Comparison of Sodium Lactate Infusion and Carbon Dioxide Inhalation Panic Provocation Tests: A Meta-analysis

2021 ◽  
Author(s):  
Umit Tural ◽  
Dan V. Iosifescu
Keyword(s):  
Carbon Dioxide ◽  
Meta Analysis ◽  
Provocation Test ◽  
Sodium Lactate ◽  
Panic Attacks ◽  
Provocation Tests ◽  
Inhalation Challenge ◽  
Carbon Dioxide Co2 ◽  
Lactate Infusion ◽  
The Brain

Abstract Background Sodium lactate (NaL) infusion and carbon dioxide (CO2) inhalation are proven to provoke acute panic attacks (PAs) in patients with panic disorder (PD). A systematic literature search and meta-analysis were performed to compare the effect sizes of these methods. Methods Odds ratios were calculated for each of the original studies and were pooled using the random-effects model. Results Either NaL or CO2 provocations significantly increased the rates of PAs in individuals with PD compared to those in healthy controls. However, the effect size of NaL infusion (OR=25.13, 95% CI=15.48–40.80) was significantly greater than that of CO2 inhalation (OR=10.58, 95%CI=7.88–14.21). Conclusion The evidence for the efficacy of the two panic provocation tests is very strong. Yet, the results support the superiority of NaL infusion over CO2 inhalation challenge as a panic provocation test. Thus, lactate seems a much stronger stimulus than CO2 for the brain suffocation detector.

scholarly journals Effect of lactate administration on brain lactate levels during hypoglycemia in patients with type 1 diabetes

2018 ◽  
Vol 39 (10) ◽  
pp. 1974-1982 ◽  
Author(s):  
Evita C Wiegers ◽  
Hanne M Rooijackers ◽  
Cees J Tack ◽  
Bart WJ Philips ◽  
Arend Heerschap ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Sodium Lactate ◽  
Saline Infusion ◽  
Modest Increase ◽  
Impaired Awareness ◽  
Lactate Levels ◽  
Lactate Infusion ◽  
The Brain ◽  
Brain Lactate

Administration of lactate during hypoglycemia suppresses symptoms and counterregulatory responses, as seen in patients with type 1 diabetes and impaired awareness of hypoglycemia (IAH), presumably because lactate can substitute for glucose as a brain fuel. Here, we examined whether lactate administration, in a dose sufficient to impair awareness of hypoglycemia, affects brain lactate levels in patients with normal awareness of hypoglycemia (NAH). Patients with NAH ( n = 6) underwent two euglycemic-hypoglycemic clamps (2.8 mmol/L), once with sodium lactate infusion (NAH w|lac) and once with saline infusion (NAH w|placebo). Results were compared to those obtained during lactate administration in patients with IAH ( n = 7) (IAH w|lac). Brain lactate levels were determined continuously with J-difference editing 1H-MRS. During lactate infusion, symptom and adrenaline responses to hypoglycemia were considerably suppressed in NAH. Infusion of lactate increased brain lactate levels modestly, but comparably, in both groups (mean increase in NAH w|lac: 0.12 ± 0.05 µmol/g and in IAH w|lac: 0.06 ± 0.04 µmol/g). The modest increase in brain lactate may suggest that the excess of lactate is immediately metabolized by the brain, which in turn may explain the suppressive effects of lactate on awareness of hypoglycemia observed in patients with NAH.

scholarly journals Carbon dioxide test as an additional clinical measure of treatment response in panic disorder

2002 ◽  
Vol 60 (2B) ◽  
pp. 358-361 ◽  
Author(s):  
Alexandre M. Valença ◽  
Antonio Egidio Nardi ◽  
Isabella Nascimento ◽  
Walter A. Zin ◽  
Márcio Versiani
Keyword(s):  
Carbon Dioxide ◽  
Panic Disorder ◽  
Panic Attack ◽  
Challenge Test ◽  
Panic Attacks ◽  
Test Results ◽  
Carbon Dioxide Co2 ◽  
Drug Free ◽  
Free Status ◽  
Co2 Challenge

OBJECTIVE: We aim to determine if a treatment with a dose of clonazepam - 2 mg/day, for 6 weeks, blocks spontaneous panic attacks and the ones induced by the inhalation of 35% carbon dioxide (CO2) in panic disorder (PD) patients. The CO2 challenge-test may be a useful addition tool for measuring the pharmacological response during the initial phase (6 weeks) in the treatment of PD. METHOD: Eighteen PD patients drug free for a week participated in a carbon dioxide challenge test. Fourteen had a panic attack and were openly treated for a 6-week period with clonazepam. At the end of the 6-week period they were submitted again to the CO2 challenge test. RESULTS: After 6 weeks of treatment with clonazepam, 12 of 14 PD patients (85.7%) did not have a panic attack after the CO2 challenge test. Just 2 of 14 patients (14.3%) had a panic attack after the CO2 challenge test. Ten of 14 (71.4%) PD patients had panic free status after clonazepam treatment. The 2 patients who had a panic attack in the sixth week, after the CO2 test, did not have panic free status after the treatment with clonazepam. CONCLUSION: The CO2-test may be a valid tool for testing and predicting the drug response.

scholarly journals Neurobiology of panic and pH chemosensation in the brain

2011 ◽  
Vol 13 (4) ◽  
pp. 475-483 ◽  
Keyword(s):  
Animal Models ◽  
Panic Disorder ◽  
Ph Regulation ◽  
Ph Sensitive ◽  
Panic Attacks ◽  
Brain Ph ◽  
Neuron Function ◽  
Lactate Infusion ◽  
The Brain ◽  
Insight Into

Panic disorder is a common and disabling illness for which treatments are too frequently ineffective. Greater knowledge of the underlying biology could aid the discovery of better therapies. Although panic attacks occur unpredictably, the ability to provoke them in the laboratory with challenge protocols provides an opportunity for crucial insight into the neurobiology of panic. Two of the most well-studied panic provocation challenges are CO(2) inhalation and lactate infusion. Although it remains unclear how these challenges provoke panic animal models of CO(2) and lactate action are beginning to emerge, and offer unprecedented opportunities to probe the molecules and circuits underlying panic attacks. Both CO(2) and lactate alter pH balance and may generate acidosis that can influence neuron function through a growing list of pH-sensitive receptors. These observations suggest that a key to better understanding of panic disorder may He in more knowledge of brain pH regulation and pH-sensitive receptors.

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