25] Cochrane review in this area also highlighted lack of quality studies and emphasized the need of large scale RCTs.[24] Nonpharmacologicalmanagements, for example, Yoga, Tai-Chi, Self-helpmindfulness, andrelaxationtechniquescanoffersomebenefitinthemanagementofPSA(C).[2627] Therefore, SSRIs, SNRIs, andevenTCAscanbeusedinthetreatmentofPSA(S, D)alongwithnon-pharmacologicalinterventions(C). However, as in case of PSD, psychiatrists and neurologists should be aware of potential drug-drug interactions. Posttraumatic stress disorder following stroke PTSD develops following an event which pose actual or imagined threat to physical and psychological integrity of an individual and stroke is no less than a catastrophe. Symptoms of PTSD include intrusive flashbacks/memories, autonomic arousal, emotional numbness, and avoidance behavior. Poststroke PTSD often has associated PSD and PSA (in up to 40% of the cases).[28] A meta-analysis reported 1-year prevalence of poststroke PTSD to be around 23%.[29] Furthermore, persons with PTSD have higher risk of developing stroke compared to people without PTSD.[30] There is dearth of RCTs in treatment of PTSD. SSRIs, SNRIs, andTCAscanbetried(D). Othermedications, e.g., antipsychotics, anticonvulsants, andanxiolyticshavealsobeentried(D).[31] Psychotherapeutic approaches, e.g., trauma-focused therapies, CBT, and exposure therapy appears to be helpful in resolution of symptoms but they need to be tested in large scale studies (D).[32] Poststroke mania Prevalence of poststroke mania (PSM) is rather low (<2%).[33] Most of the data in this area are in the form of case report or case series.[33] Majority of the subject developed PSM between 1 day to 24 months after stroke.[34] In 1978, Kraut-hammer and Klerman gave the concept of secondary mania in which a manic episode is produced by metabolic, neurological, or toxic disorder.[34] The criteria of secondary mania (PSM in this case) are as follows: (1) symptoms lasting for at least 1 week; (2) presence of elevated or irritable mood; and (3) presence of at least two symptoms out of the followings: Pressured speech, grandiosity, hyperactivity, flight of ideas, distractibility, lack of judgment, and decreased sleep; and (4) no history of affective illness or delirium co-occurring with the mania. Lesions responsible for PSM are usually found in the caudate nucleus, parietal, temporal, and frontal lobes and thalamus. Mania is more common with right-sided lesions, although left sided lesions have also been reported.[3536] Treatment of PSM is in line with treatment of an acute manic episode. Moodstabilizers, e.g., valproate, carbamazepine, oxcarbazepine, etc.;antipsychotics, e.g., olanzapine, quetiapine, risperidone, etc.;andbenzodiazepinesarethemainstayoftreatment(S. D). It is better to avoid lithium in this population because of the presence of multiple comorbidities and potential drug-drug interactions. Furthermore, choosing a mood stabilizer which allows antiepileptic coverage is beneficial. Poststroke emotional lability Poststroke emotional lability is also known by various other names, for example, pathological laughter/crying, emotional incontinence, hyperemotionality, pseudobulbar affect, etc. The symptoms appeared to be dramatic but transient. Patients can present with sudden onset laughter or crying while speaking on a rather inconspicuous matter. Sometimes, it may be difficult to differentiate it from depression. If symptoms are long-lasting, it may result in distress, depression, social avoidance, and embarrassment. The prevalence of poststroke emotional lability varies between 8% to 32%.[37] Quality research in the management of poststroke emotional lability is lacking, thereby precluding any meaningful recommendation. ACochranereviewwithtotal293participantsreported, antidepressantsreducedthefrequencyoflaughingandcryingepisodesbutthequalityofevidencewaslow(A). The effect was not specific to any particular drug or class of drugs. The review pointed our several methodological deficiencies.[38] Poststroke fatigue Poststroke fatigue (PSF) is common sequalae of both ischemic and hemorrhagic stroke. Nearly half of the stroke survivors suffer from PSF. A systematic review put the prevalence of PSF between 25% and 85%.[39] Uniform definition of PSF is lacking. Most commonly PSF is described as, subject lack of mental and physical energy which interferes with individual's day to day activities. PSF has been found to be associated with old age, neurological deficits, diabetes, hypertension, heart failure, kidney disease, pain, anxiety, depression, sleep disturbances, prestroke fatigue, and cognitive impairment.[40] Few studies have pointed to a link between PSF and subcortical and infra-tentorial infarcts.[40] Considering the multifactorial causation of PSF, any one particular pharmacological agent is unlikely to provide any benefit. Modafinil, amoodawakenerhasbeenfoundtobeusefulinPSFfollowingbrainstem-diencephalicstrokebecauseofitseffectonreticularactivatingsystem(C).[41] A small RCT also favoured the use of Modafinil up to a dose of 400 mg/day (B).[42] SSRIs including fluoxetine, escitalopram, sertraline and SNRI, duloxetine has been studied in PSF but none were proven beneficial except for anxiety symptoms.[4344] Clinicians often try vitamin supplementations in PSF. Vitamin B12, Vitamin B1, and idebenone, a synthetic coenzyme Q10 analog have all been studied, but results are inconclusive (C).[454647] JointAmericanStrokeAssociationandAmericanHeartAssociationstatementencouragesregularphysicalexercisetoreducePSF(D, S).[48] A Cochrane review which included two nonpharmacological interventions, mindfulness-based stress reduction program and a fatigue education program found no conclusive evidence of any intervention having any efficacy to treat PSF (A).[49] Poststroke apathy Post-stroke apathy is of stroke. It is by a lack of with and criteria for poststroke apathy for weeks or and two other symptoms cognitive or and functional There are conditions, particularly depression, which can mimic poststroke In that case, should be put on of cognitive symptoms of depression, for example, low lack of attention and ideas, etc. prevalence of poststroke apathy was in a large Poststroke apathy is more common in less and in of and depression in 40% of Patients with poststroke apathy have been found to have higher risk of depression and worse functional Quality evidence for the treatment of poststroke apathy is lacking. There is one RCT with mg and mg which in in Scale score and more There are Poststroke personality disorders There can be of personality or patient can personality after a stroke. There are that patient and/or Personality are more in case of frontal Studies have put the prevalence of and at and The in the prevalence was because of the in which the study was population of stroke, and used to assess personality changes. There are very RCTs which have looked into the treatment of poststroke personality disorders have been extrapolated from studies conducted in SSRIs, for example, in this group of patients OF PSYCHIATRIC DISORDERS FOLLOWING TRAUMATIC BRAIN INJURY For management of psychiatric disorders following TBI, we are not to the same for stroke for of this Rather, we will management and treatment evidences as The first report of psychiatric disorder following TBI was of a who an in when an and frontal which personality form a responsible to and not to take A of psychiatric disorders can be seen following TBI. Posttraumatic agitation, and are common in Posttraumatic has been to posttraumatic consciousness and in cognitive The of posttraumatic varies between to sleep and underlying delirium can promote can be physical and and often than not is sudden and in The of is the severity of injury and of The of in TBI varies between 25% to is although a rather form compared to and it is common in post-TBI patients which as excessive with The of post-TBI varies between to as per the of the studies consequences of TBI are apathy, and We have discussed apathy in in the of psychiatric disorders following stroke. The prevalence of post-TBI apathy varies between 20% to As discussed it may be difficult to differentiate apathy from depression. Furthermore, apathy can to available pharmacological anxiety, and psychosis are other common psychiatric disorders following TBI. The prevalence of depression after TBI was higher compared to population and was put at having depression at the time of injury, cognitive deficits, of left and and pain was associated with depression in TBI All of anxiety for example, anxiety social anxiety and PTSD are common in TBI patients. The prevalence of anxiety disorders varies between and following between psychosis and TBI is less A meta-analysis suggested that, risk of was in TBI group as compared to the control but of studies included any meaningful and are higher in TBI group as compared to the population and some have found it to be as high as Around 20% participants with TBI all of for example, mood antipsychotics, and have been used in the treatment of psychiatric disorders following TBI [Table but in the of study and large of the studies recommendations are difficult to In clinical many of these alone or in There is evidence in of nonpharmacological Cochrane review did not any evidence in of any nonpharmacological for example, mindfulness-based cognitive therapy or CBT for depression following There are a psychiatrist should be aware while such patients, for example, level of cognitive function, neuroimaging done or presence or of clinical subconvulsive status medications received by the patient, drug-drug etc. [Box of medications for should be prescribed to improve patient compliance (S). or should be used because of risk of and cognitive (S). but not the attending psychiatrist should also use depending on of comorbid physical conditions 1].Table used to treat psychiatric disorders following traumatic brain injury and their of to for treating psychiatrist in patients with traumatic brain 1: of psychiatric management of a patient with traumatic brain Psychiatric disorders following stroke and TBI present for the treating a who is with brain psychiatrists of should in of brain and its the other being a behavioral should be the of the patient, the need of the and the emotional need of The link between psychiatric disorders following stroke and TBI is not an Therefore, treatment also to be one drug for Psychiatrist often has to do and before the As already been there is dearth of large scale RCTs for most of the conditions and treatment recommendations are often extrapolated from primary disorders. However, that may not a or brain may not function in the same as a or However, this guideline an to of the available evidences in this area and recommendations were based on has to while this is in a particular clinical support and of There are no of

The non-invasive delivery of electric currents through the scalp (transcranial electrical stimulation) is a popular tool for neuromodulation, mostly due to its highly adaptable nature (waveform, montage) and tolerability at low intensities (< 2mA). Applied rhythmically, transcranial alternating current stimulation (tACS) may entrain neural oscillations in a frequency- and phase-specific manner, providing a causal perspective on brain-behaviour relationships. While the past decade has seen many behavioural and electrophysiological effects of tACS that suggest entrainment-mediated effects in the brain, it has been difficult to reconcile such reports with the weak intracranial field strengths (< 1 V/m)achievable at conventional intensities. In this review, we first describe the ongoing challenges faced by users of tACS. We outline the biophysics of electrical brain stimulation and the factors that contribute to the weak field intensities achievable in the brain. Since the applied current predominantly shunts through the scalp-stimulating the nerves that innervate it-the plausibility of transcutaneous (rather than transcranial) effects of tACS is also discussed. In examining the effects of tACS on brain activity, the complex problem of salvaging electrophysiological recordings from artefacts of tACS is described. Nevertheless, these challenges by no means mark the rise and fall of tACS: the second part of this review outlines the recent advancements in the field. We describe some ways in which artefacts of tACS may be better managed using high-frequency protocols, and describe innovative methods for current interactions within the brain that offer either dynamic or more focal current distributions while also minimising transcutaneous effects.

European reclassification of non-invasive brain stimulation as class III medical devices: A call to action

Brain electrical stimulation, particularly non-invasive brain stimulation (NIBS) techniques such as transcranial electrical stimulation (tES), have emerged as a promising treatment for various psychiatric disorders, including depression, anxiety, and post-traumatic stress disorder. tES techniques, such as transcranial direct current stimulation (tDCS), transcranial alternating current stimulation (tACS), and transcranial random noise stimulation (tRNS), are cost-effective and safe interventions that are designed to affect neuronal circuits in the brain using various modalities. Although tES has shown effectiveness in the treatment of psychiatric disorders, there is a lack of comprehensive papers that consider its clinical implications. Therefore, this review aims to evaluate the clinical implications of tES and provide practical guidance for the treatment of psychiatric illnesses. Moreover, this review provides an overview of tES techniques and their mechanisms of action and summarizes recent clinical studies that have examined the use of tES for psychiatric disorders.

Cerebral blood flow changes after transcranial direct current stimulation for a patient with schizophrenia: a case report.

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Treatment for brain diseases has been disappointing because available medications have failed to produce clinical response across all the patients. Many patients either do not respond or show partial and inconsistent effect, and even in patients who respond to the medications have high relapse rates. Brain stimulation has been seen as an alternative and effective remedy. As a result, brain stimulation has become one of the most valuable therapeutic tools for combating against brain diseases. In last decade, studies with the application of brain stimulation techniques not only have grown exponentially but also have expanded to wide range of brain disorders. Brain stimulation involves passing electric currents into the cortical and subcortical area brain cells with the use of noninvasive as well as invasive methods to amend brain functions. Over time, technological advancements have evolved into the development of precise devices; however, at present, most used noninvasive techniques are repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS), whereas the most common invasive technique is deep brain stimulation (DBS). In the current review, we will provide an overview of the potential of noninvasive (rTMS and tDCS) and invasive (DBS) brain stimulation techniques focusing on the treatment of mental, psychiatric, and cognitive disorders.

Review Raises Questions About Low-Intensity Transcranial Stimulation

Transcranial magnetic and electrical stimulation compared: Does TES activate intracortical neuronal circuits?

Context: Transcranial electrical stimulation (tES) is a non-invasive method to stimulate the brain, which has recently been used to treat psychiatric and neurological disorders. Transcranial direct current stimulation (tDCS) is one of the most widely used tES protocols. This study aimed to review the effectiveness of tDCS for the treatment of various mental disorders. Evidence Acquisition: The present study is a narrative review type, for which more than 55 articles and scientific reports were downloaded using MeSH terms related to the subject of the study by reliable and international databases. Considering the inclusion and exclusion criteria, 25 studies were selected, and the results of those studies were recorded. Results: Transcranial direct current stimulation significantly affected the treatment of various mental disorders, including depressive disorder, obsessive-compulsive disorder, autism spectrum disorder, attention deficit hyperactivity disorder, and anxiety disorders. In addition, this treatment method improved the symptoms of each of the aforementioned mental disorders. Conclusions: Based on the findings, the use of tDCS can be effective in improving mental disorders. However, it seems necessary to conduct more studies to achieve reassuring findings due to limited results in some areas.

Background Fibromyalgia syndrome (FMS) is a complex disorder where a widespread musculoskeletal pain (without a clear lesion basis) is associated with a great variety of symptoms including affective disturbances, central fatigue, cognitive dysfunction and even a particular skin reactivity to several chemical substances. Despite intense research effort, especially in the last years, the pathophysiology of the disease remains to be explained. The treatment recommendations were classified as pharmacological therapies, non-pharmacological treatments, and complementary non-pharmacological therapies. Also, particular interest has been raised by techniques able to perform effective modulation of brain areas through magnetic or electric currents applied to the scalp like transcranial magnetic and electrical stimulation such as direct current (TMS and tDCS). Objective: To compare the efficacy of Repetitive transcranial magnetic stimulation (r-TMS) and transcranial direct current stimulation (t-DCS) as non- invasive brain stimulation techniques in the rehabilitation of patients with primary (1ry) fibromyalgia (FM). Patients and Methods The present study included 30 patients with 1ry FM, equally divided into 2 groups. Group I included 15 patients who received 8 sessions of rTMS and Group II included 15 patients who received 8 sessions of anodal tDCS. Differences in visual analogue scale (VAS) of pain, tender point scale, Fibromyalgia Impact Questionnaire (FIQ) and Hospital Anxiety and Depression Scale (HADS) were assessed before and after completion of assigned treatment sessions. Results Pain VAS, tender point scale, FIQ and HADS showed significant decrease between baseline and follow-up assessments for both groups. Moreover, a significant change in all assessment scales was observed post treatment when compared between both groups with more significant improvement in the group received rTMS. Conclusion Both rTMS and tDCS techniques showed marked improvement in symptoms of pain, functional status and quality of life in patients with 1ry fibromyalgia. Both techniques can be considered as promising alternatives therapeutic options in the treatment of FM in order to reduce side effects of long-term use of drugs.

Transcranial electrical stimulation (tES) is a widely used noninvasive brain stimulation method to improve motor performance. Transcranial alternating current stimulation (tACS), which modulates oscillatory brain activity, has been extensively investigated as a tES method to enhance motor skills. However, few studies have investigated the effects of tACS on sports performance. The purpose of this study was to determine the effects of cerebellar tACS on basketball shooting skills in college students with basketball experience. This study was conducted as a single-blind, randomized controlled trial. A total of 36 healthy young women (average age: 20.2years) who were with former basketball players were included in the study. tACS (1.0mA, 70Hz) was administered for 15min with 25cm2 electrodes placed on the scalp over the bilateral cerebellar hemispheres. The stimulus frequency was selected based on prior findings showing effectiveness in gamma-band modulation. Shooting skills were assessed with a two-handed free throw shooting task. Shooting skills were scored on a 6-point scale per shot, and 30 shots (10 shots×3 sets) were taken before and after the tACS intervention. This task has been validated as a reliable measure of shooting accuracy in previous studies. Shooting scores significantly increased after stimulation in the tACS group (Median [IQR]: 34.8 [27.3-37.9]-37.0 [30-40.1], p=0.028, r_rb=-0.661); however, no significant differences in shooting scores were detected before and after stimulation in the sham group (33 [29.9-36.9]-32 [25.4-36.9], p=0.310, r_rb=0.404). There was no significant change in shooting success rates before and after the intervention in either group (tACS group: 62.5 [38.8-75]-65 [43.8-76.3], p=0.751, r_rb=-0.258, sham group: 57.5 [45-76.3]-55 [26.3-67.5], p=0.810, r_rb=0.235). Our results indicate that 70Hz tACS over the cerebellum may improve basketball shooting skills. These results provide valuable insights into the practical application of tACS in sports. l The purpose of this study was to determine the effects of cerebellar tACS on basketball shooting skills. l A total of 36 healthy young women with basketball experience received cerebellar tACS (1.0mA, 70Hz) for 15min. l Shooting scores significantly increased after cerebellar tACS intervention.

Objective To assess the influence of transcranial electric stimulation (TES) on the recovery of motor function after cerebral focal ischemia and reperfusion and to explore the mechanisms in terms of neural plasticity.Methods An acute focal ischemia-reperfusion model was established by transient occlusion of the right middle cerebral artery (MCAO).Seventy-two male Sprague-Dawley rats were randomly divided into a TES group,a model group,a sham-operation group and a normal group.The TES group was given TES 24 h after MCAO;the model group received the operation without any treatment.Forelimb placing (FPT) and beam walking (BWT) were mea-sured at the 3rd,7th,14th and 28th day after reperfusion.Microtubule-associated protein-2 (MAP-2) and growth-associated protein-43 (GAP-43) and grey levels of reaction products in the peri-infarct region were examined by immunohistochemical techniques.Results The TES group rats had markedly better FPT and BWT performance at the 7th,14th and 28th day after MCAO,compared with the model group.Expression of MAP-2 had increased significantly more at the 14th and 28th day in the peri-infarct region in the TES group compared with the model group.Expression of GAP-43 was significantly elevated in the peri-infarct region in the TES group compared with the model group at all time points.Conclusions TES can improve motor function and neural plasticity following cerebral ischemia and reperfusion damage.The functional enhancement may be partly due to up-regulation of the expression of GAP-43 and MAP-2 in the peri-infarct region. Key words: Cerebral ischemia and reperfusion; Transcranial electrical stimulation; Microtubule-asso-ciated protein-2; Growth associated protein-43; Forelimb placing test; Beam walking test