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4 results

  • The neurobiology of obsessive–compulsive personality disorder: a systematic review

  • Clara Marincowitz, Christine Lochner, Dan J. Stein
  • Journal:
    CNS Spectrums / Volume 27 / Issue 6 / December 2022
    Published online by Cambridge University Press:
    11 August 2021, pp. 664-675
  • Background

    A number of recent investigations have focused on the neurobiology of obsessive–compulsive personality disorder (OCPD). However, there have been few reviews of this literature with no detailed model proposed. We therefore undertook a systematic review of these investigations, aiming to map the available evidence and investigate whether it is possible to formulate a detailed model of the neurobiology of OCPD.

    Methods

    OCPD can be considered from both categorical and dimensional perspectives. An electronic search was therefore conducted using terms that would address not only OCPD as a category, but also related constructs, such as perfectionism, that would capture research on neuropsychology, neuroimaging, neurochemistry, and neurogenetics.

    Results

    A total of 1059 articles were retrieved, with 87 ultimately selected for abstract screening, resulting in a final selection of 49 articles focusing on neurobiological investigations relevant to OCPD. Impaired executive function and cognitive inflexibility are common neuropsychological traits in this condition, and suggest that obsessive–compulsive disorder (OCD) and OCPD may lie on a continuum. However, neuroimaging studies in OCPD indicate the involvement of specific neurocircuitry, including the precuneus and amygdala, and so suggest that OCD and OCPD may have important differences. Although OCPD has a heritable component, we found no well-powered genetic studies of OCPD.

    Conclusion

    Although knowledge in this area has advanced, there are insufficient data on which to base a comprehensive model of the neurobiology of OCPD. Given the clinical importance of OCPD, further work to understand the mechanisms that underpin this condition is warranted.

  • The psychosis risk timeline: can we improve our preventive strategies? Part 3: primary common pathways and preventive strategies

  • Karen Romain, Alexandra Eriksson, Richard Onyon, Manoj Kumar
  • Journal:
    BJPsych Advances / Volume 25 / Issue 5 / September 2019
    Published online by Cambridge University Press:
    21 June 2019, pp. 321-332
    Print publication:
    September 2019
    • Article
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  • Psychosis is a recognised feature of several psychiatric disorders and it causes patients significant distress and morbidity. It is therefore important to keep knowledge of possible risk factors for psychosis up to date and to have an overview model on which further learning can be structured. This article concludes a three-part series. It gives a review of evidence regarding common pathways by which many risk factors come together to influence the development of psychosis and finalises our suggested overview model, a psychosis risk timeline. The three primary pathways considered are based on the major themes identified in this narrative review of recent literature and they focus on neurological, neurochemical and inflammatory changes. We link each back to the factors discussed in the first and second parts of this series that alter psychosis risk through different mechanisms and at different stages throughout life. We then consider and summarise key aspects of this complex topic with the aim of providing current and future clinicians with a model on which to build their knowledge and begin to access and understand current psychosis research and implications for future preventive work.

    LEARNING OBJECTIVES

    After reading this article you will be able to:

    • • give an overview of common pathways thought to link identified risk factors with psychosis development

    • • understand neurochemical, neurostructural and inflammatory changes associated with psychosis

    • • demonstrate increased knowledge of possible preventive strategies.

    DECLARATION OF INTEREST

    None.

  • Magnetic resonance spectroscopy in anxiety disorders

  • Clarissa Trzesniak, David Araújo, José Alexandre S. Crippa
  • Journal:
    Acta Neuropsychiatrica / Volume 20 / Issue 2 / April 2008
    Published online by Cambridge University Press:
    24 June 2014, pp. 56-71
  • Objective:

    Magnetic resonance spectroscopy (MRS) is a non-invasive in vivo method used to quantify metabolites that are relevant to a wide range of brain processes. This paper briefly describes neuroimaging using MRS and provides a systematic review of its application to anxiety disorders.

    Method:

    A literature review was performed in the PubMed, Lilacs and Scielo databases using the keywords spectroscopy and anxiety disorder. References of selected articles were also hand-searched for additional citations.

    Results:

    Recent studies have shown that there are significant metabolic differences between patients with anxiety disorders and healthy controls in various regions of the brain. Changes were mainly found in N-acetylaspartate, which is associated with neuronal viability, but some of them were also seen in creatine, a substance that is thought to be relatively constant among individuals with different pathological conditions.

    Conclusions:

    MRS is a sophisticated neuroimaging technique that has provided useful insights into the biochemical and neurobiological basis of many anxiety disorders. Nevertheless, its utilization in some anxiety disorders is still modest, particularly social phobia and generalised anxiety. Although it is an extremely useful advance in neuroimaging, further research in other brain areas and patient populations is highly advisable.

  • Chapter 10 - Sleep deprivation: biomarkers for identifying and predicting individual differences in response to sleep loss

  • from Section 2 - Sleep Disorders and Excessive Sleepiness
  • Edited by Michael J. Thorpy, Michel Billiard
  • Book:
    Sleepiness
    Published online:
    04 February 2011
    Print publication:
    27 January 2011, pp 101-110

  • Summary

    This chapter discusses the neurochemistry of excessive daytime sleepiness (EDS) with various etiologies. It presents a brief discussion of basic sleep physiology and narcolepsy symptoms to explain the specific neurochemistry of hypersomnia. The significant roles hypocretin deficiency and postnatal cell death of hypocretin neurons as the major pathophysiological process underlying narcolepsy with cataplexy emerged from a decade of investigation, employing both animal and human models. The chapter talks about idiopathic hypersomnia and hypocretin non-deficient primary hypersomnia. It explains how hypocretin ligand deficiency may cause narcolepsy phenotype. Narcolepsy symptoms can also occur during the course of other neurological conditions, and discovery of hypocretin ligand deficiency in idiopathic narcolepsy has led to new insights into the pathophysiology of symptomatic narcolepsy and EDS. The metabolic data may support the hypothesis of a primary deficient arousal system in patients with idiopathic hypersomnia.