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Studies suggest deep brain stimulation (DBS) as a treatment modality for the refractory obsessive-compulsive disorder (OCD). It is unclear where to place the DBS. Various sites are proposed for placement with the ventral capsule/ventral striatum (VC/VS) among the most studied. Herein, we aim to summarize both quantitative Yale-Brown Obsessive-Compulsive Scale (YBOCS) data and qualitative descriptions of the participants' symptoms when given. A literature search conducted via PubMed yielded 32 articles. We sought to apply a standard based on the utilization of YBOCS. This yielded 153 distinct patients. The outcome measure we focused on in this review is the latest YBOCS score reported for each patient/cohort in comparison to the location of the DBS. A total of 32 articles were found in the search results. In total, 153 distinct patients' results were reported in these studies. Across this collection of papers, a total of 9 anatomic structures were targeted. The majority of studies showed a better response at the last time point as compared to the first time point. Most patients had DBS at nucleus accumbens followed by VC/VS and the least patients had DBS at the bilateral superolateral branch of the median forebrain bundle and the bilateral basolateral amygdala. The average YBOCS improvement did not seem to directly correlate with the percentile of patients responding to the intervention.

Well-controlled, randomized studies with larger sample sizes with close follow up are needed to provide a more accurate determination for placement of DBS for OCD.

Drive and motivation are central to affective neuroscience. Here, we describe the development of conceptualizations from early behaviorist theories to contemporary theories linking motivation closely to reward. Current experimental data suggest key roles of drive and motivation in the wanting, liking, and learning processes underlying the pleasure cycle supporting survival of individuals and species. In particular, the underlying functional neuroanatomy of drive and motivation is now becoming clearer in humans and other mammals, which provides hope for novel more effective interventions for the pervasive problems of drive and motivation in affective and addictive disorders.

Classical definitions of motivation typically involve two main components: direction and activation. Motivated behavior is directed toward or away from particular stimuli (i.e., appetitive and aversive motivation). Furthermore, activational aspects of motivation refer to the observation that motivated behavior is characterized by substantial activity, vigor, persistence, and exertion of effort in both the initiation and maintenance of behavior. Although separate neural systems direct organisms toward distinct motivational stimuli (e.g., food, water, sex), there appears to be a common circuitry regulating behavioral activation and the exertion of effort. Mesolimbic dopamine is one of the brain systems mediating activational aspects of motivation and exertion of effort. This system integrates aspects of motivation and motor control functions involved in the instigation of action. Research on the neurobiology of effort has contributed to our understanding of the pathophysiology of neurological and psychiatric disorders that are characterized by motivational dysfunction.

This study aims to review the relationship between neurological processes and financial behavior from an interdisciplinary perspective. Individual decision-making is influenced by cognitive and affective biases; hence, it becomes pertinent to understand the origin of these biases. Neurofinance is an emerging field of finance budding from neuroeconomics and explains the relationship between human brain activity and financial behavior, drawn from interdisciplinary fields, including neurology, psychology and finance.

This conceptual paper extensively reviews the extant literature and performs meta-analysis to attain its research objectives.

The paper highlights the use of neuroimaging techniques in mapping the brain areas to help understand the processes in the higher cognitive areas of brain. The paper raises some new questions regarding individual preferences and choices while making financial or non-financial decisions.

The special focus on dysfunctions arising in brain because of injury and their impact on decision-making is also a key point in this paper and is summarized using meta-analytic forest plot. The existing literature provides instances where emotional processing is altered by injury in brain and may lead to more advantageous decisions, especially in risky situations.

How does the human brain absorb information and turn it into skills of its own in psychotherapy? In an attempt to answer this question, the authors will review the intricacies of processing channels in psychotherapy and propose the term transprocessing (as in transduction and processing combined) for the underlying mechanisms. Through transprocessing the brain processes multimodal memories and creates reparative solutions in the course of psychotherapy. Transprocessing is proposed as a stage-sequenced mechanism of deconstruction of engrained patterns of response. Through psychotherapy, emotional-cognitive reintegration and its consolidation is accomplished. This process is mediated by cellular and neural plasticity changes.

Performance feedback about whether responses are correct or incorrect provides valuable information to help guide learning. Although feedback itself has no extrinsic value, it can produce subjective feelings similar to “rewards” and “punishments.” Therefore, feedback can play both an informative and a motivational role. Over the past decade, researchers have identified a neural circuit that processes reward value and promotes reinforcement learning, involving target regions of dopaminergic input (e.g., striatum and ventromedial prefrontal cortex). Importantly, this circuit is engaged by performance feedback even in the absence of reward. Recent research suggests that feedback-related brain activity can be modulated by motivational context, such as whether feedback reflects goal achievement, whether learners are oriented toward the informative versus evaluative aspect of feedback, and whether individual learners are motivated to perform well relative to their peers. This body of research suggests that the brain responds flexibly to feedback, based on the learner’s goals.

Although first rank symptoms focus on positive symptoms of psychosis they are shared by a number of psychiatric conditions. The difficulty in differentiating bipolar disorder from schizophrenia with affective features has led to a third category of patients often loosely labeled as schizoaffective. Research in schizophrenia has attempted to render the presence or absence of negative symptoms and their relation to etiology and prognosis more explicit. A dichotomous population is a recurring theme in experimental paradigms. Thus, schizophrenia is defined as process or reactive, deficit or non-deficit and by the presence or absence of affective symptoms. Laboratory tests confirm the clinical impression showing conflicting responses to dexamethasone suppression and clearly defined differences in autonomic responsiveness, but their patho-physiological significance eludes mainstream theory. Added to this is the difficulty in agreeing to what exactly constitutes useful clinical features differentiating, for example, negative symptoms of a true deficit syndrome from features of depression. Two recent papers proposed that the general and specific cognitive features of schizophrenia and major depression result from a monoamine-cholinergic imbalance, the former due to a relative muscarinic receptor hypofunction and the latter, in contrast, to a muscarinic hypersensitivity exacerbated by monoamine depletion. Further development of these ideas will provide pharmacological principles for what is currently an incomplete and largely, descriptive nosology of psychosis. It will propose a dimensional view of affective and negative symptoms based on relative muscarinic integrity and is supported by several exciting intracellular signaling and gene expression studies. Bipolar disorder manifests both muscarinic and dopaminergic hypersensitivity. The greater the imbalance between these two receptor signaling systems, the more the clinical picture will resemble schizophrenia with bizarre, incongruent delusions and increasingly disorganized thought. The capacity for affective expression, by definition a non-deficit syndrome, will remain contingent on the degree of preservation of muscarinic signaling, which itself may be unstable and vary between trait and state examinations. At the extreme end of muscarinic impairment, a deficit schizophrenia subpopulation is proposed with a primary and fixed muscarinic receptor hypofunction.

The genomic profile of bipolar disorder and schizophrenia overlap and both have a common dopaminergic intracellular signaling which is hypersensitive to various stressors. It is proposed that the concomitant muscarinic receptor upregulation differentiates the syndromes, being marked in bipolar disorder and rather less so in schizophrenia. From a behavioral point of view non-deficit syndromes and bipolar disorder appear most proximate and could be reclassified as a spectrum of affective psychosis or schizoaffective disorders. Because of a profound malfunction of the muscarinic receptor, the deficit subgroup cannot express a comparable stress response. None -theless, a convergent principle of psychotic features across psychiatric disorders is a relative monoaminergic-muscarinic imbalance in signal transduction.

Genetic risk for depressive disorders is poorly understood despite consistent suggestions of a high heritable component. Most genetic studies have focused on risk associated with single variants, a strategy which has so far only yielded small (often non-replicable) risks for depressive disorders. In this paper we argue that more substantial risks are likely to emerge from genetic variants acting in synergy within and across larger neurobiological systems (polygenic risk factors). We show how knowledge of major integrated neurobiological systems provides a robust basis for defining and testing theoretically defensible polygenic risk factors. We do this by describing the architecture of the overall stress response. Maladaptation via impaired stress responsiveness is central to the aetiology of depression and anxiety and provides a framework for a systems biology approach to candidate gene selection. We propose principles for identifying genes and gene networks within the neurosystems involved in the stress response and for defining polygenic risk factors based on the neurobiology of stress-related behaviour. We conclude that knowledge of the neurobiology of the stress response system is likely to play a central role in future efforts to improve genetic prediction of depression and related disorders.

Chinese herbal medicine is effective in treating some addictions using, for example, aural acupuncture. Its application outside of China is limited due to a lack of clinical trials and ‘scientific’ evidence. U'finer™ is one of the first herbal remedies to undergo clinical trials, and is so far demonstrating a remarkable ability to improve brain function, restore physical health and enhance recovery from opiate addiction. The drug's pioneer Dr Wei Wang explains his methods and the drug's unique ability to treat the body and mind.