The vexing role of baseline: Implications for neuroimaging studies of panic disorder

The role of the amygdala in the pathophysiology of panic disorder: evidence from neuroimaging studies

“…Theoretically, disruption in any of these brain areas and connections along these areas, or any imbalance in the network can cause maladaptive and exaggerated fear responses such as panic attacks, increased basal anxiety or arousal [19], and excessive worrying [18,20]. Consistent with this postulation, structural, chemical, and functional alterations in these amygdalar areas have been reported in neuroimaging studies in patients with PD (Tables 1, 2, 3, 4, 5; Additional files 1, 2, 3).…”

“…In a relatively small sample size, the heterogeneity with regard to genetic polymorphism and sex may make it hard to detect the increased amygdalar activation, if any [99]. Baseline anxiety and associated physiologic changes may also confound functional neuroimaging findings [19]. …”

“…Findings from chemical neuroimaging studies suggest metabolic disturbances in the brain of patients with PD [19] (Table 5). Hypermetabolic state was suspected based on the findings that show depletion of phosphocreatine and creatine [92,109] in patients with PD, consistent with functional neuroimaging findings.…”

“…Inorganic phosphate is known to be accumulated when creatine phosphate is broken down during anaerobic metabolism [110]. A rapid rise of the brain lactate level in response to physiological challenge (vigilance task with visual stimuli) also suggests an intrinsic metabolic disturbance [19,36]. …”

Further Commentary on Mitochondrial Dysfunction in Autism Spectrum Disorder: Assessment and Treatment Considerations

“…Our laboratory has substantial experience measuring brain lactate in clinical populations (Dager 2010;Dager et al 1999;Dager et al 2004;Dager and Steen, 1992;Friedman et al 2000). Previously, using similar 1 H MRS acquisition methods, but a less sensitive analytic technique, there was sufficient sensitivity to detect subtle brain lactate elevations in untreated individuals with bipolar disorder, which we interpreted to reflect brain mitochondrial dysfunction (Dager et al 2004).…”