Morphing voxels: The hype around structural imaging of headache patients

Department of Systems Neuroscience, Universitäts-Krankenhaus Eppendorf , Martinistrasse 52, Hamburg, Germany.
Brain (Impact Factor: 9.2). 06/2009; 132(Pt 6):1419-25. DOI: 10.1093/brain/awp116
Source: PubMed


Neuroimaging analysis using structural data has begun to provide insights into the pathophysiology of headache syndromes. Several independent studies have suggested a decrease in grey matter in pain-transmitting areas in migraine patients. Most of these data are discussed as damage or loss of brain grey matter, reinforcing the idea of migraine as a progressive disease. However, given what we know about the nature of morphometric changes detectable by the methods we have to date, this interpretation is highly speculative and not supported by the data. It is likely that these changes are the consequence and not the cause of the respective headache syndromes, as they are probably not irreversible and only mirror the proportion or duration of pain suffered. Moreover, structural changes are not headache specific and have to be seen in the light of a wealth of pain studies using these methods. The studies in cluster headache patients prompted the use of stereotactic stimulation of the hypothalamic target point identified by functional and structural neuroimaging. Due to the nature of the methods used and due to a high anatomical variance it is more than questionable to use this point as a definite answer to the source of the headache in clusters and even more so when it is uncritically used in individuals. We need a way to study each patient individually using the functional imaging method with the highest spatial and temporal resolution available to enable us to target the seed point for deep brain stimulation on this individual basis. One of the major future challenges is to understand the behavioural consequences and cellular mechanisms underlying neuroanatomic changes in pain and headache.

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Available from: Arne May, Dec 29, 2013
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    • "Interestingly, a very recent, but small longitudinal study in CH showed GM increase in bout-state compared to o.b. in some regions including the cingulate and insular cortex (Yang et al., 2013). A possible explanation for GM increase in acute pain may be that the brain only reacts with local GM increase until a particular task/stimulus is learned or processed adequately and further on recedes (May, 2009). Regarding acute pain as part of the experience of learning is further supported by our finding in the hippocampus. "
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    ABSTRACT: Cluster headache (CH) is characterized by recurrent episodes of excruciatingly painful, unilateral headache attacks typically accompanied by trigeminal autonomic symptoms. Due to its rhythm with alternating episodes of pain and no-pain, it is an excellent model to investigate whether structural brain changes detected by magnetic resonance based voxel-based-morphometry (VBM) reflect the cause of the disease, may be a consequence of the underlying disease other than pain, or may simply be caused by the sensation of pain itself. We investigated 91 patients with CH in different stages of their disease using VBM and compared them to 78 age- and gender-matched healthy controls. We detected distinct regional gray matter (GM) changes in different brain regions including the temporal lobe, the hippocampus, the insular cortex and the cerebellum. The extent, location and direction of observed GM alterations depended on the state of disease and appeared dynamic in relation to pain state (i.e., pain vs. no-pain). No hypothalamic changes were detected in CH patients compared to healthy controls. The GM changes observed in this study are highly dynamic and thereby reflect the cortical plasticity of the brain in regard to pain. This observed dynamic may provide an explanation of the diverse results of previous VBM studies in pain. Regarding CH the results suggest that the disease is more likely to be caused by a network dysfunction rather than by a single malfunctioning structure.
    Full-text · Article · Dec 2014 · Clinical neuroimaging
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    • "It is known that chronic pain (May, 2008) and also depression (Li et al., 2010) may change brain gray matter. These changes usually correlate with disease duration (May, 2009) but are, in principle, reversible (Rodriguez-Raecke et al., 2009, 2013). The functional consequences – if any – of such changes are not known. "
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    ABSTRACT: Longitudinal studies of experimental pain are rare and little is known about the differences regarding sensitization and habituation over longer periods in patients with chronic pain or depression compared with controls. We used a standardized longitudinal painful heat paradigm that was designed to induce long-term habituation in 19 patients with chronic low back pain (CLBP), 21 patients with depression (DEP) and 21 healthy participants (controls) over a time course of eight consecutive days. We applied functional magnetic resonance imaging on the first and last day of this period and after 3 months. Although the pain paradigm was standardized, patients with DEP exhibited significantly higher pain thresholds and a trend to higher pain ratings and, in functional imaging, showed less activation of the operculum and the secondary somatosensory cortex (S2) as compared to patients with CLBP and controls. Conversely, patients with CLBP showed increased activation in the anterior insula and parietal operculum as compared to patients with DEP and controls. Within session, all participants sensitized to pain, which was associated with higher activation levels in the thalamus, amygdala, midcingulate cortex, and sensory and motor areas. However, patients with depression showed significantly less activation in midbrain and brainstem areas. Given that pain and depression potentiate each other clinically, our data suggest that this may involve different cortical pain areas.
    Full-text · Article · May 2014 · European journal of pain (London, England)
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    • "Neuroimaging techniques such as positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) have been especially helpful in furthering our understanding of how chronic pain affects the brain, and evidence is accumulating for structural and functional alterations from the cerebral cortex down to the level of receptors. Neuroanatomical changes have been indicated across studies of chronic pain conditions including chronic back pain (Schmidt-Wilcke et al., 2006), osteoarthritic hip pain (Rodriguez-Raecke et al., 2009), irritable bowel syndrome (Davis, 2008), and migraines (May, 2009). Negative volumetric changes have also been observed across a variety of regions involved in the processing of pain, with significant overlap in the cingulate cortex, orbitofrontal and prefrontal cortex, and insula (Apkarian et al., 2004; May, 2008) Frontal areas in particular are known to house higherlevel cognitive functions including attention, working memory, decision-making, and goal-directed behavior (Metz et al., 2009), as well as cognitive and emotional self-regulation (Solberg, Roach, & Segerstrom, 2009), and have been implicated as part of the pain network. "
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    ABSTRACT: Background: The pervasive disease of chronic pain is a common challenge for the clinical rehabilitation professional. Concurrent with physical and emotional symptoms, pain-related cognitive impairment has been reported. Although opioid analgesics are frequently prescribed, concern exists that opioids possess adverse cognitive effects of their own. Objectives: To review the neuropsychological and neuroanatomical sequelae of chronic non-malignant pain and opioid therapy, to clarify roles and benefits of neuropsychological assessment in a chronic pain population, and to provide recommendations for clinical practice and future research. Methods: This non-systematic review sought to provide a comprehensive synthesis of relevant neurobiology, neuroimaging, neuropsychological, and rehabilitation research literatures. We included citations from seminal and current texts as well as relevant original and review articles from 1980-2012 in PubMed and PubMedCentral online research databases. Discussion and summary/conclusions: To date, evidence from opioid studies suggests only mild deficits in specific cognitive domains (e.g., memory, attention/concentration) and only under specific conditions (e.g., dose escalations). Additionally, neuroimaging and neuropsychological evidence suggests that pain itself results in cognitive sequelae. Methodological improvements in future research will allow for better delineation of the contributing effects of pain and opioids, with an overall goal of improving evidence-based clinical treatment recommendations.
    Full-text · Article · Jul 2013 · Neurorehabilitation
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