Central Processing (central + processing)

Distribution by Scientific Domains
Medical Sciences75%

Terms modified by Central Processing

  • central processing unit
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    Selected Abstracts

    Habits of the heart: Life history and the developmental neuroendocrinology of emotion

    AMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 6 2009
    Carol M. Worthman
    The centrality of emotion in cognition and social intelligence as well as its impact on health has intensified investigation into the causes and consequences of individual variation in emotion regulation. Central processing of experience directly informs regulation of endocrine axes, essentially forming a neuro-endocrine continuum integrating information intake, processing, and physiological and behavioral response. Two major elements of life history,resource allocation and niche partitioning,are served by linking cognitive-affective with physiologic and behavioral processes. Scarce cognitive resources (attention, memory, and time) are allocated under guidance from affective co-processing. Affective-cognitive processing, in turn, regulates physiologic activity through neuro-endocrine outflow and thereby orchestrates energetic resource allocation and trade-offs, both acutely and through time. Reciprocally, peripheral activity (e.g., immunologic, metabolic, or energetic markers) influences affective-cognitive processing. By guiding attention, memory, and behavior, affective-cognitive processing also informs individual stances toward, patterns of activity in, and relationships with the world. As such, it mediates processes of niche partitioning that adaptively exploit social and material resources. Developmental behavioral neurobiology has identified multiple factors that influence the ontogeny of emotion regulation to form affective and behavioral styles. Evidence is reviewed documenting roles for genetic, epigenetic, and experiential factors in the development of emotion regulation, social cognition, and behavior with important implications for understanding mechanisms that underlie life history construction and the sources of differential health. Overall, this dynamic arena for research promises to link the biological bases of life history theory with the psychobehavioral phenomena that figure so centrally in quotidian experience and adaptation, particularly, for humans. Am. J. Hum. Biol. 2009. © 2009 Wiley-Liss, Inc. [source]

    Sensorimotor integration in movement disorders

    MOVEMENT DISORDERS, Issue 3 2003
    Giovanni Abbruzzese MD
    Abstract Although current knowledge attributes movement disorders to a dysfunction of the basal ganglia,motor cortex circuits, abnormalities in the peripheral afferent inputs or in their central processing may interfere with motor program execution. We review the abnormalities of sensorimotor integration described in the various types of movement disorders. Several observations, including those of parkinsonian patients' excessive reliance on ongoing visual information during movement tasks, suggest that proprioception is defective in Parkinson's disease (PD). The disturbance of proprioceptive regulation, possibly related to the occurrence of abnormal muscle-stretch reflexes, might be important for generating hypometric or bradykinetic movements. Studies with somatosensory evoked potentials (SEPs), prepulse inhibition, and event-related potentials support the hypothesis of central abnormalities of sensorimotor integration in PD. In Huntington's disease (HD), changes in SEPs and long-latency stretch reflexes suggest that a defective gating of peripheral afferent input to the brain might impair sensorimotor integration in cortical motor areas, thus interfering with the processing of motor programs. Defective motor programming might contribute to some features of motor impairment in HD. Sensory symptoms are frequent in focal dystonia and sensory manipulation can modify the dystonic movements. In addition, specific sensory functions (kinaesthesia, spatial,temporal discrimination) can be impaired in patients with focal hand dystonia, thus leading to a "sensory overflow." Sensory input may be abnormal and trigger focal dystonia, or defective "gating" may cause an input,output mismatch in specific motor programs. Altogether, several observations strongly support the idea that sensorimotor integration is impaired in focal dystonia. Although elemental sensation is normal in patients with tics, tics can be associated with sensory phenomena. Some neurophysiological studies suggest that an altered "gating" mechanism also underlies the development of tics. This review underlines the importance of abnormal sensorimotor integration in the pathophysiology of movement disorders. Although the physiological mechanism remains unclear, the defect is of special clinical relevance in determining the development of focal dystonia. [source]

    Role of spinal cord glia in the central processing of peripheral pain perception

    NEUROGASTROENTEROLOGY & MOTILITY, Issue 5 2010
    S. Bradesi
    Abstract Background, The discovery that glial activation plays a critical role in the modulation of neuronal functions and affects the spinal processing of nociceptive signalling has brought new understanding on the mechanisms underlying central sensitization involved in chronic pain facilitation. Spinal glial activation is now considered an important component in the development and maintenance of allodynia and hyperalgesia in various models of chronic pain, including neuropathic pain and pain associated with peripheral inflammation. In addition, spinal glial activation is also involved in some forms of visceral hyperalgesia. Purpose, We discuss the signalling pathways engaged in central glial activation, including stress pathways, and the neuron,glia bidirectional relationships involved in the modulation of synaptic activity and pain facilitation. In this expanding field of research, the characterization of the mechanisms by which glia affect spinal neuro-transmission will increase our understanding of central pain facilitation, and has the potential for the development of new therapeutic agents for common chronic pain conditions. [source]

    Neuronal correlates of gastric pain induced by fundus distension: a 3T-fMRI study

    NEUROGASTROENTEROLOGY & MOTILITY, Issue 5 2004
    C.-L. Lu
    Abstract Visceral hypersensitivity in gastric fundus is a possible pathogenesis for functional dyspepsia. The cortical representation of gastric fundus is still unclear. Growing evidence shows that the insula, but not the primary or secondary somatosensory region (SI or SII), may be the cortical target for visceral pain. Animal studies have also demonstrated that amygdala plays an important role in processing visceral pain. We used fMRI to study central projection of stomach pain from fundus balloon distension. We also tested the hypothesis that there will be neither S1 nor S2 activation, but amygdala activation with the fundus distension. A 3T-fMRI was performed on 10 healthy subjects during baseline, fullness (12.7 ± 0.6 mmHg) and moderate gastric pain (17.0 ± 0.8 mmHg). fMRI signal was modelled by convolving the predetermined psychophysical response. Statistical comparisons were performed between conditions on a group level. Gastric pain activated a wide range of cortical and subcortical structures, including thalamus and insula, anterior and posterior cingulate cortices, basal ganglia, caudate nuclei, amygdala, brain stem, cerebellum and prefrontal cortex (P < 0.001). A subset of these neuronal substrates was engaged in the central processing of fullness sensation. SI and SII were not activated during the fundus stimulation. In conclusion, the constellation of neuronal structures activated by fundus distension overlaps the pain matrices induced musculocutaneous pain, with the exception of the absence of SI or SII activation. This may account for the vague nature of visceral sensation/pain. Our data also confirms that the insula and amygdala may act as the central role in visceral sensation/pain, as well as in the proposed sensory-limbic model of learning and memory of pain. [source]