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Dive into the research topics where C. Mancini is active.

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Featured researches published by C. Mancini.


Depression and Anxiety | 2009

Childhood maltreatment linked to greater symptom severity and poorer quality of life and function in social anxiety disorder.

Naomi M. Simon; Nannette N. Herlands; Elizabeth H. Marks; C. Mancini; Andrea Letamendi; Zhonghe Li; Mark H. Pollack; Michael Van Ameringen; Murray B. Stein

Background: There is a paucity of data examining the prevalence and impact of childhood maltreatment in patients presenting with a primary diagnosis of social anxiety disorder (SAD). We thus examined the presence of a broad spectrum of childhood maltreatment, including physical, sexual, and emotional abuse and neglect, in treatment‐seeking individuals with the generalized subtype of SAD (GSAD). We hypothesized that a history of childhood maltreatment would be associated with greater SAD symptom severity and poorer associated function. Methods: One hundred and three participants with a primary diagnosis of GSAD (mean age 37±14; 70% male) completed the well‐validated, self‐rated Childhood Trauma Questionnaire (CTQ), as well as measures of SAD symptom severity and quality of life. Results: Fully 70% (n=72) of the GSAD sample met severity criteria for at least one type of childhood abuse or neglect as measured by the CTQ subscales using previously established thresholds. CTQ total score adjusted for age and gender was associated with greater SAD severity, and poorer quality of life, function, and resilience. Further, the number of types of maltreatment present had an additive effect, with specific associations for emotional abuse and neglect with SAD severity. Conclusions: Despite the use of validated assessments, our findings are limited by the retrospective and subjective nature of self‐report measures used to assess childhood maltreatment. Nonetheless, these data suggest a high rate of childhood maltreatment in individuals seeking treatment for GSAD, and the association of maltreatment with greater disorder severity suggests that screening is clinically prudent. Depression and Anxiety 26:1027–1032, 2009.


Expert Opinion on Investigational Drugs | 2000

Drugs in development for social anxiety disorder: more to social anxiety than meets the SSRI

Michael Van Ameringen; C. Mancini; Peter Farvolden; Jonathan Oakman

Individuals with social phobia (SP) fear and avoid a wide variety of social and performance situations in which they are exposed to unfamiliar persons or to possible scrutiny by others. The lifetime prevalence of SP is estimated to be as high as 13%. It is frequently co-morbid with and usually precedes the onset of other psychiatric illnesses and is associated with significant occupational and social impairment, including academic and vocational underachievement. Fortunately, there are effective treatments for this common and debilitating condition. There is currently considerable evidence for the efficacy of pharmacotherapy and especially the monoamine oxidase inhibitors (MAOIs) and selective serotonin re-uptake inhibitors (SSRIs) in the treatment of this disorder. However, SSRIs are generally preferred as the first-line treatment of choice due to the advantages of SSRIs over MAOIs in terms of safety and tolerability. Despite encouraging results, current treatments most often produce partial symptomatic improvement, rather than high end-state functioning. While current first line treatments for social phobia target the serotonergic system, it is important to remember that different social fears are likely to have different developmental roots and may be based on quite different neurobiological systems. In this article we provide a review of current pharmacotherapeutic options for SP, current knowledge of the neurobiology of SP, and a review of new and promising directions in pharmacological research. It is increasingly clear that serotonin (5-HT) is unlikely to be the whole story in SP and that other brain chemical systems, especially the dopaminergic, noradrenaline-corticotropin releasing hormone and γ-aminobutyric acid (GABA) dependent systems, most probably have an important role to play in a substantial percentage of cases. A number of new and novel agents, including the substance P antagonists, GABA agonists and CRF antagonists show considerable promise in the treatment of SP. However, in order to enhance the understanding of the neurobiology and treatment response of SP, we need to develop more sophisticated theory-driven typologies of SP.


Journal of Affective Disorders | 2002

Does SSRI augmentation with antidepressants that influence noradrenergic function resolve depression in obsessive–compulsive disorder?

C. Mancini; Michael Van Ameringen; Peter Farvolden

BACKGROUNDnObsessive compulsive disorder (OCD) often coexists with major depressive disorder (MDD). Serotonergic antidepressant medications have emerged as the treatment of choice for both OCD and MDD. In the usual course of events, both the patients OCD and depressive symptoms improve in parallel following initiation of serotonin reuptake inhibitor (SRI) treatment for OCD. However, such is not always the case. We report here on a series of ten patients whose OCD but not depression improved following a trial of SRI therapy.nnnMETHODnTen patients with OCD and comorbid MDD who experienced a worsening or exacerbation of depressive symptoms while being maintained on an adequate dose of SRI therapy were treated using a combination of SRIs and agents with effects on noradrenergic reuptake. Response to treatment was based on clinician-ratings of severity and improvement of OCD and MDD (CGI-S and CGI-I).nnnRESULTSnFollowing augmentation, nine of the ten patients had a significant improvement/resolution of their MDD, with little further change in the severity of their OCD.nnnLIMITATIONSnInferences from the results of this study are limited by the lack of a control group, the small sample size, and the use of nonstandardized ratings as measures of symptom severity.nnnCONCLUSIONSnThese results are of practical significance to clinicians insofar as they suggest a possible guideline to clinicians treating depression in OCD with SSRIs without success.


International Journal of Neuroscience | 2007

BEHAVIORAL AND PSYCHOPHYSIOLOGICAL CHARACTERISTICS OF CHILDREN OF PARENTS WITH SOCIAL PHOBIA: A PILOT STUDY

Mira J. Campbell; Louis A. Schmidt; Diane L. Santesso; Michael Van Ameringen; C. Mancini; Jonathan M. Oakman

Recent studies have noted a relation between the pattern of resting frontal EEG activity and individual differences in affective style in typically developing infants, children, and adults. The authors conducted a pilot study to investigate the pattern of frontal EEG activity during a resting condition (eyes-open, eyes-closed) in a group of children who had one parent clinically diagnosed with social phobia (SP; n = 6) and in a group of typically developing children of similar age with healthy parents (n = 7). Patients with a primary DSM-IV diagnosis of SP with at least one biological child were recruited from the Anxiety Disorders Clinic at McMaster University Medical Centre. We found that children of parents clinically diagnosed with SP tended to exhibit higher overall resting frontal EEG activity compared with the children of healthy parents. This pattern of overall high EEG activity that is specific to the frontal region is similar to that observed in socially anxious profiles. Preliminary findings are discussed in terms of how overall resting frontal brain activation may be an early psychophysiological marker for placing children of parents with social phobia at risk for socioemotional problems before such problems emerge.


Biological Psychiatry | 1998

101. A pilot study of PET in social phobia

M. Van Ameringen; C. Mancini; Jonathan M. Oakman; M. Kamath; Claude Nahmias; Henry Szechtman

bydorsolateral prefrontalcortexardor its relatedsubcortical circuitry.For instance,duringantiaaccadetaskssubjectsarerequiredto lookto themirror imageof a cue(Sameamplitude, oppositedirection). SCbiZO#rrenia p tients andtheirrelativesgenerateanincreasedproportionof errorstowardthecue (McDowell8cClementz,1997).Patientswith lesionsof dorsolateral prefrontalmrtex,butnotthosewithlesionsofothercorticalregions(including frontaland parietaleye fields;Pierrot-Deseilligny, Rivaud Gaymardt% A@&1991)also generatean increasedproportionof errors.To evaluate whetherantiaaccadeperformanceis associatedwithprefrontal cortexactivity, we presentedsubjectswithfixtion, proaaccade, andandsacmdetasks whilecollectingfunctionalmagnetic” [email protected] subjectsweretestedwhhfour5minuteblocksofalternatm “ g40 secondtlisk (saccadekmtisaccade, fixationkacadc,tixationhrhaccade,saccaddantisaccade).whole head images(12 slices,8mmthickness,TR=3 see) were collectedusinga 1.5Tesla magnet.Activationof prefrontal,motor,and parietalcortexwasobservedin all subjectsduringsaccadetasks.Thisis the expectedpatternof results.Thesefindingssuggesthatstudyingschizophrenia patientsusing this paradigmwill help identifythe neuroanatornicrd correlatesof the illness.


Expert Opinion on Pharmacotherapy | 2005

An evaluation of paroxetine in generalised social anxiety disorder.

Michael Van Ameringen; C. Mancini; Beth Patterson; Mark Bennett

It is estimated that social anxiety disorder affects ∼ 13.3% individuals within the community at some point in their lifetime and is associated with significant functional impairment. A variety of drug groups have demonstrated efficacy in treating social anxiety disorder, including selective serotonin reuptake inhibitors (SSRIs). Paroxetine is an SSRI approved by the FDA and Health Canada for the treatment of a variety of psychiatric conditions. Paroxetine has been the most studied agent in social anxiety disorder and has been shown to be effective in short-term, fixed- and flexible-dose placebo-controlled trials, as well as in long-term treatment. The pharmacotherapy of social phobia will be reviewed, with a special focus on investigations with paroxet-ine.


Current Psychiatry Reports | 2000

The neurobiology of social phobia: from pharmacotherapy to brain imaging.

Michael Van Ameringen; C. Mancini; Peter Farvolden; Jonathan M. Oakman


European Neuropsychopharmacology | 2006

P.4.a.008 A randomized placebo controlled trial of olanzapine in trichotillomania

M. Van Ameringen; C. Mancini; Beth Patterson; Mark Bennett; Jonathan M. Oakman


European Neuropsychopharmacology | 2002

Predictors of remission in patients treated with sertraline for moderate to severe generalized social phobia

M. Van Ameringen; C. Mancini; H. Chung; E. Batzar; R. Yang


European Neuropsychopharmacology | 2011

P.4.b.005 Panic attacks and generalised anxiety disorder

M. Van Ameringen; C. Mancini; W. Simpson; Beth Patterson

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Peter Farvolden

McMaster University Medical Centre

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W. Simpson

McMaster University Medical Centre

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Mark Bennett

McMaster University Medical Centre

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