Acclimatization to cold in humans

This review focuses on the responses and mechanisms of both natural and artificial acclimatization to a cold environment in mammals, with specific reference to human beings. The purpose is to provide basic information for designers of thermal protection systems for astronauts during intra- and extravehicular activities. Hibernation, heat production, heat loss, vascular responses, body insulation, shivering thermogenesis, water immersion, exercise responses, and clinical symptoms and hypothermia in the elderly are discussed

Exploring Biosignals for Quantitative Pain Assessment in Cancer Patients: A Proof of Concept

Perception and expression of pain in cancer patients are influenced by distress levels, tumor type and progression, and the underlying pathophysiology of pain. Relying on traditional pain assessment tools can present limitations due to the highly subjective and multifaceted nature of the symptoms. In this scenario, objective pain assessment is an open research challenge. This work introduces a framework for automatic pain assessment. The proposed method is based on a wearable biosignal platform to extract quantitative indicators of the patient pain experience, evaluated through a self-assessment report. Two preliminary case studies focused on the simultaneous acquisition of electrocardiography (ECG), electrodermal activity (EDA), and accelerometer signals are illustrated and discussed. The results demonstrate the feasibility of the approach, highlighting the potential of EDA in capturing skin conductance responses (SCR) related to pain events in chronic cancer pain. A weak correlation (R = 0.2) is found between SCR parameters and the standard deviation of the interbeat interval series (SDRR), selected as the Heart Rate Variability index. A statistically significant (p < 0.001) increase in both EDA signal and SDRR is detected in movement with respect to rest conditions (assessed by means of the accelerometer signals) in the case of motion-associated cancer pain, thus reflecting the relationship between motor dynamics, which trigger painful responses, and the subsequent activation of the autonomous nervous system. With the objective of integrating parameters obtained from biosignals to establish pain signatures within different clinical scenarios, the proposed framework proves to be a promising research approach to define pain signatures in different clinical contexts

Manipulating the perceived shape and color of a virtual limb can modulate pain responses

Changes in body representation may affect pain perception. The effect of a distorted body image, such as the telescoping effect in amputee patients, on pain perception, is unclear. This study aimed to investigate whether distorting an embodied virtual arm in virtual reality (simulating the telescoping effect in amputees) modulated pain perception and anticipatory responses to pain in healthy participants. Twenty-seven right-handed participants were immersed in virtual reality and the virtual arm was shown with three different levels of distortion with a virtual threatening stimulus either approaching or contacting the virtual hand. We evaluated pain/discomfort ratings, ownership, and skin conductance responses (SCRs) after each condition. Viewing a distorted virtual arm enhances the SCR to a threatening event with respect to viewing a normal control arm, but when viewing a reddened-distorted virtual arm, SCR was comparatively reduced in response to the threat. There was a positive relationship between the level of ownership over the distorted and reddened-distorted virtual arms with the level of pain/discomfort, but not in the normal control arm. Contact with the threatening stimulus significantly enhances SCR and pain/discomfort, while reduced SCR and pain/discomfort were seen in the simulated-contact condition. These results provide further evidence of a bi-directional link between body image and pain perception

Neurophysiological mechanisms of longer-lasting experimental pain in humans

Pain serves the protection of the body. Consequently, noxious stimuli or, more precisely, the thereby induced neurophysiological processes commonly lead to pain perception. Identical noxious stimuli, however, do not always translate into the same pain experience depending on multiple factors. To acknowledge this variability, the distinction between nociception as the neural process elicited by noxious stimuli and pain as subjective multifactorial experience is essential. During longer-lasting experimental pain and chronic pain, nociception and pain can substantially dissociate. Moreover, longer-lasting experimental pain resembles chronic pain regarding certain perceptual features such as prolonged pain duration and intensity fluctuations. Thus, longer-lasting experimental pain offers the opportunity to gain new insights into both the differential neural representation of noxious stimuli and pain and the neuronal mechanisms associated with the state of longer- lasting pain. We applied 10 minutes of painful heat stimulation to the left and right hand of 39 healthy participants while we recorded continuous pain ratings, electroencephalography (EEG), and autonomic responses. Data were analyzed in three distinct projects aiming at different aspects of neuronal mechanisms underlying longer-lasting pain. Project 1 assessed whether stimulus intensity as proxy of nociception and pain intensity relate to distinct patterns of oscillatory brain activity. EEG recordings revealed that increases in stimulus intensity were reflected by suppressions of alpha and beta oscillations in sensorimotor areas contralateral to the stimulated hand. In contrast, increases in pain intensity were associated with enhanced gamma oscillations in the medial prefrontal cortex. More importantly, the encoding of stimulus intensity by alpha and beta oscillations in the sensorimotor areas was spatially specific, i.e. depended on the stimulus location, whereas the encoding of pain intensity by gamma oscillations in the medial prefrontal cortex was independent of stimulus location. Thus, prefrontal gamma oscillations might reflect higher- order aspects of noxious stimuli, such as salience, valence, and motivational aspects rather than precise sensory features. Project 2 investigated the relationship between stimulus intensity, pain intensity, autonomic responses, and brain activity. Skin conductance measures, as markers of sympathetic activity, co-varied more closely with stimulus intensity than with pain intensity. Correspondingly, skin conductance measures were related to suppressions of alpha and beta oscillations in the sensorimotor area contralateral to the stimulated hand. These finding suggest that skin conductance measures are in part directly elicited by nociceptive processes and, thus, at least partially independent of perceptual processes during longer-lasting pain. Hence, these observations corroborate concepts of pain in which sensory, motivational, and autonomic processes partially independently contribute to the experience of pain. Finally, project 3 incorporated the systematic and comprehensive assessment of oscillatory brain activity, functional connectivity, and graph- theory based network measures during the state of longer-lasting pain. Longer-lasting pain was associated with suppressions of oscillatory brain activity at alpha frequencies in addition to stronger connectivity at alpha and beta frequencies in sensorimotor areas. Furthermore, sensorimotor areas contralateral to stimulation showed increased connectivity to a common area in the medial prefrontal cortex at alpha frequencies and built a sensorimotor-prefrontal network during longer-lasting pain. This network might be involved in the integration of sensory, cognitive, and motivational-affective information and, consequently, in the translation of a noxious stimulus into a subjective pain experience. All three projects contribute to a better understanding of neuronal mechanisms underlying longer-lasting experimental pain, which serves as an experimental model for chronic pain. Since the treatment of chronic pain has remained insufficient and unsatisfactory, the current results might provide EEG-based targets for urgently needed new treatment approaches, such as non-invasive brain stimulation and neurofeedback

Social interactions, emotion and sleep: a systematic review and research agenda

Sleep and emotion are closely linked, however the effects of sleep on socio-emotional task performance have only recently been investigated. Sleep loss and insomnia have been found to affect emotional reactivity and social functioning, although results, taken together, are somewhat contradictory. Here we review this advancing literature, aiming to 1) systematically review the relevant literature on sleep and socio-emotional functioning, with reference to the extant literature on emotion and social interactions, 2) summarize results and outline ways in which emotion, social interactions, and sleep may interact, and 3) suggest key limitations and future directions for this field. From the reviewed literature, sleep deprivation is associated with diminished emotional expressivity and impaired emotion recognition, and this has particular relevance for social interactions. Sleep deprivation also increases emotional reactivity; results which are most apparent with neuro-imaging studies investigating amygdala activity and its prefrontal regulation. Evidence of emotional dysregulation in insomnia and poor sleep has also been reported. In general, limitations of this literature include how performance measures are linked to self-reports, and how results are linked to socio-emotional functioning. We conclude by suggesting some possible future directions for this field

Theoretical aspects of metal-electrolyte interfaces Final report

Skin surface electrode and electrochemical cell characteristics for human bioelectric response determination

Neurophysiological mechanisms of longer-lasting experimental pain in humans

Pain serves the protection of the body. Consequently, noxious stimuli or, more precisely, the thereby induced neurophysiological processes commonly lead to pain perception. Identical noxious stimuli, however, do not always translate into the same pain experience depending on multiple factors. To acknowledge this variability, the distinction between nociception as the neural process elicited by noxious stimuli and pain as subjective multifactorial experience is essential. During longer-lasting experimental pain and chronic pain, nociception and pain can substantially dissociate. Moreover, longer-lasting experimental pain resembles chronic pain regarding certain perceptual features such as prolonged pain duration and intensity fluctuations. Thus, longer-lasting experimental pain offers the opportunity to gain new insights into both the differential neural representation of noxious stimuli and pain and the neuronal mechanisms associated with the state of longer- lasting pain. We applied 10 minutes of painful heat stimulation to the left and right hand of 39 healthy participants while we recorded continuous pain ratings, electroencephalography (EEG), and autonomic responses. Data were analyzed in three distinct projects aiming at different aspects of neuronal mechanisms underlying longer-lasting pain. Project 1 assessed whether stimulus intensity as proxy of nociception and pain intensity relate to distinct patterns of oscillatory brain activity. EEG recordings revealed that increases in stimulus intensity were reflected by suppressions of alpha and beta oscillations in sensorimotor areas contralateral to the stimulated hand. In contrast, increases in pain intensity were associated with enhanced gamma oscillations in the medial prefrontal cortex. More importantly, the encoding of stimulus intensity by alpha and beta oscillations in the sensorimotor areas was spatially specific, i.e. depended on the stimulus location, whereas the encoding of pain intensity by gamma oscillations in the medial prefrontal cortex was independent of stimulus location. Thus, prefrontal gamma oscillations might reflect higher- order aspects of noxious stimuli, such as salience, valence, and motivational aspects rather than precise sensory features. Project 2 investigated the relationship between stimulus intensity, pain intensity, autonomic responses, and brain activity. Skin conductance measures, as markers of sympathetic activity, co-varied more closely with stimulus intensity than with pain intensity. Correspondingly, skin conductance measures were related to suppressions of alpha and beta oscillations in the sensorimotor area contralateral to the stimulated hand. These finding suggest that skin conductance measures are in part directly elicited by nociceptive processes and, thus, at least partially independent of perceptual processes during longer-lasting pain. Hence, these observations corroborate concepts of pain in which sensory, motivational, and autonomic processes partially independently contribute to the experience of pain. Finally, project 3 incorporated the systematic and comprehensive assessment of oscillatory brain activity, functional connectivity, and graph- theory based network measures during the state of longer-lasting pain. Longer-lasting pain was associated with suppressions of oscillatory brain activity at alpha frequencies in addition to stronger connectivity at alpha and beta frequencies in sensorimotor areas. Furthermore, sensorimotor areas contralateral to stimulation showed increased connectivity to a common area in the medial prefrontal cortex at alpha frequencies and built a sensorimotor-prefrontal network during longer-lasting pain. This network might be involved in the integration of sensory, cognitive, and motivational-affective information and, consequently, in the translation of a noxious stimulus into a subjective pain experience. All three projects contribute to a better understanding of neuronal mechanisms underlying longer-lasting experimental pain, which serves as an experimental model for chronic pain. Since the treatment of chronic pain has remained insufficient and unsatisfactory, the current results might provide EEG-based targets for urgently needed new treatment approaches, such as non-invasive brain stimulation and neurofeedback