Anxiety Disorders: Hermann B

LaFrance WC, Kanner AM, Hermann B. · Brown Medical School, Rhode Island Hospital, Departments of Psychiatry and Neurology, Providence, Rhode Island 02903, USA. · Int Rev Neurobiol. · Pubmed #18929092 No free full text.

Abstract: Psychiatric disorders can be identified in 25-50% of patients with epilepsy, with higher prevalence among patients with poorly controlled seizures. These disturbances include depression, anxiety, psychotic disorders, cognitive, and personality changes occurring in the interictal or ictal/postictal states. In this chapter, we describe four areas of focus in women with epilepsy: comorbid primary psychiatric processes, integrated symptoms secondary to epilepsy, stigma and psychosocial consequences of epilepsy, and nonepileptic seizures.

Rupprecht R, di Michele F, Hermann B, Ströhle A, Lancel M, Romeo E, Holsboer F. · Department of Psychiatry, Ludwig Maximilian University, Munich, Germany. · Brain Res Brain Res Rev. · Pubmed #11744074 No free full text.

Abstract: Besides their binding to cognate intracellular receptors gonadal steroids may also act as functional antagonists at the 5-HT3 receptor. A structure-activity relationship for the actions of a variety of steroids at the 5-HT3 receptor was elaborated that differed considerably from that known for GABA(A) receptors. Steroids appear to interact allosterically with ligand-gated ion channels at the receptor membrane interface. The functional antagonism of gonadal steroids at the 5-HT3 receptor may play a role for the development and course of nausea during pregnancy and of psychiatric disorders. Moreover, we could demonstrate that 3alpha-reduced neuroactive steroids concurrently modulate the GABA(A) receptor and regulate gene expression via the progesterone receptor after intracellular oxidation. Animal studies showed that progesterone is converted rapidly into GABAergic neuroactive steroids in vivo. Progesterone reduces locomotor activity in a dose dependent fashion in male Wister rats. Moreover, progesterone and 3alpha,5alpha-tetrahydroprogesterone produce a benzodiazepine-like sleep EEG profile in rats and humans. In addition, there is a dysequilibrium of such 3alpha-reduced neuroactive steroids during major depression which is corrected by successful treatment with antidepressants. Neuroactive steroids may further be involved in the treatment of depression and anxiety with antidepressants in patients during ethanol withdrawal. First studies in patients with panic disorder suggest that neuroactive steroids may also play a pivotal role in human anxiety. The genomic and non-genomic effects of steroids in the brain contribute to the pathophysiology of psychiatric disorders and the mechanisms of action of antidepressants. Neuroactive steroids affect a broad spectrum of behavioral functions through their unique molecular properties and may constitute a yet unexploited class of drugs.

Brand S, Hermann B, Muheim F, Beck J, Holsboer-Trachsler E. · Psychiatric University Clinics Basel, Depression Research Unit, Whilhelm Klein-Strasse 27, 4025 Basel, Switzerland. · Ind Health. · Pubmed #18544879 links to  free full text

Abstract: OBJECTIVE: Good and sufficient sleep is crucial for a good quality of life. We investigated the associations between sleep patterns, work, and strain among students of hospitality and tourism. METHODS: 92 students completed psychological and sleep-related questionnaires, and a sleep/work log for one week. Results: Sleeping hours were inversely correlated with working hours. Decreased sleep quality was associated with increased scores of strain, depression and anxiety. Participants with increased working hours were 3.2 times more likely to report heightened insomnia scores than those with lower weekly working hours. Working on weekends was associated with increased strain with family life and peers. CONCLUSIONS: In hospitality and tourism, the employees' 'personal costs' for a 24/7 service may be underestimated; unfavourable work schedules are linked with decreased sleep quality, symptoms of depression, anxiety, and with social problems.

Jones JE, Watson R, Sheth R, Caplan R, Koehn M, Seidenberg M, Hermann B. · Department of Neurology, University of Wisconsin School of Medicine and Public Health, 600 N. Highland, Madison, WI 53742, USA. · Dev Med Child Neurol. · Pubmed #17593119 No free full text.

Abstract: The aim of this study was to characterize the distribution, timing, and risk factors for psychiatric comorbidity in children with recent onset epilepsy. Children aged 8 to 18 years with recent onset epilepsy (<1 year in duration) of idiopathic etiology (n=53) and a healthy comparison group (n=50) underwent a structured psychiatric diagnostic interview to characterize the spectrum of lifetime-to-date history of comorbid psychiatric disorder. There was no significant difference between the children with recent onset epilepsy and healthy comparison children in sex (31 males, 22 females vs 23 males, 27 females) or mean age 12.7y [SD 3.3] vs 12.7y [SD 3.2]). Children with recent onset epilepsy exhibited an elevated rate of lifetime-to-date Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) Axis I disorders compared with the comparison group. They showed significantly higher rates of depressive disorders (22.6 vs. 4%, p=0.01), anxiety disorders (35.8 vs 22%, p<0.05), and attention-deficit-hyperactivity disorder (26.4 vs 10%, p=0.01) with elevated but less prevalent rates of oppositional defiant and tic disorders. A subset of children with epilepsy (45%) exhibited DSM-IV Axis I disorders before the first recognized seizure, suggesting the potential influence of antecedent neurobiological factors that remain to be identified. The increased prevalence of psychiatric comorbidity antedating epilepsy onset may be consistent with the presence of underlying neurobiological influences independent of seizures, epilepsy syndrome, and medication treatment.

Hermann B, Landgraf R, Keck ME, Wigger A, Morrow AL, Ströhle A, Holsboer F, Rupprecht R. · Max Planck Institute of Psychiatry, Munich, Germany. · World J Biol Psychiatry. · Pubmed #12607222 No free full text.

Abstract: Two Wistar rat lines that have been selectively bred for high-anxiety-related behaviour (HAB) and low-anxiety-related behaviour (LAB) in the elevated plusmaze test may be considered as a genetically prone animal model to study the neurochemical correlates of anxiety-related behaviour. Because there are pronounced differences between the two lines both in baseline levels of open-arm exploration in the elevated plus-maze test and in sensitivity to the anxiolytic effects of 1 mg/kg diazepam, we used these lines to investigate the pharmacology of the benzodiazepine binding site and the GABA binding site of cortical GABAA receptors. No difference in characteristics of flunitrazepam, zolpidem or muscimol binding to cortical GABAA receptors could be detected between the two lines. Although there was an increase in the brain concentration of the anxiolytic neuroactive steroid allopregnanolone, a potent positive allosteric modulator of GABAA receptors, both in HAB and LAB animals after a forced swim stress, allopregnanolone concentrations did not differ between the two lines. Moreover, plasma dehydroepiandrosterone (DHEA) concentrations were similar in HAB and LAB animals. We conclude that anxiety-related behaviour and benzodiazepine sensitivity in these rat lines are likely to be independent of the pharmacology of cortical GABAA receptors.

Ströhle A, Romeo E, di Michele F, Pasini A, Hermann B, Gajewsky G, Holsboer F, Rupprecht R. · Max Planck Institute of Psychiatry, Munich, Germany. · Arch Gen Psychiatry. · Pubmed #12578433 links to  free full text

Abstract: BACKGROUND: Certain metabolites of progesterone such as 3alpha,5alpha-tetrahydroprogesterone (3alpha,5alpha-THP; allopregnanolone) and 3alpha,5beta-THP (pregnanolone) are potent, positive allosteric modulators of gamma-aminobutyric acid type A receptors. Although animal studies suggest anxiolytic properties of these endogenous modulators of central nervous excitability, no clinical data indicate whether they are also involved in the pathophysiology of anxiety disorders and panic attacks. METHODS: We quantified the concentrations of 3alpha,5alpha-THP, 3alpha,5beta-THP, the isomer 3beta,5alpha-THP, and their precursors in the plasma of 10 patients with panic disorder and matched control subjects during panic attacks induced by means of sodium lactate and cholecystokinin tetrapeptide administration, using a highly sensitive gas chromatography-mass spectrometry analysis. RESULTS: Panic attacks induced by sodium lactate and cholecystokinin tetrapeptide in patients with panic disorder were accompanied by pronounced decreases in the concentrations of 3alpha,5alpha-THP and 3alpha,5beta-THP and a concomitant increase in the concentrations of the functional antagonistic isomer 3beta,5alpha-THP, findings that are compatible with a decreased gamma-aminobutyric acid-ergic tone. No changes in neuroactive steroid concentrations were observed after placebo administration in patients with panic disorder or after placebo, sodium lactate, or cholecystokinin tetrapeptide administration in controls. CONCLUSIONS: The association between changes in plasma neuroactive steroid concentrations and experimentally induced panic attacks and the well-documented pharmacological properties of these compounds as gamma-aminobutyric acid type A receptor modulators suggest that neuroactive steroids may play a role in the pathophysiology of panic attacks in patients with panic disorder.