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candidate loci and genes in schizophrenic and affective disorders. Recently, a genomic duplication on human chromosome 15q24-26 has been suggested as a susceptibility factor for panic and phobic disorders associated with joint hyper- mobility syndrome and mitral valve prolaps (Gratacos et al., Cell 106:367-378, 2001). In fact, increased anxiety and anxiety disorders have been reported for a series of chromosomal aberrations. They include Turner syndrome and fragile x syndrome on chromosome Xq, Prader-Willi- syndrome on chromosome 15q11 and velo-cardio-facial syndrome on chromosome 22q11. The phenotypic ex- pression of anxiety varies from social phobia in individu- als with premutation status in fragile x syndrome over panic disorder in the 15q24-26 duplication to separation anxiety in velo-cardio-facial syndrome. Some of these anxiety syndromes have been shown to occur indepen- dently from intellectual impairment and thus appear not to be secondary to it. In a replication study on a possible association of panic disorder with joint hypermobility syndrome we have sys- tematically investigated patients and gender- and age- matched controls for joint hypermobility syndrome ac- cording to the criteria of Beighton. Preliminary results (n=10) do not support the hypothesis of an increased rate of joint hypermobility syndrome in our German sample. A deletion of the short arm of chromosome 18 (18p) was observed in a woman who was admitted to our depart- ment with phobias and depression as well as intellectual impairment. This observation is consistent with linkage findings on chromosome 18p in bipolar affective disorder and harm avoidance. Searching for the gene on chromo- some 22q11.2, which causes increased separation anxiety in velo-cardio-facial-syndrome, we studied the functional valine/methionine polymorphism of the COMT gene. In accordance with observations of Hamilton et al. (2000) we observed an association in women with panic disorder. However, this association was due to an excess of the functionally more active valine COMT variant and not the functionally less active methionine COMT variant. Genes contributing to the pathogenesis of anxiety disor- ders in most instances do so to a rather small degree. Linkage studies have so far failed to provide unambiguous results. Observations of increased anxiety and anxiety syndromes in patients with chromosomal aberrations may thus help to define candidate genes for molecular studies.

References Gratacos M et al., A polymorphic genomic duplication on human chromosome 15 is a susceptibility factor for panic and phobic disorders, Cell 106:367-379, 2001 Hamilton et al., Evidence for a susceptibility locus for panic disorder near the catechol-o-methlytranferase gene on chromosome 22, Am J Med Genet 96:485, 2000)

German J Psychiatry 2001; 4: S5 Heart rate variability in experimentally indu- ced panic attacks

A. Siegmund1, R. Heese2, F. Strian2, A. Ströhle2 1Justus-Liebig-University, Gießen; 2Max Planck Institute of Psychiatry, Munich

To further study the pathophysiology of panic disorder and possible new treatment approaches, panic attacks can be experimentally induced. The aim of this study was to discern the differential effects of two different panico- genic challenges on autonomic function in 23 patients with panic disorder and 13 healthy control subjects. In a double-blind randomized design each subject received

tetrapeptide (CCK-4) intravenously on separate days. Heart rate variability was assessed using an analogous ECG and subsequent power spectral analysis of RR- intervals. 17/18 of the patients and 2/3 of the controls developed a panic attack following the administration of CCK-4/sodium lactate. In patients and controls the heart rate increased in both active treatments conditions. In both groups a shift from mid frequency power (PMID) to high frequency power (PHIGH) occurred after sodium lactate, indicating vagal predominance. Following CCK-4 only the patients showed an increase of the PLOW (low frequency power): PHIGH ratio, representing increased sympathic activity. The differential effects of the two panicgenic substances point to differential mechanisms in the development and regression of panic attacks. Whether the PMID to PHIGH shift during lactate induced panic attacks represents counterregulatory mechanisms and whether they may be used in the treatment of panic dis- order is studied.

German J Psychiatry 2001; 4: S5 GABAA receptor modulatory neuroactive ste- roids in panic disorder

A. Ströhle, E. Romeo1, A. Pasini, F. Holsboer, R. Rupp- recht Max Planck Institute of Psychiatry, Munich, Germany 1University Tor Vergata, IRCCS Santa Lucia, Rome, Italy

are potent positive allosteric modulaturs of GABAA recep- tors. Altough animal studies suggest anxiolytic properties of these endogenous modulators of central nervous exci- tability no data exist whether they are also involved in anxiety disorders. We quantified the concentrations of

precursors of patients with panic disorder and healthy control subjects during experimentally induced panic attacks and during paroxetine treatment using a highly sensitive gaschromatography/mass spectrometry analysis.


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