Pathological Fear Research Articles

Intrinsic functional connectivity of the central extended amygdala.

The central extended amygdala (EAc)-including the bed nucleus of the stria terminalis (BST) and central nucleus of the amygdala (Ce)-plays a critical role in triggering fear and anxiety and is implicated in the development of a range of debilitating neuropsychiatric disorders. Although it is widely believed that these disorders reflect the coordinated activity of distributed neural circuits, the functional architecture of the EAc network and the degree to which the BST and the Ce show distinct patterns of functional connectivity is unclear. Here, we used a novel combination of imaging approaches to trace the connectivity of the BST and the Ce in 130 healthy, racially diverse, community-dwelling adults. Multiband imaging, high-precision registration techniques, and spatially unsmoothed data maximized anatomical specificity. Using newly developed seed regions, whole-brain regression analyses revealed robust functional connectivity between the BST and Ce via the sublenticular extended amygdala, the ribbon of subcortical gray matter encompassing the ventral amygdalofugal pathway. Both regions displayed coupling with the ventromedial prefrontal cortex (vmPFC), midcingulate cortex (MCC), insula, and anterior hippocampus. The BST showed stronger connectivity with the thalamus, striatum, periaqueductal gray, and several prefrontal territories. The only regions showing stronger functional connectivity with the Ce were neighboring regions of the dorsal amygdala, amygdalohippocampal area, and anterior hippocampus. These observations provide a baseline against which to compare a range of special populations, inform our understanding of the role of the EAc in normal and pathological fear and anxiety, and showcase image registration techniques that are likely to be useful for researchers working with "deidentified" neuroimaging data.

Potential of microRNAs as novel targets in the alleviation of pathological fear.

The current treatment of post-traumatic stress disorder (PTSD), phobias and other anxiety disorders, remains insufficient particularly in producing long-lasting full symptom control. Dysfunctional fear processing is common in these disorders, including a deficiency in fear-inhibitory mechanisms and impairment in the ability to discriminate between safety and danger cues. Research has aimed to elucidate brain circuitries, neurotransmitters and downstream signaling pathways important in the alleviation of aberrant fear, with a specific focus on mechanisms modulating fear memory and its behavioral expression. MicroRNAs (miRNA) as "fine tuners" of gene expression at the post-transcriptional level have emerged as critical regulators of such mechanisms important in both, the generation and the inhibition of fear memories. Along these lines, abnormal expression of miRNAs has been associated with different fear-related disorders. After providing an updated overview on the involvement of miRNAs in fear learning mechanisms, we summarize and discuss in particular those studies in which the implication of miRNAs in successful inhibition of fear has been explored. For a better overview, we dissociate the different modes of fear alleviation investigated in this regard and present studies in rodents demonstrating that specific miRNAs are involved in the destabilization of fear by interfering with consolidation/reconsolidation mechanisms or that they are associated with the generation of fear extinction or safety learning. Finally, we discuss the potential of miRNAs as biomarkers and novel therapeutic targets, as well as the challenges involved in applying the discovered mechanisms in the development of improved treatments of fear- and trauma-related disorders.

Pathological Fear of Students in Mathematics: Gender Differences

The study explored the pathological fear in Mathematics of male and female college students. The study utilized the mixed method of research with 199 first year non-Math students as participants to determine the causes, effects, and ways of overcoming this fear. It made use of the cross-sectional design to explore the strategies of overcoming this pathological fear among the students. Results revealed that the students fear Math because of the influence of their friends, personal capacity, and the complex nature of Math. The male and female students differ in the prime cause of pathological fear. The cause as identified for the males is nature of the subject while personal capacity for the females. The students’ fear in Mathematics affects their performance in the subject. The main effect of the students’ fear in Math is recalling what had been learned when preparing for an examination. As a way of overcoming this fear, the female students cited that the teaching of mathematics should be made enjoyable. The male students suggested that they should be taught how mathematics is applied in everyday life situations. The students also need their parents’ support, encouragement, and motivation. On the part of the teachers, the students suggest the use of appropriate teaching strategies to make mathematics learning more meaningful.

Body dysmorphic disorder: Latest neuroanatomical and neuropsychological findings.

Body dysmorphic disorder (BDD) is characterized by a preoccupation with a perceived defect or flaw in physical appearance that is not observable or appears slight to others. It leads to severe distress and functional impairment. Cognitive-behavioural and neurobiological similarities to obsessive compulsive disorder (OCD) have led to its newly conceived classification as an obsessive compulsive related disorder (OCRD). In the process of investigating the neurobiology of BDD, neuroimaging and neuropsychological studies have been conducted. This review presents the most recent research findings and their connection with BDD clinical features. Imaging studies have shown increased total white matter volume and caudate volume asymmetry in BDD patients. These findings are consistent with the striatal topography model of OCRDs. Other studies have showed perfusion deficits in bilateral anterior-medial temporal and occipital regions and asymmetric perfusion in parietal lobes. In addition, correlation between symptom severity and left inferior frontal gyrus volume reflects the degree of detailed, analytic encoding that occurs on day-to-day basis when viewing others and themselves, and that likely underlies their symptoms. Finally, positive correlation between right amygdala volume and symptom severity signifies pathological fear circuitry engagement, hypervigilance and heightened sensitivity to social situations. Neuropsychological studies of BDD reveal deficits in strategic organization, learning and free recall after short and long delays. Executive function deficits are related to spatial working memory and subsequent thinking speed as well as impaired higher level planning ability. BDD patients' organizational strategies tend to focus on detail rather than on larger, global clustering features. They are characterized by abnormal visual processing of both details and global elements, inaccurate processing of global elements and reduced flexibility in switching visual attention between global and local features. Moreover, BDD patients seem to have deficits in identifying facial emotional expressions and they tend to misinterpret expressions of disgust (and others) as anger. Poor insight and ideas of reference, common in BDD, might be related to emotion recognition biases for angry expressions. These findings have been supplemented by combined neuroimaging and neuropsychological studies. Left hemisphere hyperactivity for low and normal spatial frequency face tasks and abnormal activation of the amygdala for high and low spatial frequency face tasks suggests detail encoding and analysis in BDD. Patients may primarily perceive details but they are impaired in their ability to contextualize them holistically.

Neurobiology of fear and specific phobias.

Fear, which can be expressed innately or after conditioning, is triggered when a danger or a stimulus predicting immediate danger is perceived. Its role is to prepare the body to face this danger. However, dysfunction in fear processing can lead to psychiatric disorders in which fear outweighs the danger or possibility of harm. Although recognized as highly debilitating, pathological fear remains insufficiently treated, indicating the importance of research on fear processing. The neurobiological basis of normal and pathological fear reactions is reviewed in this article. Innate and learned fear mechanisms, particularly those involving the amygdala, are considered. These fear mechanisms are also distinguished in specific phobias, which can indeed be nonexperiential (implicating innate, learning-independent mechanisms) or experiential (implicating learning-dependent mechanisms). Poor habituation and poor extinction are presented as dysfunctional mechanisms contributing to persistence of nonexperiential and experiential phobias, respectively.

The Prevalence and Psychological Symptoms of Nomophobia among University Students

T his empirical study investigates the prevalence and symptoms of Nomophobia among university students in Saudi Arabia. An anonymous and self-reported survey was distributed from Feb 2015 to June 2015. Out of around 1800 potential candidates, 335 undergraduate students comprised the study sample. Scores were calculated to assess demographic data and patterns of Smartphone use in terms of duration, frequency, context and purpose. Depression, Anxiety and Stress Scales (DASS) was used to assess the psychological status of the participants, and Nomophobia Questionnaire (NMP-Q) was used to assess the prevalence of Nomophobia dimensions. Statistical analysis and tests were used to identify associations among the study variables and to test the hypotheses. The findings showed that there was a high level of mobile phone involvement, high levels of the Nomophobia dimensions; females were significantly more involved than males with a mean of 3.3 (SD = 0.93) versus 2.8 (SD = 1.05) with a (t = 3.54, p-value < 0.001). The findings also showed a “Mild” level of depression with average score was 8.55 (Z = 0.83) (SD = 3.41, ranging from 1 to 17), a “Normal” level of anxiety with average score was 5.96 (Z = -0.03) (SD = 2.9, ranging from 0 to 12), and a “Normal” level of stress with average score was 6.55 (Z = -1.90) (SD = 4.8, ranging from 0 to 18). Based on the findings, it can be concluded that the duration of use was significant with both mobile phone involvement and psychological health factors. The psychological Health factors using DASS are all correlated significantly with Mobile phone involvement factors. The findings suggest that they way a person interacts with their Smart-device, mainly duration of use, can predict the pathological fear and psychological symptoms caused by modern digital and virtual means.

Genetics of generalized anxiety disorder and related traits

This review serves as a systematic guide to the genetics of generalized anxiety disorder (GAD) and further focuses on anxiety-relevant endophenotypes, such as pathological worry fear of uncertainty, and neuroticism. We inspect clinical genetic evidence for the familialityl heritability of GAD and cross-disorder phenotypes based on family and twin studies. Recent advances of linkage studies, genome-wide association studies, and candidate gene studies (eg, 5-HTT, 5-HT1A, MAOA, BDNF) are outlined. Functional and structural neuroimaging and neurophysiological readouts relating to peripheral stress markers and psychophysiology are further integrated, building a multilevel disease framework. We explore etiologic factors in gene-environment interaction approaches investigating childhood trauma, environmental adversity, and stressful life events in relation to selected candidate genes (5-HTT, NPSR1, COMT, MAOA, CRHR1, RGS2), Additionally, the pharmacogenetics of selective serotonin reuptake inhibitor/serotonin-norepinephrine reuptake inhibitor treatment are summarized (5-HTT, 5-HT2A, COMT, CRHR1). Finally, GAD and trait anxiety research challenges and perspectives in the field of genetics, including epigenetics, are discussed.

Causes and frequency of tocophobia - own experiences.

The phenomenon of tocophobia (pathological fear of labor) has not been fully explored. Currently, there are no diagnostic criteria that would enable its detection or make it recognizable as a disease entity. The aim of study was to determine the degree of anxiety/tocophobia as well as to learn about and analyze the causes of this phenomenon in Polish pregnant women. The prospective study included 120 pregnant women in the third trimester of gestation from February to May 2016. The study was performed with the use of a standardized and revised version of the Labor Anxi-ety Questionnaire (KLP II) designed by Putyński and Paciorek (1997) as well as a proprietary interview questionnaire and structured data documentation form. In 6.7% of the subjects, the level of labor anxiety was very high (> 18 in KLP II). It was the highest in women over 30 years of age (Pearson's chi squared test = 0.00422; p < 0.05). It has been shown that successive childbirths have an im-pact on the degree of anxiety (p = 0.04217).The highest level of anxiety was noted in primiparous women. In 85% of the subjects, anxiety was caused by fear of labor pain. 56.7% of the tested women did not use any professional help in the preparation for childbirth and motherhood. Primiparas and women over 30 years of age experience very high levels of fear significantly more frequently. The lack of proper preparation for childbirth determines the occurrence of tocophobia. Ante-natal classes and prenatal education based on standards of obstetric care should be promoted in order to reduce or eliminate fear of natural labor.

Use of a Brief Fear Memory Reactivation Procedure for Enhancing Exposure Therapy

We tested postretrieval extinction as an augmentation strategy for enhancing in vivo exposure therapy for naturally acquired pathological fear. Participants displaying marked phobic responding to either spiders or snakes were randomized to receive a standard one session in vivo exposure therapy protocol under one of two conditions. The experimental group (RFM-EXP) completed a 10-s fear reactivation procedure 30 min prior to initiating exposure therapy. Controls (EXP-RFM) completed the reactivation procedure after completing exposure therapy. Expected and peak fear during confrontation with live spiders or snakes were collected at pretreatment, posttreatment, and 1-month follow-up. RFM-EXP participants displayed significantly lower phobic responding at the 1-month follow-up relative to EXP-RFM controls. Unexpectedly, RFM-EXP participants showed more rapid fear attenuation during exposure relative to controls. Results provide preliminary support for further investigation of this exposure augmentation strategy across a wider range of anxiety-related disorders.

Hippocampal Contribution to Context Encoding across Development Is Disrupted following Early-Life Adversity.

Context can drastically influence responses to environmental stimuli. For example, a gunshot should provoke a different response at a public park than a shooting range. Little is known about how contextual processing and neural correlates change across human development or about individual differences related to early environmental experiences. Children (N = 60; 8-19 years, 24 exposed to interpersonal violence) completed a context encoding task during fMRI scanning using a delayed match-to-sample design with neutral, happy, and angry facial cues embedded in realistic background scenes. Outside the scanner, participants completed a memory test for context-face pairings. Context memory and neural correlates of context encoding did not vary with age. Larger hippocampal volume was associated with better context memory. Posterior hippocampus was recruited during context encoding, and greater activation in this region predicted better memory for contexts paired with angry faces. Children exposed to violence had poor memory of contexts paired with angry faces, reduced hippocampal volume, and atypical neural recruitment on encoding trials with angry faces, including reduced hippocampal activation and greater functional connectivity between hippocampus and ventrolateral prefrontal cortex (vlPFC). Greater hippocampus-vlPFC connectivity was associated with worse memory for contexts paired with angry faces. Posterior hippocampus appears to support context encoding, a process that does not exhibit age-related variation from middle childhood to late adolescence. Exposure to dangerous environments in childhood is associated with poor context encoding in the presence of threat, likely due to greater vlPFC-dependent attentional narrowing on threat cues at the expense of hippocampus-dependent processing of the broader context.SIGNIFICANCE STATEMENT The ability to use context to guide reactions to environmental stimuli promotes flexible behavior. Remarkably little research has examined how contextual processing changes across development or about influences of the early environment. We provide evidence for posterior hippocampus involvement in context encoding in youth and lack of age-related variation from middle childhood to late adolescence. Children exposed to interpersonal violence exhibited poor memory of contexts paired with angry faces and atypical neural recruitment during context encoding in the presence of threatening facial cues. Heightened attention to threat following violence exposure may come at the expense of encoding contextual information, which may ultimately contribute to pathological fear expressed in safe contexts.

The OptiMUM-study: EMDR therapy in pregnant women with posttraumatic stress disorder after previous childbirth and pregnant women with fear of childbirth: design of a multicentre randomized controlled trial

ABSTRACTBackground: Approximately 3% of women develop posttraumatic stress disorder (PTSD) after giving birth, and 7.5% of pregnant women show a pathological fear of childbirth (FoC). FoC or childbirth-related PTSD during (a subsequent) pregnancy can lead to a request for an elective caesarean section as well as adverse obstetrical and neonatal outcomes. For PTSD in general, and several subtypes of specific phobia, eye movement desensitization and reprocessing (EMDR) therapy has been proven effective, but little is known about the effects of applying EMDR during pregnancy.Objective: To describe the protocol of the OptiMUM-study. The main aim of the study is to determine whether EMDR therapy is an effective and safe treatment for pregnant women with childbirth-related PTSD or FoC. In addition, the cost-effectiveness of this approach will be analysed.Method: The single-blind OptiMUM-study consists of two two-armed randomized controlled trials (RCTs) with overlapping design. In several hospitals and community midwifery practices in Amsterdam, the Netherlands, all eligible pregnant women with a gestational age between eight and 20 weeks will be administered the Wijma delivery expectations questionnaire (WDEQ) to asses FoC. Multiparous women will also receive the PTSD checklist for DSM-5 (PCL-5) to screen for possible PTSD. The clinician administered PTSD scale (CAPS-5) will be used for assessing PTSD according to DSM-5 in women scoring above the PCL-5 cut-off value. Fifty women with childbirth-related PTSD and 120 women with FoC will be randomly allocated to either EMDR therapy carried out by a psychologist or care-as-usual. Women currently undergoing psychological treatment or women younger than 18 years will not be included. Primary outcome measures are severity of childbirth-related PTSD or FoC symptoms. Secondary outcomes are percentage of PTSD diagnoses, percentage caesarean sections, subjective childbirth experience, obstetrical and neonatal complications, and health care costs.Results: The results are meant to provide more insight about the safety and possible effectiveness of EMDR therapy during pregnancy for women with PTSD or FoC.Conclusion: This study is the first RCT studying efficacy and safety of EMDR in pregnant women with PTSD after childbirth or Fear of Childbirth.

Characterization of controlled gamblers and pathological gamblers using the social representation theory

IntroductionIn industrialized countries, gambling disorder tends to become a major issue. The use of the social representation theory provides clues for a better understanding of pathological gamblers. ObjectiveThis paper investigates the representation of risk in a gambling context among lay people (Study 1) and among controlled gamblers and probable pathological gamblers (Study 2). MethodIn the first study, 1106 people answered a free association task based on the target expression ‘risk in a gambling context’. In the second study, a small sample of gamblers, half of them being probable pathological gamblers (based on their score at the SOGS), participated in a semi-structured interview about risk in a gambling context. Interview guidelines were constructed based on the results obtained from Study 1. ResultsIn Study 1, results indicate that the overall representation of risk in a gambling context differs from the one in a general context. The results are interpreted through the prospect theory and the decision-making dual-process model. Results from Study 2 show that, contrarily to those being probable pathological gamblers, controlled gamblers orient their discourse around the notion of pleasure and do not perceive gambling as a threat for their ego. ConclusionControlled gamblers fear to lose money, while probable pathological gamblers fear to lose the game.

Childbirth Fear Influence On Delivery Process And The Choice Of Analgesia Method

Labor, as a life event, is characterized by tremendous physiological and psychological changes that require major behavioral adjustments in a short period of time. These changes may negatively impact the state of the pregnant woman and the fetus and may even complicate pregnancy and childbirth. Clinically significant fear of childbirth is estimated to affect 20-25% of pregnant women and the prevalence of pathological fear is thought to be 6-10%. Objective. To examine the influence of fear of childbirth on the process of delivery and the choice of analgesia. Methods. The study composed of two stages was carried. During the first stage of this study 245 lowrisk pregnant women in their 3rd trimester of pregnancy completed A version of The Wijma Delivery Expectancy/Experience Questionnaire (W-DEQ) and the fear of childbirth was evaluated. During the second stage of the study medical records (including information about the exact time of labor, the beginning of labor, duration of labor, labor progress, mode of delivery, the medicinal pain relief used during delivery) of 189 respondents were examined. Statistical analysis was carried out using SPSS 17.0. Results. Study showed that the majority of respondents (47,8 %) experienced moderate fear, 34,7% respondents suffered from severe fear, 16,3% respondents experienced mild fear, while 1,2% respondents suffered from pathological fear. Severe fear was more common in unemployed, single women and women with lower education. The fear of childbirth intensifies closer to the birth. Statistically significant links between the fear of childbirth and the beginning of spontaneous labor, premature rupture of membranes, induced labor and the use medicinal pain relief have been found. The study could not show an important connection between the mode of delivery and the fear of childbirth. However, respondents who had vacuum delivery were experiencing higher level of fear of childbirth than those respondents who had spontaneous delivery or caesarean section. Conclusions. Pregnant women experience moderate or severe fear of childbirth closer to the birth. Greater fear of childbirth increased the risk of protracted and inducted labor and using medicinal pain relief during the labor. The fear of childbirth is not connected with the mode of delivery.

Fear Erasure Facilitated by Immature Inhibitory Neuron Transplantation

Transplantation of embryonic γ-aminobutyric acid (GABA)ergic neurons has been shown to modify disease phenotypes in rodent models of neurologic and psychiatric disorders. However, whether transplanted interneurons modulate fear memory remains largely unclear. Here, we report that transplantation of embryonic interneurons into the amygdala does not alter host fear memory formation. Yet approximately 2weeks after transplantation, but not earlier or later, extinction training produces a marked reduction in spontaneous recovery and renewal of fear response. Further analyses reveal that transplanted interneurons robustly form functional synapses with neurons of the host amygdala and exhibit similar developmental maturation in electrophysiological properties as native amygdala interneurons. Importantly, transplanted immature interneurons reduce the expression of perineuronal nets, promote long-term synaptic plasticity, and modulate both excitatory and inhibitory synaptic transmissions ofthe host circuits. Our findings demonstrate that transplanted immature interneurons modify amygdala circuitry and suggest a previously unknown strategy for the prevention of extinction-resistant pathological fear.

Infralimbic Neurotrophin-3 Infusion Rescues Fear Extinction Impairment in a Mouse Model of Pathological Fear.

The inability to properly extinguish fear memories constitutes the foundation of several anxiety disorders, including panic disorder. Recent findings show that boosting prefrontal cortex synaptic plasticity potentiates fear extinction, suggesting that therapies that augment synaptic plasticity could prove useful in rescue of fear extinction impairments in this group of disorders. Previously, we reported that mice with selective deregulation of neurotrophic tyrosine kinase receptor, type 3 expression (TgNTRK3) exhibit increased fear memories accompanied by impaired extinction, congruent with an altered activation pattern of the amygdala-hippocampus-medial prefrontal cortex fear circuit. Here we explore the specific role of neurotrophin 3 and its cognate receptor in the medial prefrontal cortex, and its involvement in fear extinction in a pathological context. In this study we combined molecular, behavioral, in vivo pharmacology and ex vivo electrophysiological recordings in TgNTRK3 animals during contextual fear extinction processes. We show that neurotrophin 3 protein levels are increased upon contextual fear extinction in wild-type animals but not in TgNTRK3 mice, which present deficits in infralimbic long-term potentiation. Importantly, infusion of neurotrophin 3 to the medial prefrontal cortex of TgNTRK3 mice rescues contextual fear extinction and ex vivo local application improves medial prefrontal cortex synaptic plasticity. This effect is blocked by inhibition of extracellular signal-regulated kinase phosphorylation through peripheral administration of SL327, suggesting that rescue occurs via this pathway. Our results suggest that stimulating neurotrophin 3-dependent medial prefrontal cortex plasticity could restore contextual fear extinction deficit in pathological fear and could constitute an effective treatment for fear-related disorders.

Editorial: Extinction Learning from a Mechanistic and Systems Perspective.

Editorial: Extinction Learning from a Mechanistic and Systems Perspective.

Dynamic changes in neural circuitry during adolescence are associated with persistent attenuation of fear memories.

Fear can be highly adaptive in promoting survival, yet it can also be detrimental when it persists long after a threat has passed. Flexibility of the fear response may be most advantageous during adolescence when animals are prone to explore novel, potentially threatening environments. Two opposing adolescent fear-related behaviours—diminished extinction of cued fear and suppressed expression of contextual fear—may serve this purpose, but the neural basis underlying these changes is unknown. Using microprisms to image prefrontal cortical spine maturation across development, we identify dynamic BLA-hippocampal-mPFC circuit reorganization associated with these behavioural shifts. Exploiting this sensitive period of neural development, we modified existing behavioural interventions in an age-specific manner to attenuate adolescent fear memories persistently into adulthood. These findings identify novel strategies that leverage dynamic neurodevelopmental changes during adolescence with the potential to extinguish pathological fears implicated in anxiety and stress-related disorders.

I’m really fat!

Introduction The eating disorders are changes in eating behaviour associated with distortions in the self-concept and self-image, pathological fear of getting fat, morbid motivation for thinness and changes in appetite and its control, with or without compensatory attitudes. In the DSM-5 and in the CID-10, the two fundamental diagnostics are anorexia nervosa and bulimia nervosa. Purpose Characterization of the Portuguese population concerning eating disorders incidence. Methods Bibliographic revision through Pubmed until 2013, using the keywords: anorexia nervosa, bulimia nervosa, eating disorders. Psychometric instruments like the Eating Disorder Examination 12th version (Cooper and Fairburn, 1987), Eating Attitudes Test/EAT-25 (Garner e Garfinkel, 1979) and the Eating Disorder Inventory (Garner et al., 1983; Machado et al., 2001) contributed for the characterization of the Eating Disorders in the Portuguese population. Results The Eating Disorders have a higher incidence in the young Caucasian woman, living in the urban area. The combination of the restrictive diet with intense physical exercise in the anorexia nervosa very often evolves with negative emotions. The emotional instability, namely the dysphoria, the anxiety and the sleep pattern changes are frequent. The bulimia nervosa initially manifests itself by restrictive diet, which evolves to excessive food intake episodes getting increasingly frequent and intense. Conclusions The Eating Disorders come from the gene-environment interaction and risk premorbid biological and psychological changes may result. These are inseparable from the interaction with the social context where the epigenetic mechanisms may play an important role. The reason for thinness, limitations at the level of interoception and obsessive-compulsive character traits are predisposing factors.

Applying Research Domain Criteria (RDoC) to the study of fear and anxiety: A critical comment.

The goal of the Research Domain Criteria (RDoC) is to develop an interdisciplinary science of psychopathology, forming a template for research and disconnecting conceptual and empirical questions from traditional diagnostic entities. In this article, we review some of the challenges in the implementation of this framework within the field of pathological fear and anxiety, specifically commenting on the article by Hamm and colleagues (2016). The study of pathological fear and anxiety has had considerable, yet stalled, success in its understanding of underlying mechanisms, prevention, and treatment. With a shift toward RDoC, it is unclear what to do with the existing diagnostic labels, and the importance of defining and measuring phenotypes becomes paramount. Additional concerns include the role of psychological constructs and mechanisms, the use of self-report measures, the examination of replication and clinical utility, and the measurement of the role of the environment. Though a laudable and potentially necessary shift in focus, it remains to be seen whether new overall insights into psychopathology will emerge from focusing on small units of analyses and piecing them together and whether these insights will directly translate into the prevention of psychopathology, more efficacious treatments, and improved lives of patients.

Efficacy and Tolerability of Pregabalin vs Sertralin in Generalised Anxiety Disorder Concise Communication

Copyright: © 2015 Cvjetkovic-Bosnjak M. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Generalised Anxiety Disorder(GAD) represent a chronic mental illness characterized with pathological fear,extremely persistant worry usually about minor everyday problems and with numerous of vegetative symptoms [1-17]. It represent difficult problem in Mental Health,as life occurance of GAD is 5-7% Symptoms of GAD, according to ICD-X and DSM-V even today can be misdiagnosed, and unadeqvatelly treated [8-24] . If the symptoms are long lasting and untreated, often comorbidity with depression,alcohol abuse,and high suicidality level make extremely serious mental problem [2-9]. GAD interfered significantly with everyday activities and causes substantional personall distres so proper diagnosis and adeqvate treatment have to become priority in medical practice. WFSBP (World Federation of Societes of Biological Psychiatry) recommend SSRI (Selective Serotonin Reutake Inhibitors), SNRI (Serotonin and Norepinefrin Reuptake Inhibiors) and pregabaline, atypical anxiolytc as first line treatment, in combination with psychotherapy [7-19]. In present study, efficacy and tolerability of pregabaline vs.sertraline in patient with diagnoses of GAD was observed.The study included 107 in-patients age 20-60,both gender. Duration of disorder was in average of 4,7+0,3 years in group of patients treated with sertraline and about 4,6+0,4 in group treated with pregabalin.In previous episodes, 98% of all included patients were treated with SSRI and SNRI, in adeqvately therapeutical doses. Actually, patients were admitted in daily treatment due to new episode of GAD. In included patients, washup period was one week. At the begining of the study, all patients were reqvired to have a Covi Anxiety Scale, total score >9 and total score on HAMA (Hamilton Anxiety Scale) >20.In first group, patients were treated with sertraline, (doses began from 50 mg up to mean value of 150 mg/die). Doses was titrated during one week.In second group patient were treated with pregabalin, doses at first day were 75 mg, and titrated to 225 mg/die during one week. In all included patients cognitive-behavioral therapy ,individual and group was performed, during investigation. The primary analysis was change in Hamilton Raiting Scale for Anxiety (HAMA), a total score from baseline to endpoint. Secondary indicator of efficacy was change in HAMA psychic (emotional) and somatic (physical) scores weekly till endpoint. Global clinical assessment was conducted by using the Clinical Global Impression change raiting (CGI).