Neuroscience and biobehavioral reviews
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Neurosci Biobehav Rev · Feb 2014
ReviewPsychological processing in chronic pain: a neural systems approach.
Our understanding of chronic pain involves complex brain circuits that include sensory, emotional, cognitive and interoceptive processing. The feed-forward interactions between physical (e.g., trauma) and emotional pain and the consequences of altered psychological status on the expression of pain have made the evaluation and treatment of chronic pain a challenge in the clinic. ⋯ These changes are ongoing, vary in their magnitude, and their hierarchical manifestations, and may be temporally and sequentially altered by treatments, and all contribute to an overall pain phenotype. Furthermore, we link altered psychological processes to specific evidence-based treatments to put forth a model of pain neuroscience psychology.
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Neurosci Biobehav Rev · Jan 2014
ReviewFactors modulating neural reactivity to drug cues in addiction: a survey of human neuroimaging studies.
Human neuroimaging studies suggest that neural cue reactivity is strongly associated with indices of drug use, including addiction severity and treatment success. However, little is known about factors that modulate cue reactivity. The goal of this review, in which we survey published fMRI and PET studies on drug cue reactivity in cocaine, alcohol, and tobacco cigarette users, is to highlight major factors that modulate brain reactivity to drug cues. ⋯ We then discuss major factors that have been shown to modulate cue reactivity and review specific evidence as well as outstanding questions related to each factor. Building on previous model-building reviews on the topic, we then outline a simplified model that includes the key modulatory factors and a tentative ranking of their relative impact. We conclude with a discussion of outstanding challenges and future research directions, which can inform future neuroimaging studies as well as the design of treatment and prevention programs.
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Neurosci Biobehav Rev · Jan 2014
ReviewStress, serotonin, and hippocampal neurogenesis in relation to depression and antidepressant effects.
Chronic stressful life events are risk factors for developing major depression, the pathophysiology of which is strongly linked to impairments in serotonin (5-HT) neurotransmission. Exposure to chronic unpredictable stress (CUS) has been found to induce depressive-like behaviours, including passive behavioural coping and anhedonia in animal models, along with many other affective, cognitive, and behavioural symptoms. The heterogeneity of these symptoms represents the plurality of corticolimbic structures involved in mood regulation that are adversely affected in the disorder. ⋯ In addition, by decreasing neurogenesis, CUS decreases hippocampal inhibition of the hypothalamic-pituitary-adrenal (HPA) axis, exacerbating stress axis overactivity. Similarly, we discuss the possibility that adult hippocampal neurogenesis mediates antidepressant effects via the ventral (in rodents; anterior in humans) hippocampus' influence on the HPA axis, and mechanisms by which antidepressants may reverse chronic stress-induced 5-HT and neurogenic changes. Although data are as yet equivocal, antidepressant modulation of 5-HT neurotransmission may well serve as one of the factors that could drive neurogenesis-dependent antidepressant effects through these stress regulation-related mechanisms.
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Memory loss is the key symptom of dementia-related disorders, including the prevalent Alzheimer's disease (AD). To date, pharmacological treatments for AD have limited and short-lasting effects. Therefore, researchers are investigating novel therapies such as deep brain stimulation (DBS) to treat memory impairment and to reduce or stop the progression of it. ⋯ The mechanisms underlying memory enhancement may include the release of specific neurotransmitters and neuroplasticity. Some authors suggest that DBS might even be disease-modifying. Nevertheless, it is still premature to conclude that DBS can be used in the treatment of AD, and the field will wait for the results of ongoing clinical trials.
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Neurosci Biobehav Rev · Dec 2013
ReviewThe downward spiral of chronic pain, prescription opioid misuse, and addiction: cognitive, affective, and neuropsychopharmacologic pathways.
Prescription opioid misuse and addiction among chronic pain patients are emerging public health concerns of considerable significance. Estimates suggest that more than 10% of chronic pain patients misuse opioid analgesics, and the number of fatalities related to nonmedical or inappropriate use of prescription opioids is climbing. ⋯ Addictive use of opioids is described as the outcome of a cycle initiated by chronic pain and negative affect and reinforced by opioidergic-dopamingeric interactions, leading to attentional hypervigilance for pain and drug cues, dysfunctional connectivity between self-referential and cognitive control networks in the brain, and allostatic dysregulation of stress and reward circuitry. Implications for clinical practice are discussed; multimodal, mindfulness-oriented treatment is introduced as a potentially effective approach to disrupting the downward spiral and facilitating recovery from chronic pain and opioid addiction.