BACKGROUND:Electroconvulsive therapy (ECT) is a well-accepted intervention for treatment-resistant, serious mental illnesses. Its acceptability, efficacy, and tolerability are well documented in high-income settings, but less so in lower- and middle-income countries (LMICs). This report is a narrative review of ECT practice in the latter setting.METHODS:A literature search was conducted using Medline and PubMed. Initial results yielded 81 publications in English. Following the screening, 19 papers were included to evaluate the information on ECT practice and perceptions.RESULTS:Reports from LMICs on efficacy, tolerability, and perceptions of ECT were relatively sparse. In general, they confirm its use mostly for treatment-resistant major mental illnesses (i.e., depression, schizophrenia, bipolar disorder). Both modified and unmodified forms of ECT are used and considered equally effective, although the former is better tolerated. Use of unmodified ECT remains significant in LMICs due to its low cost and limited resource requirements. In general, there is satisfaction with ECT and its outcomes. The education of patients and families, content process, and research have been noted as areas to improve.CONCLUSIONS:ECT is perceived as an effective intervention in LMICs, but use of unmodified ECT remains controversial. There is a need for the development and use of global guidelines to improve clinician training, knowledge sharing with patients and their families, and outcome research.

OBJECTIVE:We measured the neurophysiological responses of both active and sham transcranial magnetic stimulation (TMS) for both single pulse (SP) and paired pulse (PP; long interval cortical inhibition (LICI)) paradigms using TMS-EEG (electroencephalography).METHODS:Nineteen healthy subjects received active and sham (coil 90° tilted and touching the scalp) SP and PP TMS over the left dorsolateral prefrontal cortex (DLPFC). We measured excitability through SP TMS and inhibition (i.e., cortical inhibition (CI)) through PP TMS.RESULTS:Cortical excitability indexed by area under the curve (AUC(25-275ms)) was significantly higher in the active compared to sham stimulation (F(1,18) = 43.737, p < 0.001, η2 = 0.708). Moreover, the amplitude of N100-P200 complex was significantly larger (F(1,18) = 9.118, p < 0.01, η2 = 0.336) with active stimulation (10.38 ± 9.576 µV) compared to sham (4.295 ± 2.323 µV). Significant interaction effects were also observed between active and sham stimulation for both the SP and PP (i.e., LICI) cortical responses. Finally, only active stimulation (CI = 0.64 ± 0.23, p < 0.001) resulted in significant cortical inhibition.CONCLUSION:The significant differences between active and sham stimulation in both excitatory and inhibitory neurophysiological responses showed that active stimulation elicits responses from the cortex that are different from the non-specific effects of sham stimulation.SIGNIFICANCE:Our study reaffirms that TMS-EEG represents an effective tool to evaluate cortical neurophysiology with high fidelity.

Electroconvulsive therapy (ECT) is effective for treatment-resistant depression, but its use is limited owing largely to stigma and its cognitive adverse effects. Magnetic seizure therapy (MST) is a new, alternative seizure treatment for treatmentresistant depression (TRD), and early studies suggest that MST does not produce any adverse effects on memory.1 These differences between ECT and MST are best illustrated in the clinical case of a 34-year-old patient with a longstanding history of TRD. Numerous trials of antidepressant medications (selective serotonin reuptake inhibitors, tricyclic antidepressants) had failed while she continued to experience marked depressive symptoms with passive suicidal ideation. She began a course of ECT in 2012. She experienced a marked improvement in depressive symptoms following 10 right-unilateral ultrabrief ECT treatments delivered 2–3 times per week on nonconsecutive days. She also reported subjective worsening of memory; ECT was discontinued as she could no longer tolerate this memory impairment. Unfortunately, she experienced a marked worsening of depressed mood within 1 month of discontinuing ECT. At that time, her 24-item Hamilton Rating Scale for Depression (HAM-D) score was 29. Given her response to ECT and lack of response to numerous antidepressants, the only viable option to be considered was an alternative seizure treatment. She was offered a course of MST as part of a clinical trial at the Centre for Addiction and Mental Health. She received 9 MST treatments, delivered bilaterally over the frontal cortex using the Tonica MagPro MST and twin coil, and she experienced complete remission of her depressive symptoms as indexed by the 24-item HAM-D. Subjectively, she reported no memory loss. This patient continues to be treated with MST on a maintenance basis, and she remains in remission of depressive symptoms. Electroconvulsive therapy was first introduced in Italy by Ugo Cerletti and Lucio Bini in 1938.2 Within a few years, the therapeutic benefit of ECT became widely recognized, and it was quickly adopted as a treatment for severe and persistent mental illness across the globe. Evidence suggests that 50%–75% of patients with TRD experience significant improvement with ECT — more than any other treatment option for this disorder.3 By delivering a series of electrical stimuli to the cortex, ECT produces a generalized seizure. This seizure has been shown to release neurotransmitters, including serotonin, dopamine and noradrenaline.4 It has been postulated that deficiencies in these neurotransmitters are associated with depression and that the release of these neuro transmitters has been linked to the therapeutic effects of ECT.4 Additionally, ECT may also have antidepressant effects by increasing cerebral blood flow and by improving synaptic plasticity.5 Many patients, however, are reluctant to undergo ECT, and fewer than 1% of patients with TRD receive ECT.6 There are likely 2 main reasons. The first is that ECT is highly stigmatized in our society, in part because of the negative stereotype of ECT delivery — as shown in One Flew Over the Cukoo’s Nest. A second reason limiting the use of ECT is its effect on memory. Most patients receiving ECT experience some degree of both anterograde and retrograde amnesia. Magnetic seizure therapy was first developed in 1998 as a potential alternative treatment to ECT in patients with TRD.7 It delivers a focused magnetic field that produces a seizure; MST activates the cortex in a focal manner, as magnetic fields are not shunted by the skull and are not volume-conducted by the cerebrospinal fluid, unlike with ECT.8 As such, studies suggest that MST does not interfere with memory, as it does not affect deeper brain regions (e.g., hippocampus).1 Studies suggest that MST produces significant mood improvements without any significant cognitive impairment9,10 and show that MST can produce remission of suicidal ideation.11 However, further research is needed to determine if the clinical efficacy of MST is comparable to that of ECT.12 Although studies comparing ECT with MST report comparable clinical efficacy with superiority of MST in relation to cognition,9,10 to our knowledge there are no case reports illustrating within-patient effects of ECT and MST in relation to clinical outcomes and adverse effects on memory. The present case highlights these differences in adverse effects in a single patient and emphasizes the importance of offering advancements in seizure treatments to patients with TRD.

Introduction: Resting state electroencephalographic (EEG) activity is regarded as a measure of excitability in the cortex. Transcranial magnetic stimulation combined with EEG (TMS-EEG) is, however, conventionally regarded as a more precide measure of excitability in the cortex. The relationship between resting state EEG and TMS-EEG has never been probed. We hypothesized that TMS-EEG measures of excitability from the prefrontal cortex would be associated resting state EEG activity.

Patients with schizophrenia (SCZ) exhibit a variety of symptoms related to altered processing of somatosensory information. Little is known, however, about the neural substrates underlying somatosensory impairments in SCZ. This study endeavored to evaluate somatosensory processing in patients with SCZ compared to healthy individuals by generating somatosensory evoked potentials through stimulation of the right median nerve. The median nerve was stimulated by a peripheral nerve stimulator in 34 SCZ and 33 healthy control (HC) participants. The peripheral nerve stimulus (PNS) intensity was adjusted to 300 percent of sensory threshold and delivered at 0.1 Hz. The EEG data were acquired through 64-channels per 10-20 montage. We collected and averaged 100 trials and the recording electrodes of interest were the F3/F5 electrodes representing the dorsolateral prefrontal cortex (DLPFC) and C3/CP3 representing the somatosensory cortex (S1). In response to PNS, SCZ participants experienced over the DLPFC N30 amplitude that was significantly smaller than that of HC participants. By contrast, S1 N20 was of similar amplitude between the two groups. In addition, we found an association between N20 and N30 amplitudes in SCZ but not in HC participants. Our findings suggest that patients with SCZ demonstrate aberrant processing of somatosensory activation by the DLPFC locally and not due to a connectivity disruption between S1 and DLPFC. These results could help to develop a model through which to DLPFC hypofunctioning could be studied. Our findings may also help to identify a potential biological target to treat somatosensory information processing related deficits in SCZ. (C) 2019 Elsevier B.V. All rights reserved.

Many patients with schizophrenia exhibit a variety of symptoms relating to alterations in the somatosensory system. Little is known, however, about the neural substrates underlying somatosensory impairments in schizophrenia.

Introduction: Many patients with schizophrenia exhibit a variety of symptoms relating to alterations in the somatosensory system. Little is known, however, about the neural substrates underlying somatosensory impairments in schizophrenia.