Imaging CNS Modulation of Pain in Humans

ArticleinPhysiology 23(6):371-80 · January 2009with16 Reads
DOI: 10.1152/physiol.00024.2008 · Source: PubMed
Pain is a highly complex and subjective experience that is not linearly related to the nociceptive input. What is clear from anecdotal reports over the centuries and more recently from animal and human experimentation is that nociceptive information processing and consequent pain perception is subject to significant pro- and anti-nociceptive modulations. These modulations can be initiated reflexively or by contextual manipulations of the pain experience including cognitive and emotional factors. This provides a necessary survival function since it allows the pain experience to be altered according to the situation rather than having pain always dominate. The so-called descending pain modulatory network involving predominantly medial and frontal cortical areas, in combination with specific subcortical and brain stem nuclei appears to be one key system for the endogenous modulation of pain. Furthermore, recent findings from functional and anatomical neuroimaging support the notion that an altered interaction of pro- and anti-nociceptive mechanisms may contribute to the development or maintenance of chronic pain states. Research on the involved circuitry and implemented mechanisms is a major focus of contemporary neuroscientific research in the field of pain and should provide new insights to prevent and treat chronic pain states.
    • "In adults, top-down connections play a key role in modulating pain perception [1]. This involves an extensive network of brain regions that include the anterior cingulate cortex, insular cortices, and brainstem [1]. In full-term infants, these brain regions are actively involved in processing nociceptive input [4] and may contribute toward the generation of the electrophysiological nociceptive activity characterized here [15]. "
    [Show abstract] [Hide abstract] ABSTRACT: In adults, nociceptive reflexes and behavioral responses are modulated by a network of brain regions via descending projections to the spinal dorsal horn [1]. Coordinated responses to noxious inputs manifest from a balance of descending facilitation and inhibition. In contrast, young infants display exaggerated and uncoordinated limb reflexes [2]. Our understanding of nociceptive processing in the infant brain has been advanced by the use of electrophysiological and hemodynamic imaging [3–6]. From approximately 35 weeks’ gestation, nociceptive-specific patterns of brain activity emerge [7], whereas prior to this, non-specific bursts of activity occur in response to noxious, tactile, visual, and auditory stimulation [7–10]. During the preterm period, refinement of spinal cord excitability is also observed: reflex duration shortens, response threshold increases, and improved discrimination between tactile and noxious events occurs [2, 11, 12]. However, the development of descending modulation in human infants remains relatively unexplored. In 40 infants aged 28–42 weeks’ gestation, we examined the relationship between nociceptive brain activity and spinal reflex withdrawal activity in response to a clinically essential noxious procedure. Nociceptive-specific brain activity increases in magnitude with gestational age, whereas reflex withdrawal activity decreases in magnitude, duration, and latency across the same developmental period. By recording brain and spinal cord activity in the same infants, we demonstrate that the maturation of nociceptive brain activity is concomitant with the refinement of noxious-evoked limb reflexes. We postulate that, consistent with studies in animals, infant reflexes are influenced by the development of top-down inhibitory modulation from maturing subcortical and cortical brain networks.
    Full-text · Article · Jun 2016
    • "The non-primary auditory cortex is loosely located surrounding AC1 in the planum temporal and planum polare. Its function is less known, and it is thought to process broadband sounds (bandwidth), sound motion and location, and integration of other elements of the sounds (Bingel & Tracey, 2008; Hall, Hart, & Johnsrude, 2003; Jensen & Sindrup, 2002). The auditory and frontal cortices are able to extract regularities and form hierarchical structures from the music (Fields, 2000; Koelsch, 2006; Koelsch et al., 2001; Näätänen, 1995; Tracey & Dickenson, 2012; Wiech, Ploner, & Tracey, 2008b). "
    [Show abstract] [Hide abstract] ABSTRACT: Book Description: Music has been used as a mood altering intervention for thousands of years. There are numerous examples of the healing powers of music in the historical records of different cultures. In the last few decades, investigators have developed a more scientific approach to exploring the mechanisms by which music exerts its effects on the brain and other organs. Music interventions are now being used in medicine and nursing throughout the world, and “music therapy” has become an accepted discipline alongside other paramedical professions. This book is a timely and comprehensive review of the use of music as a complementary therapy, and for management of some “otherwise difficult to treat” conditions. The authors, each experts in their chosen field of medicine, have come together to compile an excellent, clear and precise update regarding the use of music therapy in different illnesses and neuropsychiatric conditions. This book contains information useful to psychologists, psychiatrists and physicians involved in primary care in other branches of medicine, as well as health science students and other health professionals interested in music as a complementary and alternative therapy (CAM). This book adds music as a potent, enlightening, and life-enriching addition to our armamentarium for the management of complex medical conditions. The content of some chapters may foster more ideas for future research. Throughout the book, there is an emphasis on the greater need for large, blinded, controlled studies to better support music therapy.
    Chapter · May 2016 · Human Brain Mapping
    • "For example, in placebo analgesia studies, increased dlPFC activity was associated with analgesia and correlated with activity in the PAG [Wager et al., 2004], and the analgesic effects of perceived pain control is correlated with dlPFC activity [Wiech et al., 2006] . It has been postulated that the prefrontal cortex " represents the pivotal source of modulation that, at least within one conceivable pathway, initiates downstream analgesic activity and/or emotional modulation " [Bingel and Tracey, 2008]. Our data furthers this idea and we add that activity within the dlPFC may indeed prevent the expression of an analgesic response such as that mediated by the brainstem circuitry responsible for CPM. "
    [Show abstract] [Hide abstract] ABSTRACT: Conditioned pain modulation (CPM) is a powerful endogenous analgesic mechanism which can completely inhibit incoming nociceptor signals at the primary synapse. The circuitry responsible for CPM lies within the brainstem and involves the subnucleus reticularis dorsalis (SRD). While the brainstem is critical for CPM, the cortex can significantly modulate its expression, likely via the brainstem circuitry critical for CPM. Since higher cortical regions such as the anterior, mid-cingulate, and dorsolateral prefrontal cortices are activated by noxious stimuli and show reduced activations during other analgesic responses, we hypothesized that these regions would display reduced responses during CPM analgesia. Furthermore, we hypothesized that functional connectivity strength between these cortical regions and the SRD would be stronger in those that express CPM analgesia compared with those that do not. We used functional magnetic resonance imaging to determine sites recruited during CPM expression and their influence on the SRD. A lack of CPM analgesia was associated with greater signal intensity increases during each test stimulus in the presence of the conditioning stimulus compared to test stimuli alone in the mid-cingulate and dorsolateral prefrontal cortices and increased functional connectivity with the SRD. In contrast, those subjects exhibiting CPM analgesia showed no change in the magnitude of signal intensity increases in these cortical regions or strength of functional connectivity with the SRD. These data suggest that during multiple or widespread painful stimuli, engagement of the prefrontal and cingulate cortices prevents the generation of CPM analgesia, raising the possibility altered responsiveness in these cortical regions underlie the reduced CPM observed in individuals with chronic pain. Hum Brain Mapp, 2016. © 2016 Wiley Periodicals, Inc.
    Article · Apr 2016
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