Neural Mechanisms of Antinociceptive Effects of Hypnosis

2000 ◽  
Vol 92 (5) ◽  
pp. 1257-1267 ◽  
Author(s):  
Marie Elisabeth Faymonville ◽  
Steven Laureys ◽  
Christian Degueldre ◽  
Guy DelFiore ◽  
André Luxen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Pain Perception ◽  
Cingulate Cortex ◽  
Neural Mechanisms ◽  
Anterior Cingulate ◽  
Noxious Stimulation ◽  
Pain Sensation ◽  
Brain Areas ◽  
Noxious Stimuli

Background The neural mechanisms underlying the modulation of pain perception by hypnosis remain obscure. In this study, we used positron emission tomography in 11 healthy volunteers to identify the brain areas in which hypnosis modulates cerebral responses to a noxious stimulus. Methods The protocol used a factorial design with two factors: state (hypnotic state, resting state, mental imagery) and stimulation (warm non-noxious vs. hot noxious stimuli applied to right thenar eminence). Two cerebral blood flow scans were obtained with the 15O-water technique during each condition. After each scan, the subject was asked to rate pain sensation and unpleasantness. Statistical parametric mapping was used to determine the main effects of noxious stimulation and hypnotic state as well as state-by-stimulation interactions (i.e., brain areas that would be more or less activated in hypnosis than in control conditions, under noxious stimulation). Results Hypnosis decreased both pain sensation and the unpleasantness of noxious stimuli. Noxious stimulation caused an increase in regional cerebral blood flow in the thalamic nuclei and anterior cingulate and insular cortices. The hypnotic state induced a significant activation of a right-sided extrastriate area and the anterior cingulate cortex. The interaction analysis showed that the activity in the anterior (mid-)cingulate cortex was related to pain perception and unpleasantness differently in the hypnotic state than in control situations. Conclusions Both intensity and unpleasantness of the noxious stimuli are reduced during the hypnotic state. In addition, hypnotic modulation of pain is mediated by the anterior cingulate cortex.

Reduced cerebral blood flow in anterior cingulate cortex (ACC) during stroop performance in chronic cocaine users

NeuroImage ◽  
2001 ◽  
Vol 13 (6) ◽  
pp. 772 ◽  
Author(s):  
Karen Bolla ◽  
Monique Ernst ◽  
Maria Mouratidis ◽  
John Matochik ◽  
Carlo Contoreggi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Anterior Cingulate Cortex ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Chronic Cocaine ◽  
Cocaine Users

Decreased cerebral blood flow of the right anterior cingulate cortex in long-term and short-term abstinent methamphetamine users☆

2006 ◽  
Vol 82 (2) ◽  
pp. 177-181 ◽  
Author(s):  
Jaeuk Hwang ◽  
In Kyoon Lyoo ◽  
Seog Ju Kim ◽  
Young Hoon Sung ◽  
Soojeong Bae ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Anterior Cingulate Cortex ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Short Term ◽  
The Right

scholarly journals Hypoglycemic thalamic activation in type 1 diabetes is associated with preserved symptoms despite reduced epinephrine

2019 ◽  
Vol 40 (4) ◽  
pp. 787-798 ◽  
Author(s):  
Munachiso Nwokolo ◽  
Stephanie A Amiel ◽  
Owen O'Daly ◽  
Megan L Byrne ◽  
Bula M Wilson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Type 1 Diabetes ◽  
Cerebral Blood Flow ◽  
Anterior Cingulate Cortex ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Regional Cerebral Blood ◽  
Cerebral Blood Flow Change ◽  
Global Cerebral Blood Flow

Brain responses to low plasma glucose may be key to understanding the behaviors that prevent severe hypoglycemia in type 1 diabetes. This study investigated the impact of long duration, hypoglycemia aware type 1 diabetes on cerebral blood flow responses to hypoglycemia. Three-dimensional pseudo-continuous arterial spin labeling magnetic resonance imaging was performed in 15 individuals with type 1 diabetes and 15 non-diabetic controls during a two-step hyperinsulinemic glucose clamp. Symptom, hormone, global cerebral blood flow and regional cerebral blood flow responses to hypoglycemia were measured. Epinephrine release during hypoglycemia was attenuated in type 1 diabetes, but symptom score rose comparably in both groups. A rise in global cerebral blood flow did not differ between groups. Regional cerebral blood flow increased in the thalamus and fell in the hippocampus and temporal cortex in both groups. Type 1 diabetes demonstrated lesser anterior cingulate cortex activation; however, this difference did not survive correction for multiple comparisons. Thalamic cerebral blood flow change correlated with autonomic symptoms, and anterior cingulate cortex cerebral blood flow change correlated with epinephrine response across groups. The thalamus may thus be involved in symptom responses to hypoglycemia, independent of epinephrine action, while anterior cingulate cortex activation may be linked to counterregulation. Activation of these regions may have a role in hypoglycemia awareness and avoidance of problematic hypoglycemia.

Altered cerebral blood flow in the anterior cingulate cortex is associated with neuropathic pain

2018 ◽  
Vol 89 (10) ◽  
pp. 1082-1087 ◽  
Author(s):  
Keisuke Watanabe ◽  
Shigeki Hirano ◽  
Kazuho Kojima ◽  
Kengo Nagashima ◽  
Hiroki Mukai ◽  
...  
Keyword(s):  
Blood Flow ◽  
Neuropathic Pain ◽  
Cerebral Blood Flow ◽  
Pain Relief ◽  
Anterior Cingulate Cortex ◽  
Rating Scale ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Pharmacological Intervention ◽  
Emission Computed Tomography

ObjectiveTo assess the cerebral blood flow (CBF) in patients with diabetic neuropathic pain, and its changes after duloxetine therapy.MethodsUsing iodine-123-N-isopropyl-p-iodoamphetamine single-photon emission computed tomography (IMP-SPECT), we performed a cross-sectional study of 44 patients with diabetes, and compared CBF in those with (n = 24) and without neuropathic pain (n = 20). In patients with neuropathic pain, we also longitudinally assessed changes in CBF 3 months after treatment with duloxetine.ResultsIMP-SPECT with voxel-based analyses showed a significant increase in cerebral blood flow in the right anterior cingulate cortex and a decrease in the left ventral striatum in patients with neuropathic pain, compared with those without pain. After duloxetine treatment, volume of interest analyses revealed a decrease in cerebral blood flow in the anterior cingulate cortex in patients with significant pain relief but not in non-responders. Furthermore, voxel-based whole brain correlation analyses demonstrated that greater baseline CBF in the anterior cingulate cortex was associated with better pain relief on the numerical rating scale.ConclusionsOur results suggest that the development of neuropathic pain is associated with increased activity in the anterior cingulate cortex, and greater baseline activation of this region may predict treatment responsiveness to pharmacological intervention.Trial registration numberUMIN000017130;Results.

Dose-dependent Effects of Propofol on the Central Processing of Thermal Pain

2004 ◽  
Vol 100 (2) ◽  
pp. 386-394 ◽  
Author(s):  
Robert K. Hofbauer ◽  
Pierre Fiset ◽  
Gilles Plourde ◽  
Steven B. Backman ◽  
M. Catherine Bushnell
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Anterior Cingulate Cortex ◽  
Regional Cerebral Blood Flow ◽  
Insular Cortex ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Regional Cerebral Blood ◽  
Central Processing ◽  
Dose Dependent

Background Anatomic and physiologic data show that multiple regions of the forebrain are activated by pain. However, the effect of anesthetic level on nociceptive input to these regions is not well understood. Methods The authors used positron emission tomography to measure the effect of various concentrations of propofol on pain-evoked changes in regional cerebral blood flow. Fifteen volunteers were scanned while warm and painful heat stimuli were presented to the volar forearm using a contact thermode during administration of target propofol concentrations of 0.0 microg/ml (alert control), 0.5 microg/ml (mild sedation), 1.5 microg/ml (moderate sedation), and 3.5 microg/ml (unconsciousness). Results During the 0.5-microg/ml target propofol concentration (mild sedation), the subjects' pain ratings increased relative to the alert control condition; correspondingly, pain-evoked regional cerebral blood flow increased in the thalamus and the anterior cingulate cortex. In contrast, when subjects lost consciousness (3.5 microg/ml), pain-evoked responses in the thalamus and the anterior cingulate cortex were no longer observed, whereas significant pain-evoked activation remained in the insular cortex. Conclusion These data show that propofol has a dose-dependent effect on thalamocortical transfer of nociceptive information but that some pain-evoked cortical activity remains after loss of consciousness.

scholarly journals Cerebral blood flow alterations specific to auditory verbal hallucinations in schizophrenia

2017 ◽  
Vol 210 (3) ◽  
pp. 209-215 ◽  
Author(s):  
Chuanjun Zhuo ◽  
Jiajia Zhu ◽  
Wen Qin ◽  
Hongru Qu ◽  
Xiaolei Ma ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Superior Temporal Gyrus ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Resonance Imaging ◽  
Auditory Verbal Hallucinations ◽  
The Right ◽  
Parietal Cortices ◽  
Left Middle

BackgroundAuditory verbal hallucinations (AVHs) have been associated with deficits in auditory and speech-related networks. However, the resting-state cerebral blood flow (CBF) alterations specific to AVHs in schizophrenia remain unknown.AimsTo explore AVH-related CBF alterations in individuals with schizophrenia.MethodIn total, 35 individuals with schizophrenia with AVHs, 41 individuals with schizophrenia without AVHs and 50 controls underwent arterial spin labelling magnetic resonance imaging. The CBF differences were voxel-wise compared across the three groups.ResultsWe found AVH-specific CBF increase in the right superior temporal gyrus and caudate, and AVH-specific CBF decrease in the bilateral occipital and left parietal cortices. We also observed consistent CBF changes in both schizophrenia subgroups (i.e. those with and without AVHs) including decreased CBF in the bilateral occipital regions, the left lateral prefrontal and insular cortices, and the right anterior cingulate cortex and increased CBF in the bilateral lateral temporal regions and putamen, the left middle cingulate cortex and the right thalamus.ConclusionsThe AVH-specific CBF increases in the auditory and striatal areas and CBF reductions in the visual and parietal areas suggest that there exists a CBF redistribution associated with AVHs.

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