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 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.

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

scholarly journals Effects of hypoglycaemia on working memory and regional cerebral blood flow in type 1 diabetes: a randomised, crossover trial

Diabetologia ◽  
2017 ◽  
Vol 61 (3) ◽  
pp. 551-561 ◽  
Author(s):  
Michael Gejl ◽  
Albert Gjedde ◽  
Birgitte Brock ◽  
Arne Møller ◽  
Eelco van Duinkerken ◽  
...  
Keyword(s):  
Working Memory ◽  
Blood Flow ◽  
Type 1 Diabetes ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Crossover Trial ◽  
Regional Cerebral Blood

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 Acute Hyperglycemia Increases Brain Pregenual Anterior Cingulate Cortex Glutamate Concentrations in Type 1 Diabetes Mellitus

2020 ◽  
Author(s):  
Ada Admin ◽  
Nicolas R. Bolo ◽  
Alan M. Jacobson ◽  
Gail Musen ◽  
Matcheri S. Keshavan ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Depressive Symptoms ◽  
Anterior Cingulate Cortex ◽  
Emotional Processing ◽  
Response Times ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Emotional Stroop ◽  
Chronic Hyperglycemia

The brain mechanisms underlying the association of hyperglycemia with depressive symptoms are unknown. We hypothesized that disrupted glutamate metabolism in pregenual anterior cingulate cortex (ACC) in type 1 diabetes (T1D) without depression affects emotional processing. Using proton magnetic resonance spectroscopy (MRS), we measured glutamate concentrations in ACC and occipital cortex (OCC) in 13 T1D without major depression (HbA1c=7.1±0.7% [54±7mmol/mol]) and 11 healthy non-diabetic controls (HbA1c=5.5±0.2% [37±3mmol/mol]) during fasting euglycemia (EU) followed by a 60-minute +5.5mmol/l hyperglycemic clamp (HG). Intrinsic neuronal activity was assessed using resting-state blood oxygen level dependent functional MRI to measure the fractional amplitude of low frequency fluctuations in slow-band 4 (fALFF4). Emotional processing and depressive symptoms were assessed using emotional tasks (Emotional-Stroop, Self-Referent-Encoding-Task SRET) and clinical ratings (HAM-D, SCL-90-R), respectively. During HG, ACC glutamate increased (1.2mmol/kg, +10%, p=0.014) while ACC fALFF4 was unchanged (-0.007, -2%, p=0.449) in T1D; in contrast, glutamate was unchanged (-0.2mmol/kg, -2%, p=0.578) while fALFF4 decreased (-0.05, -13%, p=0.002) in controls. OCC glutamate and fALFF4 were unchanged in both groups. T1D had longer SRET negative-word response-times (p=0.017) and higher depression-rating scores (HAM-D p=0.020; SCL-90-R-depression p=0.008). Higher glutamate change tended to associate with longer Emotional-Stroop response-times in T1D only. Brain glutamate must be tightly controlled during hyperglycemia due to the risk for neurotoxicity with excessive levels. Results suggest that ACC glutamate control mechanisms are disrupted in T1D, which affects glutamatergic neurotransmission related to emotional or cognitive processing. Increased prefrontal glutamate during acute hyperglycemic episodes could explain our previous findings of associations between chronic hyperglycemia, cortical thinning and depressive symptoms in T1D.

scholarly journals Acute Hyperglycemia Increases Brain Pregenual Anterior Cingulate Cortex Glutamate Concentrations in Type 1 Diabetes Mellitus

2020 ◽  
Author(s):  
Ada Admin ◽  
Nicolas R. Bolo ◽  
Alan M. Jacobson ◽  
Gail Musen ◽  
Matcheri S. Keshavan ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Depressive Symptoms ◽  
Anterior Cingulate Cortex ◽  
Emotional Processing ◽  
Response Times ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Emotional Stroop ◽  
Chronic Hyperglycemia

The brain mechanisms underlying the association of hyperglycemia with depressive symptoms are unknown. We hypothesized that disrupted glutamate metabolism in pregenual anterior cingulate cortex (ACC) in type 1 diabetes (T1D) without depression affects emotional processing. Using proton magnetic resonance spectroscopy (MRS), we measured glutamate concentrations in ACC and occipital cortex (OCC) in 13 T1D without major depression (HbA1c=7.1±0.7% [54±7mmol/mol]) and 11 healthy non-diabetic controls (HbA1c=5.5±0.2% [37±3mmol/mol]) during fasting euglycemia (EU) followed by a 60-minute +5.5mmol/l hyperglycemic clamp (HG). Intrinsic neuronal activity was assessed using resting-state blood oxygen level dependent functional MRI to measure the fractional amplitude of low frequency fluctuations in slow-band 4 (fALFF4). Emotional processing and depressive symptoms were assessed using emotional tasks (Emotional-Stroop, Self-Referent-Encoding-Task SRET) and clinical ratings (HAM-D, SCL-90-R), respectively. During HG, ACC glutamate increased (1.2mmol/kg, +10%, p=0.014) while ACC fALFF4 was unchanged (-0.007, -2%, p=0.449) in T1D; in contrast, glutamate was unchanged (-0.2mmol/kg, -2%, p=0.578) while fALFF4 decreased (-0.05, -13%, p=0.002) in controls. OCC glutamate and fALFF4 were unchanged in both groups. T1D had longer SRET negative-word response-times (p=0.017) and higher depression-rating scores (HAM-D p=0.020; SCL-90-R-depression p=0.008). Higher glutamate change tended to associate with longer Emotional-Stroop response-times in T1D only. Brain glutamate must be tightly controlled during hyperglycemia due to the risk for neurotoxicity with excessive levels. Results suggest that ACC glutamate control mechanisms are disrupted in T1D, which affects glutamatergic neurotransmission related to emotional or cognitive processing. Increased prefrontal glutamate during acute hyperglycemic episodes could explain our previous findings of associations between chronic hyperglycemia, cortical thinning and depressive symptoms in T1D.

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.

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