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Following arm amputation the region that represented the missing hand in primary somatosensory cortex (S1) becomes deprived of its primary input, resulting in changed boundaries of the S1 body map. This remapping process has been termed ‘reorganisation’ and has been attributed to multiple mechanisms, including increased expression of previously masked inputs. In a maladaptive plasticity model, such reorganisation has been associated with phantom limb pain (PLP). Brain activity associated with phantom hand movements is also correlated with PLP, suggesting that preserved limb functional representation may serve as a complementary process. Here we review some of the most recent evidence for the potential drivers and consequences of brain (re)organisation following amputation, based on human neuroimaging. We emphasise other perceptual and behavioural factors consequential to arm amputation, such as non-painful phantom sensations, perceived limb ownership, intact hand compensatory behaviour or prosthesis use, which have also been related to both cortical changes and PLP. We also discuss new findings based on interventions designed to alter the brain representation of the phantom limb, including augmented/virtual reality applications and brain computer interfaces. These studies point to a close interaction of sensory changes and alterations in brain regions involved in body representation, pain processing and motor control. Finally, we review recent evidence based on methodological advances such as high field neuroimaging and multivariate techniques that provide new opportunities to interrogate somatosensory representations in the missing hand cortical territory. Collectively, this research highlights the need to consider potential contributions of additional brain mechanisms, beyond S1 remapping, and the dynamic interplay of contextual factors with brain changes for understanding and alleviating PLP. •Technological advancements provide new insight into the neural basis of phantom pain.•Traditional mechanistic accounts of remapping in somatosensory cortex are incomplete.•Related contextual factors such as adaptive behaviour will contribute to brain plasticity.•A broader mechanistic focus beyond primary sensorimotor cortex is needed.•Plasticity and stability of the sensorimotor body maps may vary across time scales.

How we use our voice is central to how we express information about ourselves to others. A speaker’s dispositional social reactivity might contribute to how well they can volitionally modulate their voice to manage listener impressions. Here, we investigated individual differences in social vocal control performance in relation to social reactivity indices and underlying neural mechanisms. Twenty-four right-handed speakers of British English (twenty females) modulated their voice to communicate social traits (sounding likeable, hostile, intelligent) while undergoing a rapid-sparse fMRI protocol. Performance in social vocal control was operationalized as the specificity with which speakers evoked trait percepts in an independent group of naïve listeners. Speakers’ empathy levels, as well as psychopathic and Machiavellian traits, were assessed using self-report questionnaires. The ability to express specific social traits in voices was associated with activation in brain regions involved in vocal motor and social processing (left posterior TPJ, bilateral SMG, premotor cortex). While dispositional cognitive empathy predicted general vocal performance, self-reported levels of Machiavellianism were specifically related to better performance in expressing likeability. These findings highlight the psychological and neural mechanisms involved in strategic social voice modulation, suggesting differential processing in a combined network of vocal control and social processing streams.

Major depressive disorder (MDD) is characterized by altered emotional and cognitive functioning. We performed a voxel-based whole-brain meta-analysis of functional neuroimaging data on altered emotion and cognition in MDD. Forty peer-reviewed studies in English-language published between 1998 and 2010 were included, which used functional neuroimaging during cognitive–emotional challenge in adult individuals with MDD and healthy controls. All studies reported between-groups differences for whole-brain analyses in standardized neuroanatomical space and were subjected to Activation Likelihood Estimation (ALE) of brain cluster showing altered responsivity in MDD. ALE resulted in thresholded and false discovery rate corrected hypo- and hyperactive brain regions. Against the background of a complex neural activation pattern, studies converged in predominantly hypoactive cluster in the anterior insular and rostral anterior cingulate cortex linked to affectively biased information processing and poor cognitive control. Frontal areas showed not only similar under- but also over-activation during cognitive–emotional challenge. On the subcortical level, we identified activation alterations in the thalamus and striatum which were involved in biased valence processing of emotional stimuli in MDD. These results for active conditions extend findings from ALE meta-analyses of resting state and antidepressant treatment studies and emphasize the key role of the anterior insular and rostral anterior cingulate cortex for altered emotion and cognition in MDD. ► Meta-analysis of 40 neuroimaging studies on cognitive-emotional challenge in MDD. ► Hypoactivity was found in the anterior insular and anterior cingulate cortex. ► Prefrontal regions showed both hypo- and hyperactivity. ► Subcortical activation alterations were identified in the thalamus and striatum.

Chronic peer victimization has long-term impacts on mental health; however, the biological mediators of this adverse relationship are unknown. We sought to determine whether adolescent brain development is involved in mediating the effect of peer victimization on psychopathology. We included participants (n = 682) from the longitudinal IMAGEN study with both peer victimization and neuroimaging data. Latent profile analysis identified groups of adolescents with different experiential patterns of victimization. We then associated the victimization trajectories and brain volume changes with depression, generalized anxiety, and hyperactivity symptoms at age 19. Repeated measures ANOVA revealed time-by-victimization interactions on left putamen volume (F = 4.38, p = 0.037). Changes in left putamen volume were negatively associated with generalized anxiety (t = −2.32, p = 0.020). Notably, peer victimization was indirectly associated with generalized anxiety via decreases in putamen volume (95% CI = 0.004–0.109). This was also true for the left caudate (95% CI = 0.002–0.099). These data suggest that the experience of chronic peer victimization during adolescence might induce psychopathology-relevant deviations from normative brain development. Early peer victimization interventions could prevent such pathological changes.

Phantom limb pain (PLP) is a common phenomenon occurring after the amputation of a limb and can be accompanied by serious suffering. Psychological factors have been shown to play an important role in other types of chronic pain, where they are pivotal in the acquisition and maintenance of pain symptoms. For PLP, however, the interaction between pain and psychological variables is less well documented. In this review, we summarize research on the role of emotional, motivational, cognitive, and perceptual factors in PLP. The reported findings indicate that emotional factors modulate PLP but might be less important compared to other types of chronic pain. Additional factors such as the amount of disability and adjustment to the amputation appear to also play a role. Bidirectional relationships between stress and PLP have been shown quite consistently, and the potential of stress and tension reduction in PLP treatment could be further exploited. Little is known about the role of cognitive variables such as attention or expectation. Catastrophizing seems to aggravate PLP and could be targeted in treatment. Body perception is altered in PLP and poses a potential target for novel mechanistic treatments. More research on psychological factors and their interactions in PLP is needed.

Key Points With suitable standardization and validation, brain imaging could provide objective biomarkers of key characteristics and mechanisms related to chronic pain, that could guide personalized pain management Brain imaging shows promise in the assessment of risk factors for chronic pain and in identification of the mechanisms that underlie transition to, and maintenance of, chronic pain Identification of brain-based markers of chronic pain requires technological advances, large-scale data acquisition across diverse groups of individuals, and strict application of standards of evidence Brain-based biomarkers should be used as an adjunct to rather than a replacement for subjective reports of the pain experience Use of brain imaging as legal evidence of an individual's pain is not advisable until the specificity and sensitivity of such tests are improved, and validated protocols exist Current brain-based measures should be used only to understand brain mechanisms underlying pain, factors that lead to persistence of pain, and targets in the brain for safe and effective pain management Chronic pain is the greatest source of disability globally and claims related to chronic pain feature in many insurance and medico-legal cases. In this Consensus Statement, a presidential task force of the International Association for the Study of Pain examines the capabilities of brain imaging in the diagnosis of chronic pain, and the ethical and legal implications of such uses of brain imaging. Chronic pain is the greatest source of disability globally and claims related to chronic pain feature in many insurance and medico-legal cases. Brain imaging (for example, functional MRI, PET, EEG and magnetoencephalography) is widely considered to have potential for diagnosis, prognostication, and prediction of treatment outcome in patients with chronic pain. In this Consensus Statement, a presidential task force of the International Association for the Study of Pain examines the capabilities of brain imaging in the diagnosis of chronic pain, and the ethical and legal implications of its use in this way. The task force emphasizes that the use of brain imaging in this context is in a discovery phase, but has the potential to increase our understanding of the neural underpinnings of chronic pain, inform the development of therapeutic agents, and predict treatment outcomes for use in personalized pain management. The task force proposes standards of evidence that must be satisfied before any brain imaging measure can be considered suitable for clinical or legal purposes. The admissibility of such evidence in legal cases also strongly depends on laws that vary between jurisdictions. For these reasons, the task force concludes that the use of brain imaging findings to support or dispute a claim of chronic pain — effectively as a pain lie detector — is not warranted, but that imaging should be used to further our understanding of the mechanisms underlying pain.

Phantom limb pain (PLP) impacts the majority of individuals who undergo limb amputation. The PLP experience is highly heterogenous in its quality, intensity, frequency and severity. This heterogeneity, combined with the low prevalence of amputation in the general population, has made it difficult to accumulate reliable data on PLP. Consequently, we lack consensus on PLP mechanisms, as well as effective treatment options. However, the wealth of new PLP research, over the past decade, provides a unique opportunity to re-evaluate some of the core assumptions underlying what we know about PLP and the rationale behind PLP treatments. The goal of this review is to help generate consensus in the field on how best to research PLP, from phenomenology to treatment. We highlight conceptual and methodological challenges in studying PLP, which have hindered progress on the topic and spawned disagreement in the field, and offer potential solutions to overcome these challenges. Our hope is that a constructive evaluation of the foundational knowledge underlying PLP research practices will enable more informed decisions when testing the efficacy of existing interventions and will guide the development of the next generation of PLP treatments.

Phantom limb pain (PLP) is a common consequence of the amputation of a limb. Individuals with congenital limb absence (here: congenital amputees), however, seem to rarely experience PLP. Previous results suggest that the experience of PLP in the waking state affects the recalled body appearance in dreams of individuals with acquired limb amputation, with PLP being associated with the recall of an impaired rather than an intact body. However, it remains unclear how congenital amputees – who never experienced an intact body and rarely PLP – recall their body appearance in dreams. In the present cross-sectional study, we assessed body-related dream content in a sample of adult congenital amputees and compared their reports with those from adult persons with an acquired limb amputation early in life. We found that congenital amputees reported the least frequent dreams with an intact body, and after birth, the age at amputation positively predicted the recall of an intact body in dreams. The effects were not explained by time since amputation and the presence or absence of PLP. This suggests that life experiences of an intact body find expression in self-related dream content.

There is an extensive body of literature linking ADHD to overweight and obesity. Research indicates that impulsivity features of ADHD account for a degree of this overlap. The neural and polygenic correlates of this association have not been thoroughly examined. In participants of the IMAGEN study, we found that impulsivity symptoms and body mass index (BMI) were associated (r = 0.10, n = 874, p = 0.014 FWE corrected), as were their respective polygenic risk scores (PRS) (r = 0.17, n = 874, p = 6.5 × 10−6 FWE corrected). We then examined whether the phenotypes of impulsivity and BMI, and the PRS scores of ADHD and BMI, shared common associations with whole-brain grey matter and the Monetary Incentive Delay fMRI task, which associates with reward-related impulsivity. A sparse partial least squared analysis (sPLS) revealed a shared neural substrate that associated with both the phenotypes and PRS scores. In a last step, we conducted a bias corrected bootstrapped mediation analysis with the neural substrate score from the sPLS as the mediator. The ADHD PRS associated with impulsivity symptoms (b = 0.006, 90% CIs = 0.001, 0.019) and BMI (b = 0.009, 90% CIs = 0.001, 0.025) via the neuroimaging substrate. The BMI PRS associated with BMI (b = 0.014, 95% CIs = 0.003, 0.033) and impulsivity symptoms (b = 0.009, 90% CIs = 0.001, 0.025) via the neuroimaging substrate. A common neural substrate may (in part) underpin shared genetic liability for ADHD and BMI and the manifestation of their (observable) phenotypic association.

Phantom-limb pain is a common sequela of amputation, occurring in up to 80% of people who undergo the procedure. It must be differentiated from non-painful phantom phenomena, residual-limb pain, and non-painful residual-limb phenomena. Central changes seem to be a major determinant of phantom-limb pain; however, peripheral and psychological factors may contribute to it. A comprehensive model of phantom-limb pain is presented that assigns major roles to pain occurring before the amputation and to central as well as peripheral changes related to it. So far, few mechanism-based treatments for phantom-limb pain have been proposed. Most published reports are based on anecdotal evidence. Interventions targeting central changes seem promising. The prevention of phantom-limb pain by peripheral analgesia has not yielded consistent results. Additional measures that reverse or prevent the formation of central memory processes might be more effective.