Sexually dimorphic gray matter volume reduction in patients with panic disorder.

While clinical features of panic disorder show significant sexual dimorphism, previous structural MRI studies have not sufficiently controlled for sex when looking at regional brain abnormalities in panic disorder. Using optimized voxel-based morphometry (VBM), regional gray matter volume was compared between 24 patients (male/female: 9/15) with panic disorder and 24 healthy subjects matched for age and sex. Significant gray matter volume reductions were found in the bilateral dorsomedial and right ventromedial prefrontal cortices, right amygdala, anterior cingulate cortex, bilateral insular cortex, occipitotemporal gyrus and left cerebellar vermis in the patients compared with the controls. Among these regions, the VBM revealed significant sexual dimorphism: volume reduction in the right amygdala and the bilateral insular cortex was significantly greater in the males, while reduction in the right superior temporal gyrus was greater in females. Furthermore, a significant reduction in the dorsolateral and ventrolateral prefrontal cortices, thalamus, and parietal cortex was specific to the female patients. The present study demonstrated the morphological changes in extensive brain regions of patients with panic disorder compared with the sex-matched controls. The current results further suggested that the sexually dimorphic clinical phenotypes of panic disorder might have a neurobiological background even at the structural level of the brain.

Anterior cingulate cortex volume reduction in patients with panic disorder.

AIM: Recent neuroimaging studies have suggested that the anterior cingulate cortex (ACC) has an important role in the pathology of panic disorder. Despite numerous functional neuroimaging studies that have elucidated the strong relationship between functional abnormalities of the ACC and panic disorder and its symptoms and response to emotional tasks associated with panic disorder, there has been no study showing volumetric changes of the ACC or its subregions. METHODS: To clarify the structural abnormalities of ACC and its subregions, the combination of region of interest (ROI) and optimized voxel-based morphometry (VBM) methods were performed on 26 patients with panic disorder, and 26 age and sex-matched healthy subjects. In the ROI study, ACC was divided into four subregions: dorsal, rostral, subcallosal and subgenual ACC. RESULTS: The results of the manually traced ROI volume comparison showed significant volume reduction in the right dorsal ACC. VBM also showed a volume reduction in the right dorsal as well as a part of the rostral ACC as a compound mass. CONCLUSIONS: Both manual ROI tracing and optimized VBM suggest a subregion-specific pattern of ACC volume deficit in panic disorder. In addition to functional abnormalities, these results suggest that structural abnormalities of the ACC contribute to the pathophysiology of panic disorder.

Psychiatric symptoms typical of patients with dementia with Lewy bodies - similarity to those of levodopa-induced psychosis.

We examined psychiatric symptoms in eight cases with dementia with Lewy bodies (DLB), which included visual hallucination of persons or small animals, visual illusion, metamorphosia, leibhaftige Bewusstheit, personal or topographical misidentification, Capgras' syndrome and reduplicative paramnesia as well as depressive state and delusion of persecution. These psychiatric symptoms are identical to those of levodopa-induced psychosis, although these symptoms appeared before medication with anti-Parkinson drugs. The hypersensitivity of the dopamine receptor in the meso-limbic dopaminergic system has been presumed in levodopa-induced psychosis. We previously showed disturbance of the nigro-amygdaloid dopaminergic connections in DLB brains on pathological studies. Hypoperfusion or glucose hypometabolism in the occipital lobe has been demonstrated in DLB patients using SPECT or PET. The amygdala has reciprocal connections with the visual cortex in the occipital lobe. From these findings, it is supposed that the disturbance of the nigro-amygdaloid connections induces hypersensitivity of the dopamine receptor in the amygdala, causing psychiatric symptoms with dysfunction of the visuo-amygdaloid connections.