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Neurotherapeutics : the Journal of the... Sep 2022Pain is an unpleasant sensory and emotional experience. Understanding the neural mechanisms of acute and chronic pain and the brain changes affecting pain factors is... (Review)
Review
Pain is an unpleasant sensory and emotional experience. Understanding the neural mechanisms of acute and chronic pain and the brain changes affecting pain factors is important for finding pain treatment methods. The emergence and progress of non-invasive neuroimaging technology can help us better understand pain at the neural level. Recent developments in identifying brain-based biomarkers of pain through advances in advanced imaging can provide some foundations for predicting and detecting pain. For example, a neurologic pain signature (involving brain regions that receive nociceptive afferents) and a stimulus intensity-independent pain signature (involving brain regions that do not show increased activity in proportion to noxious stimulus intensity) were developed based on multivariate modeling to identify processes related to the pain experience. However, an accurate and comprehensive review of common neuroimaging techniques for evaluating pain is lacking. This paper reviews the mechanism, clinical application, reliability, strengths, and limitations of common neuroimaging techniques for assessing pain to promote our further understanding of pain.
Topics: Humans; Pain Measurement; Reproducibility of Results; Neuroimaging; Brain; Chronic Pain; Magnetic Resonance Imaging
PubMed: 35902535
DOI: 10.1007/s13311-022-01274-z -
International Journal of Hyperthermia :... 2022Noxious acute cold stimuli cause cold shock the sympathetic nervous system. However, no studies have investigated respiratory "heat shock" in response to noxious acute...
Noxious acute cold stimuli cause cold shock the sympathetic nervous system. However, no studies have investigated respiratory "heat shock" in response to noxious acute heat stimuli (≥ 42 °C). In the present study, we examined whether short-duration whole-body immersion (for 5 min) in noxious hot water (45 °C) is a sufficient stimulus to induce a respiratory acute shock response. Our results indicate that short-duration whole-body immersion in noxious 45 °C water produces a significantly greater body temperature, heart rate, and perceptual and respiratory strain than immersion in innocuous warm 37 °C water ( < .05). The initial first minute of hot water immersion (HWI) at 45 °C (vs. immersion at 37 °C) caused a cardiorespiratory shock response, which manifested as acute hyperventilation, and increased ventilatory tidal volume, respiratory exchange ratio, and heart rate ( < .05). Adjustment to this initial respiratory heat shock response within the first minute of immersion was observed as compared with remaining HWI time (1-5 min). Intriguingly, the time-course kinetics of breathing frequency, oxygen uptake, and carbon dioxide washout did not differ between whole-body immersion at 37 °C and immersion at 45 °C, but were higher than in control thermoneutral conditions of an empty bath ( < .05). This may be because of events initiated not only by the water temperature but also by the change in the hydrostatic pressure acting upon the body when immersed in the water bath.
Topics: Body Temperature; Cold Temperature; Heart Rate; Heat-Shock Response; Humans; Water
PubMed: 35000494
DOI: 10.1080/02656736.2021.2023225 -
Neuron Aug 2007In order to deal effectively with danger, it is imperative to know about it. This is what nociceptors do--these primary sensory neurons are specialized to detect intense... (Review)
Review
In order to deal effectively with danger, it is imperative to know about it. This is what nociceptors do--these primary sensory neurons are specialized to detect intense stimuli and represent, therefore, the first line of defense against any potentially threatening or damaging environmental inputs. By sensing noxious stimuli and contributing to the necessary reactions to avoid them--rapid withdrawal and the experience of an intensely unpleasant or painful sensation, nociceptors are essential for the maintenance of the body's integrity. Although nociceptive pain is clearly an adaptive alarm system, persistent pain is maladaptive, essentially an ongoing false alarm. Here, we highlight the genesis of nociceptors during development and the intrinsic properties of nociceptors that enable them to transduce, conduct, and transmit nociceptive information and also discuss how their phenotypic plasticity contributes to clinical pain.
Topics: Animals; Cell Differentiation; Embryonic Development; Humans; Ion Channels; Nerve Endings; Neural Crest; Neuronal Plasticity; Nociceptors; Pain; Peptides; Phenotype; Physical Stimulation; Presynaptic Terminals; Receptors, Cell Surface; Stem Cells
PubMed: 17678850
DOI: 10.1016/j.neuron.2007.07.016 -
Frontiers in Immunology 2017The sensory nervous and immune systems, historically considered autonomous, actually work in concert to promote host defense and tissue homeostasis. These systems... (Review)
Review
The sensory nervous and immune systems, historically considered autonomous, actually work in concert to promote host defense and tissue homeostasis. These systems interact with each other through a common language of cell surface G protein-coupled receptors and receptor tyrosine kinases as well as cytokines, growth factors, and neuropeptides. While this bidirectional communication is adaptive in many settings, helping protect from danger, it can also become maladaptive and contribute to disease pathophysiology. The fundamental logic of how, where, and when sensory neurons and immune cells contribute to either health or disease remains, however, unclear. Our lab and others' have begun to explore how this neuro-immune reciprocal dialog contributes to physiological and pathological immune responses and sensory disorders. The cumulative results collected so far indicate that there is an important role for nociceptors (noxious stimulus detecting sensory neurons) in driving immune responses, but that this is highly context dependent. To illustrate this concept, we present our findings in a model of airway inflammation, in which nociceptors seem to have major involvement in type 2 but not type 1 adaptive immunity.
PubMed: 29163530
DOI: 10.3389/fimmu.2017.01463 -
The Journal of Neuroscience : the... Oct 2022Anterolateral system (AS) neurons transmit pain signals from the spinal cord to the brain. Their morphology, anatomy, and physiological properties have been extensively...
Anterolateral system (AS) neurons transmit pain signals from the spinal cord to the brain. Their morphology, anatomy, and physiological properties have been extensively characterized and suggest that specific AS neurons and their brain targets are concerned with the discriminatory aspects of noxious stimuli, such as their location or intensity, and their motivational/emotive dimension. Among the recently unraveled molecular markers of AS neurons is the developmentally expressed transcription factor Phox2a, providing us with the opportunity to selectively disrupt the embryonic wiring of AS neurons to gain insights into the logic of their adult function. As mice with a spinal-cord-specific loss of the netrin-1 receptor deleted in colorectal carcinoma (DCC) have increased AS neuron innervation of ipsilateral brain targets and defective noxious stimulus localization or topognosis, we generated mice of either sex carrying a deletion of in Phox2a neurons. Such mice displayed impaired topognosis along the rostrocaudal axis but with little effect on left-right discrimination and normal aversive responses. Anatomical tracing experiments in mice revealed defective targeting of cervical and lumbar AS axons within the thalamus. Furthermore, genetic labeling of AS axons revealed their expression of DCC on their arrival in the brain, at a time when many of their target neurons are being born and express Our experiments suggest a postcommissural crossing function for netrin-1:DCC signaling during the formation of somatotopically ordered maps and are consistent with a discriminatory function of some of the Phox2a AS neurons. How nociceptive (pain) signals are relayed from the body to the brain remains an important question relevant to our understanding of the basic physiology of pain perception. Previous studies have demonstrated that the AS is a main effector of this function. It is composed of AS neurons located in the spinal cord that receive signals from nociceptive sensory neurons that detect noxious stimuli. In this study, we generate a genetic miswiring of mouse AS neurons that results in a decreased ability to perceive the location of a painful stimulus. The precise nature of this defect sheds light on the function of different kinds of AS neurons and how pain information may be organized.
Topics: Animals; Mice; Colorectal Neoplasms; DCC Receptor; Homeodomain Proteins; Nerve Growth Factors; Netrin Receptors; Netrin-1; Neurons; Pain; Receptors, Cell Surface; Transcription Factors; Tumor Suppressor Proteins; Thalamus
PubMed: 36028316
DOI: 10.1523/JNEUROSCI.1164-22.2022 -
NeuroImage Mar 2017Noxious stimuli induce physiological processes which commonly translate into pain. However, under certain conditions, pain intensity can substantially dissociate from...
Noxious stimuli induce physiological processes which commonly translate into pain. However, under certain conditions, pain intensity can substantially dissociate from stimulus intensity, e.g. during longer-lasting pain in chronic pain syndromes. How stimulus intensity and pain intensity are differentially represented in the human brain is, however, not yet fully understood. We therefore used electroencephalography (EEG) to investigate the cerebral representation of noxious stimulus intensity and pain intensity during 10min of painful heat stimulation in 39 healthy human participants. Time courses of objective stimulus intensity and subjective pain ratings indicated a dissociation of both measures. EEG data showed that stimulus intensity was encoded by decreases of neuronal oscillations at alpha and beta frequencies in sensorimotor areas. In contrast, pain intensity was encoded by gamma oscillations in the medial prefrontal cortex. Contrasting right versus left hand stimulation revealed that the encoding of stimulus intensity in contralateral sensorimotor areas depended on the stimulation side. In contrast, a conjunction analysis of right and left hand stimulation revealed that the encoding of pain in the medial prefrontal cortex was independent of the side of stimulation. Thus, the translation of noxious stimulus intensity into pain is associated with a change from a spatially specific representation of stimulus intensity by alpha and beta oscillations in sensorimotor areas to a spatially independent representation of pain by gamma oscillations in brain areas related to cognitive and affective-motivational processes. These findings extend the understanding of the brain mechanisms of nociception and pain and their dissociations during longer-lasting pain as a key symptom of chronic pain syndromes.
Topics: Adult; Affect; Alpha Rhythm; Beta Rhythm; Brain; Brain Mapping; Electroencephalography; Female; Functional Laterality; Gamma Rhythm; Healthy Volunteers; Hot Temperature; Humans; Male; Pain; Physical Stimulation; Prefrontal Cortex; Sensorimotor Cortex; Young Adult
PubMed: 28069543
DOI: 10.1016/j.neuroimage.2017.01.011