Large-scale intrinsic brain systems have been identified for exteroceptive senses (such as sight, hearing and touch). We introduce an analogous system for representing sensations from within the body, called interoception, and demonstrate its relation to regulating peripheral systems in the body, called allostasis. Employing the recently introduced Embodied Predictive Interoception Coding (EPIC) model, we used tract-tracing studies of macaque monkeys, followed by two intrinsic functional magnetic resonance imaging samples (N = 280 and N = 270) to evaluate the existence of an intrinsic allostatic–interoceptive system in the human brain. Another sample (N = 41) allowed us to evaluate the convergent validity of the hypothesized allostatic–interoceptive system by showing that individuals with stronger connectivity between system hubs performed better on an implicit index of interoceptive ability related to autonomic fluctuations. Implications include insights for the brain’s functional architecture, dissolving the artificial boundary between mind and body, and unifying mental and physical illness.

Electrodermal activity (EDA) is a noninvasive measure of sympathetic activation often used to study emotions, decision making, and health. The use of "ambulatory" EDA in everyday life presents novel challenges-frequent artifacts and long recordings-with inconsistent methods available for efficiently and accurately assessing data quality. We developed and validated a simple, transparent, flexible, and automated quality assessment procedure for ambulatory EDA data. A total of 20 individuals with autism (5 females, 5-13 years) provided a combined 181 h of EDA data in their home using the Affectiva Q Sensor across 8 weeks. Our procedure identified invalid data using four rules: First, EDA out of range; second, EDA changes too quickly; third, temperature suggests the sensor is not being worn; and fourth, transitional data surrounding segments identified as invalid via the preceding rules. We identified invalid portions of a pseudorandom subset of our data (32.8 h, 18%) using our automated procedure and independent visual inspection by five EDA experts. Our automated procedure identified 420 min (21%) of invalid data. The five experts agreed strongly with each other (agreement: 98%, Cohen's κ: 0.87) and, thus, were averaged into a "consensus" rating. Our procedure exhibited excellent agreement with the consensus rating (sensitivity: 91%, specificity: 99%, accuracy: 92%, κ: 0.739 [95% CI = 0.738, 0.740]). We developed a simple, transparent, flexible, and automated quality assessment procedure for ambulatory EDA data. Our procedure can be used beyond this study to enhance efficiency, transparency, and reproducibility of EDA analyses, with free software available at http://www.cbslab.org/EDAQA.

Chemotherapy-induced peripheral neuropathy (CIPN) is a common, debilitating, and dose-limiting side effect of many chemotherapy regimens yet has limited treatments due to incomplete knowledge of its pathophysiology. Research on the pathophysiology of CIPN has focused on peripheral nerves because CIPN symptoms are felt in the hands and feet. However, better understanding the role of the brain in CIPN may accelerate understanding, diagnosing, and treating CIPN. The goals of this review are to (1) investigate the role of the brain in CIPN, and (2) use this knowledge to inform future research and treatment of CIPN. We identified 16 papers using brain interventions in animal models of CIPN and five papers using brain imaging in humans or monkeys with CIPN. These studies suggest that CIPN is partly caused by (1) brain hyperactivity, (2) reduced GABAergic inhibition, (3) neuroinflammation, and (4) overactivation of GPCR/MAPK pathways. These four features were observed in several brain regions including the thalamus, periaqueductal gray, anterior cingulate cortex, somatosensory cortex, and insula. We discuss how to leverage this knowledge for future preclinical research, clinical research, and brain-based treatments for CIPN.

Chemotherapy-induced peripheral neuropathy (CIPN) is an adverse effect of neurotoxic antineoplastic agents commonly used to treat cancer. Patients with CIPN experience debilitating signs and symptoms, such as combinations of tingling, numbness, pain, and cramping in the hands and feet that inhibit their daily function. Among the limited prevention and treatment options for CIPN, exercise has emerged as a promising new intervention that has been investigated in approximately two dozen clinical trials to date. As additional studies test and suggest the efficacy of exercise in treating CIPN, it is becoming more critical to develop mechanistic understanding of the effects of exercise in order to tailor it to best treat CIPN symptoms and identify who will benefit most. To address the current lack of clarity around the effect of exercise on CIPN, we reviewed the key potential mechanisms (e.g., neurophysiological and psychosocial factors), mediators (e.g., anti-inflammatory cytokines, self-efficacy, and social support), and moderators (e.g., age, sex, body mass index, physical fitness, exercise dose, exercise adherence, and timing of exercise) that may illuminate the relationship between exercise and CIPN improvement. Our review is based on the studies that tested the use of exercise for patients with CIPN, patients with other types of neuropathies, and healthy adults. The discussion presented herein may be used to (1) guide oncologists in predicting which symptoms are best targeted by specific exercise programs, (2) enable clinicians to tailor exercise prescriptions to patients based on specific characteristics, and (3) inform future research and biomarkers on the relationship between exercise and CIPN.