CNS spectrums Journal Impact Factor & Information

Publisher: International Neuropsychiatric Assoc, Cambridge University Press (CUP)

Journal description

CNS Spectrums is a monthly Index Medicus/MEDLINE journal designed to bridge the clinical information needs of 48,000 psychiatrists and neurologists. Introduced in 1996, CNS Spectrums reaches more physicians than any other peer-reviewed neuropsychiatric journal in the world. CNS Spectrums' editorial mission is to address relevant neuropsychiatric topics, including the prevalence of comorbid diseases among patients, and original research and reports that emphasize the profound diagnostic and physiologic connections made within the neurologic and psychiatric fields. The journal's goal is to serve as a resource to psychiatrists and neurologists seeking to understand and treat disturbances of cognition, emotion, and behavior as a direct consequence of central nervous system disease, illness, or trauma.

Current impact factor: 2.71

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.71
2013 Impact Factor 1.304
2012 Impact Factor 1.727
2011 Impact Factor 2.197
2010 Impact Factor 2.667
2009 Impact Factor 2.197
2008 Impact Factor 1.974
2007 Impact Factor 2.222
2006 Impact Factor 2.051
2005 Impact Factor 2.037

Impact factor over time

Impact factor

Additional details

5-year impact 2.38
Cited half-life 7.10
Immediacy index 0.87
Eigenfactor 0.00
Article influence 0.65
Website CNS Spectrums website
Other titles CNS spectrums, International journal of neuropsychiatric medicine
ISSN 1092-8529
OCLC 36426249
Material type Periodical
Document type Journal / Magazine / Newspaper

Publisher details

Cambridge University Press (CUP)

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Author's Pre-print on author's personal website, departmental website, social media websites, institutional repository, non-commercial subject-based repositories, such as PubMed Central, Europe PMC or arXiv
    • Author's post-print on author's personal website on acceptance of publication
    • Author's post-print on departmental website, institutional repository, non-commercial subject-based repositories, such as PubMed Central, Europe PMC or arXiv, after a 6 months embargo
    • Publisher's version/PDF cannot be used
    • Published abstract may be deposited
    • Pre-print to record acceptance for publication
    • Publisher copyright and source must be acknowledged with set statement
    • Must link to publisher version
    • Publisher last reviewed on 07/10/2014
    • This policy is an exception to the default policies of 'Cambridge University Press (CUP)'
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Binge eating disorder (BED) is the most common of eating disorders and is characterized by excessive, out-of-control, rapid food intake. This review focuses on cognitive impairments in BED, which represent an endophenotype that mediates brain function and behavior. Here we focus on reviewing impulsivity, compulsivity, attentional biases to food cues, and executive function. Behavioral regulation in BED appears to be influenced by the context of motivationally salient food cues and the degree of obesity. Deficits in delay discounting and risk taking under ambiguity are impaired in obesity irrespective of BED status. However, in BED subjects with milder obesity, greater risk seeking under explicit probabilistic risk is observed to monetary rewards, whereas this shifts to risk aversion and enhanced delay discounting in more severe obesity. Relative to non-BED obese subjects, BED is characterized by enhanced behavioral inflexibility or compulsivity across multiple domains, with subjects selecting the same choices despite change in relevance (set shifting), being no longer rewarding (habit formation), or irrespective of outcome (perseveration). The context of food cues was associated with multiple attentional and early and late inhibitory impairments and enhanced memory bias, although BED patients also have generalized cognitive interference in working memory. These findings may help explain the phenotype of binge eating. Motivationally salient food cues provoke attentional and memory biases along with impairing response inhibitory processes. Those with BED are also more susceptible to cognitive interference and have impaired decisional impulsivity, with the tendency to inflexibly stick with the same choices irrespective of changes in context. These findings suggest critical cognitive domains that may guide therapeutic interventions.
    CNS spectrums 12/2015; 20(06):566-573. DOI:10.1017/S1092852915000681
  • [Show abstract] [Hide abstract]
    ABSTRACT: We performed a qualitative review of treatment studies of binge eating disorder (BED), focusing on randomized clinical trials (RCTs). Limited effectiveness has been demonstrated for self-help strategies, and substantial effectiveness has been shown for cognitive behavioral therapy (CBT) and interpersonal therapy (IPT). CBT and IPT may each be more effective than behavior weight loss therapy (BWLT) for reducing binge eating over the long term. The stimulant pro-drug lisdexamfetamine dimesylate (LDX) is the only drug approved by the FDA for the treatment of BED in adults based on 2 pivotal RCTs. Topiramate also decreases binge eating behavior, but its use is limited by its adverse event profile. Antidepressants may be modestly effective over the short term for reducing binge eating behavior and comorbid depressive symptoms, but are not associated with clinically significant weight loss. A RCT presented in abstract form suggests that intranasal naloxone may decrease time spent binge eating. There is no RCT of obesity surgery in BED, but many patients with BED seek and receive such surgery. While some studies suggest patients with BED and obesity do just as well as patients with obesity alone, other studies suggest that patients with BED have more post-operative complications, less weight loss, and more weight regain. This evidence suggests that patients with BED would benefit from receiving highly individualized treatment.
    CNS spectrums 12/2015; 20(06):546-556. DOI:10.1017/S1092852915000759

  • CNS spectrums 12/2015; 20(06):520-521. DOI:10.1017/S109285291500067X
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    ABSTRACT: Objective Antidepressants are frequently associated with treatment-emergent sexual dysfunction (TESD). Vortioxetine, which was approved for patients with major depressive disorder (MDD), has a receptor profile that suggests limited impact on sexual functioning. Methods Arizona Sexual Experiences Scale (ASEX) patient-level data were pooled from 7 short-term vortioxetine trials (6 in MDD, 1 in generalized anxiety disorder) and analyzed for incidence of TESD at any post-baseline visit in patients without sexual dysfunction at baseline (defined as ASEX total score ≥19; individual ASEX item score ≥5; or a score ≥4 on any 3 ASEX items). The primary objective was to confirm the non-inferiority of vortioxetine 5–20 mg/day to placebo on the incidence of TESD. Comparisons were based on the common risk difference (95% confidence interval). Additional analyses compared vortioxetine to duloxetine and duloxetine to placebo. A sensitivity analysis, defined as TESD at 2 consecutive post-baseline visits, was conducted. Results TESD incidence, relative to placebo, generally increased with vortioxetine dose with vortioxetine 5 mg non-inferior to placebo. Vortioxetine 10, 15, and 20 mg did not meet the non-inferiority criterion, but no dose had a significantly higher risk of developing TESD versus placebo. Changes in ASEX individual item scores supported the similarity of vortioxetine doses to placebo. Significantly higher TESD risk occurred with duloxetine 60 mg/day versus placebo and versus vortioxetine 5 or 10 mg. The sensitivity analysis was generally consistent with the primary analysis. Rates of spontaneously reported sexual adverse events were low. Conclusions Vortioxetine was associated with rates of TESD that were not significantly different from placebo in short-term clinical trials.
    CNS spectrums 11/2015; DOI:10.1017/S1092852915000553

  • CNS spectrums 11/2015; DOI:10.1017/S1092852915000541
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    ABSTRACT: Biobehavioral features associated with binge-eating disorder (BED) have been investigated; however, few systematic reviews to date have described neuroimaging findings from studies of BED. Emerging functional and structural studies support BED as having unique and overlapping neural features as compared with other disorders. Neuroimaging studies provide evidence linking heightened responses to palatable food cues with prefrontal areas, particularly the orbitofrontal cortex (OFC), with specific relationships to hunger and reward-sensitivity measures. While few studies to date have investigated non-food-cue responses; these suggest a generalized hypofunctioning in frontostriatal areas during reward and inhibitory control processes. Early studies applying neuroimaging to treatment efforts suggest that targeting neural function underlying motivational processes may prove important in the treatment of BED.
    CNS spectrums 11/2015; DOI:10.1017/S1092852915000814
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    ABSTRACT: Obesity has reached epidemic prevalence, and much research has focused on homeostatic and nonhomeostatic mechanisms underlying overconsumption of food. Mesocorticolimbic circuitry, including dopamine neurons of the ventral tegmental area (VTA), is a key substrate for nonhomeostatic feeding. The goal of the present review is to compare changes in mesolimbic dopamine function in human obesity with diet-induced obesity in rodents. Additionally, we will review the literature to determine if dopamine signaling is altered with binge eating disorder in humans or binge eating modeled in rodents. Finally, we assess modulation of dopamine neurons by neuropeptides and peripheral peptidergic signals that occur with obesity or binge eating. We find that while decreased dopamine concentration is observed with obesity, there is inconsistency outside the human literature on the relationship between striatal D 2 receptor expression and obesity. Finally, few studies have explored how orexigenic or anorexigenic peptides modulate dopamine neuronal activity or striatal dopamine in obese models. However, ghrelin modulation of dopamine neurons may be an important factor for driving binge feeding in rodents.
    CNS spectrums 10/2015; DOI:10.1017/S1092852915000693
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    ABSTRACT: Binge eating is seen across the spectrum of eating disorder diagnoses as well as among individuals who do not meet diagnostic criteria. Analyses of the specific types of foods that are frequently binged upon reveal that sugar-rich items feature prominently in binge-type meals, making the effects of binge consumption of sugar an important focus of study. One avenue to do this involves the use of animal models. Foundational and recent studies of animal models of sugar bingeing, both outlined here, lend insight into the various neurotransmitters and neuropeptides that may participate in or be altered by this behavior. Further, several preclinical studies incorporating sugar bingeing paradigms have explored the utility of pharmacological agents that target such neural systems for reducing sugar bingeing in an effort to enhance clinical treatment. Indeed, the translational implications of findings generated using animal models of sugar bingeing are considered here, along with potential avenues for further study.
    CNS spectrums 10/2015; DOI:10.1017/S1092852915000656
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: Dextromethorphan (DM)/quinidine (Q) is an approved treatment for pseudobulbar affect (PBA) based on trials in amyotrophic lateral sclerosis or multiple sclerosis. PRISM II evaluated DM/Q effectiveness and tolerability for PBA secondary to dementia, stroke, or traumatic brain injury; dementia cohort results are reported. Methods: This was an open-label, multicenter, 90 day trial; patients received DM/Q 20/10 mg twice daily. Primary outcome was change in Center for Neurologic Study-Lability Scale (CNS-LS) score. Secondary outcomes included PBA episode count and Clinical and Patient/Caregiver Global Impression of Change scores with respect to PBA (CGI-C/PGI-C). Results: 134 patients were treated. CNS-LS improved by a mean (SD) of 7.2 (6.0) points at Day 90/Endpoint (P<.001) vs. baseline. PBA episodes were reduced 67.7% (P<.001) vs. baseline; global measures showed 77.5% CGI-C and 76.5% PGI-C "much"/"very much" improved. Adverse events included headache (7.5%), urinary tract infection (4.5%), and diarrhea (3.7%); few patients dropped out for adverse events (10.4%). Conclusions: DM/Q significantly reduced PBA symptoms in patients with dementia; reported adverse events were consistent with the known safety profile of DM/Q. Trial Registration identifier: NCT01799941.
    CNS spectrums 10/2015; DOI:10.1017/S1092852915000620

  • CNS spectrums 10/2015; 20(5):466-468. DOI:10.1017/S1092852915000607
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    ABSTRACT: Introduction Behavioral addictions refer to repeated dysfunctional behaviors that do not involve the ingestion of addictive substances. Studies on the association between behavioral addictions and personality traits have noted in individuals with problematic behaviors a high proclivity toward impulsivity and sensation-seeking and a low predisposition to harm avoidance. The majority of these studies have focused on adults, while far fewer have involved adolescents. The study population was 109 high school students (age range 15-18 years) in Turin, Italy. Participants completed an assessment that comprised a demographic questionnaire and 3 self-report questionnaires: the Shorter PROMIS Questionnaire (SPQ), the Internet Addiction Test (IAT), and the Multidimensional Questionnaire for Adolescents (QMA). A gender-related difference in the risk of developing an addictive behavior was observed, with a significantly higher percentage of risk seen for several addiction tendencies among the males. Statistically significant correlations emerged between some personality determinants and certain addictive behaviors. Discussion The study pinpoints epidemiological indicators for the extent of this growing problem among adolescents. The findings have implications for identifying protection factors and risk factors for addictive behaviors and related psychiatric disorders, and the development of primary prevention strategies derived from such factors.
    CNS spectrums 08/2015; -1:1-7. DOI:10.1017/S1092852915000474