scholarly journals Chronic pain as a brain imbalance between pain input and pain suppression

2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Sven Vanneste ◽  
Dirk De Ridder
Keyword(s):  
Chronic Pain ◽  
Anterior Cingulate Cortex ◽  
Somatosensory Cortex ◽  
Subjective Experience ◽  
Effective Connectivity ◽  
Cingulate Cortex ◽  
Brain Network ◽  
Anterior Cingulate ◽  
Dorsal Anterior Cingulate Cortex ◽  
Density Ratios

Abstract Chronic pain is pain that persists beyond the expected period of healing. The subjective experience of chronic pain results from pathological brain network interactions, rather than from persisting physiological sensory input of nociceptors. We hypothesize that pain is an imbalance between pain evoking dorsal anterior cingulate cortex and somatosensory cortex and pain suppression (i.e. pregenual anterior cingulate cortex). This imbalance can be measured objectively by current density ratios between pain input and pain inhibition. A balance between areas involved in pain input and pain suppression requires communication, which can be objectively identified by connectivity measures, both functional and effective connectivity. In patients with chronic neuropathic pain, electroencephalography is performed with source localization demonstrating that pain is reflected by an abnormal ratio between the dorsal anterior cingulate cortex, somatosensory cortex and pregenual anterior cingulate cortex. Functional connectivity demonstrates decreased communication between these areas, and effective connectivity puts the culprit at the dorsal anterior cingulate cortex, suggesting that the problem is related to abnormal behavioral relevance attached to the pain. In conclusion, chronic pain can be considered as an imbalance between pain input and pain suppression.

scholarly journals Musical Hallucinations in Chronic Pain: The Anterior Cingulate Cortex Regulates Internally Generated Percepts

2021 ◽  
Vol 12 ◽  
Author(s):  
Ashlyn Schmitgen ◽  
Jeremy Saal ◽  
Narayan Sankaran ◽  
Maansi Desai ◽  
Isabella Joseph ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Electrical Stimulation ◽  
Anterior Cingulate Cortex ◽  
Case Series ◽  
Cingulate Cortex ◽  
Brain Network ◽  
Anterior Cingulate ◽  
Functional Brain Network ◽  
Band Activity ◽  
Stimulation Of

The anterior cingulate cortex (ACC) has been extensively implicated in the functional brain network underlying chronic pain. Electrical stimulation of the ACC has been proposed as a therapy for refractory chronic pain, although, mechanisms of therapeutic action are still unclear. As stimulation of the ACC has been reported to produce many different behavioral and perceptual responses, this region likely plays a varied role in sensory and emotional integration as well as modulating internally generated perceptual states. In this case series, we report the emergence of subjective musical hallucinations (MH) after electrical stimulation of the ACC in two patients with refractory chronic pain. In an N-of-1 analysis from one patient, we identified neural activity (local field potentials) that distinguish MH from both the non-MH condition and during a task involving music listening. Music hallucinations were associated with reduced alpha band activity and increased gamma band activity in the ACC. Listening to similar music was associated with different changes in ACC alpha and gamma power, extending prior results that internally generated perceptual phenomena are supported by circuits in the ACC. We discuss these findings in the context of phantom perceptual phenomena and posit a framework whereby chronic pain may be interpreted as a persistent internally generated percept.

132 The Underlying Effect of Burst Stimulation on Chronic Pain Using Multimodal Neuroimaging - EEG, fMRI and PET

Neurosurgery ◽  
2017 ◽  
Vol 64 (CN_suppl_1) ◽  
pp. 230-230 ◽  
Author(s):  
Shaheen Ahmed ◽  
Sven Vanneste
Keyword(s):  
Anterior Cingulate Cortex ◽  
Somatosensory Cortex ◽  
Premotor Cortex ◽  
Cingulate Cortex ◽  
Posterior Cingulate Cortex ◽  
Anterior Cingulate ◽  
Leg Pain ◽  
Burst Stimulation ◽  
Dorsal Anterior Cingulate Cortex ◽  
Tonic Stimulation

Abstract INTRODUCTION Minimally invasive neuromodulation such as spinal cord stimulation (SCS) and occipital nerve stimulation (ONS) have shown to be successful for treatment of different types of pain such as chronic back or leg pain, complex regional pain syndrome (CRPS), and fibromyalgia. Recently, novel stimulation paradigm called burst stimulation was developed that suppresses pain to better extent than classical tonic stimulation. From clinical point of view, burst stimulation is very promising; however, little is known about its underlying mechanism. Hence, in this work we investigate mechanism of action for burst stimulation in different patient groups and controls using different neuroimaging multimodalities such as EEG, fMRI and PET. METHODS Control subjects and patients with chronic back or leg pain, CRPS, or fibromyalgia enrolled for study. Both controls and patients received SCS or ONS and sham, tonic, and burst stimulation in fMRI, PET, and EEG. RESULTS >EEG shows significant changes for burst stimulation compared to tonic and sham stimulation; evident by increased activity at dorsal anterior cingulate cortex (dACC), dorsolateral prefrontal cortex (dPFC), primary somatosensory cortex, and posterior cingulate cortex (PSC) in alpha frequency band. PET further confirmed by showing increased tracer capitation for burst in dACC, pregenual anterior cingulate cortex (pgACC), parahippocampus, and fusiform gyrus. Furthermore, fMRI showed burst changes in dACC, dPFC, pgACC, cerebellum, hypothalamus, and premotor cortex. A conjunction analysis between tonic and burst stimulation demonstrated theta activity is commonly modulated in somatosensory cortex and PSC. CONCLUSION Our data suggest that burst and tonic stimulation modulate ascending lateral and descending pain inhibitory pathways. Burst stimulation adds by modulating the medial pain pathway, possibly by direct modulation of spinothalamic pathway, as suggested by animal research. Burst normalizes an imbalance between ascending pain via medial system and descending pain inhibitory activity, which could be a plausible reason it's better than to tonic stimulation.

scholarly journals Anterior Cingulate Cortex Signals the Need to Control Intrusive Thoughts During Motivated Forgetting

2021 ◽  
Author(s):  
Maité Crespo García ◽  
Yulin Wang ◽  
Mojun Jiang ◽  
Michael Anderson ◽  
Xu Lei
Keyword(s):  
Anterior Cingulate Cortex ◽  
Inhibitory Control ◽  
Effective Connectivity ◽  
Cingulate Cortex ◽  
Blood Oxygen Level Dependent ◽  
Anterior Cingulate ◽  
Reactive Control ◽  
Dorsal Anterior Cingulate Cortex ◽  
Dynamic Interactions ◽  
Hippocampal Activity

How do people limit awareness of unwanted memories? Evidence suggests that when unwelcome memories intrude, a retrieval stopping process engages the right dorsolateral prefrontal cortex (rDLPFC; Michael C. Anderson et al., 2004) to inhibit hippocampal activity (Benoit & Anderson, 2012; Benoit, Hulbert, Huddleston, & Anderson, 2015; Gagnepain, Hulbert, & Anderson, 2017) and disrupt retrieval. It remains unknown how and when the need to engage prefrontal control is detected, and whether control operates proactively to prevent an unwelcome memory from being retrieved, or must respond reactively, to counteract its intrusion. We hypothesized that dorsal anterior cingulate cortex (dACC) achieves this function by detecting signals indicating that an unwanted trace is emerging in awareness, and transmitting the need for inhibitory control to right DLPFC (Alexander & Brown, 2011; Botvinick, Braver, Barch, Carter, & Cohen, 2001). During a memory suppression task, we measured trial-by-trial variations in dACC's theta power and N2 amplitude, two electroencephalographic (EEG) markers of the need for enhanced control (Cavanagh & Frank, 2014). With simultaneous EEG-fMRI recordings, we tracked dynamic interactions between the dACC, rDLPFC and hippocampus during suppression. EEG analyses revealed a clear role of dACC in detecting the need for memory control, and in upregulating prefrontal inhibition. Importantly, we identified dACC contributions before episodic retrieval could have occurred (500 ms) and afterwards, indicating distinct proactive and reactive control signalling. Stronger proactive control by the dACC led to reduced hippocampal activity and diminished overall blood-oxygen-level-dependent (BOLD) signal in dACC and rDLPFC, suggesting that pre-empting retrieval early reduced overall control demands. However, when dACC activity followed the likely onset of recollection, retrieval was cancelled reactively: effective connectivity analyses revealed robust communication from dACC to rDLPFC and from rDLPFC to hippocampus, tied to successful forgetting. Together, our findings support a model in which dACC detects the emergence of unwanted content, triggering top-down inhibitory control, and in which rDLPFC countermands intruding thoughts that penetrate awareness.

scholarly journals Suppressing Anterior Cingulate Cortex Modulates Default Mode Network and Behavior in Awake Rats

2020 ◽  
Vol 31 (1) ◽  
pp. 312-323 ◽  
Author(s):  
Wenyu Tu ◽  
Zilu Ma ◽  
Yuncong Ma ◽  
David Dopfel ◽  
Nanyin Zhang
Keyword(s):  
Anterior Cingulate Cortex ◽  
Default Mode Network ◽  
Cingulate Cortex ◽  
Brain Network ◽  
Anterior Cingulate ◽  
Mammalian Brain ◽  
Dorsal Anterior Cingulate Cortex ◽  
Default Mode ◽  
Network Function ◽  
And Behavior

Abstract The default mode network (DMN) is a principal brain network in the mammalian brain. Although the DMN in humans has been extensively studied with respect to network structure, function, and clinical implications, our knowledge of DMN in animals remains limited. In particular, the functional role of DMN nodes, and how DMN organization relates to DMN-relevant behavior are still elusive. Here we investigated the causal relationship of inactivating a pivotal node of DMN (i.e., dorsal anterior cingulate cortex [dACC]) on DMN function, network organization, and behavior by combining chemogenetics, resting-state functional magnetic resonance imaging (rsfMRI) and behavioral tests in awake rodents. We found that suppressing dACC activity profoundly changed the activity and connectivity of DMN, and these changes were associated with altered DMN-related behavior in animals. The chemo-rsfMRI-behavior approach opens an avenue to mechanistically dissecting the relationships between a specific node, brain network function, and behavior. Our data suggest that, like in humans, DMN in rodents is a functional network with coordinated activity that mediates behavior.

scholarly journals Chronic Pain is Associated With Reduced Sympathetic Nervous System Reactivity During Simple and Complex Walking Tasks: Potential Cerebral Mechanisms

2021 ◽  
Vol 5 ◽  
pp. 247054702110302
Author(s):  
Taylor D. Yeater ◽  
David J. Clark ◽  
Lorraine Hoyos ◽  
Pedro A. Valdes-Hernandez ◽  
Julio A. Peraza ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Anterior Cingulate Cortex ◽  
Gray Matter ◽  
Dual Task ◽  
Brain Region ◽  
Skin Conductance Level ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Autonomic Responses ◽  
The Difference

Background Autonomic dysregulation may lead to blunted sympathetic reactivity in chronic pain states. Autonomic responses are controlled by the central autonomic network (CAN). Little research has examined sympathetic reactivity and associations with brain CAN structures in the presence of chronic pain; thus, the present study aims to investigate how chronic pain influences sympathetic reactivity and associations with CAN brain region volumes. Methods Sympathetic reactivity was measured as change in skin conductance level (ΔSCL) between a resting reference period and walking periods for typical and complex walking tasks (obstacle and dual-task). Participants included 31 people with (n = 19) and without (n = 12) chronic musculoskeletal pain. Structural 3 T MRI was used to determine gray matter volume associations with ΔSCL in regions of the CAN (i.e., brainstem, amygdala, insula, and anterior cingulate cortex). Results ΔSCL varied across walking tasks (main effect p = 0.036), with lower ΔSCL in chronic pain participants compared to controls across trials 2 and 3 under the obstacle walking condition. ΔSCL during typical walking was associated with multiple CAN gray matter volumes, including brainstem, bilateral insula, amygdala, and right caudal anterior cingulate cortex (p’s < 0.05). The difference in ΔSCL from typical-to-obstacle walking were associated with volumes of the midbrain segment of the brainstem and anterior segment of the circular sulcus of the insula (p’s < 0.05), with no other significant associations. The difference in ΔSCL from typical-to-dual task walking was associated with the bilateral caudal anterior cingulate cortex, and left rostral cingulate cortex (p’s < 0.05). Conclusions Sympathetic reactivity is blunted during typical and complex walking tasks in persons with chronic pain. Additionally, blunted sympathetic reactivity is associated with CAN brain structure, with direction of association dependent on brain region. These results support the idea that chronic pain may negatively impact typical autonomic responses needed for walking performance via its potential impact on the brain.

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