Objective

Repetitive transcranial magnetic stimulation (rTMS) is an emerging treatment for neuropsychiatric disorders. Patients in rTMS treatment typically receive concomitant psychotropic medications, which affect neuronal excitability and plasticity and may interact to affect rTMS treatment outcomes. A greater understanding of these drug effects may have considerable implications for optimizing multi-modal treatment of psychiatric patients, and elucidating the mechanism(s) of action (MOA) of rTMS.

Method

We summarized the empirical literature that tests how psychotropic drugs affect cortical excitability and plasticity, using varied experimental TMS paradigms.

Results

Glutamate antagonists robustly attenuate plasticity, largely without changes in excitability per se; antiepileptic drugs show the opposite pattern of effects, while calcium channel blockers attenuate plasticity. Benzodiazepines have moderate and variable effects on plasticity, and negligible effects on excitability. Antidepressants with potent 5HT transporter inhibition reduce both excitability and alter plasticity, while antidepressants with other MOAs generally lack either effect. Catecholaminergic drugs, cholinergic agents and lithium have minimal effects on excitability but exhibit robust and complex, non-linear effects in TMS plasticity paradigms.

Limitations

These effects remain largely untested in sustained treatment protocols, nor in clinical populations. In addition, how these medications impact clinical response to rTMS remains largely unknown.

Conclusions

Psychotropic medications exert robust and varied effects on cortical excitability and plasticity. We encourage the field to more directly and fully investigate clinical pharmaco-TMS studies to improve outcomes.

The study objective was to evaluate the usefulness of Classification and Regression Trees (CART), to classify clinical responders to antidepressant and placebo treatment, utilizing symptom severity and quantitative EEG (QEEG) data. Patients included 51 adults with unipolar depression who completed treatment trials using either fluoxetine, venlafaxine or placebo. Hamilton Depression Rating Scale (HAM-D) and single electrodes data were recorded at baseline, 2, 7, 14, 28 and 56 days. Patients were classified as medication and placebo responders or non-responders. CART analysis of HAM-D scores showed that patients with HAM-D scores lower than 13 by day 7 were more likely to be treatment responders to fluoxetine or venlafaxine compared to non-responders (p=0.001). Youden's index γ revealed that CART models using QEEG measures were more accurate than HAM-D-based models. For patients given fluoxetine, patients with a decrease at day 2 in θ cordance at AF2 were classified by CART as treatment responders (p=0.02). For those receiving venlafaxine, CART identified a decrease in δ absolute power at day 7 at the PO2 region as characterizing treatment responders (p=0.01). Using all patients receiving medication, CART identified a decrease in δ absolute power at day 2 in the FP1 region as characteristic of nonresponse to medication (p=0.003). Optimal trees from the QEEG CART analysis primarily utilized cordance values, but also incorporated some δ absolute power values. The results of our study suggest that CART may be a useful method for identifying potential outcome predictors in the treatment of major depression.

Purpose

We conducted a randomized clinical trial evaluating the efficacy of a cognitive rehabilitation (CR) intervention compared with a wait list (WL) control condition on cognitive complaints, neuropsychological and brain functioning in breast cancer survivors (BCS).

Methods

The small group intervention of five sessions included psychoeducation and cognitive exercises.

Eligibility

Disease-free BCS with cognitive complaints, diagnosed with stage I, II or III breast cancer, completed primary treatment 18 months to 5 years earlier. Neurocognitive test data and cognitive complaints on the Patient's Assessment of Own Functioning Inventory (PAOFI) were assessed at baseline (T1), immediately post-intervention (T2), and 2 months later (T3). A subgroup of participants underwent resting state quantitative electroencephalography (qEEG) at all three assessment time points.

Results

Forty-eight participants [mean age (SD) 53.8 (8.2)] completed T1 assessments, and 29 participants had analyzable qEEG data. The CR group improved significantly over time compared with the WL group on PAOFI total and memory scores (both p = .01) and on Rey Auditory Verbal Learning Test (RAVLT) total (trials I-V) (p = .02) and RAVLT delayed recall (p = .007) scores. On qEEG, the CR group showed a significant decrease in delta 'slow wave' power (p = .02) and an increase in the frontal distribution of alpha power (p = .04) from T1 to T2.

Conclusions

BCS in the CR group showed immediate and sustained improvements in self-reported cognitive complaints and memory functioning on neurocognitive testing. Results of the qEEG substudy provide some support for neurophysiological changes underlying the intervention. Copyright © 2015 John Wiley & Sons, Ltd.