Vol 5 n° 3 - Anxiety II
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The State of the art article in this second issue of Dia- logues in Clinical Neuroscience devoted to anxiety provides the reader with a major review by Dennis S. Charney (page 207) about the neurotransmitter and neurohormone sys- tems known to play a role in the different clinical entities within the anxiety disorders (eg, monoamines, corticos- teroids, and sex hormones). He also discusses compounds that probably play a role in anxiety, but have not yet been extensively discussed in this respect (eg, galanin and neu- ropeptide Y). His review describes how these compounds are involved in various brain systems and during different challenges to the individual. Thus, the complete domain covered by the author includes brain structures and neu- rotransmitters before, during, and after states of stress, pleasure, social exchanges, behavioral conditioning, and resilience. Evolutionary psychology and evolutionary psychiatry can be defined as the application of Darwinian theories of evo- lution  to  behaviors  of  men  (or  animals).  The  central hypothesis is that many—if not all—behaviors have been selected  because  of  a  survival  advantage.  The  Basic research review by John S. Price on the evolutionary aspects of anxiety (page 223) illustrates this hypothesis, and contains a list of strategies that might have been life- saving in ancient times, but that nowadays only represent unwanted sequelae of hard-wired behavioral tendencies to establish safety. In the modern world, where ritual behaviors play a lesser role than in animal societies and where individuals are overloaded with information, the persistence of all or some of these ancient behavioral ten- dencies might explain some of the clinical symptoms in psychiatry.  The  review  has  been  placed  in  the  Basic research category not because of the results acquired to date, but because this new approach has generated a wealth of research questions that bridge the gap between social behaviors, psychiatric syndromes, and the biology of the brain. The therapeutic and beneficial aspects of the pharmaco- logical treatment were reviewed in the first issue on anxi- ety (see Dialogues in Clinical Neuroscience, 2002, Volume 4, No. 3). In this, the second issue on anxiety, the Phar- macological aspects article discusses dependence on anxiolytic medications. Lisa L. von Moltke and David J. Greenblatt (page 237) document the statements that benzo- diazepines are efficacious, that they are not widely abused, and that tapering the dose towards treatment interruption can be achieved in many patients. The authors underline that a history of addiction should lead to the restriction of benzodiazepine prescriptions. Finally, since selective sero- tonin reuptake inhibitors (SSRIs) are useful in several anxi- ety disorders, the authors confirm that cases of dependence have not been reported. They discuss the discontinuation syndrome, a series of symptoms that follow the abrupt ces- sation of some SSRIs and that can be mistaken for several other conditions in anxious patients. In the Poster, Thérèse Schunck, Gilles Erb, Christian Gilles, Yann Hode, Izzie J. Namer, Hermann Fuder, and Rémy Luthringer give an illustration of the usefulness of functional magnetic resonance imaging (fMRI) to explore the biologi- cal changes in models of anxiety induced in normal subjects (page 246). They used the pharmacological model with cholecystokinin-4 (CCK-4) injection and a behavioral model where the subject is anxious during periods of unpre- dictable transcutaneous electrical stimulations. The authors found that several paralimbic structures are active during anticipatory anxiety in both models. Of interest, they find that the activation of other regions varies according to the phenomenon that the subject anticipates, ie, in the tran- scutaneous electrical stimulation model, brain regions are activated that are known to be related to the physical and the psychological aspects of pain perception. The Clinical research article by Luc Staner (page 249) offers  a  compact  review  of  sleep  physiology  and  an extended analysis of the interactions between anxiety dis- orders and sleep disturbances, showing the high rate of comorbidity. The author reminds us that increased arousal is inherent to anxiety states, whether these are justified or not. He then explains how two components of the stress system, the corticotropin-releasing hormone system and the locus ceruleus noradrenergic system, interact with sleep regulation. The rates of insomnia and hypersomnia increase in all anxiety disorders, but some changes in sleep are specific to given disorders: nocturnal panics in panic disorder, possibly shorter rapid-eye movement (REM) laten- cy in obsessive-compulsive disorder, and recurrent night- mares in posttraumatic stress disorder. The treatment of 2 0 5 I n   t h i s   i s s u e . . .