Brain Stimulation For Depression Research Articles

Medial forebrain bundle deep brain stimulation in depression: preliminary results showing shift and sustained response

Medial forebrain bundle deep brain stimulation in depression: preliminary results showing shift and sustained response

Genetics of non-invasive brain stimulation in depression: a narrative review

Genetics of non-invasive brain stimulation in depression: a narrative review

Deep Brain Stimulation in Depression: Even if Successful, Will It Ever Be Scalable?

Deep Brain Stimulation in Depression: Even if Successful, Will It Ever Be Scalable?

New buzz on brain stimulation for depression [News

Here are three things we know for sure about deep brain stimulation (DBS) as a treatment for severe depression: 1. When the pacemaker-like brain implants do help depressed people, those people get dramatically better. "I have patients who got their implants 10 years ago now," says Helen Mayberg, a professor of psychiatry and neurology at Emory University, in Atlanta. "These people get well and they stay well," she says. 2. Unfortunately, DBS doesn't help everybody. Experimental trials by Mayberg and others have consistently had a subset of people who simply don't respond to the treatment. And two big industry-sponsored trials were counted as failures by the companies involved, squashing hopes that the treatment would soon be available for mainstream clinical use. 3. Researchers must figure out why some depressed patients respond to DBS while others don't; otherwise their experiments will never lead to a truly practical treatment that can gain regulators' approval. Two new academic studies show that researchers are progressing toward that understanding.

Cogntive functions following Deep Brain Stimulation in depression

Cogntive functions following Deep Brain Stimulation in depression

Deep Brain Stimulation for Depression: An Update

Depression is an often debilitating disorder affecting a person’s ability to work and function. Treatment-resistant depression (TRD) leads to many interventions and significant health care costs. Deep brain stimulation (DBS) is an emerging potential intervention for those with TRD who have undergone adequate medication, therapy, and rTMS/ECT trials, but who continue to suffer from unremitting depressive symptoms. The latest clinical safety and efficacy data of DBS for TRD is presented in this review. Since the origin of DBS is rooted in specific neuroanatomical targets, the discussion is organized according to target brain region. Relevant neuroimaging and animal studies are discussed, when available, as to how they shed light on possible mechanisms of action. Lastly, critical ethical issues related to informed consent and decision-making capacity are considered.

Deep brain stimulation in depression.

Deep brain stimulation in depression.

Use of Deep Brain Stimulation in Depression?- Opportunities and Risks. Conclusions Based On the Results of Author's Research.

Currently work is underway on the use of DBS in psychiatry, particularly in the population of patients with treatment-resistant depression. Authors summarize the current state of knowledge, risks and benefits associated with the use of DBS and try to specify the position of DBS in the treatment of depression. Conclusions are based on a review of the literature and the results of research conducted in the Department of Neurosurgery in Institute of Psychiatry and Neurology (Warsaw). The study group included 60 patients with Parkinson's disease surgically treated by implantation of subthalamic nucleus stimulator (STN -DBS). The aim of the study was to assess the mental state of patients before and after implantation of STN-DBS, with particular attention to the presence of depression and anhedonia. This study showed an improvement in mental status, which has followed within a month after the start of stimulation and manifested in the improvement of mood, reduction of sadness, apathy and anhedonia. The trend towards improvement was maintained over the following months. The assessment carried out six months after DBS implantation showed reduction in score in HADRS, MADRS, BDI compared to the state before the operation. Anhedonia reduction observed during the first 30 days after initiating the stimulation persisted in the assessment six months after DBS implantation. There is a need of systematic study of population treated with DBS using standardized measures. Data on effectivness and side-effects of DBS would be extremely useful for further research on the use of DBS in psychiatric disorders.

Cardiac autonomic function before and after deep brain stimulation for depression

Cardiac autonomic function before and after deep brain stimulation for depression

P.2.a.016 Electrode implantation produces an early response to deep brain stimulation in depression: potential role of regional neuroinflammation

P.2.a.016 Electrode implantation produces an early response to deep brain stimulation in depression: potential role of regional neuroinflammation

Early responses to deep brain stimulation in depression are modulated by anti-inflammatory drugs

Deep brain stimulation (DBS) in the subgenual cingulated gyrus (SCG) is a promising new technique that may provide sustained remission in resistant major depressive disorder (MDD). Initial studies reported a significant early improvement in patients, followed by a decline within the first month of treatment, an unexpected phenomenon attributed to potential placebo effects or a physiological response to probe insertion that remains poorly understood. Here we characterized the behavioural antidepressant-like effect of DBS in the rat medial prefrontal cortex, focusing on modifications to rodent SCG correlate (prelimbic and infralimbic (IL) cortex). In addition, we evaluated the early outcome of DBS in the SCG of eight patients with resistant MDD involved in a clinical trial. We found similar antidepressant-like effects in rats implanted with electrodes, irrespective of whether they received electrical brain stimulation or not. This effect was due to regional inflammation, as it was temporally correlated with an increase of glial-fibrillary-acidic-protein immunoreactivity, and it was blocked by anti-inflammatory drugs. Indeed, inflammatory mediators and neuronal p11 expression also changed. Furthermore, a retrospective study indicated that the early response of MDD patients subjected to DBS was poorer when they received anti-inflammatory drugs. Our study demonstrates that electrode implantation up to the IL cortex is sufficient to produce an antidepressant-like effect of a similar magnitude to that observed in rats receiving brain stimulation. Moreover, both preclinical and clinical findings suggest that the use of anti-inflammatory drugs after electrode implantation may attenuate the early anti-depressive response in patients who are subjected to DBS.

P.2.b.013 Does the early response to deep brain stimulation in depression represent a placebo or electrode insertion effect?

P.2.b.013 Does the early response to deep brain stimulation in depression represent a placebo or electrode insertion effect?

Diffusion Tensor Imaging to Aid Subgenual Cingulum Target Selection for Deep Brain Stimulation in Depression

Background: The most investigated target for deep brain stimulation in depression is the subgenual cingulate gyrus (Cg25) which has been shown to be a critical hub for signalling in the condition. Diffusion tensor imaging (DTI) is a form of MR sequence that can visualise white matter connections and potentially aid target selection. Objectives: To assess whether targets selected using DTI to find the area of maximal tract crossover (maximal isotropy) underlying the subgenual cingulum differ significantly in location from those selected using standard T₂ sequences. Methods: Fifty-nine non-depressed adult volunteers underwent MR imaging using T₁, T₂ and DTI sequences of the brain. Each patient had targets selected for both hemispheres using both T₂ and DTI sequences. The significance of the differences in coordinates in all three dimensions was tested using the paired t test. Results: There was a significant difference in the mediolateral (x) and dorsoventral (z) coordinates of DTI targets when compared with T₂ targets (p < 0.001). Conclusions: Targets within Cg25 selected using DTI are significantly different in location from those selected using T₂ sequences and have the potential to enhance treatment outcome by reducing the impact of interindividual variability.

Circuits, Cells, and Synapses: Toward a New Target for Deep Brain Stimulation in Depression

Understanding the pathophysiology of depression requires knowledge of the anatomical pathways that malfunction in this disorder. The anatomy of depression involves limbic and hypothalamic activation mediating stress and anxiety. These interact with cortical areas, primarily the medial prefrontal cortex (mPFC), which appears to mediate the cognitive aspects of depression. The mPFC in turn innervates the thalamus and lateral habenula (l. habenula). The anatomy of melancholia has recently been advanced through an understanding of the role of the l. habenula and incorporation of this structure between the cortical and limbic inputs and the monoaminergic nuclei. The l. habenula controls the midbrain monoaminergic nuclei, whose output pathways interact with each other, as well as providing strong modulatory control of limbic and cortical areas. Recently understanding of how the dopamine system is regulated by the l. habenula in normal (Matsumoto and Hikosaka, 2009) and affectively disturbed states (Li et al, 2011) has been investigated. Over activity in the l. habenula is seen in both the learned helplessness model (Li et al, 2011) and in patients who express depressive symptoms following tryptophan depletion (Roiser et al, 2009). This over activity causes decreased dopaminergic stimuation, suppressing reward signals (Matsumoto and Hikosaka, 2009). It also depresses 5HT signals (Wang and Aghajanian, 1997), which feed back further increasing l. habenular activity. The l. habenula receives strong inputs from both the limbic system, through the basal nucleus of the stria terminalis, which carries information from the amygdala related to anxiety and from the mPFC, which may be related to the cognitive aspects of depression (Li et al, 2011) and sends its output to the midbrain aminergic nuclei.

PL.03.01 Deep brain stimulation for depression: present and future

PL.03.01 Deep brain stimulation for depression: present and future

Serotonin affects transcranial direct current-induced neuroplasticity in humans

Background Modulation of the serotonergic system affects long-term potentiation (LTP) and long-term depression (LTD), the likely neurophysiologic derivates of learning and memory formation, in animals and slice preparations. Serotonin-dependent modulation of plasticity has been proposed as an underlying mechanism for depression. However, direct knowledge about the impact of serotonin on neuroplasticity in humans is missing. Here we explore the impact of the serotonin reuptake blocker citalopram on plasticity induced by transcranial direct current stimulation (tDCS) in humans in a single-blinded, placebo-controlled, randomized crossover study. Methods In 12 healthy subjects, anodal excitability-enhancing or cathodal excitability-diminishing tDCS was applied to the motor cortex under a single dose of 20-mg citalopram or placebo medication. Motor cortex excitability was monitored by single-pulse transcranial magnetic stimulation (TMS). Results Under placebo medication, anodal tDCS enhanced, and cathodal tDCS reduced, excitability for about 60–120 min. Citalopram enhanced and prolonged the facilitation induced by anodal tDCS, whereas it turned cathodal tDCS-induced inhibition into facilitation. Conclusions Serotonin has a prominent impact on neuroplasticity in humans, which is in favor for facilitatory plasticity. Taking into account serotonergic hypoactivity in depression, this might explain deficits of learning and memory formation. Moreover, the results suggest that for therapeutic brain stimulation in depression and other neuropsychiatric diseases (e.g., in neurorehabilitation), serotonergic reinforcement may enhance facilitatory aftereffects and thereby increase the efficacy of these tools.

Serotonin Affects Transcranial Direct Current–Induced Neuroplasticity in Humans

Modulation of the serotonergic system affects long-term potentiation (LTP) and long-term depression (LTD), the likely neurophysiologic derivates of learning and memory formation, in animals and slice preparations. Serotonin-dependent modulation of plasticity has been proposed as an underlying mechanism for depression. However, direct knowledge about the impact of serotonin on neuroplasticity in humans is missing. Here we explore the impact of the serotonin reuptake blocker citalopram on plasticity induced by transcranial direct current stimulation (tDCS) in humans in a single-blinded, placebo-controlled, randomized crossover study. In 12 healthy subjects, anodal excitability-enhancing or cathodal excitability-diminishing tDCS was applied to the motor cortex under a single dose of 20-mg citalopram or placebo medication. Motor cortex excitability was monitored by single-pulse transcranial magnetic stimulation (TMS). Under placebo medication, anodal tDCS enhanced, and cathodal tDCS reduced, excitability for about 60-120 min. Citalopram enhanced and prolonged the facilitation induced by anodal tDCS, whereas it turned cathodal tDCS-induced inhibition into facilitation. Serotonin has a prominent impact on neuroplasticity in humans, which is in favor for facilitatory plasticity. Taking into account serotonergic hypoactivity in depression, this might explain deficits of learning and memory formation. Moreover, the results suggest that for therapeutic brain stimulation in depression and other neuropsychiatric diseases (e.g., in neurorehabilitation), serotonergic reinforcement may enhance facilitatory aftereffects and thereby increase the efficacy of these tools.