Converging evidence suggests that patients with
panic disorder have a metabolic disturbance that may influence the regulation of arousal systems and confer vulnerability to 'spontaneous'
panic attacks. The consistent finding of elevated brain
lactate responses to various metabolic challenges in
panic disorder appears to support this model, although the mechanism of this effect is not understood. Several mechanisms have been proposed to account for elevated brain
lactate responses in
panic disorder, including (1)
brain hypoxia due to excessive cerebral vasoconstriction, and (2) a metabolic disturbance affecting
lactate metabolism. Recent studies have shown that neural activation (for example, sensory stimulation) causes local
lactate accumulation in the presence of increased
oxygen availability. The current study used
proton magnetic resonance spectroscopic measures of visual cortex
lactate changes during visual stimulation in 15 untreated patients with
panic disorder and 15 matched volunteers to critically test these two proposed mechanisms of elevated brain
lactate responses in
panic disorder. Visual cortex
lactate/
N-acetylaspartate increased during visual stimulation in both groups. The increase was significantly greater in the panic patients than in the comparison group. There were no group differences in end-tidal pCO(2). The finding that visual stimulation leads to significantly greater visual cortex
lactate responses in panic patients is not predicted by the
hypoxia model. These results suggest that a metabolic disturbance affecting the production or clearance of
lactate is the cause of the elevated brain
lactate responses consistently observed in
panic disorder and provide further support for metabolic models of vulnerability to this illness.