Cerebral Glucose Utilization Is Reduced in Second Test Session

Stapleton, June M.; Morgan, Michael J.; Liu, Xiang; Yung, Babington C. K.; Phillips, Robert L.; Wong, Dean F.; Shaya, Elias K.; Dannals, Robert F.; London, Edythe D.

doi:10.1097/00004647-199706000-00012

Cited by 43 publications

(24 citation statements)

References 19 publications

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“…However, there is no reason to suspect that the regional cerebral metabolic changes seen in controls would have been significantly different if the period between their first and second scans was shorter. The decrease in ACC metabolism seen in controls replicated the findings of several prior PET studies [65][66][67][68] and likely reflects habituation to the scanning environment and procedures. 67 However, this study also had several strengths that afford confidence in its findings.…”

Section: Discussionsupporting

confidence: 79%

Rapid effects of brief intensive cognitive-behavioral therapy on brain glucose metabolism in obsessive-compulsive disorder

Saxena

Gorbis²,

O’Neill³

et al. 2008

Mol Psychiatry

124

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Brief intensive cognitive-behavioral therapy (CBT) using exposure and response prevention significantly improves obsessive-compulsive disorder (OCD) symptoms in as little as 4 weeks. However, it has been thought that much longer treatment was needed to produce the changes in brain function seen in neuroimaging studies of OCD. We sought to elucidate the brain mediation of response to brief intensive CBT for OCD and determine whether this treatment could induce functional brain changes previously seen after longer trials of pharmacotherapy or standard CBT. [ 18 F]-fluorodeoxyglucose positron emission tomography brain scans were obtained on 10 OCD patients before and after 4 weeks of intensive individual CBT. Twelve normal controls were scanned twice, several weeks apart, without treatment. Regional glucose metabolic changes were compared between groups. OCD symptoms, depression, anxiety and overall functioning improved robustly with treatment. Significant changes in normalized regional glucose metabolism were seen after brief intensive CBT (P = 0.04). Compared to controls, OCD patients showed significant bilateral decreases in normalized thalamic metabolism with intensive CBT but had a significant increase in right dorsal anterior cingulate cortex activity that correlated strongly with the degree of improvement in OCD symptoms (P = 0.02). The rapid response of OCD to intensive CBT is mediated by a distinct pattern of changes in regional brain function. Reduction of thalamic activity may be a final common pathway for improvement in OCD, but response to intensive CBT may require activation of dorsal anterior cingulate cortex, a region involved in reappraisal and suppression of negative emotions.

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Section: Discussionsupporting

confidence: 79%

Rapid effects of brief intensive cognitive-behavioral therapy on brain glucose metabolism in obsessive-compulsive disorder

Saxena

Gorbis²,

O’Neill³

et al. 2008

Mol Psychiatry

124

View full text Add to dashboard Cite

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“…18 F]deoxyglucose PET studies of metabolism performed 1 to 18 days apart show no changes in thalamic uptake normalized for whole brain counts, as was done here (37,38). In the present study, the regional CBF patterns during euglycemia on day 2 were not different from these on day 1.…”

Section: Discussionsupporting

confidence: 60%

Attenuation of Counterregulatory Responses to Recurrent Hypoglycemia by Active Thalamic Inhibition

et al. 2008

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OBJECTIVE-Hypoglycemia, the limiting factor in the glycemic management of diabetes, is the result of the interplay of therapeutic insulin excess and compromised glycemic defenses. The key feature of the latter is an attenuated sympathoadrenal response to hypoglycemia that typically follows an episode of recent antecedent iatrogenic hypoglycemia, a phenomenon termed hypoglycemia-associated autonomic failure (HAAF) in diabetes. We investigated the role of cerebral mechanisms in HAAF by measuring regional brain activation during recurrent hypoglycemia with attenuated counterregulatory responses and comparing it with initial hypoglycemia in healthy individuals. RESEARCH DESIGN AND METHODS-We used [15 O]water and positron emission tomography to measure regional cerebral blood flow as a marker of brain synaptic activity during hyperinsulinemic hypoglycemic clamps (55 mg/dl [3.0 mmol/l]) in the naïve condition (day 1) and after ϳ24 h of interval interprandial hypoglycemia (day 2) in nine healthy adults.RESULTS-Interval hypoglycemia produced attenuated sympathoadrenal, symptomatic, and other counterregulatory responses to hypoglycemia on day 2, a model of HAAF. Synaptic activity in the dorsal midline thalamus during hypoglycemia was significantly greater on day 2 than day 1 (P ϭ 0.004).CONCLUSIONS-Greater synaptic activity associated with attenuated counterregulatory responses indicates that the dorsal midline thalamus plays an active inhibitory role in reducing sympathoadrenal and symptomatic responses to hypoglycemia when previous hypoglycemia has occurred, the key feature of HAAF in diabetes. Diabetes 57:470-475, 2008 I atrogenic hypoglycemia is the limiting factor in the glycemic management of diabetes (1). It causes recurrent morbidity in most people with type 1 diabetes and many with advanced type 2 diabetes and is sometimes fatal. Furthermore, the barrier of hypoglycemia precludes maintenance of euglycemia over a lifetime of diabetes and thus full realization of the longterm benefits of glycemic control. Finally, episodes of hypoglycemia further impair defenses against falling plasma glucose concentrations and therefore cause a vicious cycle of recurrent hypoglycemia.Hypoglycemia in diabetes is the result of the interplay of therapeutic insulin excess and compromised physiological and behavioral defenses against falling plasma glucose concentrations (1-3). The key feature of the latter is an attenuated sympathoadrenal response to hypoglycemia that causes the clinical syndromes of hypoglycemia unawareness, which is largely the result of a reduced sympathetic neural response (4), and defective glucose counterregulation, which is the result of a reduced adrenomedullary epinephrine response in the setting of absent decrements in insulin and absent increments in glucagon in insulin-deficient diabetes--type 1 diabetes and advanced (i.e., absolutely insulin deficient) type 2 diabetes. These syndromes increase the risk of severe iatrogenic hypoglycemia ϳ6-fold (5) and 25-fold or more (6,7), respectively, in type 1 diabet...

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“…Healthy subjects with high-trait anxiety showed greater right/left ratios of cerebral metabolism than low-trait anxiety subjects, particularly during the second PET session (Stapleton et al 1997). Healthy male subjects showed increased connectivity between the right but not the left amygdala and the pulvinar and superior colliculus during presentations of unseen (masked) fearconditioned faces compared to seen (unmasked) fearconditioned faces (Morris et al 1999).…”

Section: Discussionmentioning

confidence: 92%