PD is associated with WM connectivity enhancement in cingulate region, which probably compensate the WM structural abnormalities derived from PD symptoms.1 In this case, white matter increased after escitalopram treatment, which might suggest that WM volume could be lower through PD illness course and the increase probably represent WM restore phenomenon. PD is also associated with GM deficits in rostral anterior cingulate, dorsal anterior cingulate, left superior temporal gyrus and middle temporal gyrus,2 which represent possible consequences of panic attacks or pathophysiology. The GM increase in this PD patient is different from our previous finding in PD with depression,3 which showed that residual GM deficits were still obvious and widespread without global increase of GM volume. The results of this case probably suggested pure PD patients should not be severe as comorbid patients with significant residual GM deficits. PD patients can recover with faster and significant “re-growth” of GM volume. Escitalopram can increase the cytogenesis of ventral hippocampal formation through its modulation of brain-derived neurotrophic factor (BDNF) release in the chronic stress rat model.4 Escitalopram contributes to synaptic plasticity through enhancing BDNF calcium-dependent intracellular signal transduction in prefrontal, frontal and hippocampal regions,5 which probably produce neurogenesis phenomenon in this case.