AGBG. Neurociencias - UDES

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https://repositorio.udes.edu.co/handle/001/9429

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Examinando AGBG. Neurociencias - UDES por Autor "Beissner, Florian"

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  • Publicación
    Acceso abierto
    Brain Circuitry Supporting Multi-Organ Autonomic Outflow in Response to Nausea
    (2016-02) García, Ronald G.; Kim, Jieun; Sheehan, James D.; Beissner, Florian; Bianchi, Anna M.; Cerutti, Sergio; Kuo, Braden; Barbieri, Riccardo; Napadow, Vitaly; Sclocco, Roberta
    While autonomic outflow is an important co-factor of nausea physiology, central control of this outflow is poorly understood. We evaluated sympathetic (skin conductance level) and cardiovagal (high-frequency heart rate variability) modulation, collected synchronously with functional MRI (fMRI) data during nauseogenic visual stimulation aimed to induce vection in susceptible individuals. Autonomic data guided analysis of neuroimaging data, using a stimulus-based (analysis windows set by visual stimulation protocol) and percept-based (windows set by subjects’ ratings) approach. Increased sympathetic and decreased parasympathetic modulation was associated with robust and anti-correlated brain activity in response to nausea. Specifically, greater autonomic response was associated with reduced fMRI signal in brain regions such as the insula, suggesting an inhibitory relationship with premotor brainstem nuclei. Interestingly, some sympathetic/parasympathetic specificity was noted. Activity in default mode network and visual motion areas was anti-correlated with parasympathetic outflow at peak nausea. In contrast, lateral prefrontal cortical activity was anticorrelated with sympathetic outflow during recovery, soon after cessation of nauseogenic stimulation. These results suggest divergent central autonomic control for sympathetic and parasympathetic response to nausea. Autonomic outflow and the central autonomic network underlying ANS response to nausea may be an important determinant of overall nausea intensity and, ultimately, a potential therapeutic target.
  • Publicación
    Acceso abierto
    Neuroimaging brainstem circuitry supporting cardiovagal response to pain : A combined heart rate variability/ultrahigh-field (7 T) functional magnetic resonance imaging study
    (2016-01) García, Ronald G.; Sclocco, Roberta; Beissner, Florian; Desbordes, Gaelle; Polimeni, Jonathan R.; Wald, Lawrence L.; Kettner, Norman W.; Kim, Jieun; Renvall, Ville; Bianchi, Anna M.; Cerutti, Sergio; Napadow, Vitaly; Barbieri, Riccardo
    Central autonomic control nuclei in the brainstem have been difficult to evaluate non-invasively in humans. We applied ultrahigh-field (7 T) functional magnetic resonance imaging (fMRI), and the improved spatial resolution it affords (1.2 mm isotropic), to evaluate putative brainstem nuclei that control and/or sense pain-evoked cardiovagal modulation (high-frequency heart rate variability (HF-HRV) instantaneously estimated through a point-process approach). The time-variant HF-HRV signal was used to guide the general linear model analysis of neuroimaging data. Sustained (6 min) pain stimulation reduced cardiovagal modulation, with the most prominent reduction evident in the first 2 min. Brainstem nuclei associated with pain-evoked HF-HRV reduction were previously implicated in both autonomic regulation and pain processing. Specifically, clusters consistent with the rostral ventromedial medulla, ventral nucleus reticularis (Rt)/nucleus ambiguus (NAmb) and pontine nuclei (Pn) were found when contrasting sustained pain versus rest. Analysis of the initial 2-min period identified Rt/NAmb and Pn, in addition to clusters consistent with the dorsal motor nucleus of the vagus/nucleus of the solitary tract and locus coeruleus. Combining high spatial resolution fMRI and high temporal resolution HF-HRV allowed for a non-invasive characterization of brainstem nuclei, suggesting that nociceptive afference induces pain-processing brainstem nuclei to function in concert with known premotor autonomic nuclei in order to affect the cardiovagal response to pain.
  • Publicación
    Acceso abierto
    The somatosensory link : S1 functional connectivity is altered by sustained pain and associated with clinical/autonomic dysfunction in fibromyalgia
    (2015-05) Kim, Jieun; Loggia, Marco L.; Cahalan, Christine M.; Harris, Richard E.; Beissner, Florian; García, Ronald G.; Kim, Hyungjun; Wasan, Ajay D.; Edwards, Robert R.; Napadow, Vitaly
    Objective—Fibromyalgia (FM) is a chronic functional pain syndrome characterized by widespread pain, significant pain catastrophizing, sympathovagal dysfunction, and amplified temporal summation for evoked pain. While several studies have found altered resting brain connectivity in FM, studies have not specifically probed the somatosensory system, and its role in both somatic and non-somatic FM symptomatology. Our objective was to evaluate resting primary somatosensory cortex (S1) connectivity, and explore how sustained, evoked deep-tissue pain modulates this connectivity.Methods—We acquired fMRI and electrocardiography data from FM patients and healthy controls (HC) during rest (REST) and sustained mechanical pressure pain (PAIN) over the lower leg. Functional connectivity associated with different S1 subregions was calculated, while S1leg (leg representation) connectivity was contrast between REST and PAIN, and correlated with clinically-relevant measures in FM. Results—At REST, FM showed decreased connectivity between multiple ipsilateral and cross-hemispheric S1 subregions, which was correlated with clinical pain severity. PAIN, compared to REST, produced increased S1legconnectivity to bilateral anterior insula in FM, but not in HC. Moreover, in FM, sustained pain-altered S1legconnectivity to anterior insula was correlated with clinical/behavioral pain measures and autonomic responses. Conclusion—Our study demonstrates that both somatic and non-somatic dysfunction in FM, including clinical pain, pain catastrophizing, autonomic dysfunction, and amplified temporal summation, are all closely linked with the degree to which evoked deep-tissue pain alters S1 connectivity to salience/affective pain processing regions. Additionally, diminished connectivity between S1 subregions at REST in FM may result from ongoing widespread clinical pain.