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.

Mirth and laughter elicited by electrical stimulation of the human anterior cingulate cortex

Cortex ◽  
2015 ◽  
Vol 71 ◽  
pp. 323-331 ◽  
Author(s):  
Fausto Caruana ◽  
Pietro Avanzini ◽  
Francesca Gozzo ◽  
Stefano Francione ◽  
Francesco Cardinale ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Anterior Cingulate Cortex ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Stimulation Of

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.

Tractography Study of Deep Brain Stimulation of the Anterior Cingulate Cortex in Chronic Pain: Key to Improve the Targeting

2016 ◽  
Vol 86 ◽  
pp. 361-370.e3 ◽  
Author(s):  
Sandra G.J. Boccard ◽  
Henrique M. Fernandes ◽  
Saad Jbabdi ◽  
Tim J. Van Hartevelt ◽  
Morten L. Kringelbach ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Deep Brain Stimulation ◽  
Anterior Cingulate Cortex ◽  
Brain Stimulation ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Deep Brain ◽  
Stimulation Of

scholarly journals Transcranial Ultrasound Stimulation of the Anterior Cingulate Cortex Reduces Neuropathic Pain in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Xiangjun Feng ◽  
Lili Niu ◽  
Meng Long ◽  
Kaixuan Luo ◽  
Xiaowei Huang ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Neuropathic Pain ◽  
Anterior Cingulate Cortex ◽  
Intervention Group ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Control Group ◽  
Mechanical Threshold ◽  
Stimulation Of

Focused ultrasound (FUS) is a potential tool for treating chronic pain by modulating the central nervous system. Herein, we aimed to determine whether transcranial FUS stimulation of the anterior cingulate cortex (ACC) effectively improved chronic pain in the chronic compress injury mice model at different stages of neuropathic pain. The mechanical threshold of pain was recorded in the nociceptive tests. We found FUS stimulation elevated the mechanical threshold of pain in both short-term ( p < 0.01 ) and long-term ( p < 0.05 ) experiments. Furthermore, we determined protein expression differences in ACC between the control group, the intervention group, and the Sham group to analyze the underlying mechanism of FUS stimulation in improving neuropathic pain. Additionally, the results showed FUS stimulation led to alterations in differential proteins in long-term experiments, including cellular processes, cellular signaling, and information storage and processing. Our findings indicate FUS may effectively alleviate mechanical neuropathic pain via the ACC’s stimulation, especially in the chronic state.

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.

scholarly journals Pra-C exerts analgesic effect through inhibiting microglial activation in anterior cingulate cortex in complete Freund’s adjuvant-induced mouse model

2021 ◽  
Vol 17 ◽  
pp. 174480692199093
Author(s):  
Dan-jie Su ◽  
Long-fei Li ◽  
Sai-ying Wang ◽  
Qi Yang ◽  
Yu-jing Wu ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Mouse Model ◽  
Anterior Cingulate Cortex ◽  
Analgesic Effect ◽  
Microglial Activation ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Freund’S Adjuvant ◽  
Complete Freund's Adjuvant ◽  
Freund's Adjuvant

Chronic pain is highly prevalent worldwide and severely affects daily lives of patients and family members. Praeruptorin C (Pra-C) is a main active ingredient derived from Peucedanum praeruptorum Dunn, traditionally used as antibechic, anti-bronchitis and anti-hypertension drug. Here, we evaluated the effects of Pra-C in a chronic inflammatory pain mouse model induced by complete Freund’s adjuvant (CFA) injection. Pra-C (3 mg/kg) treatment for just 3 days after CFA challenge relieved CFA-induced mechanical allodynia and hindpaw edema in mice. In the anterior cingulate cortex (ACC), Pra-C treatment inhibited microglia activation and reduced levels of proinflammatory cytokines, TNF-α and IL-1β, and suppressed upregulation of glutamate receptors caused by CFA injection. In addition, Pra-C attenuated neuronal hyperexcitability in ACC of CFA-injected mice. In vitro studies confirmed the analgesic effect of Pra-C was due to its inhibitory ability on microglial activation. In conclusion, Pra-C administration had a certain effect on relieving chronic pain by inhibiting microglial activation, attenuating proinflammatory cytokine releasing and regulating excitatory synaptic proteins in the ACC of the CFA-injected mice.

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