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 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.

Dose-dependent Regional Cerebral Blood Flow Changes during Remifentanil Infusion in Humans

2001 ◽  
Vol 94 (5) ◽  
pp. 732-739 ◽  
Author(s):  
Klaus J. Wagner ◽  
Frode Willoch ◽  
Eberhard F. Kochs ◽  
Thomas Siessmeier ◽  
Thomas R. Tölle ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Correlation Analysis ◽  
Regional Cerebral Blood Flow ◽  
Statistical Parametric Mapping ◽  
Occipital Lobe ◽  
Anterior Cingulate ◽  
Pain Processing ◽  
Regional Cerebral Blood ◽  
Dose Dependent

Background The current study investigated dose-dependent effects of the mu-selective agonist remifentanil on regional cerebral blood flow (rCBF) in volunteers using positron emission tomography (PET). Methods Ten right-handed male volunteers were included in a 15O-water PET study. Seven underwent three conditions: control (saline), low remifentanil (0.05 microg x kg(-1) x min(-1)), and moderate remifentanil (0.15 microg x kg(-1) x min(-1)). The remaining three participated in the low and moderate conditions. A semirandomized study protocol was used with control and remifentanil conditions 3 or more months apart. The order of low and moderate conditions was randomized. Cardiovascular and respiratory parameters were monitored. Categoric comparisons between the control, low, and moderate conditions and a pixelwise correlation analysis across the three conditions were performed (P < 0.05, corrected for multiple comparisons) using statistical parametric mapping. Results Cardiorespiratory parameters were maintained constant over time. At the low remifentanil dose, significant increases in relative rCBF were noted in the lateral prefrontal cortices, inferior parietal cortices, and supplementary motor area. Relative rCBF decreases were observed in the basal mediofrontal cortex, cerebellum, superior temporal lobe, and midbrain gray matter. Moderate doses further increased rCBF in mediofrontal and anterior cingulate cortices, occipital lobe transition, and caudal periventricular grey. Significant decreases were detected in the inferior parietal lobes. These dose-dependent effects of remifentanil on rCBF were confirmed by a correlation analysis. Conclusion Remifentanil induced dose-dependent changes in relative rCBF in areas involved in pain processing. At moderate doses, rCBF responses were additionally detected in structures known to participate in modulation of vigilance and alertness. Insight into the mechanisms of opioid analgesia within the pain-processing neural network may lead to a better understanding of antinociception and opioid treatment.

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

Imaging Human Cerebral Pain Modulation by Dose-dependent Opioid Analgesia

2007 ◽  
Vol 106 (3) ◽  
pp. 548-556 ◽  
Author(s):  
Klaus J. Wagner ◽  
Till Sprenger ◽  
Eberhard F. Kochs ◽  
Thomas R. Tölle ◽  
Michael Valet ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Periaqueductal Gray ◽  
Emission Tomography ◽  
Regional Cerebral Blood ◽  
Heat Stimulation ◽  
Positron Emission ◽  
Dose Dependent

Background Previous imaging studies have demonstrated a number of cortical and subcortical brain structures to be activated during noxious stimulation and infusion of narcotic analgesics. This study used O-water and positron emission tomography to investigate dose-dependent effects of the short-acting mu-selective opioid agonist remifentanil on regional cerebral blood flow during experimentally induced painful heat stimulation in healthy male volunteers. Methods Positron emission tomography measurements were performed with injection of 7 mCi O-water during nonpainful heat and painful heat stimulation of the volar forearm. Three experimental conditions were used during both sensory stimuli: saline, 0.05 microg x kg x min remifentanil, and 0.15 microg x kg x min remifentanil. Cardiovascular and respiratory parameters were monitored noninvasively. Across the three conditions, dose-dependent effects of remifentanil on regional cerebral blood flow were analyzed on a pixel-wise basis using a statistical parametric mapping approach. Results During saline infusion, regional cerebral blood flow increased in response to noxious thermal stimulation in a number of brain regions as previously reported. There was a reduction in pain-related activations with increasing doses of remifentanil in the thalamus, insula, and anterior and posterior cingulate cortex. Increasing activation occurred in the cingulofrontal cortex (including the perigenual anterior cingulate cortex) and the periaqueductal gray. Conclusions Remifentanil induced regional cerebral blood flow increases in the cingulofrontal cortex and periaqueductal gray during pain stimulation, indicating that mu-opioidergic activation modulates activity in pain inhibitory circuitries. This provides direct evidence that opioidergic analgesia is mediated by activation of established descending antinociceptive pathways.

scholarly journals Intranasal insulin increases regional cerebral blood flow in the insular cortex in men independently of cortisol manipulation

2013 ◽  
Vol 35 (5) ◽  
pp. 1944-1956 ◽  
Author(s):  
Thomas M. Schilling ◽  
Diana S. Ferreira de Sá ◽  
René Westerhausen ◽  
Florian Strelzyk ◽  
Mauro F. Larra ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Insular Cortex ◽  
Intranasal Insulin ◽  
Regional Cerebral Blood
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