Abstract
Panic patients consistently show exaggerated lactic acid response to alkalosis, whether produced by hyperventilation or by sodium lactate infusion. Understanding why this occurs may provide important clues to the pathogenesis of panic disorder. Although brain hypoxia from excessive hypocapnia-induced cerebral vasoconstriction is often cited as the mechanism of elevated brain lactic acid in panic disorder, studies of brain metabolism show that hypocapnia rarely leads to brain hypoxia. Increased lactic acid production is a normal response to intracellular alkalosis and to intracellular cyclic AMP. Thus, other possible mechanisms of the exaggerated lactic acid response in panic disorder include a disturbance of mechanisms regulating intracellular pH and factors increasing intracellular cyclic AMP. Both mechanisms are consistent with the suffocation false alarm theory of panic disorder. This review suggests a theoretical framework for future magnetic resonance spectroscopy studies that can test some of the predictions of these competing models.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 22-34 |
| Number of pages | 13 |
| Journal | Journal of Neuropsychiatry and Clinical Neurosciences |
| Volume | 13 |
| Issue number | 1 |
| DOIs | |
| State | Published - 2001 |
Fingerprint
ASJC Scopus subject areas
- Neuropsychology and Physiological Psychology
- Neuroscience(all)
Cite this
The lactic acid response to alkalosis in panic disorder : An integrative review. / Maddock, Richard J.
In: Journal of Neuropsychiatry and Clinical Neurosciences, Vol. 13, No. 1, 2001, p. 22-34.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The lactic acid response to alkalosis in panic disorder
T2 - An integrative review
AU - Maddock, Richard J
PY - 2001
Y1 - 2001
N2 - Panic patients consistently show exaggerated lactic acid response to alkalosis, whether produced by hyperventilation or by sodium lactate infusion. Understanding why this occurs may provide important clues to the pathogenesis of panic disorder. Although brain hypoxia from excessive hypocapnia-induced cerebral vasoconstriction is often cited as the mechanism of elevated brain lactic acid in panic disorder, studies of brain metabolism show that hypocapnia rarely leads to brain hypoxia. Increased lactic acid production is a normal response to intracellular alkalosis and to intracellular cyclic AMP. Thus, other possible mechanisms of the exaggerated lactic acid response in panic disorder include a disturbance of mechanisms regulating intracellular pH and factors increasing intracellular cyclic AMP. Both mechanisms are consistent with the suffocation false alarm theory of panic disorder. This review suggests a theoretical framework for future magnetic resonance spectroscopy studies that can test some of the predictions of these competing models.
AB - Panic patients consistently show exaggerated lactic acid response to alkalosis, whether produced by hyperventilation or by sodium lactate infusion. Understanding why this occurs may provide important clues to the pathogenesis of panic disorder. Although brain hypoxia from excessive hypocapnia-induced cerebral vasoconstriction is often cited as the mechanism of elevated brain lactic acid in panic disorder, studies of brain metabolism show that hypocapnia rarely leads to brain hypoxia. Increased lactic acid production is a normal response to intracellular alkalosis and to intracellular cyclic AMP. Thus, other possible mechanisms of the exaggerated lactic acid response in panic disorder include a disturbance of mechanisms regulating intracellular pH and factors increasing intracellular cyclic AMP. Both mechanisms are consistent with the suffocation false alarm theory of panic disorder. This review suggests a theoretical framework for future magnetic resonance spectroscopy studies that can test some of the predictions of these competing models.
UR - http://www.scopus.com/inward/record.url?scp=0035121673&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0035121673&partnerID=8YFLogxK
U2 - 10.1176/appi.neuropsych.13.1.22
DO - 10.1176/appi.neuropsych.13.1.22
M3 - Article
C2 - 11207326
AN - SCOPUS:0035121673
VL - 13
SP - 22
EP - 34
JO - Journal of Neuropsychiatry and Clinical Neurosciences
JF - Journal of Neuropsychiatry and Clinical Neurosciences
SN - 0895-0172
IS - 1
ER -