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Managing cancer-related chronic pain is challenging to health care professionals as well as cancer patients and survivors. The management of cancer-related pain has largely consisted of pharmacological treatments, which has caused researchers to focus on neurotransmitter activity as a mediator of patients’ perception of pain rather than the electrical activity during neurobiological processes of cancer-related pain. Consequently, brain-based pain treatment has focused mainly on neurotransmitters and not electrical neuromodulation. Neuroimaging research has revealed that brain activity is associated with patients’ perceptions of symptoms across various diagnoses. The brain modulates internally generated neural activity and adjusts perceptions according to sensory input from the peripheral nervous system. Cancer-related pain may result not only from changes in the peripheral nervous system but also from changes in cortical activity over time. Thus, cortical reorganization by way of the brain’s natural, plastic ability (neuroplasticity) may be used to manage pain symptoms. Physical and psychological distress could be modulated by giving patients tools to regulate neural activity in symptom-specific regions of interest. Initial research in nononcology populations suggests that encouraging neuroplasticity through a learning paradigm can be a useful technique to help treat chronic pain. Here we review evidence that indicates a measurable link between brain activity and patient-reported psychological and physical distress. We also summarize findings regarding both the neuroelectrical and neuroanatomical experience of symptoms, review research examining the mechanisms of the brain’s ability to modify its own activity, and propose a brain-computer interface as a learning paradigm to augment neuroplasticity for pain management. [ABSTRACT FROM PUBLISHER]

Introduction: Cancer survivors experienced poorer health-related quality of life (HRQoL) and greater psychological distress during the COVID-19 pandemic than those without cancer. However, the underlying mechanisms that may explain how negative experiences during the pandemic are associated with distress and HRQoL remain unknown. We examined whether psychosocial risk factors (i.e., healthcare disruption, disruption to daily activities and social interaction [DDASI], and financial hardship) mediated the relationship between negative COVID-19-related experiences and cancer survivors' HRQoL and psychological distress (i.e., depressive symptoms, and anxiety) and whether the mediating effects were moderated by psychosocial protective factors (i.e., stress management ability and social support)., Methods: A total of 9,651 cancer survivors completed a questionnaire assessing negative COVID-19-related experiences, psychosocial and practical experiences, and HRQoL. Conditional process analysis was used to evaluate the proposed moderated mediation models., Results: Participants had a mean age of 63.8 years (SD = 12.3) and were mostly non-Hispanic White (82.3%). DDASI and financial hardship mediated the relationship between negative COVID-19-related experiences and cancer survivor's HRQoL and psychological distress. Stress management ability buffered the indirect effect of DDASI on cancer survivors' HRQoL and psychological distress. Social support buffered the indirect effect of financial hardship on HRQoL and depressive symptoms., Conclusion: Financial resources and social interactions may buffer negative effects of major disruptions such as the COVID-19 pandemic. Future studies should assess the longitudinal impact of these associations., Competing Interests: Antoni and Penedo are paid consultants for Blue Note Therapeutics. Antoni is a paid consultant for Atlantis Healthcare. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision., (Copyright © 2024 Noriega Esquives, Natori, Antoni, Otto, Prinsloo, Wagner, Gomez, Hathaway, Ulrich, Peoples, Cohen and Penedo.)

Like other forms of neuropathology, gliomas appear to spread along neural pathways. Accordingly, our group and others have previously shown that brain network connectivity is highly predictive of glioma survival. In this study, we aimed to examine the molecular mechanisms of this relationship via imaging transcriptomics. We retrospectively obtained presurgical, T1-weighted MRI datasets from 669 adult patients, newly diagnosed with diffuse glioma. We measured brain connectivity using gray matter networks and coregistered these data with a transcriptomic brain atlas to determine the spatial co-localization between brain connectivity and expression patterns for 14 proto-oncogenes and 3 neural network construction genes. We found that all 17 genes were significantly co-localized with brain connectivity (p < 0.03, corrected). The strength of co-localization was highly predictive of overall survival in a cross-validated Cox Proportional Hazards model (mean area under the curve, AUC = 0.68 +/- 0.01) and significantly (p < 0.001) more so for a random forest survival model (mean AUC = 0.97 +/- 0.06). Bayesian network analysis demonstrated direct and indirect causal relationships among gene-brain co-localizations and survival. Gene ontology analysis showed that metabolic processes were overexpressed when spatial co-localization between brain connectivity and gene transcription was highest (p < 0.001). Drug-gene interaction analysis identified 84 potential candidate therapies based on our findings. Our findings provide novel insights regarding how gene-brain connectivity interactions may affect glioma survival.

Objective: Patients with low-grade glioma (LGG) in eloquent regions often present with seizures, and findings on detailed neuropsychological testing are often abnormal. This study evaluated the association between cortical excitability, seizures, and cognitive function in patients with LGG., Methods: LGG patients who underwent transcranial magnetic stimulation (TMS) from January 2021 to December 2022 were studied. Cortical excitability was measured using the resting motor thresholds (RMTs) of the upper and lower extremities. Early postoperative seizures served as the seizure endpoint. Neuropsychological assessment was completed prior to surgery contemporaneous with the TMS studies., Results: A total of 31 patients were analyzed for seizure outcome. Median (interquartile range [IQR]) upper-extremity RMT was 39% (34%-46%) of maximum stimulator output, and the median (IQR) lower-extremity RMT was 69% (51%-79%). Lower-extremity RMT was higher in patients with early postoperative seizures, especially in those with motor region tumors (p = 0.02); however, RMT was not associated with seizures at presentation or long-term seizure control. A total of 26 patients completed neuropsychological assessment. There were significant negative correlations between upper-extremity RMT and psychomotor processing speed (Wechsler Adult Intelligence Scale-Fourth Edition [WAIS-IV] Processing Speed Index r = -0.42, p = 0.031; WAIS-IV Coding r = -0.41, p = 0.036; WAIS-IV Symbol Search r = -0.39, p = 0.048), executive function (Trail Making Test Part B r = -0.41, p = 0.036), and hand dexterity (Grooved Pegboard Test r = -0.50, p = 0.047)., Conclusions: RMT was positively correlated with early postoperative seizure risk and negatively correlated with psychomotor processing speed, executive function, and hand dexterity. These findings support the theory of local and regional resting oscillatory network dysfunction from a glioma-brain network.

As Antonio Damasio highlighted back in 1994, Descartes' division of mind and body slowed the full realization of the connectedness of the brain and the body by centuries. The simple fact that homeostasis in the brain was fully interconnected with the body has eluded researchers and clinicians even after the connection was well established. Recent studies reporting the central role in dysfunction of mental systems as a result of inflammation in the gut and the autonomic nervous system (ANS) was yet one more reminder that the entire system is connected and interdependent. Central to this discovery and its application to mental function has been the growing field of study of the microbiome. This article is an attempt to situate those who are active in the variety of ways and means of treating the brain in the essential role that is likely being played by a vast community of bacteria living in the bowels of the human being and influencing all of the higher and most "sophisticated" aspects of human interchange and thought. It is the authors hope that this brief introduction will remind and inform researchers and clinicians that the organism is more interconnected and more complex than we have tended to think and that disorders of the mind are likely also, often disorders of the gut.