Müller-Tasch T, Frankenstein L, Holzapfel N, Schellberg D, Löwe B, Nelles M, Zugck C, Katus H, Rauch B, Haass M, Jünger J, Remppis A, Herzog W.

Department of Psychosomatic and General Internal Medicine, University of Heidelberg, Heidelberg, Germany. Thomas.Mueller-Tasch@med.uni-heidelberg.de

OBJECTIVE: Our objective was to assess the prevalence of panic disorder, its influence on quality of life (QoL), and the presence of further anxiety and depressive comorbid disorders in outpatients with chronic heart failure (CHF). METHODS: In a cross-sectional study, anxiety and depressive disorders were diagnosed according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition diagnostic criteria in patients with CHF who were aged > or =18 years and had New York Heart Association (NYHA) Functional Classes I-IV, using the Patient Health Questionnaire. Health-related QoL was evaluated using the Short-Form 36 Health Survey (SF-36). RESULTS: Of the 258 participating patients, 24 (9.3%) fulfilled diagnostic criteria for panic disorder. Seven of these (29.2%) were diagnosed with comorbid anxiety disorders, 11 (47.3%) were diagnosed with comorbid depressive disorder, and 5 (20.8%) were diagnosed with other anxiety disorders and any depressive disorder. Female gender [odds ratio (OR)=3.1; 95% confidence interval (95% CI)=1.2-7.8; P=.02] and a lower level of education (OR=0.3; 95% CI=0.1-0.9; P=.04) were associated with the presence of panic disorder. In patients with panic disorder, QoL was significantly more restricted on all subscales of the SF-36 as compared to those without panic disorder, even when age, gender, and NYHA functional class were controlled for (P=.05 to <.01). CONCLUSION: Approximately 1 of 10 patients with CHF suffers from panic disorder, many of whom also have additional anxiety or depressive comorbid disorders. Female gender and a low level of education are positively associated with the presence of panic disorder. QoL is severely limited by the presence of panic disorder. Diagnosis of mental disorders and treatment offers for affected patients should be available in patient care.

Publication Types:

• Research Support, Non-U.S. Gov’t

PMID: 18291245 [PubMed – indexed for MEDLINE]

Galderisi S, Mancuso F, Mucci A, Garramone S, Zamboli R, Maj M.

Department of Psychiatry, University of Naples SUN, Naples, Italy. sgalderi@tin.it

BACKGROUND: In patients with panic disorder (PD), the difficulty to identify and manage emotional experience might contribute to the enduring vulnerability to panic attacks. Such a difficulty might reflect a dysfunction of fronto-temporo-limbic circuits. The present study was designed to test the hypothesis that drug-free patients with PD, as compared with healthy subjects (HS), show a higher prevalence of alexithymia, greater difficulty in emotional stimuli processing and poorer performance on neuropsychological tests exploring the activity of fronto-temporo-limbic circuits. METHODS: Alexithymia, general cognitive abilities, focused and sustained attention, working memory, secondary memory, incidental learning, susceptibility to interference from both cognitive and emotional stimuli, and ability to recognize facial emotional expressions were assessed in 32 drug-free patients with PD and 32 HS. RESULTS: Alexithymia was more frequent in patients with PD than in HS. Patients with PD, as compared to HS, had lower verbal cognitive abilities and more difficulty to inhibit interference from nonverbal stimuli and from panic-related words; they performed better than HS on the test assessing spatial incidental learning. Anxiety, panic symptomatology and verbal cognitive abilities (VIQ) were associated with alexithymia. CONCLUSIONS: Findings are compatible with a dysfunction of frontolimbic circuits, in particular orbitofrontal and cingulate cortices. A reduction in verbal cognitive abilities was also observed, which might suggest reduced abstraction and symbolization in these patients. Copyright (c) 2008 S. Karger AG, Basel.

Publication Types:

• Research Support, Non-U.S. Gov’t

PMID: 18332616 [PubMed – indexed for MEDLINE]

Maddock RJ, Buonocore MH, Copeland LE, Richards AL.

[1] 1Department of Psychiatry, University of California Davis Medical Center, Sacramento, CA, USA [2] 3Imaging Research Center, University of California Davis Medical Center, Sacramento, CA, USA.

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.Molecular Psychiatry advance online publication, 8 January 2008; doi:10.1038/sj.mp.4002137.

PMID: 18180759 [PubMed – as supplied by publisher]