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Personality Disorders: Theory, Research, and Treatment

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Journal scope statement

Personality Disorders: Theory, Research, and Treatment ® ( PD:TRT ) publishes a wide range of cutting-edge research on personality disorders and related psychopathology from a categorical and/or dimensional perspective including laboratory and treatment outcome studies, as well as integrative conceptual manuscripts and practice reviews that bridge science and practice.

Equity, diversity, and inclusion

Personality Disorders: Theory, Research, and Treatment supports equity, diversity, and inclusion (EDI) in its practices. More information on these initiatives is available under EDI Efforts .

Call for papers

• General call for papers

Open science

The APA Journals Program is committed to publishing transparent, rigorous research; improving reproducibility in science; and aiding research discovery. Open science practices vary per editor discretion. View the initiatives implemented by this journal .

Editor’s Choice

In each issue of Personality Disorders: Theory, Research, and Treatment one accepted manuscript will be selected to serve as an “ Editor’s Choice ” paper. Selection will follow discussion by the editor and associate editor and consider issues such as overall contribution, clinical implications, or the highlighting of important theoretical, methodological, or quantitative issues or advances in the study of personality pathology.

Author and editor spotlights

Explore journal highlights : free article summaries, editor interviews and editorials, journal awards, mentorship opportunities, and more.

Prior to submission, please carefully read and follow the submission guidelines detailed below. Manuscripts that do not conform to the submission guidelines may be returned without review.

Personality Disorders: Theory, Research, and Treatment ® ( PD:TRT ) is now using a software system to screen submitted content for similarity with other published content. The system compares each submitted manuscript against a database of 25+ million scholarly publications, as well as content appearing on the open web.

This allows APA to check submissions for potential overlap with material previously published in scholarly journals (e.g., lifted or republished material). A similarity report will be generated by the system and provided to the PD:TRT Editorial office for review immediately upon submission.

To submit to the editorial office of Joshua D. Miller, PhD, please submit manuscripts electronically through the Manuscript Submission Portal (.rtf, .doc, or .pdf files).

Prepare manuscripts according to the Publication Manual of the American Psychological Association using the 7 th edition. Manuscripts may be copyedited for bias-free language (see Chapter 5 of the Publication Manual ). APA Style and Grammar Guidelines for the 7 th edition are available.

New to 2021 and beyond submissions

An emphasis of PDTRT moving forward is to publish studies with larger sample sizes given the problems associated with smaller samples including lack of statistical power, lower precision and poorer stability of effect sizes (e.g., Schönbrodt & Perugini, 2013), and the increased odds that statistically significant effect sizes from small samples may be substantial overestimates. Studies submitted with very small samples are likely to be rejected without review (even when reporting patient data). Given the importance of power, all submissions must discuss how they decided upon the current sample size, report power analyses that influenced such decisions (if conducted), and if power was not part of the original plan, must report sensitivity analyses as to the smallest effects of interest the study was powered to find. Post-hoc power analyses based on the current effect sizes should not be reported. For case control designs (e.g., borderline PD vs. healthy groups), our strong preference will be that a third group be included (e.g., major depressive disorder) so as to speak to the specificity of the findings. Submissions must also note whether attempts were made to screen for data validity (e.g., with self-report data, reporting on tests of inconsistent or invariant responding, use of validity scales, attention checks, or cut-offs for timing deemed implausible). If data were not screened for validity, this must be noted explicitly. If participants were removed for invalid responding, the details (i.e., how many and for what reasons) must be provided.

Another goal of PDTRT is to increase transparency. In that vein, it is our hope that authors will submit work that was pre-registered . As such, authors must report in the first footnote of the study whether the study was pre-registered and, if so, provide an anonymized link to the pre-registration so that it can be examined by reviewers. Similarly, please note whether the data and code for the study are publicly available and, if so, where these can be found. Although pre-registration itself is not required for submission to PDTRT, it is our goal that an increasing percentage of PDTRT submissions will have been pre-registered across our 6 year term. We also welcome Registered Report submissions . If interested authors have questions about Registered Reports, please contact Josh Miller .

Submit Manuscript

Joshua D. Miller Department of Psychology 153 Psychology Building University of Georgia Athens, GA 30602 Email

In addition to addresses and phone numbers, please supply email addresses and fax numbers for use by the editorial office and later by the production office. Most correspondence between the editorial office and authors is handled by email, so a valid email address is important for the timely flow of communication during the editorial process.

Keep a copy of the manuscript to guard against loss.

Masked review policy

PD:TRT uses a masked reviewing system for all submissions. Omit the authors' names and affiliations on the first page of the manuscript, but include the title of the manuscript and the submission date. Authors are to make every effort to see that the manuscript itself contains no clues to their identities, including grant numbers, names of institutions providing IRB approval, self-citations, and links to online repositories for data, materials, code, or preregistrations (e.g., Create a View-only Link for a Project ).

Please ensure that the final version for production includes a byline and full author note for typesetting.

List five keywords on the title page to facilitate the selection of peer reviewers. Additionally, provide a cover letter indicating the proposed category under which the manuscript was submitted (e.g., Brief Report) and up to four suggestions for potential reviewers. Suggested reviewers should generally not include those with possible conflicts of interest (COI). In most cases, this would include frequent collaborators, mentors, departmental colleagues, current or previous lab mates, or close personal friends. In some rarer cases in which the research is done in a very small, niche area it may be impossible to avoid suggestions with some COI. In these cases, please include information pertaining to this issue in the cover letter.

Transparency and openness

APA endorses the Transparency and Openness Promotion (TOP) Guidelines by a community working group in conjunction with the Center for Open Science ( Nosek et al. 2015 ).

Empirical research, including meta-analyses, submitted to the PD:TRT must at least meet the “requirement” level (Level 2) for citation; data, code, and materials transparency; design and analysis transparency; and study and analysis plan preregistration. Authors should include a subsection in the method section titled “Transparency and Openness.” This subsection should detail the efforts the authors have made to comply with the TOP guidelines.

For example:

• We report how we determined our sample size, all data exclusions (if any), all manipulations, and all measures in the study, and we follow JARS (Appelbaum et al., 2018). All data, analysis code, and research materials are available at [stable link to repository]. Data were analyzed using R, version 4.0.0 (R Core Team, 2020) and the package ggplot , version 3.2.1 (Wickham, 2016). This study’s design and its analysis were not pre-registered.

Data, materials, and code

Authors must state whether data and study materials are posted to a trusted repository and, if so, how to access them, including their location and any limitations on use. If they cannot be made available, authors must state the legal or ethical reasons why they are not available. Trusted repositories adhere to policies that make data discoverable, accessible, usable, and preserved for the long term. Trusted repositories also assign unique and persistent identifiers. Recommended repositories include APA’s repository on the Open Science Framework (OSF), or authors can access a full list of other recommended repositories .

In a subsection titled “Transparency and Openness” at the end of the method section, specify whether and where the data and materials are available or note the legal or ethical reasons for not doing so. For submissions with quantitative or simulation analytic methods, state whether the study analysis code is posted to a trusted repository, and, if so, how to access it (or the legal or ethical reason why it is not available).

• All data have been made publicly available at the [trusted repository name] and can be accessed at [persistent URL or DOI].
• Materials and analysis code for this study are not available [for ethical or legal reason].
• The code behind this analysis/simulation has been made publicly available at the [trusted repository name] and can be accessed at [persistent URL or DOI].

If you cannot make your data available on a public site, authors are required to follow current APA policy to make the materials and data used in a published study available in a timely manner to other researchers upon request.

If an author has multiple studies, the repository landing page should clearly identify how to access the specific type of information for each study and the links.

Disclosure of prior uses of data

Upon submission of a manuscript, the authors must disclose any prior uses in published, accepted, or under review papers of data reported in the manuscript. The cover letter should include a complete reference list of these articles as well as a description of the extent and nature of any overlap between the present submission and the previous work.

Citation standards

Upon submission, all data sets, materials, and program code created by others must be appropriately cited in the text and listed in the reference section. Such materials should be recognized as original intellectual contributions and afforded recognition through citation.

Where possible, references for data sets and program code should include a persistent identifier assigned by digital archives, such as a Digital Object Identifier (DOI).

Data set citation example:

Campbell, Angus, & Kahn, Robert L. (1948). American National Election Study [Data set]. ICPSR07218v3. Interuniversity Consortium for Political and Social Research (Ann Arbor, MI) [distributor] (1999). [Data set]. http://doi.org/10.3886/ICPSR07218.v3

Design and analysis transparency

Authors must adhere to the Journal Article Reporting Standards (JARS) (PDF, 220KB) . See also the specific section editorials and instructions on information to include in method and results sections. It is particularly important to provide justifiable power considerations and specific details related to sample characteristics.

Preregistration of studies and analysis plans

Preregistration of studies and specific hypotheses can be a useful tool for making strong theoretical claims. Likewise, preregistration of analysis plans can be useful for distinguishing confirmatory and exploratory analyses. Investigators may reregister prior to conducting the research via a publicly accessible registry system (e.g., OSF , ClinicalTrials.gov, or other trial registries in the WHO Registry Network). There are many available templates; for example, APA, the British Psychological Society, and the German Psychological Society partnered with the Leibniz Institute for Psychology and Center for Open Science to create Preregistration Standards for Quantitative Research in Psychology (Bosnjak et al., 2022).

At the same time, we recognize that there may be good reasons to change a study or analysis plan after it has been preregistered, and thus encourage authors to do so when appropriate so long as all changes are clearly and transparently disclosed in the manuscript. Articles must state whether or not any work was preregistered and, if so, where to access the preregistration. Preregistrations must be available to reviewers; authors may submit a masked copy via stable link or supplemental material. Links in the method section should be replaced with an identifiable copy on acceptance.

• This study’s design was preregistered; see [STABLE LINK OR DOI].
• This study’s design and hypotheses were preregistered; see [STABLE LINK OR DOI].
• This study’s analysis plan was preregistered; see [STABLE LINK OR DOI].
• This study was not preregistered.

Whether or not a study is preregistered, PD:TRT stresses the importance of transparency in reporting and expects researchers to fully disclose in their manuscript all decisions that were data-dependent (e.g., deciding when to stop data collection, what observations to exclude, what covariates to include, and what analyses to conduct after rather than before seeing the data).

Replication and Registered Reports

Personality Disorders: Theory, Research, and Treatment acknowledges the significance of replication in building a cumulative knowledge base in our field. We therefore encourage submissions that attempt to replicate important findings. Major criteria for publication of replication papers include (i) theoretical significance of the finding being replicated, (ii) statistical power of the study that is carried out, and (iii) the number and power of previous replications of the same finding.

Other factors that would weigh in favor of a replication submission include: pre-registration of hypotheses, design, and analysis; submissions by researchers other than the authors of the original findings; and attempts to replicate more than one study of a multi-study original publication. Personality Disorders: Theory, Research, and Treatment publishes Registered Reports, which are particularly well-suited for planned replications (but not limited to such content). Such submissions will consist of a detailed research proposal, including an abstract, introduction, hypotheses, method, planned analyses, and implications of the expected results. We recommend that authors initially contact the editor before submitting a Registered Report. For Registered Reports, the proposed research will be reviewed and, if approved, should then be carried out in accordance with the proposed plan. To the extent that the study is judged to have been competently performed, the paper will be accepted (pending any necessary revisions) regardless of the outcome of the study.

Types of manuscripts

Four types of manuscripts will be accepted:

• full-length articles
• brief reports
• target conceptual articles
• practice reviews (jointly written by a researcher and primary clinician)

Further, the journal will operate an open-access message board to foster continuing dialogue on the target conceptual article.

Full-length articles

Manuscripts presenting empirical findings may be submitted as full-length articles. Full-length articles should not exceed 36 pages total (including cover page, abstract, text, references, tables, and figures), with margins of at least 1 inch on all sides and a standard font (e.g., Times New Roman) of 12 points (no smaller). The entire paper (text, references, tables, etc.) must be double-spaced.

PD:TRT requires that reports of randomized clinical trials conform to CONSORT reporting standards , including the submission of a flow diagram and checklist. Nonrandomized clinical trials must conform to TREND criteria .

Brief reports

In addition to full-length manuscripts, PD:TRT will consider brief reports of empirical findings. Brief reports are to be prepared in line with the guidelines for full-length articles, yet they may not exceed 18 pages.

Target conceptual articles

Manuscripts that evaluate and synthesize the research literature and/or make important theoretical contributions are sought for target conceptual articles. Four commentaries invited by the journal will be published on the PD:TRT homepage, along with the author's response to the commentaries.

Target conceptual articles are to be prepared in line with the guidelines for full-length articles, yet they may not exceed 40 pages. Please note that these are typically invited submissions. If you have an idea for a manuscript or a prepared manuscript that may be relevant for this mechanism, please email the editor-in-chief prior to submission for initial consideration.

Meta-analytic and narrative reviews are appropriate for submission to PD:TRT with a preference for quantitative reviews when possible. These reviews can be a maximum of 40 pages; for meta-analyses, references to studies summarized can be included in supplemental materials, if necessary. Narrative reviews in particular must provide a systematic, integrative synthesis of the empirical literature in a given area and/or should be a springboard to the development of a new theory or model. Mere reviews of the literature without integrative synthesis or model/theory development will not be considered.

Practice reviews

In line with the journal's commitment to bridging science and practice, practice reviews will present an issue from clinical practice, review relevant research, and provide a practical recommendation informed by the reviewed research.

Practice reviews must be coauthored by at least one individual with a primary focus in clinical practice and at least one individual with a primary focus in research. This partnering of individuals with a different professional emphasis is crucial for practice reviews to provide a credible bridge between research and practice.

When submitting a practice review, provide a description of each individual's primary professional focus in the cover letter. Manuscripts not meeting this partnering requirement will be returned without review. New collaborations are especially encouraged.

Practice reviews are to be prepared in line with the guidelines for full-length articles, yet they may not exceed 30 pages.

Manuscript preparation

Prepare manuscripts according to the Publication Manual of the American Psychological Association using the 7th edition. Manuscripts may be copyedited for bias-free language (see Chapter 5 of the Publication Manual ).

Review APA's Journal Manuscript Preparation Guidelines before submitting your article.

Double-space all copy. Other formatting instructions, as well as instructions on preparing tables, figures, references, metrics, and abstracts, appear in the Manual . Additional guidance on APA Style is available on the APA Style website .

Below are additional instructions regarding the preparation of display equations, computer code, and tables.

Display equations

We strongly encourage you to use MathType (third-party software) or Equation Editor 3.0 (built into pre-2007 versions of Word) to construct your equations, rather than the equation support that is built into Word 2007 and Word 2010. Equations composed with the built-in Word 2007/Word 2010 equation support are converted to low-resolution graphics when they enter the production process and must be rekeyed by the typesetter, which may introduce errors.

To construct your equations with MathType or Equation Editor 3.0:

• Go to the Text section of the Insert tab and select Object.
• Select MathType or Equation Editor 3.0 in the drop-down menu.

If you have an equation that has already been produced using Microsoft Word 2007 or 2010 and you have access to the full version of MathType 6.5 or later, you can convert this equation to MathType by clicking on MathType Insert Equation. Copy the equation from Microsoft Word and paste it into the MathType box. Verify that your equation is correct, click File, and then click Update. Your equation has now been inserted into your Word file as a MathType Equation.

Use Equation Editor 3.0 or MathType only for equations or for formulas that cannot be produced as Word text using the Times or Symbol font.

Computer code

Because altering computer code in any way (e.g., indents, line spacing, line breaks, page breaks) during the typesetting process could alter its meaning, we treat computer code differently from the rest of your article in our production process. To that end, we request separate files for computer code.

In online supplemental material

We request that runnable source code be included as supplemental material to the article. For more information, visit Supplementing Your Article With Online Material .

In the text of the article

If you would like to include code in the text of your published manuscript, please submit a separate file with your code exactly as you want it to appear, using Courier New font with a type size of 8 points. We will make an image of each segment of code in your article that exceeds 40 characters in length. (Shorter snippets of code that appear in text will be typeset in Courier New and run in with the rest of the text.) If an appendix contains a mix of code and explanatory text, please submit a file that contains the entire appendix, with the code keyed in 8-point Courier New.

Use Word's insert table function when you create tables. Using spaces or tabs in your table will create problems when the table is typeset and may result in errors.

Author contribution statements using CRediT

The APA Publication Manual (7th ed.) stipulates that "authorship encompasses…not only persons who do the writing but also those who have made substantial scientific contributions to a study." In the spirit of transparency and openness, PD:TRT has adopted the Contributor Roles Taxonomy (CRediT) to describe each author's individual contributions to the work. CRediT offers authors the opportunity to share an accurate and detailed description of their diverse contributions to the manuscript. During submission, the corresponding author will be asked to identify the contribution(s) of each author so each may be tagged with metadata that is both visible and trackable. Authors can claim credit for more than one contributor role, and the same role can be attributed to more than one author. If the manuscript is accepted for publication, the CRediT designations will be published as an author contributions statement in the author note. All authors should have reviewed and agreed to their individual contribution(s) before submission.

Academic writing and English language editing services

Authors who feel that their manuscript may benefit from additional academic writing or language editing support prior to submission are encouraged to seek out such services at their host institutions, engage with colleagues and subject matter experts, and/or consider several vendors that offer discounts to APA authors .

Please note that APA does not endorse or take responsibility for the service providers listed. It is strictly a referral service.

Use of such service is not mandatory for publication in an APA journal. Use of one or more of these services does not guarantee selection for peer review, manuscript acceptance, or preference for publication in any APA journal.

Submitting supplemental materials

APA can place supplemental materials online, available via the published article in the APA PsycArticles ® database. Please see Supplementing Your Article With Online Material for more details.

Abstract and keywords

All manuscripts must include an abstract containing a maximum of 250 words typed on a separate page. After the abstract, please supply up to five keywords or brief phrases.

List references in alphabetical order. Each listed reference should be cited in text, and each text citation should be listed in the References section.

Examples of basic reference formats:

Journal article

McCauley, S. M., & Christiansen, M. H. (2019). Language learning as language use: A cross-linguistic model of child language development. Psychological Review , 126 (1), 1–51. https://doi.org/10.1037/rev0000126

Authored book

Brown, L. S. (2018). Feminist therapy (2nd ed.). American Psychological Association. https://doi.org/10.1037/0000092-000

Chapter in an edited book

Balsam, K. F., Martell, C. R., Jones. K. P., & Safren, S. A. (2019). Affirmative cognitive behavior therapy with sexual and gender minority people. In G. Y. Iwamasa & P. A. Hays (Eds.), Culturally responsive cognitive behavior therapy: Practice and supervision (2nd ed., pp. 287–314). American Psychological Association. https://doi.org/10.1037/0000119-012

Data, code, and methods

All data, program code and other methods must be cited in the text and listed in the References section.

Data Set Citation:

Alegria, M., Jackson, J. S., Kessler, R. C., & Takeuchi, D. (2016). Collaborative Psychiatric Epidemiology Surveys (CPES), 2001–2003 [Data set]. Inter-university Consortium for Political and Social Research. http://doi.org/10.3886/ICPSR20240.v8

Preferred formats for graphics files are TIFF and JPG, and preferred format for vector-based files is EPS. Graphics downloaded or saved from web pages are not acceptable for publication. Multipanel figures (i.e., figures with parts labeled a, b, c, d, etc.) should be assembled into one file. When possible, please place symbol legends below the figure instead of to the side.

• All color line art and halftones: 300 DPI
• Black and white line tone and gray halftone images: 600 DPI

Line weights

• Color (RGB, CMYK) images: 2 pixels
• Grayscale images: 4 pixels
• Stroke weight: 0.5 points

APA offers authors the option to publish their figures online in color without the costs associated with print publication of color figures.

The same caption will appear on both the online (color) and print (black and white) versions. To ensure that the figure can be understood in both formats, authors should add alternative wording (e.g., “the red (dark gray) bars represent”) as needed.

For authors who prefer their figures to be published in color both in print and online, original color figures can be printed in color at the editor's and publisher's discretion provided the author agrees to pay:

• $900 for one figure
• An additional $600 for the second figure
• An additional $450 for each subsequent figure

Permissions

Authors of accepted papers must obtain and provide to the editor on final acceptance all necessary permissions to reproduce in print and electronic form any copyrighted work, including test materials (or portions thereof), photographs, and other graphic images (including those used as stimuli in experiments).

On advice of counsel, APA may decline to publish any image whose copyright status is unknown.

• Download Permissions Alert Form (PDF, 13KB)

Open science badges

Articles are eligible for open science badges recognizing publicly available data, materials, and/or preregistered plans and analyses. These badges are awarded on a self-disclosure basis.

At submission, authors must confirm that criteria have been fulfilled in a signed badge disclosure form (PDF, 42KB) that must be submitted as supplemental material. If all criteria are met as confirmed by the editor, the form will then be published with the article as supplemental material.

Authors should also note their eligibility for the badge(s) in the cover letter.

For all badges, items must be made available on an open-access repository with a persistent identifier in a format that is time-stamped, immutable, and permanent. For the preregistered badge, this is an institutional registration system.

Data and materials must be made available under an open license allowing others to copy, share, and use the data, with attribution and copyright as applicable.

Available badges are:

Note that it may not be possible to preregister a study or to share data and materials. Applying for open science badges is optional.

Publication policies

For full details on publication policies, including use of Artificial Intelligence tools, please see APA Publishing Policies .

APA policy prohibits an author from submitting the same manuscript for concurrent consideration by two or more publications.

See also APA Journals ® Internet Posting Guidelines .

APA requires authors to reveal any possible conflict of interest in the conduct and reporting of research (e.g., financial interests in a test or procedure, funding by pharmaceutical companies for drug research).

• Download Full Disclosure of Interests Form (PDF, 41KB)

In light of changing patterns of scientific knowledge dissemination, APA requires authors to provide information on prior dissemination of the data and narrative interpretations of the data/research appearing in the manuscript (e.g., if some or all were presented at a conference or meeting, posted on a listserv, shared on a website, including academic social networks like ResearchGate, etc.). This information (2–4 sentences) must be provided as part of the Author Note.

Ethical Principles

It is a violation of APA Ethical Principles to publish "as original data, data that have been previously published" (Standard 8.13).

In addition, APA Ethical Principles specify that "after research results are published, psychologists do not withhold the data on which their conclusions are based from other competent professionals who seek to verify the substantive claims through reanalysis and who intend to use such data only for that purpose, provided that the confidentiality of the participants can be protected and unless legal rights concerning proprietary data preclude their release" (Standard 8.14).

APA expects authors to adhere to these standards. Specifically, APA expects authors to have their data available throughout the editorial review process and for at least 5 years after the date of publication.

Authors are required to state in writing that they have complied with APA ethical standards in the treatment of their sample, human or animal, or to describe the details of treatment.

• Download Certification of Compliance With APA Ethical Principles Form (PDF, 26KB)

The APA Ethics Office provides the full Ethical Principles of Psychologists and Code of Conduct electronically on its website in HTML, PDF, and Word format. You may also request a copy by emailing or calling the APA Ethics Office (202-336-5930). You may also read "Ethical Principles," December 1992, American Psychologist , Vol. 47, pp. 1597–1611.

Other information

See APA’s Publishing Policies page for more information on publication policies, including information on author contributorship and responsibilities of authors, author name changes after publication, the use of generative artificial intelligence, funder information and conflict-of-interest disclosures, duplicate publication, data publication and reuse, and preprints.

Visit the Journals Publishing Resource Center for more resources for writing, reviewing, and editing articles for publishing in APA journals.

Joshua D. Miller, PhD University of Georgia, United States

Associate editor

Carla Sharp, PhD University of Houston, United States

Open science consulting editor

Leigha Rose Waikel, BS University of Georgia, United States

Editorial board reviewers

Jaime L. Anderson, PhD Sam Houston State University, United States

Bo Bach, PhD Slagelse Psychiatric Hospital, Denmark

Mitja D. Back, PhD University of Münster, Germany

R. Michael Bagby, PhD, ABAP University of Toronto, Canada

Arielle Baskin-Sommers, PhD Yale University, United States

Daniel M. Blonigen, PhD VA Palo Alto Health Care System, United States

Marina A. Bornovalova, PhD University of South Florida, United States

Alexander L. Chapman, PhD, RPsych Simon Fraser University, United States

Jennifer S. Cheavens, PhD The Ohio State University, United States

Lois W. Choi-Kain, MD, MEd Gunderson Personality Disorders Institute, Harvard Medical School, United States

John F. Clarkin, PhD Weill Cornell Medical College, New York Presbyterian Hospital, United States

Allan D. Clifton, PhD Vassar College, United States

Christopher Conway, PhD Fordham University, United States

Sheila Crowell, PhD University of Utah, United States

Barbara J. De Clercq, PhD Ghent University, Belgium

Filip De Fruyt, PhD Ghent University, Belgium

Karen J. Derefinko, PhD University of Tennessee Health Science Center, United States

Katherine Lee Dixon-Gordon, PhD University of Massachusetts, Amherst, United States

Laura E. Drislane, PhD Sam Houston State University, United States

Janine D. Flory, PhD Icahn School of Medicine, Mount Sinai, United States

Peter Fonagy, OBE FMedSci FBA FAcSS University College London, United Kingdom

Andrea Fossati, PhD Vita-Salute San Raffaele University, Italy

Andrea Glenn, PhD University of Alabama, United States

Marianne Goodman, MD James J. Peters VA Medical Center, United States

Kim L. Gratz, PhD University of Toledo, United States

Brin F. S. Grenyer, PhD University of Wollongong, Australia

Michael N. Hallquist, PhD The University of North Carolina at Chapel Hill, United States

Sabine C. Herpertz, MD Heidelberg University, Germany

Christopher J. Hopwood, PhD University of Zurich, Switzerland

Joost Hutsebaut, PhD De Viersprong National Institute of Personality Disorders, Netherlands

Courtland S. Hyatt, PhD Emory University, United States

Luke Williamson Hyde, PhD University of Michigan, United States

Mie Sedoc Jørgensen, PhD, MSc Psychology. Psychiatric Research Unit, Mental Health Services of Region Zealand, Denmark

Aleksandra Kaurin, PhD Witten/Herdecke University, Germany

John G. Kerns, PhD University of Missouri, United States

Thomas R. Kwapil, PhD University of Illinois, Urbana-Champaign, United States

Justin A. Lavner, PhD University of Georgia, United States

Mark F. Lenzenweger, PhD State University of New York, Binghamton, United States

Holly F. Levin-Aspenson, PhD University of North Texas, United States

Majse Lind, PhD Aalborg University, Denmark

Patrick Luyten, PhD University of Leuven, Belgium

Donald R. Lynam, PhD Purdue University, United States

Jenny Macfie, PhD University of Tennessee, Knoxville, United States

Jessica Maples-Keller, PhD Emory University, United States

Kristian E. Markon, PhD University of Iowa, United States

Margaret McNamara McClure, PhD Fairfield University, United States

Stephanie N. Mullins-Sweatt, PhD Oklahoma State University, United States

Inga Niedtfeld, PhD Central Institute of Mental Health, Germany

Brian O'Connor, PhD University of British Columbia, Canada

Joshua R. Oltmanns, PhD Southern Methodist University, United States

Christopher J. Patrick, PhD Florida State University, United States

Jessica Peters, PhD Brown University, United States

Aaron L. Pincus, PhD Pennsylvania State University, United States

Douglas B. Samuel, PhD Purdue University, United States

Charles A. Sanislow, PhD Wesleyan University, United States

Shannon Sauer-Zavala, PhD University of Kentucky, United States

Lori N. Scott, PhD University of Pittsburgh, United States

Martin Sellbom, PhD University of Otago, New Zealand

Susan C. South, PhD Purdue University, United States

Matthew W. Southward, PhD University of Kentucky, United States

Kasey Stanton, PhD University of Wyoming, United States

Timothy Trull, PhD University of Missouri, United States

David D. Vachon, PhD McGill University, United States

Salome Vanwoerden, PhD University of Pittsburgh, United States

Edelyn Verona, PhD University of South Florida, United States

Colin Vize, PhD University of Pittsburgh, United States

Amy W. Wagner, PhD Portland VA Medical Center, United States

Rebecca Waller, PhD University of Pennsylvania, United States

Ashley L. Watts, PhD Vanderbilt University, United States

Thomas Widiger, PhD University of Kentucky, United States

Catherine Winsper, PhD University of Warwick, United Kingdom

Johannes Zimmerman, PhD University of Kassel, Germany

Peer review coordinator

Efrem Tuquabo American Psychological Association, United States

Abstracting and indexing services providing coverage of Personality Disorders: Theory, Research, and Treatment ®

• Cabell's Directory of Publishing Opportunities in Psychology
• Current Contents: Social & Behavioral Sciences
• Journal Citations Report: Social Sciences Edition
• Social Sciences Citation Index
• Studies on Women and Gender Abstracts

Special issue of the APA journal Personality Disorders: Theory, Research, and Treatment, Vol. 14, No. 1, January 2023. This special issue presents a compilation of manuscripts by leading scholars in the study of personality disorders that address a wide range of important methodological and quantitative issues.

Special issue of APA journal Personality Disorders, Vol. 13, No. 2, July 2022. In this special issue, the authors begin by summarizing the main findings and recommendations from each target review and its commentaries, as well as the shorter review articles, after which they offer additional remarks in the hopes of contributing to the setting of an agenda for the next iteration of the DSM.

Special issue of the APA journal Personality Disorders, Vol. 2, No. 1, January 2011. Articles discuss proposed changes to personality and personality disorders in the DSM-5.

APA endorses the Transparency and Openness Promotion (TOP) Guidelines by a community working group in conjunction with the Center for Open Science ( Nosek et al. 2015 ). The TOP Guidelines cover eight fundamental aspects of research planning and reporting that can be followed by journals and authors at three levels of compliance. For example:

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Personality disorder

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• Peer review
• Orestis Kanter Bax , consultant psychiatrist in medical psychotherapy 1 2 ,
• Dimitrios Chartonas , consultant psychiatrist 2 3 ,
• Jennie Parker , independent lived experience researcher , KUF development lead 2 5 ,
• Spyridon Symniakou , GP partner 6 ,
• Tennyson Lee , consultant psychiatrist in medical psychotherapy , psychoanalyst , honorary senior lecturer 2 4 7 6 8
• 1 Basildon Complex Needs Psychotherapy and Personality Disorder Service, Essex Partnership University NHS Foundation Trust, UK
• 2 Centre for Understanding Personality (CUSP), London
• 3 Camden and Islington Personality Disorder Service, Camden and Islington NHS Foundation Trust
• 4 Deancross Personality Disorder Service, East London NHS Foundation Trust
• 5 Berkshire Healthcare NHS Foundation Trust
• 6 Blithdale Health Centre, Clinical Director East End Health Network
• 7 Institute of Psychoanalysis, British Psychoanalytical Society
• 8 Wolfson Institute, Queen Mary University of London
• Correspondence to O Kanter Bax orestis.kanter-bax{at}nhs.net

What you need to know

Personality disorders are a set of complex emotional difficulties. They are common, often unrecognised, and are associated with mental and physical health comorbidities and reduced life expectancy

Personality disorders are perceived as stigmatising diagnoses. Alternative terms have been proposed. New classification systems help in moving away from rigid use of categorical diagnoses

Assessment and management in primary care require a non-judgmental approach that builds trust through attentiveness, validation, openness, and consistency

Holistic care for people with personality disorders can be improved with reflective practice structures, staff training, collaboration, and team working

Sources and selection criteria

We searched Pubmed, Medline, Embase, the Cochrane Library, CINAHL, PsycINFO, AMED, British Nursing Index, HMIC, and Health Business Elite using the term “personality disorder”. Findings from randomised controlled trials (RCTs), systematic reviews, and meta-analyses were ranked as high in quality (see table 1) and we also used our own reference archives, books, and expert contacts to supplement the structured search.

Personality disorders describe a set of long standing complex emotional difficulties, which are common, highly stigmatised, and potentially disabling. They are frequently under-recognised and may run a long course when people lack access to appropriate treatment. Recent developments in evidence, guidelines, and policy have placed an emphasis on public awareness, de-stigmatisation, training professionals in generalist settings, improving access to specialist care, and improving physical health outcomes. 1 2 This article provides an overview of the latest information on the assessment and management of personality disorders in primary care, with an emphasis on borderline personality disorder (also referred to as emotionally unstable personality disorder).

What are personality disorders?

Personality disorders are pervasive and enduring, affecting the emotional, cognitive, and behavioural functioning of a person, expressed in relation to their self (eg, identity, self-evaluation, affect regulation, direction) and others (eg, intimacy, boundaries, sense of security in relationships). People with personality disorders may face difficulties with …

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Borderline Personality Disorder (BPD): In the Midst of Vulnerability, Chaos, and Awe

Filiz kulacaoglu.

1 Department of Psychiatry, Cerkezkoy State Hospital, Tekirdag 59500, Turkey; moc.liamg@acalukf

2 Department of Psychology, Hasan Kalyoncu University, Gaziantep 27000, Turkey

3 University of Texas Medical School of Houston, Houston, TX 77065, USA

4 Center for Neurobehavioral Research on Addictions, Houston, TX 77054, USA

Borderline personality disorder (BPD) is a chronic psychiatric disorder characterized by pervasive affective instability, self-image disturbances, impulsivity, marked suicidality, and unstable interpersonal relationships as the core dimensions of psychopathology underlying the disorder. Across a wide range of situations, BPD causes significant impairments. Patients with BPD suffer considerable morbidity and mortality compared with other populations. Although BPD is more widely studied than any other personality disorder, it is not understood sufficiently. This paper briefly reviews the recent evidence on the prevalence, etiology, comorbidity, and treatment approaches of borderline personality disorder (BPD) by examining published studies, and aims to offer a more coherent framework for the understanding and management of borderline personality disorder.

1. Introduction

Borderline personality disorder (BPD) is a chronic psychiatric disorder characterized by pervasive patterns of affective instability, self-image disturbances, instability of interpersonal relationships, marked impulsivity, and suicidal behavior (suicidal ideation and attempt) causing significant impairment and distress in individual’s life [ 1 ]. Patients with BPD suffer considerable morbidity which complicates medical care compared to other individuals. BPD was initially defined in 1978 followed up with the publication of the Diagnostic and Statistical Manual of Mental Disorders, Third Edition (DSM-III) in 1980 [ 2 ] and International Classification of Diseases (ICD-10) [ 3 ] 10 years later. It has become a diagnosis based on the systematic identification of clinical features and identified as emotionally unstable personality disorder [ 2 ]. Both the DSM-5 [ 4 ] and ICD-10 [ 3 ] highlighted the affective instability as an essential criterion for BPD. Individuals with BPD have an underlying vulnerability to emotional hyperarousal states due to abnormalities in neurobiological systems sub-serving emotional regulation and stress responsibility. They also have an underlying vulnerability to social and interpersonal stressors due to abnormalities in neurobiological systems mediating social cognition, attachment, and social reward. Under stressful conditions, BPD patients are unable to regulate their emotions and quickly return to their baseline emotional states.

Since BPD is associated with receiving clinical attention and causes psychosocial impairments, it is more widely studied than other personality disorders [ 5 , 6 ]. In this brief review, we aim to elucidate epidemiology, pathogenesis, clinical features, comorbidity, and treatment approaches to BPD by critically examining published studies.

2. Epidemiology

The lifetime prevalence of BPD is approximately 5.9% and the point prevalence of BPD is 1.6% [ 6 , 7 ]. Although the prevalence of BPD is not higher than other personality disorders in the general population, BPD has a high prevalence in treatment settings; BPD was present in 6.4% of primary care visits, 9.3% of psychiatric outpatients and 20% of psychiatric inpatients according to the studies in clinical settings [ 4 , 8 , 9 ]. However, the ratio of females to males with the disorder is also greater in the clinical population. The ratio is 3:1 in clinical settings cited in the DSM-5 [ 4 ]. In contrast to the clinical setting ratio, in two epidemiologic surveys of United States general population, the lifetime prevalence of BPD was found to be similar in males and females [ 6 , 7 ]. This result can be interpreted as women with BPD are more likely to seek treatment than men. About 80% of patients who receive treatment for BPD were reported to be women.

3. Pathogenesis

The cause of BPD is not known and it is suggested that BPD is the product of an interaction between genetic, neurobiological, and psychosocial influences that affect brain development [ 10 ].

Although studies are rare and different values have been reported, there is at least moderate evidence for the genetic transmission and heritability of BPD. According to two studies, the concordance rate for BPD was found to be higher in monozygotic twins compared with dizygotic twins (36 and 35% versus 19 and 7%) [ 11 , 12 ]. However, a third twin study reported that a common genetic influence has little contribution to the development of BPD compared to environmental influences (42% versus 58%) [ 13 ]. In sum, constitutional predisposition to emotional dysregulation with a non-supporting environment leads to the development of BPD [ 14 ]. Future studies are needed to focus on interactions of specific endophenotype and environmental factors.

According to neurobiological research data, it has been suggested that neuropeptide functions may predispose to interpersonal problems of BPD patients [ 15 ]. The hypothalamic pituitary adrenal (HPA) axis dysfunction has a central role in the development of BPD. Increased levels of stress hormones, such as basal cortisol, and reduced feedback sensitivity were reported in BPD patients [ 16 ]. However, maladaptive behaviors of self–others and relationships with others are believed to be modulated by the oxytocinergic system [ 17 ]. Increased HPA activity and decreased peripheral oxytocin levels are correlated with a history of early life maltreatment and insecure attachment in patients with BPD [ 18 ]. Moreover, few studies also reported increased testosterone levels in female and male patients with BPD [ 16 ].

Neuroimaging studies that have compared BPD patients with healthy controls have reported bilateral reductions in the hippocampus, amygdala, and medial temporal lobe [ 19 , 20 ]. The neurobiology of BPD can be conceptualized as abnormalities in the top-down control, provided by the orbitofrontal cortex and the anterior cingulate cortex, and the bottom-up control drives generated in the limbic system such as amygdala, hippocampus, and insular cortex. Top-down control provides cognitive control areas and bottom-up control provides salience detection [ 21 ]. In this circuitry, serotonin regulates the prefrontal regions by acting on 5-HT2 receptors in a different role [ 22 ]. Impulsive traits, a major component of BPD, are associated with deficits in central serotonergic functioning. More specifically, increased 5-HT2A receptors and decreased 5-HT2C receptors are related with impulsivity [ 21 ]. Impulsivity is a core feature of BPD and it is related with reward and control circuits and deficient behavioral inhibition in prefrontal areas [ 23 ]. However, left amygdala hyperactivity was found in unmedicated patients with acute BPD. This feature is consistent with negative environmental stimuli [ 24 ]. Intense and variable emotions of BPD patients are related with amygdala hyperactivity. The role of the amygdala also reflects maladaptive top-down processes in evaluating negative environmental stimuli [ 25 ]. However, an enlarged hypothalamus and dysregulated HPA axis, and a reduced volume of the amygdala and hippocampus are found in patients with a history of early trauma and posttraumatic stress disorder (PTSD) [ 26 , 27 , 28 ]. In addition, the finding of reductions in gray matter volume of amygdala in older BPD patients has been interpreted as reflecting a reversible progressive pathology [ 29 ]. Emotional regulation difficulties of BPD patients are related with insufficient capacity of cognitive processes of prefrontal cortex (PFC) activity [ 30 ]. Koenigsberg et al. reported hypoactivity in orbitofrontal cortex, ventrolateral cortex, and dorsal anterior cingulate cortex (ACC) in BPD patients compared with healthy individuals [ 31 ]. This result is related with maladaptive affective regulation in BPD patients. However, lower prefronto-limbic connectivity within the affect regulation circuitry was reported to be normalized after successful psychotherapy [ 32 ]. In sum, numerous studies that have compared BPD patients with healthy controls reported a serotonergic dysfunction and reductions in amygdala, hippocampus, and medial temporal lobe volumes [ 19 , 20 ]. However, since these studies enrolled adult BPD patients, it is not clear that these neurobiological defects are the sequelae or etiologic causes of the disorder.

Life experiences are also known to be associated with the development of BPD [ 33 ]. Childhood trauma is the most significant risk factor for development of BPD [ 34 ]. Since childhood trauma is not always present in BPD, and individuals who had trauma do not always necessarily develop BPD, this relationship between childhood trauma and BPD is not clear. It can be interpreted that childhood trauma is not a mandatory precondition for the development of BPD. Childhood trauma in BPD patients can take many forms in prospective studies including sexual abuse, physical abuse and neglect, verbal abuse, and early parental separation or loss [ 35 ]. According to a prospective study with 500 individuals, more physically abused and/or neglected children met the criteria of BPD as adults. Interestingly, sexual abuse history is not found as a risk factor for BPD. However, having a parent with alcohol or substance use problems, having a diagnosis of drug abuse, major depressive disorder, and post-traumatic stress disorder have all been associated with the development of BPD but are also non-specific factors [ 36 ]. Another prospective, longitudinal study with 639 children reported that childhood abuse/neglect was significantly associated with BPD in adulthood [ 37 ]. Meta-analyses have also found that only small effect sizes for the relationship between development of BPD and childhood maltreatment [ 38 , 39 ]. As with most psychiatric disorders, no single factor can explain the development of the disorder, multiple factors can help in explaining the development of BPD. Although, there were studies that reported that childhood trauma did not play a significant role in the development of BPD, it still remains an important risk factor for BPD and more studies are needed to elucidate this relationship.

4. Clinical Features and Comorbidities

BPD is a psychiatric disorder, which was initially thought to emerge during adolescence and continue into adulthood [ 40 ]. It has also been stated that a diagnosis starts from adolescents in DSM-5 [ 4 ]. According to DSM-5 Section II, the diagnostic criteria of BPD are divided into four dimensions: (a) Interpersonal instability dimension, which has the features of fear of abandonment and intense unstable relationships; (b) cognitive and/or self-disturbance, which consists of paranoid ideations, dissociative symptoms, and identity disturbances; (c) affective and emotional dysregulation; and (d) behavioral dysregulation dimension, which has impulsivity and suicidal behavior [ 4 ].

Affective instability has been shown to be the most specific, sensitive criteria for BPD [ 41 ]. Patients with BPD are emotionally labile, react strongly, and express dysphoric emotions such as depression, anxiety, and irritable mood [ 42 ]. However, a study that examined the associations of age with affective instability of BPD patients showed an inverse relationship between age and affective instability in patients with BPD [ 43 ]. Patients with BPD have unstable and conflicted relationships. They tend to view others as all good and bad which is labeled as ‘splitting’. They can easily become dependent on others but they can also have dramatic shifts in their feelings toward others. Cognitive dysfunction in BPD patients has also been shown in a meta-analysis, where BPD patients scored poorer on tests of attention, cognitive flexibility, planning, learning, and memory [ 44 ].

Impulsive behavior is a core feature of BPD and might take many forms. Substance abuse, impulsive spending, binge eating, reckless driving, and self-damaging behavior are very common and put the patient at risk of harm [ 45 ]. Previous studies suggested that impulsivity, emotional dysregulation, and self-harm behaviors during childhood are predictive features of BPD [ 46 ].

Suicidal attempts and ideations are common manifestations of BPD and are one of the diagnostic criteria of DSM-5 [ 4 ]. In retrospective studies, the rate of suicide is found to be 8%–12% in BPD individuals [ 47 ]. Suicidal tendency is most common at age 20 [ 48 ], and completed suicide attempts are more common after the age of 30 years in patients with BPD [ 48 ]. Patients may also engage in suicidal behaviors, such as cutting themselves. These behaviors, ideation or acts might be conceptualized as non-suicidal self-injury [ 49 ]. Since non-suicidal acts and suicide attempts are so common in BPD patients, it is quite difficult to assess the current risk of a patient’s suicidal intent. Patients who have attempted suicide more than once have an increased risk for completed suicide. According to prospective studies, the predictors of suicide in patients with BPD were reported as co-occurring symptoms of dissociation, affective reactivity, self-harm, depression comorbidity, family history of suicide, and history of childhood abuse [ 50 , 51 ]. According to a recent study, which examined gender differences and similarities in aggression, psychiatric comorbidity, and suicidal behavior in patients with BPD, men with BPD were found more aggressive, impulsive and more impaired than women with BPD. Men with BPD were found at higher risk of dying due to a suicide attempt compared to women with BPD [ 52 ].

Comorbid psychiatric disorders are common in patients with BPD [ 53 ]. According to an epidemiologic survey, 85% of BPD patients have at least one comorbid psychiatric disorder [ 6 ]. Mood disorders, especially depressive disorder, bipolar disorder, anxiety disorder, posttraumatic stress disorder (PTSD), substance use disorder, or other personality disorder and neurodevelopmental disorder such as attention-deficit/hyperactivity disorder (ADHD), might be present in patients with BPD [ 54 ]. According to several large patient samples, the rate of lifetime depression comorbidity ranges from 71% to 83%, and anxiety disorder comorbidity is as high as 88% in patients with BPD [ 55 , 56 ]. More recently in a genome-association study by Witt et al., genetic overlap has been found between BPD and bipolar disorder, major depressive disorder, and schizophrenia [ 57 ]. Their findings supported the role of genetic factors having a role in the development of BPD.

4.1. Borderline Personality Disorder and Bipolar Disorder

Borderline personality disorder (BPD) and bipolar disorder can co-occur in 10%–20% of cases and since symptomatology of these disorders is very similar, many patients with BPD have been mistakenly diagnosed with bipolar disorder [ 58 ]. It has also been suggested that BPD should be conceptualized as a part of the bipolar spectrum [ 59 , 60 ]. Smith et al. reported that a significant percentage of patients with BPD were in the bipolar spectrum [ 61 ], while Paris et al. reported that no empirical evidence supported BPD’s link to the bipolar spectrum [ 62 ]. By reviewing neuroimaging studies, Sripada and Silk reported that there were both overlap and differences in certain brain regions between BPD and bipolar disorder individuals [ 63 ]. A higher but not significant prevalence of BPD in patients with bipolar II disorder was reported [ 56 ] and Vieta et al. reported that BPD was diagnosed twice as frequently in patients with bipolar II disorder and bipolar I disorder [ 64 ]. Zimmerman et al. reported that patients with major depressive disorder (MDD) and BPD had excess psychosocial morbidity compared to MDD patients without BPD, and that BPD was the third most frequent diagnosis in patients with bipolar disorder after obsessive-compulsive disorder and histrionic personality disorder, respectively [ 65 ]. In sum, these results can be interpreted as each disorder is diagnosed in the absence of the other and these findings challenge the notion that BPD can be conceptualized as the part of the bipolar spectrum [ 66 ].

4.2. Borderline Personality Disorder and Early Trauma History

Trauma history is a central feature of both PTSD and BPD. The neurobiological impairments associated with the development of BPD can be conceptualized as the predisposing factor for BPD. Both environmental and neurobiological factors contribute to the development of BPD. Genetic predisposition becomes activated during environmental experiences of trauma history. It has been reported that trauma and neglect might exacerbate both biological and behavioral tendencies [ 67 ]. However, sufficient maternal care may buffer these vulnerabilities. These results might explain why some emotionally dysregulated individuals do not develop BPD despite their genetic tendencies. There is also evidence for a strong association between traumatic events and dissociative symptoms in BPD [ 68 ]. According to retrospective studies, borderline patients have high rates of childhood abuse and dissociation [ 69 ]. Depersonalization/derealization are core symptoms of BPD and dissociation can be a prominent feature in some individuals with BPD. Research in the dissociative subtype of PTSD and depersonalization suggested that dissociation might be a form of emotional over-modulation, promoting trauma-related stressful emotions [ 70 ]. Dissociation severity was predicted by the childhood traumas such as inconsistent caretaking, sexual abuse, adult rape, emotional neglect [ 71 ].

4.3. Borderline Personality Disorder and ADHD

The comorbidity of ADHD has been reported in 20% of BPD patients in several studies [ 72 ]. Since impulsivity is considered to be a central feature of BPD and ADHD, impulsivity has been examined as part of adult ADHD symptomatology in BPD patients. According to Philipsen et al., ADHD should be considered as a potential risk factor in patients with BPD with impulsivity [ 73 ]. In a recent study that has examined the association between impulsivity and ADHD in BPD patients, we reported higher comorbidity of ADHD in BPD group, and motor impulsiveness has been shown as a potential predictor of ADHD symptoms in BPD group [ 74 ]. In terms of the relationship between BPD, ADHD, and impulsivity, BPD-ADHD has been considered a severe, more impulsive and homogeneous subtype of BPD [ 75 ].

In sum, since BPD has been associated with chronic course of other psychiatric disorders, clinicians should carefully evaluate comorbid psychiatric conditions in patients with BPD in order to plan appropriate treatments.

5. Treatment

Since patients with BPD suffer considerable morbidity and mortality, BPD causes a therapeutic challenge for clinicians. First-line treatment for BPD is psychotherapy [ 76 ]. However, symptom targeted medications have also been found effective [ 77 ].

The psychotherapies that have been adapted to treat patients with BPD are; Dialectical behavior therapy (DBT), Mentalization-based therapy, Transference-focused therapy, Cognitive-behavioral therapy (CBT), and Schema-focused therapy [ 78 ]. These therapies provide active and focused interventions that emphasize current functioning and relationships. These therapy modalities also provide; (a) a structured manual that supports the therapist and provides recommendations for common clinical problems; (b) they are structured so that they encourage increased activity, proactivity, and self-agency for the patients; (c) focus on emotional processing, particularly on creating robust connections between acts and feelings; (d) increased cognitive coherence in relation to subjective experience in the early phase of treatment by including a model of pathology that is carefully explained to the patient, and encouraging an active stance by the therapist, which invariably includes an explicit intent to validate and demonstrate empathy and generate strong attachment relationships to create a foundation of alliance. Psychoeducation is also an important part of BPD treatment. It includes informing patients and families about the disorder, signs and the symptoms of the disorder, and also possible causes and treatment options [ 79 ]. According to a 2017 systematic review and meta-analyses of 33 clinical trials with 2256 participants that examined the efficacy of psychotherapies for BPD, DBT and psychodynamic approaches were found more effective compared to other psychotherapy modalities [ 80 ]. An earlier 2012 systematic review and meta-analyses had reported DBT, mentalization-based, transference-focuses and schema-focused therapies are effective for BPD treatment. But the results for CBT have mixed results [ 81 ]. DBT is a well-studied form of CBT that puts emphasis on impulsive behavior and affective instability, and aims to regulate emotional lability using group or individual sessions. According to a clinical study that consisted of 101 women with BPD and self-injurious behavior who received DBT over a two-year period, fewer patients treated with DBT attempted suicide and required psychiatric hospitalization (23% versus 46%) compared with patients received community treatment [ 80 ]. DBT focuses on improving coping skills, self-destructive behavior and acting out. Mentalization-based and transference-focused therapies are primarily psychodynamic therapies. Mentalization therapy also includes cognitive techniques. For example, the patient is supported to observe her mind and create alternative perspectives of her thoughts to others. Transference-focused therapy includes confrontation, exploration and transference interpretations for the relationships of the BPD patients with other individuals. Schema-focused therapy is a form of CBT that includes skills training. Family education can be used adjunct to other therapies for BPD treatment [ 78 ].

According to the literature, the pharmacological treatment for BPD is limited. It is suggested that the patient with BPD who continues to experience severe, impairing symptoms (for example affective dysregulation, impulsive-behavioral dyscontrol, perceptual symptoms) despite receiving psychotherapy, should receive symptom-focused, adjunctive medication treatment [ 42 ]. According to the clinical surveys and meta-analyses, low-dose antipsychotic drugs are more effective for cognitive and perceptual symptoms such as dissociation, paranoid ideation, and hallucinations compared with antidepressants or mood stabilizers. Mood stabilizers are found to be more effective for impulsivity, aggression, and behavior control in BPD [ 77 ]. Mood stabilizers in the meta-analyses were lamotrigine, topiramate, valproate, and lithium. Lithium is also found to be effective in preventing suicide in BPD patients as reported by a retrospective study. But lithium has a limited usage due to significant side effects [ 82 ]. However, according to preliminary evidence, omega-3 fatty acids are suggested as adjunct to primary medication treatment, with mood stabilizers to prevent recurrent self-harms [ 83 ]. Meta-analyses have also found that mood stabilizers and low-dose antipsychotics are more effective for affective dysregulations in BPD compared to antidepressants [ 77 ].

Since BPD has a high rate of psychiatric comorbidity, clinicians should be aware of co-occurring mood and anxiety disorders, and substance use disorder for treating patients with BPD. For mood and anxiety disorders, clinicians should be careful to prescribe higher doses of antidepressant drugs for treating subthreshold symptoms. Thus, clinicians should focus on BPD treatment and effective treatment should be organized for comorbid psychiatric situations for patients with BPD. However, when it comes to substance use disorder, bipolar disorder comorbidity and treatment of the substance use disorder should take precedence over BPD for safety [ 84 ]. There is no evidence supporting the use of polypharmacy in personality disorder. According to the US FDA, no medication is approved and no class of psychoactive medication is dramatically effective [ 85 ]. However, The National Institute for Health and Care Excellence (NICE) guidelines have reported that psychotropic medication should not be used to treat the BPD and may be prescribed for symptoms of co-occurring disorders for a short period of time [ 86 ]. In sum, treatment of BPD is multimodal. Psychotherapy is the first line treatment and adjunctive, symptom focused pharmacotherapy is essential. Comorbid psychiatric disorders should be assessed. A positive therapeutic alliance with patient and family, as well as psychoeducation about the nature of the disorder, are useful to maintain the treatment.

6. Conclusions

Borderline personality disorder (BPD) is a psychiatric disorder that causes significant impairment with a high prevalence occurring in adolescence and early adulthood. The disorder is associated with more clinical attention than other personality disorders and has a risk for higher suicidality. The etiology is still unknown. According to the literature, a combination of genetic factors, neurobiological abnormalities and childhood trauma history can cause development of BPD. BPD can be conceptualized as a chronic and persistent disorder. However, according to prospective studies, higher rates of remission and recurrence have been reported. There is still a lack of information on which factors lead to the development of BPD. Further studies are necessary to understand the pathology of BPD and to help reach the best choices of treatment for clinicians. Most psychotropic medications were found to be effective in treatment of symptoms of affective dysregulation and impulsive aggression, which have been the core dimensions of underlying psychopathology. Polypharmacy practice is not evidence-based and is unnecessary in the management of patients with BPD.

Author Contributions

Both authors contributed to the manuscript equally.

This manuscript received no external funding.

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Moderation effects in personality disorder research

Affiliations.

• 1 Department of Psychiatry.
• 2 Department of Psychology and Neuroscience.
• 3 Department of Psychological Sciences.
• PMID: 35737564
• PMCID: PMC9990702
• DOI: 10.1037/per0000582

Tests of statistical interactions (or tests of moderation effects) in personality disorder research are a common way for researchers to examine nuanced hypotheses relevant to personality pathology. However, the nature of statistical interactions makes them difficult to reliably detect in many research scenarios. The present study used a flexible, simulation-based approach to estimate statistical power to detect trait-by-trait interactions common to psychopathy research using the Triarchic model of Psychopathy and the Psychopathic Personality Inventory. Our results show that even above-average sample sizes in these literatures (e.g., N = 428) provide inadequate power to reliably detect trait-by-trait interactions, and the sample sizes needed to detect interaction effect sizes in realistic scenarios are extremely large, ranging from 1,300 to 5,200. The implications for trait-by-trait interactions in psychopathy are discussed, as well as how the present findings might generalize to other areas of personality disorder research. We provide recommendations for how to design research studies that can provide informative tests of interactions in personality disorder research, but also highlight that a more realistic option is to abandon the traditional approach when testing for interaction effects and adopt alternative approaches that may be more productive. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

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Figure 1. Power Estimates to Detect Two-way…

Figure 1. Power Estimates to Detect Two-way Interactions when α = .80

Figure 2. Power Estimates to Detect Two-way…

Figure 2. Power Estimates to Detect Two-way Interactions when α = .90

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• Published: 24 August 2024

Examining the role of personality functioning in a hierarchical taxonomy of psychopathology using two years of ambulatory assessed data

• André Kerber   ORCID: orcid.org/0000-0002-8588-7784 1 ,
• Johannes C. Ehrenthal 2 ,
• Johannes Zimmermann 3 ,
• Carina Remmers   ORCID: orcid.org/0000-0003-1359-5747 4 ,
• Tobias Nolte 5 ,
• Leon P. Wendt 3 ,
• Phileas Heim 1 ,
• Sascha Müller   ORCID: orcid.org/0000-0002-8663-4543 6 ,
• Ina Beintner 7 &
• Christine Knaevelsrud 1  

Translational Psychiatry volume  14 , Article number:  340 ( 2024 ) Cite this article

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• Pathogenesis
• Psychiatric disorders

The Hierarchical Taxonomy of Psychopathology (HiTOP) arranges phenotypes of mental disorders based on empirical covariation, ranging from narrowly defined symptoms to higher-order spectra of psychopathology. Since the introduction of personality functioning (PF) in DSM-5 and ICD-11, several studies have identified PF as a predictor of transdiagnostic aspects of psychopathology. However, the role of PF in the HiTOP classification system has not been systematically examined. This study investigates how PF can be integrated into HiTOP, whether PF accounts for transdiagnostic variance captured in higher-order spectra, and how its predictive value for future affective well-being (AWB) and psychosocial impairment (PSI) compares to the predictive value of specific psychopathology beyond PF. To this end, we examined two years of ambulatory assessed data on psychopathology, PF, PSI, and AWB of N  = 27,173 users of a mental health app. Results of bass-ackwards analyses largely aligned with the current HiTOP working model. Using bifactor modeling, aspects of PF were identified to capture most of the internalizing, thought disorder, and externalizing higher-order factor variance. In longitudinal prediction analyses employing bifactor-(S-1) modeling, PF explained 58.6% and 30.6% of variance in PSI and AWB when assessed across one year, respectively, and 33.1% and 23.2% of variance when assessed across two years. Results indicate that personality functioning may largely account for transdiagnostic variance captured in the higher-order components in HiTOP as well as longitudinal outcomes of PSI and AWB. Clinicians and their patients may benefit from assessing PF aspects such as identity problems or internal relationship models in a broad range of mental disorders. Further, incorporating measures of PF may advance research in biological psychiatry by providing empirically sound phenotypes.

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Personality traits and dimensions of mental health

Psychosis superspectrum II: neurobiology, treatment, and implications

A critical evaluation of the p -factor literature

Introduction, hierarchical taxonomy of psychopathology.

Decades of research on psychopathology indicate that categorical approaches to assessment are limited [ 1 , 2 ]. Emerging models, such as the Hierarchical Taxonomy of Psychopathology (HiTOP [ 3 ]), adopt a dimensional perspective, prioritizing empirical data over expert consensus [ 4 ]. Following this approach, comorbidity is not a validity problem but an inherent and empirically supported aspect of the classification system. Consequently, mental health problems that tend to co-occur in individuals can aid in finding more general, higher-order factors of psychopathology that show distinct genetic, neurobiological, environmental, and behavioral correlates [ 3 , 5 , 6 , 7 ]. These empirically derived phenotypes have the potential to advance psychiatric genetics [ 8 ] and to provide clinical utility in everyday practice [ 9 ]. Current reviews on the HiTOP model propose a superspectrum of emotional dysfunction, which includes somatoform and internalizing spectra. These, in turn, encompass subfactors such as fear, distress, eating pathology, or sexual problems, which further narrow down to individual symptoms (e.g., dysphoria) and traits (e.g., separation insecurity). The superspectrum of psychosis includes spectra of thought disorder and detachment, while the superspectrum of externalizing encompasses disinhibited and antagonistic spectra, including the subfactors harmful substance use and antisocial behavior. At the highest level of the hierarchy, the “ p -factor” represents the empirical covariance between all mental disorders. In summary, HiTOP provides a comprehensive taxonomy that enables a multidimensional, hierarchical classification of mental health problems supported by meta-analytic evidence [ 10 ].

Notably, HiTOP also includes maladaptive personality traits based on the assumption that the difference between symptoms and traits primarily lies in the timeframe of occurrence [ 11 ]. It hereby incorporates findings from personality psychology regarding the convergence of HiTOP spectra and maladaptive trait domains [ 12 ]. Additionally, including dimensionally assessed traits aligns with research showing that maladaptive personality traits predict the onset of psychopathology, symptom chronicity, and functioning above and beyond categorical diagnoses [ 13 ].

Personality functioning (PF) and HiTOP

Both DSM-5, section III [ 14 ], and the new ICD-11 model of personality disorders [ 15 , 16 , 17 ] place the dimensional assessment of impairments in self- and interpersonal functioning (i.e., personality functioning) at the center of their approach. Unlike personality traits, which describe how individuals are, personality functioning (PF) focuses on basic psychological capacities individuals possess in perception, regulation, communication, and relationship formation to interact with themselves and the social world [ 18 ]. This definition of PF draws on objects relations and mentalization theories [ 14 ], which postulate that deficits in regulating the self and relationships (i.e., low levels of PF) are a result of adverse gene-environment interactions in early childhood and predispose individuals to psychopathology in general [ 19 ]. Empirically, PF shows less longitudinal stability in mean levels compared to personality traits, except for neuroticism [ 20 ], which overlaps significantly with PF [ 21 ] and appears more responsive to clinical interventions than other traits [ 22 ]. Additionally, PF is associated with various variables related to personality disorders, psychopathology, and psychosocial functioning [ 23 , 24 , 25 ]. Longitudinal research demonstrates that impairment in PF is a stronger predictor of psychosocial functioning than the sum of DSM-IV personality disorder criteria [ 26 ] or maladaptive traits [ 27 ].

Widiger et al. [ 28 ] proposed to integrate PF in the HiTOP system by mapping it largely on the p -factor of the model, which was supported by Bender [ 29 ]. Meehan et al. [ 30 ] argued that incorporating PF into HiTOP could help to “more fully capture the complexity of personality pathology over time” (p. 372). They also suggested that PF reflects the unstable and dynamic aspects of PDs while maladaptive traits may account for the stability of specific (PD) phenotypes, a hypothesis that has accumulated empirical evidence lately [ 31 , 32 ]. In a recent study investigating a large battery of established questionnaires regarding their alignment with HiTOP using a cross-sectional sample, some PF scales mapped closely onto distinct spectra, whereas other PF scales including mentalizing, negative interpersonal relationships, and problems with emotion awareness aligned with blends of spectra or lacked specificity for any particular spectrum, suggesting they are “pure markers” of the p -factor [ 33 ]. However, studies with sufficient statistical power, ecological validity, or longitudinal data on the role of PF in HiTOP are lacking.

Current study

In this study, we investigated three research questions: (1) How does PF fit into a hierarchical taxonomy of psychopathological symptoms and maladaptive traits? Does it represent a homogeneous construct that can be allocated to a specific subfactor or spectrum? (2) Does PF account for transdiagnostic variance captured in the higher-order factors? (3) If so, how much predictive validity does PF have, and how much predictive validity does specific psychopathology have beyond PF? To this aim, first, we utilized the extended bass-ackwards procedure [ 34 ] on ambulatory assessed psychopathological symptoms, traits, and PF of 27,173 users of a mental health app. We examined the placement of PF within an empirically derived hierarchical structure and explored whether PF accounted for general or specific variance in HiTOP using bifactor models. Additionally, we investigated the predictive validity of PF and residualized specific factors in relation to future affective well-being and psychosocial impairment using bifactor-(S-1) models.

Data collection

We analyzed anonymized data from the MindDoc app, which is a self-guided transdiagnostic application for individuals seeking to manage their mental health. It can be used anonymously, and according to the GDPR principle of data minimization, no sociodemographic data is collected. However, in a separate questionnaire study of N  = 1010 MindDoc users, 93.9% showed symptoms of depression and/or anxiety, 65.4% had outpatient and 49.2% had inpatient treatment in the last 6 months (see https://osf.io/swj3c/ for more details). A detailed description of all features of the app as well as its effectiveness can be found elsewhere [ 35 , 36 , 37 ]. The app is available on the Appstore and Playstore in German and English as a commercial product with both free and paid features. In addition to courses and exercises, it offers self-monitoring of psychopathology, psychosocial functioning, and personal resources. The self-monitoring feature is fully usable without a paid subscription and consists of three daily assessment blocks with three to nine questions aligned with the user’s circadian rhythm. Depending on previous answers, psychopathology, psychosocial impairment, and resources are adaptively explored using questions. Questions on psychopathology are regularly and repeatedly interspersed between all other questions in the ambulatory assessment, and the algorithm ensures that all HiTOP spectra are explored, leading to multiple assessments of the same question in regular users. Questions are first asked in a dichotomous yes/no format followed by a four-point scale assessing intensity or how much a statement applies, depending on item content, yielding a 5-point scale. Users also rate their current affective well-being after each question block (see Fig. 1 ).

Assessment system in the MindDoc app.

From a database of N  = 157,212 users, we included N  = 27,143 active users with at least one assessment of at least 90% of 201 ambulatory assessed items capturing psychopathology and psychosocial impairment. Psychopathology assessments were available for a 10-month period (2021-06-01 to 2022-04-01), while assessments of affective well-being and psychosocial impairment were available for a 24-month period (2021-06-01 to 2023-06-01). Note that for the prediction of affective well-being ( N  = 25,844 over one year; N  = 10,636 over two years) and psychosocial impairment ( N  = 27,173 over one year; N  = 5342 over two years), sample sizes were somewhat smaller because for these analyses, we only included participants with at least two assessment within these time periods. The number of assessments varied between individuals depending on app usage duration and individual psychopathology. Mean and range of assessment frequency as well as the distribution of the 98 psychopathology scales and user attrition for the included users within the two-year period of assessment are available in the Supplemental material.

The feasibility and validity of this assessment method for psychopathology was investigated in a previous version of the app [ 38 ]. The procedure of data transfer and processing was approved by a local ethics committee of FU Berlin, Department of Psychology (Nr. 047/2020). Informed consent was obtained from all subjects that provided personal data (Ethics vote Nr. 038/2022). All data collection and analysis methods were performed in accordance with the Helsinki Declaration on Medical Research Involving Human Subjects as well as the European General Data Protection Regulation.

Assessment of psychopathology

Psychopathology items were developed by a board of licensed clinical psychologists, psychiatrists, and clinical psychology researchers to capture diagnostic criteria (symptoms) for mental disorders (team including AK and IB), maladaptive traits (AK, JZ, and LW), and personality functioning (AK, JCE, and TN). Table 1 lists all psychopathology scales used in this study, including example items. Questions on symptoms of mental disorders (71 scales, 128 items) were aligned with diagnostic criteria from ICD-11. Some disorders had general opening questions that triggered further questions. For example, for eating disorders (ED), affirming the opening question “Have you set up certain rules, prohibitions, or patterns about eating?” prompts subsequent questions on eating behavior. If the opening question was negated, all subsequent questions related to that disorder were assigned a value of 0 for further analyses. PF was assessed with 11 scales (27 items) that were identified as highly indicative of the severity of personality dysfunction based on previous data from the Operationalized Psychodynamic Diagnosis - Structure Questionnaire (OPD-SQ [ 18 , 39 ]) in clinical samples [ 40 ]. The original OPD-SQ [ 39 , 41 ] and its short form (OPD-SQS [ 42 , 43 ]) are self-reports for measuring impairments in PF that are consistently associated with interview-based measures of PF according to the DSM-5 AMPD [ 44 , 45 ] and other related constructs [ 46 , 47 , 48 ]. Items were reformulated to match the format of questions in the app (e.g., from “I sometimes feel like a stranger to myself” of the original OPD-SQ to “Do you sometimes feel like a stranger to yourself?”). Questions on maladaptive traits (22 scales, 5 domains, 40 items) were aligned with Criterion B of the DSM-5 AMPD. However, a low number of items and avoidance of redundancy in item content was a prerequisite for integrating the assessment in the App. Besides leaving out interstitial trait facets submissiveness and attention seeking, this led to omission of negative affectivity facets emotional lability and anxiety due to high redundancy with PF facet affect tolerance and items for generalized anxiety disorder, respectively as well as disinhibition facet distractibility and detachment facet depressivity due to redundancy with items for depression.

We averaged all psychopathology scores within participants across 10 months prior to the subsequent analyses. Using multiple averaged assessments yields indicators for stable dispositions and minimizes measurement error [ 49 ]. Unidimensionality of all scales with at least two items was ascertained using parallel analysis followed by reliability analyses using McDonald’s ω [ 50 ]. Due to the adaptive testing algorithm implemented in the app, the number of available assessments differed substantially per scale. For example, scale hopelessness had on average 13 assessments (range 0 to 61, SD  = 12.1) whereas others such as symptoms of obsessive compulsive disorder had on average 2.1 (range 0 to 7.3, SD  = 1.53). Descriptive statistics, hierarchical McDonald’s ω, and number of pairwise complete observations for all 98 psychopathology scales can be found in the Supplemental Material.

Assessment of psychosocial impairment

Psychosocial impairment was assessed based on two broad areas (i.e., well-being and basic functioning) initially identified through a joint factor analysis of measures of quality of life, social functioning, and disability [ 51 ]. Well-being was captured using items assessing self-acceptance (“Have you been satisfied with yourself lately?”), social relations (“Is the way you’re feeling interfering with how you’re interacting with others?”), and purpose in life (“Are you spending your time on things that are meaningful to you?”). Basic functioning was captured using items assessing mobility (”Is your anxiety or another emotional issue making it difficult for you to leave the house alone or keep appointments?”), self-care (“Are you finding it difficult to maintain your personal hygiene such as taking a shower or brushing your teeth?”), and work/school (“Are you finding it difficult to take care of your responsibilities because of how you feel?”). The average number of available assessments of psychosocial impairment over two years was 78.8 (range 3 to 916, SD = 85.1).

Assessment of affective well-being

App users were asked to rate their current mood at each assessment point up to three times daily using a single-item bipolar mood rating scale. Moreover, users were allowed to give mood ratings at any time. The scale consisted of 5 emojis representing different emotions (see Fig. 1 ). The selected emojis were converted to numeric values ranging from 0 to 4, with 0 indicating the lowest affective well-being at that moment. In a previous study, averaged affective well-being assessments over 2 weeks were a significant indicator of psychopathology [ 38 ]. The average number of available momentary affective well-being assessments per user in the study sample over two years was 336.8 (range 20 to 2627, SD  = 449.0).

Data analysis

Research question 1: integrating personality functioning into hitop.

To determine the hierarchical structure of psychopathology scales in our data, we applied a bass-ackwards procedure following Forbes et al. [ 34 , 52 ], using orthogonal equamax rotation. Due to the two-step answer format in the MindDoc app, scales were expected to be zero-inflated (i.e., non-normally distributed), rendering Pearson or Spearman correlations unsuitable for the estimation of the correlation matrix. We therefore applied semi-parametric latent Gaussian copula models [ 53 ] for estimation and used the resulting correlation matrix for subsequent analyses with pairwise complete observations. Equamax rotation adjusts for the number of rotated factors, distributing the number of scales with high loadings more evenly between factors than varimax rotation does. This in turn is an important prerequisite for the following bass-ackwards analysis as more general factors are expected to be found in higher levels of the hierarchy. Compared to other rotation methods, equamax is also particularly suitable for reproducing complex data structures [ 54 ]. The number of components (n) at the bottom layer of the hierarchy was identified through parallel analysis and Velicer’s minimum average partial (MAP).

Research question 2: transdiagnostic variance of personality functioning

To explore which aspects of psychopathology (i.e., scales assessing symptoms, traits, or PF) contribute most to the transdiagnostic variance found in the higher-order components identified in the previous step, we estimated symmetrical bifactor models for every higher-order component. We iteratively specified all higher-order components identified in the previous step as a general (G) factor, and the respective lower-order components loading on this higher-order component as specific (S) factors, using the scales defining these lower-order components as indicators. Parameters and model fit of all bifactor models can be found at https://osf.io/swj3c/ . Psychopathology scales with a high G-factor loading and low S-factor loadings (highest in case of scales loading on multiple S-factors) may predominantly capture transdiagnostic variance of the mental health syndromes defining the higher-order component.

Research question 3: longitudinal prediction of affective well-being and psychosocial impairment

In case we identified a lower-order component that was both consisting of PF scales (when addressing research question 1) and capturing mainly higher-order or transdiagnostic psychopathology variance (when addressing research question 2), this component would be a candidate for a reference factor in a confirmatory bifactor-(S-1) model [ 55 , 56 ]. Thus, we aimed to establish a bifactor-(S-1) model with a lower-order component consisting of PF scales as reference factor and all other lower-order components as S-factors, while including longitudinally assessed affective well-being and psychosocial impairment as covariates for all latent factors. We planned to extract the latent covariance matrix of this model and to use it for estimating regression models by means of matrix regression. Using this approach, variance explained (i.e., squared semipartial correlation coefficient, SSPC) in affective well-being and psychosocial impairment by the reference factor (i.e., PF) can be disentangled from unique variance explained by the other factors. To evaluate model fit, we calculated the unbiased SRMR index (SRMRu; [ 57 ]) because other common fit indices such as CFI and RMSEA can be biased in scenarios with a large number of variables and a large sample size [ 58 ].

Hierarchical structure

While Velicer’s minimum average partial (MAP) calculated for 1 to 20 factors reached a minimum with 14 and 15 factors, parallel analysis indicated 14 significant components. Based on these findings, we applied the ExtendedBassAckwards function [ 34 ], that is, sequential principal component analyses with 1, 2, 3, …, 14 components using equamax rotation combined with hierarchical agglomerative clustering on a latent correlation matrix of 98 psychopathology scales. The resulting hierarchical structure is shown in Fig. 2A , depicting 14 components at the bottom layer with loadings ≥0.31 of 98 scales. Each component was assigned a distinct meaning based on the scales with highest loadings as indicated by the labels used in Fig. 2A . It is important to note that 38 scales exhibited cross-loadings with other lower-order components within one spectrum (e.g., decision problems loading on the two depression subcomponents [N2, N9] and on the generalized anxiety disorder [GAD] subcomponent [N4]). Four PF scales (affect differentiation, affect tolerance, regulation of self esteem, and identity) showed loadings on four different components across spectra.

Complete hierarchical structure of 98 symptoms, traits, and personality functioning with 1–14 components ( A ) and without redundant and artefactual components ( B ) according to Forbes (2023) based on averaged psychopathology data of N  = 27,173 MindDoc users over 10 months. Note. In A , solid lines depict the perpetuation of a component between levels ( r  < 0.9), dashed lines depict emergence of new components (0.3 ≤ | r  | ≤ 0.9), dotted black lines depict correlations from lower-level to higher-level constructs 0.3 ≤ | r  | ≤ 0.9 which are not accounted for hierarchically. Redundant components: For constructs that perpetuate to the lowest level of the hierarchy, the version at the bottom of the hierarchy is retained (light green); for constructs that perpetuate from the top or through the middle of the hierarchy, the version of the construct closest to the top is retained (dark green). Components that can be removed due to close-to-redundancy with other components are depicted in light gray. Artefactual constructs that cannot be found in a hierarchical cluster analysis (see Supplementary material) are depicted in dark gray. In B , solid lines represent the strongest component correlation for each lower-order component with the higher-order components, and dashed lines are secondary component correlations 0.3 ≤ | r  | ≤ 0.9.

The final hierarchical structure without redundant and artefactual components is depicted in Fig. 2B . A detailed description of the related bass-ackwards procedure can be found in the supplementary material, reproducible code and all results of the Bass Ackwards procedure can be found at https://osf.io/swj3c/ . We found an internalizing higher-order component consisting of fear and distress subcomponents, encompassing cognitive and somatic depression, social anxiety disorder, GAD, agoraphobia, and specific phobia. We also identified an externalizing higher-order component with subcomponents of antagonism, PF, and disinhibition, encompassing antagonistic traits, 10 out of 11 of the PF scales, impulsivity, and substance use problems, as well as a thought disorder lower-level component encompassing schizotypal traits, dissociative, and psychotic symptoms along with OCD and manic symptoms. Somatoform symptoms loaded on both distress and fear subcomponents in the internalizing spectrum. The thought disorder component, along with the externalizing component, formed an externalizing, detachment, and thought disorder superspectrum that loaded on general psychopathology (GP). All three eating disorder (ED)-related lower-order components formed a higher-order ED component that loaded directly on GP. Note that although the lower order PF component primarily loaded on the antagonism subcomponent (M8), it also showed a significant secondary correlation with G3 (GAD & PF). Detachment, while also primarily loading on the externalizing higher-order component, had a significant secondary correlation with G1 (depression).

Psychopathology scales and components capturing higher-order factor variance

All 98 scales were investigated regarding their utility in capturing higher-order factor variance using symmetrical bifactor models for every higher-order component (see https://osf.io/swj3c/ for a reproducible script and model parameters). For instance, the bifactor model for the distress (D1) component included specific factors of somatic depression (N9), cognitive depression (N2), and GAD + OCD (N4), and all indicators of these lower-order components (see Fig. 2 ) also loaded on the general factor. Figure 3 presents standardized loadings on the G-factor and S-factors (highest loading in case of scales loading on multiple S-factors) of all scales and bifactor models, ordered by the difference between G- and S-loadings. Scales higher on the list (blue color) indicate a stronger association with the common variance of mental health syndromes in the respective higher-order component. Scales in red exhibit higher loadings on specific factors (i.e., lower-order components) than on the general factor (i.e., higher-order component). For most of the higher-order components, including GP, PF scales had the highest loadings on the general factor and lowest loadings on specific factors. Identity problems, affect differentiation, and affect tolerance were most indicative of internalizing disorders (G1, D1, G3, C1). Negative internal relationship models, affect communication, restricted affectivity, and anticipating behavior of others were most indicative of externalizing disorders (H7, M8). Self-reflection, identity, and affect tolerance were most indicative of the thought disorder and externalizing higher-order component (D3). Differential loadings between spectra were found for the detachment facets withdrawal, restricted affectivity, and intimacy avoidance, which were indicators of the general factors for thought disorder and externalizing while showing mainly S-loadings within higher-order internalizing components (G1, D1). Specific phobia and agoraphobia were most indicative of the fear (D2) component, whereas excessive exercising and counting calories were most indicative of the eating disorder (B2) component.

Standardized loadings on G factor for every scale from separate bifactor models defined for each higher-order factor depicted in the column header and its respective lower-order components as specific factors. Highest loading on specific factors in brackets. Scales in red have higher loadings on specific factors scales in blue have higher loadings on the respective general factor.

Results from the bifactor models showed that PF scales seem to be pure markers of most of the higher-order components including GP. PF can therefore serve as a reference factor in a bifactor-(S-1) model by partialling out the variance in the other lower-order components that covaries with PF problems [ 56 , 59 ]. To illustrate this procedure, Fig. 4 depicts latent correlations of a correlated factors model of all lower-order components on the left (without cross-loadings of PF scales), and a bifactor-(S-1) model on the right (with the PF factor N8 as reference, i.e., setting all 13 non-PF factors orthogonal to the PF/N8 factor). The correlated factors correlogram (left panel) shows that the PF/N8 factor is highly correlated with factors from both the internalizing and externalizing spectra (highest average intercorrelation), whereas the correlogram of the bifactor-(S-1) model (right panel) shows that the correlation pattern between all lower-order factors, which is the basis of the higher-order factors found in the previous step, changes substantially if the common variance between the 13 non-PF factors and the PF factor is removed/partialled out. Furthermore, while there are still low to moderately correlated clusters of distress, fear, eating, externalizing, and thought disorder psychopathology, correlations between internalizing and externalizing/thought disorder factors become negative.

Correlations between the 14 lower-order components, modeled in a correlated factors model without cross-loadings of PF scales (left); correlations between residuals of the 13 non-PF lower-order components when variance from PF/N8 component is removed, modeled in a bifactor-(S-1) model (right).

Longitudinal prediction of affective well-being and psychosocial impairment

Table 2 shows a prediction of average psychosocial impairment and affective well-being of users during their first year of app usage including the 10 months of psychopathology assessment (left) and average psychosocial impairment and affective well-being starting 10 months after the first assessment up to two years (right) using regression coefficients and squared semipartial correlations. For the reference factor PF problems (N8), squared semipartial correlations reflect the variance overlap with the criterion while for the remaining specific factors of the bifactor-(S-1) model, they reflect the unique variance explained in the criterion beyond the reference factor and all other specific factors.

Regarding the prediction of averaged impairment in psychosocial functioning in the first year, PF accounted for 58.6% of 84.7% total variance explained, with variance specific to somatic (10.0%) and cognitive depression (7.7%), as well as social anxiety (0.5%) also contributing significantly in the multiple regression models. Concerning averaged affective well-being in the first year, PF accounted for 30.6% of 61.4% total variance explained with variance specific to cognitive depression symptoms (17.8%), somatic depression symptoms (1.3%), thought disorder (0.7%), and detachment (1.5%) significantly contributing as well. Predicting averaged impairment in psychosocial functioning from 10 months up to two years after the first assessment, PF accounted for 33.1% of 48.7% total variance explained with cognitive (2.8%) and somatic depression (7.4%) symptoms and GAD (0.8%) contributing significantly. Concerning averaged affective well-being between 10 and 24 months after the first assessment, PF accounted for 23.2% of 42.4% total variance explained with variance specific to cognitive (8.6%) and somatic (0.9%) depression symptoms and detachment (1.1%) contributing significantly. Reproducible code for bifactor-(S-1) modeling and prediction can be found at https://osf.io/swj3c/ .

The aim of this study was to investigate the role of PF within the HiTOP framework of psychopathology using ambulatory assessed longitudinal data over two years in a sample of N  = 27,173 mental health app users. We conducted a bass-ackwards analysis that yielded a hierarchical taxonomy of psychopathological symptoms, traits, and PF (research question 1), which we subsequently used for latent modeling of general and specific component variance (research question 2) and longitudinal prediction (research question 3). Using a very large sample with repeated measurements, this study achieves an unprecedented level of measurement and estimation accuracy [ 49 ] with respect to answering the present research questions.

Locating personality functioning in a hierarchical dimensional structure of psychopathology

In our sample, we replicated a hierarchical dimensional structure that largely aligns with the HiTOP model [ 3 ]. However, we identified a distinct PF component that was indicative of internalizing, externalizing, and general psychopathology. Our findings also support previous evidence on higher-order constructs, including an internalizing spectrum with subfactors of distress and fear, a thought disorder component with psychotic symptoms, manic symptoms and schizotypal traits, and an externalizing spectrum with antagonistic and disinhibited components. OCD symptoms showed comparable loadings both on the thought disorder and generalized anxiety components corroborating previous evidence on the association of OCD with both fear and thought disorder related aspects [ 60 ]. Further, we found depression to split into a somatic and a cognitive component on the lower level. This finding aligns with several studies [ 61 , 62 , 63 ] detecting the distinction between cognitive and somatic depression symptoms to be helpful in the prediction of inflammation, coronary syndrome and HPA-axis hyperactivity. Divergences were found with respect to the eating disorder higher-order component, which only had low to moderate correlation with the Internalizing higher-order component. Nevertheless, its subfactor structure encompassing restrictive, bulimic and well-being-related eating disorder components was already found previously [ 64 ]. Moreover, the detachment component exhibited stronger correlations with the externalizing spectrum, especially with antagonism, as well as with (somatic) depression symptoms than with the thought disorder spectrum. However, several other studies also found a detachment component emerging from a higher-order externalizing factor [ 65 , 66 ].

Most notably, 10 of the 11 PF scales formed a distinct PF component (N8) with the PF facets anticipating behavior of others , affect communication and internal model of relationships showing the highest loadings. These scales were highly indicative of the p -factor in Wendt et al. (2023), and all PF scales loading on the PF component were highly indicative of a general factor of personality functioning in another study [ 40 ]. In addition, we found small to moderate loadings of separation insecurity , suspiciousness , perseveration , eccentricity , and impulsivity on this component. Most of these trait scales have moderate to large correlations with the total score or subdomains of DSM-5 PF [ 31 ]. These previous findings indicate that the N8 component found in our study mainly captures variance that is due to PF.

Taken together, while our findings corroborate previous evidence on empirical covariation of psychopathological syndromes, i.e. the comorbidity problem, which led to the development of HiTOP in the first place, they also point towards PF as a construct that is identifiable as a distinct component which shows moderate to high correlations across spectra and hierarchical levels.

Personality functioning as a transdiagnostic construct capturing higher-order component variance and predicting future outcomes

The use of symmetrical bifactor models to identify central indicators for higher-order factors in combination with a bifactor-(S-1) model for assessing the predictive validity of PF compared to other residualized lower-order components were inspired by suggestions on “riskier tests” and “bringing theory to the fore” concerning research on higher-order factors of psychopathology [ 67 , 68 ]. Using this exploratory approach, several PF indicators such as identity , affect differentiation , self reflection , affect tolerance , internal relationship models , and affect communication were identified to be pure markers of the internalizing, thought disorder, and externalizing spectra. Whereas for the externalizing spectrum, more interpersonal aspects of PF ( affect communication, anticipation, internal model of relationships ) defined the higher-order factor, for the internalizing spectrum, more self-related aspects of PF ( identity, affect differentiation, self reflection, affect tolerance ) defined the higher-order factor. Most of these scales that capture what could also be called “mentalizing impairments regarding one’s own mental states” were previously described as “pure markers of p” [ 33 ]. Our findings therefore suggest that aspects of PF play a significant role in a broad range of mental disorders. This is in line with the underpinnings of PF according to psychodynamic etiological theory as summarized by Bender and colleagues [ 14 ]: “Biological and environmental problems and their interactions can lead to maladaptive mental models of self and others, and to maladaptive patterns of emotional experience and expression, cognition, and behavior. These, in turn, may lead to the development of psychopathology in general and personality pathology in particular” (p. 344).

The basis for the higher-order structure, that is, the high correlation between the 14 factors on the bottom layer, seems to change significantly if variance that is attributable to PF is partialed out using a bifactor-(S-1) approach. While small to moderately correlated clusters of eating, fear, distress, externalizing, and thought disorder still remain, correlations between residualized components of internalizing and externalizing spectra are negative after partialling out PF. This indicates that PF may explain substantial parts of the variance of higher-order constructs in HiTOP. It could also indicate why patients with different disorders share common etiological pathways and respond to the same treatments. While this hypothesis cannot be corroborated using models of covariation, it is tentatively supported by the longitudinal prediction of affective well-being and psychosocial impairment using PF and residualized lower-order components in our sample. Specifically, in the longer run (up to two years), PF accounted for more than two-thirds of total variance explained in psychosocial impairment and more than half of the total variance explained in affective well-being in multiple regression models including 13 additional predictors based on 87 psychopathology scales.

Clinical implications

Following our findings of the importance of PF in a hierarchical taxonomy of psychopathology, clinicians may assess identity problems , affect differentiation , and communication , along with internal relationship models , as etiologically informed and prognostically relevant indicators for a broad range of mental disorders. A number of well-validated PF measures may thus provide both parsimonious and reliable utility for assessment and treatment planning. This is in line with recent practical recommendations [ 69 , 70 , 71 ] which emphasize that adaptations of treatment indication, modality, and intensity may be based on individual PF assessments. Drawing on findings of PF impairments and their clinical relevance (e.g., higher drop-out rates, less therapy compliance, more risk for ruptures in the therapeutic relationship, and generally higher rates of comorbidity and chronicity), patients with mild impairments in PF may need comparably less intense or structured treatments, whereas patients with moderate and high PF impairments may need highly structured settings and more intense or process-oriented treatments, with a particular emphasis on reducing destructive tendencies towards the self and others [ 69 ]. Our findings also tentatively suggest that treatment of internalizing disorders may focus on self aspects of PF, while treatment of externalizing disorders may focus predominantly on interpersonal aspects of PF. We therefore suggest the inclusion of short measures for PF, such as LPFS-BF 2.0 [ 72 ] or OPD-SQS [ 43 ], and maladaptive traits, such as the PID5BF + M [ 73 ], in routine outcome monitoring. For time-limited settings, a recent study suggests focusing on specific subdomains of intimacy and identity to clinically approximate PF [ 74 ].

Directions for future research

First, research should investigate PF as a potential treatment indicator and target change in transdiagnostic PF features as outcome. While long-term interventions such as psychotherapy seem to be effective for changing PF [ 75 ] and traits [ 22 , 76 ], future research is needed to differentiate the impact on different PF facets. In addition, the development of scalable (digitally aided) interventions that help to support change in PF may be relevant for general healthcare.

Secondly, research on etiological processes should investigate links to transdiagnostic PF features [ 77 ]. Disentangling transdiagnostic from specific variance using psychometrically sound latent constructs could also advance studies on genetic mechanisms in psychopathology [ 8 , 78 ]. Furthermore, longitudinal research that explores the development of PF from early childhood to young adulthood up to adult age with concurrent and HiTOP-conform assessment of psychopathology and allostatic load [ 79 ] over a long period of time is needed to investigate etiological questions of causality. A useful statistical approach to disentangle “surface characteristics” from “core processes” [ 80 ] could be longitudinal bifactor-(S-1) models. This approach could also be applied to repetitive assessments of psychopathology and PF within an EMA framework. Future developments in mental health tracking apps should implement strategies to provide low time gaps between assessments to enable within-person dynamic aspects of HiTOP using dynamic structural equation modeling [ 81 ].

Finally, in addition to data-driven approaches such as HiTOP, it is also important to continue developmentally informed, theory-based, and theory-oriented research on psychopathology [ 24 , 82 , 83 , 84 ]. Integrating personality functioning into these models can help to broaden existing approaches, with its descriptive approach on capacities helping to balance or integrate more specific conceptualizations. In the long term, it may also shed light on important empirical and conceptual questions regarding the p -factor [ 68 ]. Although progress has been made in differentiating symptoms and traits in the HiTOP model [ 11 ], further differentiation with regard to personality functioning is needed. The results of the current study supports other studies that argue that personality functioning may indeed not just index different ways of expressing maladaptive traits [ 31 ]. At the same time, the general HiTOP approach has the potential of including these different perspectives into one empirically based model.

Limitations

A number of limitations should be taken into account when interpreting the results of the current study. Approximations on sample characteristics can only be obtained from a separate assessment of a subsample of MindDoc users (see https://osf.io/swj3c/ ) and a previous clinical trial [ 36 ]. The scales or components of psychopathology that were used for the bass-ackwards-procedure differed with respect to their level of abstraction. For example, the schizophrenia spectrum was assessed with one scale whereas eating pathology was assessed with a total of 14 scales and other areas of interest such as PTSD were missing completely due to the given conceptualization of the mental health app. Further, the selection of items and the labeling of constructs used in this study may be subject to “jingle-jangle-fallacies” [ 85 ]. While both the MindDoc team and authors of this study examined redundancy in item content concerning PF, traits and symptoms, it may still be objected that PF and one of the outcomes, psychosocial impairment, cannot be separated conceptually, i.e. different labels for the same phenomenon. However, items used in this study to assess psychosocial impairments were aligned with constructs previously shown to be separable of PF in terms of exploratory factor analysis [ 51 ]. Furthermore, the two-step answer format leads to high skewness. Although we were able to address this with using latent correlations, and the extracted hierarchical structure was similar to other studies using different methods, we cannot rule out consequences regarding our results. In addition, some artefactual components that were removed in the bass-ackwards procedure represent clinically valid phenomena. For example, a patient with predominant anorexic or bulimic features could primarily seek help because of depressive symptoms (K8).

Methodological issues may concern the assessments based on self-reports and the accuracy of stepwise estimation using correlation matrices. Furthermore, causal etiological conclusions cannot be drawn unambiguously from our data as the bass-ackwards analysis was based on longitudinally averaged indicators and covariation does not automatically imply a common cause for disorders [ 86 ]. However, using repetitive longitudinally averaged assessments in a very large sample both removes confounding of within- and between-person variance and reduces random measurement error, both of which represent key shortcomings of cross-sectional self-report data [ 49 ]. We could also demonstrate substantial effects of PF on outcomes in longitudinal prediction. Furthermore, the two main outcomes on prediction differed in assessment methodology as affective well-being was assessed through ambulatory assessment (three times per day) and psychosocial impairment included reverse coded items.

Our findings can be interpreted as an empirical confirmation of the assumption that PF, including problems of identity, internal models of relationships, self-reflection, emotion awareness, and regulation, lies at the core of psychopathology. The extent to which these psychological capacities are a result of early childhood gene-environment interactions, as initially predicted by psychodynamic and interpersonal theories, and whether they may serve as a fruitful target of transdiagnostic mental health interventions is subject to future studies. However, disentangling transdiagnostic and specific variance in behavioral assessments of psychopathology may be crucial for advancements in all areas of psychiatry.

Data availability

The latent correlation matrix including R markdown code generating all tables and figures of this paper are available as open data and code via the Open Science Framework repository: https://osf.io/swj3c/ .

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Kerber, A., Ehrenthal, J.C., Zimmermann, J. et al. Examining the role of personality functioning in a hierarchical taxonomy of psychopathology using two years of ambulatory assessed data. Transl Psychiatry 14 , 340 (2024). https://doi.org/10.1038/s41398-024-03046-z

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Study combines data, molecular simulations to accelerate drug discovery

New research involving the uc college of medicine may lead to finding effective therapies faster.

Researchers from the University of Cincinnati College of Medicine and Cincinnati Children’s Hospital have found a new method to increase both speed and success rates in drug discovery.

The study, published Aug. 30 in the journal Science Advances, offers renewed promise when it comes to discovering new drugs.

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Alex Thorman, PhD Co-first author and postdoctoral fellow

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“And the accuracy will only improve, hopefully offering new hope to many people who have diseases with no known cure, including those with cancer,” Thorman said.

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“An accelerated drug discovery process also could be a game changer in the ability to respond to public health crises, such as the COVID-19 pandemic,” said Thorman. “The timeline for developing effective drugs could be expedited.” 

Feature image at top: Collection of prescription drug bottles and pills. Photo/Provided.

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Borderline Personality Disorder Research Paper

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Borderline personality disorder is a term that identifies a heterogenous group of patients with serious character pathology and behavioral disturbances. The main features of this disorder are behavior that is impulsive, dramatic, and often self-destructive; moods that are labile and reactive to life circumstances; interpersonal relationships that are stormy; and a sense of self-identity that is fragile and contradictory.

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Get 10% off with 24start discount code, i. historical development of the concept of borderline personality disorder.

II. Borderline Personality Disorder Core Symptoms and Character Styles

III. Demographic and Data-Based Studies of Borderline Personality Disorder

Iv. etiology and relationship to other disorders, a. psychoanalytic hypotheses, b. bpd as an affective spectrum disorder, c. bpd as posttraumatic stress disorder secondary to childhood sexual and physical abuse, d. bpd as an impulse spectrum disorder, v. course of borderline personality disorder, vi. treatment of bpd.

More than one decade after the development and publication of DSM-III, borderline personality disorder (BPD) remains the most controversial category in the nomenclature. Disagreement persists regarding the term itself, the particular diagnostic criteria established for BPD by DSM-III and DSM-IV, the scope of applicability, and the extent of overlap with Axis I and other Axis II disorders. Ultimately, this degree and intensity of dispute reflect both the range of difficulties in identifying and working with those persons designated as borderline, as well as the more basic question of validity: whether the BPD construct describes a meaningful unitary syndrome that corresponds to an actually existing state of affairs. While this latter question can certainly be asked of any of the personality (Axis II) disorders, something about the borderline concept seems to have engendered the strongest controversy.

At least one major reason for the ongoing disputes is the fact that the very concept of borderline was born out of attempts to explain the clinical observation that certain patients seemed to do very poorly in psychodynamic psychotherapy. Thus, from the very first, this category was used to describe a disparate group of patients who had two things in common: they responded to psychotherapy by developing transient psychotic symptoms and they did not meet classical definitions of schizophrenia. It is not that they did not necessarily improve; many obsessional patients, for example, did not improve with psychotherapy. Rather, it is that these patients worsened in psychotherapy with a fairly specific pattern of acting out that showed up most dramatically in the development of severe transference problems. The difficulty confronting the predominantly psychoanalytic theoreticians and skilled therapists was how to fathom the nature of these patients who gave promise of being good psychotherapeutic cases, yet deteriorated during the course of a psychotherapy. Thus, the very origins of the borderline concept arose in the context of a clinical puzzle.

The solution to the puzzle, keeping in mind that American psychiatry held a much more encompassing concept of schizophrenia in the 1940s and 1950s than at present, was to conceptualize these patients who became worse in psychotherapy as having a schizophrenic core underlying the neurotic facade. This notion was given concrete expression in a paper by Hoch and Polatin in 1949 describing the new category of pseudoneurotic schizophrenia. The construct fit neatly into a psychoanalytic model that postulated a spectrum of psychopathology based upon increasing primitiveness of defense mechanisms, extending in an unbroken chain from mild neurotics at one end to deteriorated schizophrenics at the other. The pseudoneurotic patient served as the missing link, bridging neurosis and psychosis, and thus serving as visible proof of the continuity connecting mild and severe psychiatric disorders.

The problem with the pseudoneurotic schizophrenia construct was that the patients did not go on to develop the more classical symptoms of hallucinations and delusions nor the deteriorating course that is the usual outcome of schizophrenia. Nevertheless, the observation that there existed a group of patients who appeared neurotic, but worsened with intensive psychotherapy, was a valid finding that outlived the misleading label attached to it. The focus of what might be wrong with these difficult-to-treat patients shifted away from schizophrenia to consideration of severe character pathology, described as borderline states by Knight in 1953 and as the psychotic character by Frosch in 1964. In addition, the joint U.S.-U.K. diagnostic studies carried out in the mid-to-late 1960s demonstrated convincingly that many patients diagnosed as schizophrenic by American psychiatrists fit much better with manic-depressive and personality disorder symptoms and outcome. This diagnostic realignment tightened the diagnostic criteria for schizophrenia, thereby further emphasizing the differences between borderline conditions and schizophrenia.

In 1968, Grinker and colleagues published the results of their study of 58 hospitalized patients who fell into a broadly defined notion of borderline syndrome. These patients had difficulties in interpersonal relationships, transient losses of reality testing under stress, angry and depressive affects, and deficient self-identities. Cluster analyses of the data, primarily of measurements of ego functions, produced four major clusters. There was a “core” borderline group, two groups defined as bordering upon the psychoses and neuroses, and a fourth group embodying certain “as-if” features, most notably absence of a core self-identity. Grinker’s study, the first to utilize psychometric instruments and statistical analyses, moved the borderline concept away from the realm of schizophrenic spectrum disorders and provided the basis for future empirical studies that continued the attempt to define the still vague borderline syndrome.

It is instructive that in the next series of studies carried out by Gunderson and Singer in 1975, the primary diagnostic concern was still to demonstrate that borderlines were different than schizophrenics. At the same time that empirical studies were focusing on narrowing the construct of borderline, Kernberg developed a broader notion of borderline, based upon a fusion of ego psychology and object relations theory, to designate a form of personality organization that was characterized by the use of primitive ego defenses (denial, splitting, projective identification), intact reality testing (with transient regressions under stress), and identity diffusion. Kernberg’s construct of borderline personality organization includes the milder as well as the more severe forms of character pathology, and, in essence, encompasses most of the patients presently grouped under the Cluster B (dramatic, unstable)personality disorders: histrionic, narcissistic, borderline, and antisocial.

This was the state of affairs while the DSM-IV committee developed inclusion and exclusion criteria for the personality disorders. There were four competing and overlapping concepts of borderline, and the final result represented some degree of compromise between the various groups. Since ideological and economic considerations, in addition to empirical studies and clinical lore, influenced the final product, it is important to define these considerations in some detail. The four overlapping concepts of borderline were as follows: (1) A residual model based upon the schizophrenic spectrum concept, using the term borderline to designate those persons, usually relatives of schizophrenics, who displayed odd, eccentric thinking and schizoid interpersonal relationships; this group was given the term schizotypal personality disorder. (2) An affective disorder model, which considered BPD as an affective spectrum illness displaying prominent features of mood instability with a predominance of depression, anger, and preoccupations with suicide. (3) An empirically derived model based primarily on the research of Gunderson, with diagnostic symptoms placed into five major groupings: impulse/action patterns (including self-destructive behaviors); ego-dystonic, transient psychotic episodes; mood instability with primarily negative affects; disturbed but intense interpersonal relationships; and an unstable sense of self. (4) A psychoanalytic concept based primarily on the work of Kernberg, but encompassing theoretical formulations by Mahler relating to difficulties in the separation/individuation phase of child development.

The final configuration of BPD adopted was most influenced by Gunderson’s work, but nevertheless showed the strains inherent in a compromise between points of view that are ideologically very divergent. The results were the creation of several new personality disorders within Axis II, not based upon empirical studies, but with each reflecting to some extent components that were once loosely connected to the borderline concept. Essentially, in dividing the broad territory of the borderline syndrome, as this concept evolved during a 40-year span, the cognitive disturbances that had long been noticed were placed in the schizotypal personality disorder, the milder dramatic and attention-seeking traits were placed into the histrionic personality disorder, self-centeredness and entitlement became the core of the narcissistic personality disorder, and the affective symptoms of mood instability and negative affectivity (depression, anger, anxiety), along with impulsivity, were given prominence in the borderline personality disorder.

Borderline personality disorder was defined by DSM-III-R as a condition marked by a pervasive pattern of instability of mood, interpersonal relationships, and self-image, beginning by early adulthood and present in a variety of contexts, as indicated by at least five of the following:

• A pattern of unstable and intense interpersonal relationships characterized by alternating between extremes of overidealization and devaluation.
• Impulsiveness in at least two areas that are potentially self-damaging, e.g., spending, sex, substance use, shoplifting, reckless driving, binge eating.
• Affective instability: marked shifts from baseline mood to depression, irritability, or anxiety, usually lasting a few hours and only rarely more than a few days.
• Inappropriate, intense anger or lack of control of anger, e.g., frequent displays of temper, constant anger, physical fights.
• Recurrent suicidal threats, gestures, or behavior, or self-mutilating behavior.
• Marked and persistent identity disturbance manifested by uncertainty about at least two of the following: self-image, sexual orientation, long-term goals or career choice, type of friends desired, preferred values.
• Chronic feeling of emptiness or boredom.
• Frantic efforts to avoid real or imagined abandonment.

The revision of DSM-III-R into DSM-IV was completed by late 1993. Although the BPD construct did not undergo any major alterations, several changes were instituted which served to correct the overemphasis in DSM-III on the close relationship between BPD and the affective disorders and the omission of cognitive deficits. Criterion 3 (Criterion 6 in DSM-IV), which outlined the affective symptoms seen in BPD was changed to reflect reactivity of mood; this serves to emphasize the difference between the mood disturbances seen in BPD and the relatively situationindependent mood disturbances characteristic of the endogenous affective disorders (major depression and manic-depressive illnesses). Complementing this more accurate delineation of the type of mood disorder seen in BPD was the inclusion of a new criterion to reflect the specific cognitive disturbances of BPD. The DSM-IV calls for a ninth criterion as follows: Transient stress-related paranoid ideation or severe dissociative symptoms. There were a few additional changes to the original eight criteria, but these are relatively minor, either reflecting grammatical alterations in the interest of clarity or the result of low sensitivity/specificity ratings for a few items on further field testing. Thus, the description of the identity disturbance in Criterion 6 was reworded and the construct “boredom” was dropped from Criterion 7.

II. Borderline Personality Disorder Core Symptoms and Character Style

The clinical description of a psychiatric disorder does not correspond exactly to that disorder’s diagnostic criteria in DSM-III. The main reason for this is that a clinical description needs to be a full and rich portrayal of the condition under question, whereas the requirements for diagnostic criteria are vastly different. Diagnostic criteria must aim for those characteristics of an illness that capture a few of its core symptoms while avoiding overlap with neighboring conditions. For example, as indicated above, while boredom may very well be a characteristic mental state in BPD, it was also found in histrionic and narcissistic personality disorders and therefore was of little specific diagnostic value. It did not help discriminate between BPD and other Cluster B personality disorders. In addition, diagnostic criteria must have acceptable validity and reliability. The issue of validity of psychiatric disorders, especially of personality disorders, is a troublesome one, since there are not external validators. The construction of DSM-III had paid major attention, some would say excessively so, to reliability issues. For example, certain factors that most workers would agree are characteristic of a disorder, such as the psychological defense of splitting in BPD, were not included in the diagnostic criteria because of a preference for behavioral rather than psychological phenomena, presumably because assessment of behaviors permits greater agreement as to whether they are present or not as compared to psychological constructs.

As indicated at the beginning of this research paper, there remains considerable controversy about the core characteristics and boundaries of BPD. Workers in the field have tended to bring to the evaluation of BPD their own theoretical and clinical perspectives in the evaluation of borderlines. In addition, some of the core characteristics of BPD, such as an increase in dissociative phenomena, appear to be changing in the past decade, a possibility that raises the question of the cultural influences and even faddish quality of some of the symptoms.

Most workers would agree that BPD is a relatively severe personality disorder, seen primarily in young adults, that presents with a characteristic cognitive style, mood disturbances, problematic interpersonal relationships, negative and deficient sense of self, and a variety of dramatic and impulsive behaviors usually of a self-injurious nature. These diagnostic features represent points distributed on a continuum of personality traits with somewhat arbitrary use of social norms to determine cut-off scores separating normal from pathological. Because of this, some workers in the field have advocated use of a dimensional rather than categorical model for the personality disorders, but a categorical model has always been adopted because it is easier to use in clinical work.

The cognitive style seen in borderline individuals encompasses three overlapping features. First, borderlines tend to have altered states of consciousness; these are usually referred to as dissociative states, and vary in intensity, density, and duration. They run the gamut from brief periods of self-absorption to fugue states lasting hours. The person may be partially or fully amnestic for some of the dissociative episodes. Second, borderlines tend to split their universe into good and bad, black and white. They have difficulty conceptualizing a person, including themselves, or an event, as encompassing positive and negative features. They tend to swing between the opposite poles of idealization and devaluation in their affections toward others. Third, borderlines tend to have impressionistic and global rather than precise and focused perceptions. They tend to be intolerant of unpleasant thoughts and images and to interrupt these processes with impulsive action, dissociation, and drug and alcohol use. There is a tendency toward imprecision and exaggeration, with a loss of salient detail. All of these disturbances are increased under conditions of stress.

The affective disturbances are characteristically mood instability or lability. Mood is typically reactive to environmental circumstances, but this must be taken to include the borderline’s own thought processes too. Negative affects, such as sadness, anger, and anxiety predominate the emotional landscape, but too literal adherence to this description would belie the positive affects and interpersonal warmth that borderlines can exhibit.

Problematic interpersonal relationships are a hallmark of borderlines. Their relationships are characteristically intense, stormy, and conflictual. Dependency needs, power struggles, and the idealization/devaluation swings described earlier tend to complicate most meaningful relationships. Victimization and entitlement themes in which the borderline alternates between being exploited by others and demanding reparations from others for damages incurred are frequent patterns seen in this disorder.

Borderline individuals tend to have a deficient sense of self, and what enduring image of themselves they may have is usually negative. A deficient sense of self refers to the absence of a stable sense of core identity, of knowing who you are. A certain degree of this is expected in adolescents and young adults in Western culture, but the borderline problem with identity, by definition, must go beyond the norm for this age group. Borderlines will take on different roles and personality characteristics, depending upon the dominant features of the group they are associating with. This has been referred to as the “as-if” personality, first described by Helene Deutsch in 1942. When not caught up in a persuasive group identity, borderlines tend to have very negative notions about themselves, ranging from dislike to contemptuous loathing.

Finally, borderlines characteristically are dramatic and impulsive in their actions. The patterns of impulsivity include directly self-injurious behaviors as well as an assortment of either ill-considered or risk-taking behaviors that also may be seen as self-destructive. Alcohol and drug abuse, bulimic eating disorders, promiscuity, and attraction to predatory partners are among the impusive actions seen in borderlines. As with the other core features of borderlines, the self-injurious behaviors range from infrequent and mild delicate cutting of the wrists to deep cutting of the limbs, torso, and genitals, as well as occasional ingenious use of cigarettes, lighters, caustic solutions, and hot irons to burn themselves. Suicide threats and attempts are also hallmarks of borderlines, most frequently but not exclusively with prescription as well as nonprescription medication overdoses. There are many more threats and gestures than serious attempts, leading to the use of the term “para-suicide” to describe these provocative actions of borderlines, but often the differentiation between manipulative and serious attempts is not at all clear.

There are no accurate measures of the prevalence of BPD in the community. Most estimates range from 0.5 to 1%, but may go higher as a broader concept of borderline, such as that used by Kernberg, is applied. The prevalence of the disorder in clinical settings is influenced by the type of clinical population under consideration. An average across studies indicates that the general prevalence of BPD is 10-15%, in inpatient settings about 20%, among outpatients with a personality disorder 30-35%, and among inpatients with a personality disorder 60-65%. Prevalence figures alone may be deceptive; it is possible that borderlines in an inpatient setting may have little similarity to outpatients who have never needed hospitalization. In most studies, excepting those done in VA and prison settings, 60-75 % of BPD are women.

Although DSM-III diagnostic rules do not permit differential weighting of the different criteria, most studies have demonstrated that several items contribute disproportionately to diagnostic efficiency. The presence of two, or at most three, specific criteria (impulsivity, unstable-intense interpersonal relationships, and self-injurious behaviors) predict most strongly the diagnosis of BPD, although once again, the type of clinical setting (inpatient or outpatient) will influence this finding.

There is considerable overlap (20-60%) between BPD and the other personality disorders, especially those of Cluster B, as well as schizotypal and dependent personality disorders. This finding continues to raise the question of whether personality disorders are discrete entities truly different from each other or reflect points on a continuum of serious character pathology. There are several Axis I disorders that have substantial overlap with BPD. These are alcohol and substance abuse disorders, bulimia, and the mood disorders, primarily dysthymia and major depression. To some extent, this finding reflects overlapping criteria (e.g., substance abuse is listed as a criterion for BPD), the heterogeneity of the BPD concept, and the fact that traits such as impulsivity and mood lability do express themselves in a wide array of behaviors.

Since it appears that BPD is not a unitary disorder, and since diagnostic threshold can be met in a polythetic system by fulfilling any five of eight (or nine, under DSM-IV) criteria, it is highly unlikely that a unitary etiology will be found for this or other Cluster B personality disorders. Theories about the etiology of BPD tend to follow major trends of interest in the behavioral sciences in general. Thus, the predominance of psychoanalytic constructs as explanatory hypotheses of human health and illness has given way to a variety of biological-genetic models in the past decade. Even the recent robust correlations between childhood sexual abuse and adult BPD symptoms are increasingly explained more in terms of long-lasting neurophysiological alterations of stress-response systems rather than in terms of psychodynamic mechanisms. The major theories of the etiology of BPD are as follow:

• Psychoanalytic model of stage-specific difficulties
• Deficit model (Masterson; Adler)
• Conflict model (Kernberg)
• BPD as an affective spectrum model
• BPD as post-traumatic stress disorder secondary to childhood sexual and physical abuse
• BPD as an impulse spectrum disorder

Based upon Mahler’s theories of the importance of successful resolution of the rapprochment subphase of the separation/individuation processes in toddlerhood (ages 15-30 months), several overlapping psychodynamic hypotheses were advanced to explain those BPD features that were thought to represent the consequences of rapprochment failure. These features were the mental operation and defense of splitting, identity diffusion, and deficiencies in object constancy and object relationships. Differences of opinion and emphasis exist between various psychodynamic theories: Masterson has suggested that the mother of the borderline is herself borderline and establishes emotionally impossible conditions for the toddler to achieve age-appropriate separation and individuation, thereby resulting in the development of a borderline personality in the child. Adler has emphasized the borderline child’s inability, under circumstances similar to those described by Masterson, to form internalized soothing, holding introjects, such that the borderline child (and adult) lacks basic ego functions such as frustration tolerance, stable self-object relationships, and methods for calming itself during periods of stress. Kernberg has postulated the likelihood of an excessive aggressive drive in the infant that interferes with the fusion of sexual and aggressive drives; Kernberg’s model therefore sees borderline pathogenesis as the result of a complex interaction between infant and caregiver rather than as unilaterally caused by a “not-good-enough” mother.

The basic problem with the psychoanalytic hypotheses regarding etiology of BPD is shared by psychodynamic explanations of behavior in general: first, difficulty in operationalizing and thereby in testing various theories and second, a lack of specificity whereby certain postulated mechanisms at best appear to be general risk factors (e.g., parental psychopathology) rather than the specific and inevitable cause of a particular outcome. This latter problem, of course, applies to all unitary theories of etiology. Finally, the nature of the psychodynamic hypotheses are such that supportive evidence comes primarily from retrospective rather than prospective studies, and from individual case studies in which the investigator testing the hypothesis is also the therapist commited to the hypothesis.

The observation that borderline patients are frequently depressed, and the prominence of mood instability in the symptom picture, have led to the hypothesis that an affective disorder underlies the borderline condition. Attempts to validate this hypothesis examined a variety of biological markers, familial patterns, follow-up data, and pharmacological responses. The initial findings, varying somewhat from study to study, were that from 20 to 60% of borderline patients met diagnostic criteria for an affective disorder, usually major depressive episode. This was not particularly surprising since the diagnostic criteria for BPD were slanted toward affective type symptoms. The studies have shown that patients with depression and borderline patients who were concurrently depressed resembled each other in regard to several biological markers of depression, such as the dexamethasone suppression test, REM latency time, and thyroid stimulating hormone response to thyrotropin, but the resemblances fell away with “pure” borderline patients, i.e., borderline patients who were not depressed.

Similar results were found in the family pedigrees of borderline patients. Borderline patients with concurrent depressions had a greater prevalence of relatives with affective disorders. However, this finding is true for most of the Axis II disorders, namely, that there is a higher prevalence of depressed persons in the families of patients with any personality disorder and depression. On the other hand, borderline patients without depression tend to have increased familial linkages to other disorders, namely, borderline and antisocial personality disorders, and alcoholism and drug abuse. Studies of pharmacological efficacy with borderlines have demonstrated minimal benefit from antidepressants, even with depressed borderlines, except for some amelioration of depressive symptoms. Lithium therapy has not proven valuable in treating BPD. There have been some indications that monoamine oxidase inhibitors are effective in reducing core borderline symptoms, thereby supporting the atypical depression model of BPD, but these findings have never been sufficiently replicated to be more than suggestive. Finally, the long-term follow-up studies have shown that most borderline patients do not go on to develop depressive syndromes, again arguing against a causal linkage between BPD and affective disorders.

Despite the fairly clear evidence that BPD is not a variant of affective disorders, most studies do show that a certain percentage of borderline patients have a recurrent affective disorder (either depressive or bipolar type II, i.e., depressions and hypomanias) and evolve into a typical affective disorder pattern after the dramatic borderline symptoms recede in the 30s. Thus, it seems likely that a subclass of borderlines has a primary affective disturbance.

There has been an increasing awareness of the frequency of childhood sexual abuse in the life history of many psychiatric patients. This awareness has paralleled a growing public consciousness of domestic violence of many types. The question remains unresolved as to whether child abuse and other forms of violence have indeed become more common recently, reaching epidemic proportions, or whether the social taboos that maintained silence over such assaults have been lifted, with the result of greater case-finding and reporting of such episodes. Among psychiatric patients, rates of childhood sexual abuse range between 25 and 80%, depending on the population surveyed and the survey methods. Surveys from such varied locations as state hospitals, community hospitals, outpatient clinics, and emergency rooms have been consistent in these findings. Reported rates are highest for borderline personality disorder, in the order of 50-80%. In the borderline population, there also appears to be a correlation between severity of certain types of symptoms, such as self-injurious behaviors and dissociative episodes, and the severity of the childhood sexual abuse experiences, as judged by age of first abuse, frequency and duration of abuse, degree of force and violence employed, and absence of ameliorative factors in the life of the child. The correlations between abuse and borderline symptomatology have been robust enough to lead several workers to hypothesize that most patients who have been diagnosed BPD are really suffering from PTSD and that this latter diagnosis makes better scientific and social sense, removing the stigma that has been attached to a BPD label. The case is strengthened by the logic of borderline symptoms, such as dissociation, as a learned response of the abused child to the horrors of the abuse experience, a response that was once adaptive, but has now become generalized as a response to all emotional flooding. In a similar way, self-injurious behavior seems to make sense as an expression of the self-hatred that the abuse victim directs inwardly.

There are several obvious problems to the linear causal chain that links childhood abuse to borderline symptomatology. The major problems relate to specificity between abuse and outcome. Patients with many psychiatric diagnoses, as well as many persons who do not have psychiatric symptoms have histories of childhood sexual abuse. Only a percentage of abused persons develop the BPD or PTSD picture. Conversely, not everyone with BPD has a history of childhood abuse. In addition, the abused child was most likely raised in a chaotic home with many other disturbing features, such that it is not valid to single out the experience of sexual abuse as the cause of adult problems. There are also considerable methodological problems related to the very sensitive nature of the topic and the fact that most of the research and clinical work are based upon retrospective reports of abuse in childhood. The methodological problems slice both ways; there are persons who have been abused and who deny it, and there are patients who may distort, exaggerate or invent abuse histories. There is no easy resolution to these issues, but, in general, the detailed reports by patients about their abuse appear to have credibility and are accepted by most researchers and health care workers. The particular diagnostic question discussed here about the overlap of BPD and PTSD, however, is less an issue of data than definition of causal relationships in human behavior. Thus, it appears that childhood sexual abuse and the disturbed environment in which the abuse occurred function as general risk factors predisposing to increased severity of many types of psychiatric and physical illnesses. Within the BPD population, there does appear to be a large subgroup whose symptoms and personality styles were profoundly affected by the experiences of childhood sexual abuse and whose symptoms can be understood as a form of PTSD. It needs to be kept in mind that PTSD is still a fairly vague concept encompassing many types of traumas and responses, and that most persons suffering from PTSD do not show borderline symptoms.

Although it sounds tautological to say that a syndrome characterized by impulsivity may be an impulse spectrum disorder, more is implied in the statement than meets the eye. Essentially, such a hypothesis raises the question of whether there is a group of disorders that share some common features in addition to impulsivity, such as familial linkage, associated psychiatric disorders, and underlying neurophysiological mechanisms. Family studies have shown an increased rate of alcoholism, substance abuse, and antisocial personality in the relatives of borderline personality. Other disorders considered related to problems with impulsivity include compulsive gambling, bulimia, intermittent explosive disorder, and the other Axis II personality disorders within Cluster B (histrionic and narcissistic). Studies are presently under way to investigate serotonergic and dopaminergic mechanisms that may have some linkage to impulsive behaviors.

It is well recognized that the notion of “impulsivity” is very vague, such that the various conditions being considered as impulse disorders may turn out to have very little in common beyond surface appearances. Conceptual clarification concerning what the terms “impulsive” and “compulsive” mean, and how these relate to the notion of “addiction,” will be necessary if the hypothesis regarding impulse spectrum disorder is to be of any practical use.

The initial delineation of borderlines as encompassing a group of difficult treatment cases combined with the finding of a poor outcome on short-term follow-up led to a fairly pessimistic outlook for patients with this diagnosis. Patients who were diagnosed in their late teens or early 20s as borderline were still doing poorly 2 to 5 years later, with ongoing self-injurious behavior and suicide attempts leading to multiple hospitalizations. It was not until the late 1980s that follow-up studies covered the 10- to 20-year period after initial hospitalization. Surprisingly, the outcome was much more favorable than the early studies indicated. In several independent studies from different parts of the country, it became clear that between 50 and 60% of BPD patients were doing fairly well as they moved into their 30s. Another 30-40% of patients showed varying levels of disability. Suicide rates ranged from 8 to 15 % on 10-year follow-up. The largest follow-up series of patients was reported by Stone, who traced 502 of 550 patients (of whom 193 met DSM-III criteria for BPD) who had been hospitalized on an intensive long-term psychotherapy ward at New York State Psychiatric Institute during the years 1963-1976. As judged by Global Outcome Scores (GAS), 63% of the BPD patients were in the good to recovered categories, another 16% had made a fair adjustment, 12% were doing poorly, and 9% suicided. Less favorable outcome was correlated with the presence of major affective disorder, antisocial personality, and a pattern of alcohol and drug abuse. Poor outcome was not correlated with self-mutilative behaviors in the early years of the illness. Patients with a history of childhood neglect or sexual abuse tended to do less well than patients without these histories. Finally, there was not a good overall correlation between outcome and psychiatric treatment; some patients with very good outcomes had minimal treatment following index hospitalization and some patients with extensive treatment had poor outcomes. It is possible that averaging the outcome data washes out a treatment effect, but this remains to be demonstrated.

Three has been as much controversy about the treatment of BPD as there has been about the diagnosis. To a large extent and with some overlap, treatment modalities have tended to follow etiological hypotheses. As one might expect with a condition that drew its initial delineation from a group of difficult-to-treat patients, no single modality has yet demonstrated clear-cut superiority or even effectiveness. Studies designed to evaluate treatment of BPD have been plagued by the usual problems of therapy outcome research: differing characteristics of the patient population, despite use of DSM-III criteria; difficulty in determining what constitutes evidence of improvement; difficulty in establishing control groups.

Psychodynamic psychotherapy has been the standard and accepted form of treatment of BPD, despite the many problems that arise in this form of treatment. In a sense, the BPD population, comprising primarily young verbal adults who are dysfunctional but nonpsychotic, have appeared to be the obvious if not ideal candidates for psychotherapy. Close to 50% of psychotherapy patients seen in private practice and at most outpatient clinics will have a diagnosis of BPD or a related Axis II Cluster B (narcissistic or histrionic) disorder. While there has been no canon defining a specific therapeutic protocol for BPD (or any other disorder), the work of Kernberg has been most influential in guiding the theory and practice of psychotherapy with borderlines. The therapy has tended to be a mix of supportive and exploratory work, with special attention paid to avoiding becoming enmeshed in ill-advised rescue attempts and other acting out features that are the hallmarks of borderline patients. The outcome results of the Menninger psychotherapy project reported by Wallerstein and Stone’s follow-up study suggest that it is impossible to predict, from patient characteristics alone, which patients would benefit most from supportive and which from exploratory psychotherapy, nor is there evidence that ultimate outcome is better with exploratory than supportive psychotherapy. A single study by Stevenson and Meares employing a 12-month psychotherapy regimen that utilized a written protocol based upon self-psychology demonstrated significant improvements across a broad range of measurements. Patients served as their own controls (pre- and post-treatment measures); a separate control group of patients was not used.

There has been increasing interest in cognitive-behavioral treatment (CBT) modalities for BPD. The essence of these modalities is a focus on recognizing and eliminating the factors that reinforce self-injurious behaviors, and learning and practicing new behaviors that will enhance the quality of life of the patient. Therapy is not directed toward underlying psychodynamic causes, since the assumption of CBT is that self-injurious behavior is a learned behavior that has become relatively independent of the specific causes that originally inspired it. CBT is done individually and in groups. Techniques that are taught and practiced include behavioral skill training, contingency management, cognitive restructuring, exposure to emotional cues, distress tolerance, interpersonal skills, and emotional regulation. Linehan and colleagues reported significant improvement in self-injurious and parasuicidal behaviors in a group of SIB borderlines in CBT compared to a group receiving treatment as usual. The improvements were not accompanied by changes in severity of reported depression, suicidal ideation, or reasons for living.

The relationship of BPD to PTSD in those borderlines who experienced sexual abuse in childhood suggests that a PTSD-oriented treatment program should be helpful. To date, this has not been the case, most likely because no overall effective program for the treatment of PTSD has been demonstrated. The treatment of PTSD usually includes group therapy, desensitization techniques, and pharmacological agents. There has been a proliferation of incest and sexual abuse treatment groups, some of which seem to be very helpful and some of which have a deleterious effect on some group members. No controlled studies have been reported. Pharmacological treatment of PTSD is in its infancy; different medications have been reported to be effective with particular components of PTSD, especially the sleep disturbance and depressions that accompany PTSD, but no agents appear to interrupt the flashbacks and intrusive imagery that form the hallmark of this disorder.

The pharmacological treatment of PBD is widely used, but relatively disappointing. Tricyclic antidepressants are effective only in alleviating depressive symptoms in those borderlines who are also depressed. Monoamine oxidase inhibitors have been reported to reduce the target symptom of rejection-sensitive dysphoria, but a controlled study is still wanting. There have not been controlled studies of the efficacy of the specific serotonin reuptake blockers to date. Lithium has not appeared to be of special benefit. There are mixed reports on the benzodiazepine anti-anxiety agents; there may be some benefit to the anti-anxiety properties, but several studies have reported a worsening of impulsive behaviors in BPDs taking these agents. In addition, long-term use of benzodiazepines would not be indicated in patients with significant alcohol or drug abuse histories. The single class of medications that has demonstrated significant short-term effectiveness in several key borderline symptoms has been low-dose anti-psychotics, but here the benefits must be weighed against the serious long-term side effects of these agents. A study of Soloff and associates in 1993 failed to replicate the positive findings of their earlier study reporting improvement in borderline patients with the use of antipsychotic medications.

There has been a recent trend away from long hospitalizations for borderline patients. While much of the driving force toward brief hospitalizations in all medical fields has been concern about rising medical costs, there has also been growing awareness of the deleterious rather than helpful effect of prolonged hospitalization of borderlines. Although there are undoubtedly some patients who benefit from a controlled hospital environment that prevents major self-destructiveness, the general experience has been that borderline patients continue their self-injurious behaviors in the hospital. This behavior sets up major conflicts with staff regarding proper responses to patients who challenge staff to prevent them from hurting themselves. Placing patients on one-to-one or constant observation has seemed to encourage rather than discourage self-injurious acts. The broad, but not unanimous consensus recently is that hospitalizations should be kept as brief as possible within the boundaries of responsible patient care, with the option of brief rehospitalizations seen as preferable to lengthy hospital stays.

Bibliography:

• Druck, A. (1989). “Four Therapeutic Approaches to the Borderline Patient.” Jason Aronson, Northvale, NJ.
• Gunderson, J. G. (1984). “Borderline Personality Disorder.” American Psychiatric Press, Washington, DC.
• Herman, J. L. (1992). “Trauma and Recovery.” Basic Books, New York.
• Kernberg, O. (1984). “Severe Personality Disorders.” Yale University Press, New Haven, CT.
• Kroll, J. (1988). “The Challenge of the Borderline Patient.” WW Norton, New York.
• Kroll, J. (1993). “PTSD/Borderlines in Therapy: Finding the Balance,” Norton, New York.
• Linehan, M. M., Armstrong, H. E., Suarez, A., Allmon, D., and Heard, H. L. (1991 ). Cognitive-behavioral treatment of chronically parasuicidal borderline patients. Arch. Gen. Psychiatry 48, 1060-1064.
• Links, P. S. (1990). “Family Environment and Borderline Personality Disorder.” American Psychiatric Press, Washington, DC.
• Paris, J. (1992). “Borderline Personality Disorder: Etiology and Treatment.” American Psychiatric Press, Washington, DC.
• Soloff, P. H., Cornelius, J., George, A., Nathan, S., Perel, J. M., and Ulrich, R. F. (1993). Efficacy of phenelzine and haloperidol in borderline personality disorder. Arch. Gen. Psychiatry 50, 377-385.
• Stevenson, J., and Meares, R. (1992). An outcome study of psychotherapy for patients with borderline personality disorder. Am. J. Psychiatry 149, 358-362.
• Stone, M. (1990). “The Fate of Borderline Patients.” Guilford, New York.
• Wallerstein, R. S. (1986). “Forty-Two Lives in Treatment.” Guilford, New York.

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The IHP Interview: Rebecca Willman on Occupational Therapy as a Tool for Eating Disorder Treatment

Rebecca Willman, OTD '23, published her research paper " The potential role of occupational therapy in the treatment of avoidant/restrictive food intake disorder " earlier this year. Willman’s research on how occupational therapy could help patients with avoidant/restrictive food intake disorder (ARFID) was the culmination of her yearlong independent study with  Dr. Jennifer Thomas , the co-director of the  Eating Disorders Clinical and Research Program at Massachusetts General Hospital. 

A new lab instructor for the  Occupational Therapy in Mental Health course,  Willman recently won the OT Department's Alumni Professional Achievement Award for her work at  The Home for Little Wanderers and McLean Hospital, where she has taken a role as the first dedicated occupational therapist treating patients at McLean’s  Klarman Eating Disorders Center . In this month's IHP Interview, Strategic Communications Intern Sophie Hauck spoke with Willman about how occupational therapists play a unique role in eating disorder treatment, and why treating ARFID could be a gateway for OTs to work with people with eating disorders.

Why did you decide to specialize in eating disorder treatment as an occupational therapist?

I studied psychology and minored in nutrition in undergrad, and I saw this gap in how these two disciplines approach eating disorders. That's what occupational therapy is — the bridge between all the different aspects of eating disorder treatment. From then on, I became committed to research and advocacy for eating disorder treatment.

When you have an eating disorder, a lot of times, you're one circle, and the eating disorder is another, and you're overlapped. A lot of treatment is about separating yourself from the eating disorder, and then working through it with cognitive coping skills and different types of psychotherapy and psychoeducation. Occupational therapy is uniquely positioned to work through applying those skills in realistic context for patients in their daily life.

I take a lifestyle redesign approach, which is a framework that we use in occupational therapy where we go through every part of your day in a systematic way, and we determine, where are the problems? What are the challenges? What are some habits that are not aligned with what you want for recovery? Then we collaboratively problem-solve those things.

You spent a year conducting research with Dr. Jennifer Thomas at Mass General Hospital about how occupational therapy could help patients with avoidant/restrictive food intake disorder (ARFID). What is ARFID, and what were your findings?

Avoidant Restrictive Food Intake Disorder (ARFID) is a newer diagnosis in the DSM-5, characterized by a disturbance in eating or feeding that is not driven by body image concerns. There are three subtypes including a lack of interest in eating or food, avoidance based on the sensory characteristics of food, and fear of aversive consequences of eating — all of which have unique clinical presentations and functional implications. 

I didn't know much about ARFID before I started my research. I've always been drawn to more well-known eating disorders, like anorexia nervosa, bulimia nervosa, or binge eating disorder. Dr. Jennifer Thomas specializes in ARFID, so she pitched the idea to me to learn more about what occupational therapy can do in ARFID treatment. 

In the paper, I write about how OT has a long history of being involved in pediatric feeding disorders and feeding disorders in general. Oral motor differences often cause functional differences and physical impairments in eating and feeding. These experiences can impact someone's relationship with food psychologically or cognitively, which is where ARFID is maintained. ARFID can then persist even if those physical oral motor differences are remediated. 

With OT intervention to address oral motor differences early, an individual may have less aversive experiences with food and therefore a lower risk of developing ARFID. OTs can help prevent those issues through rehab of the muscles, and we have different tools that can promote more effective use of the mouth in eating and feeding, as well as and oral sensory function. 

There's also the sensory approach, where you can do whole-body sensory input to get somebody into a space where they're able to access higher levels of cognition. If their fight-or-flight response is on all the time because they have experienced trauma related to eating or feeding, and that's a perpetuator of their ARFID, then using those whole-body sensory inputs can help them regulate and come into a less distressed state, so they can try foods and have an appetite.  

Then there’s the component of overall occupational balance. A lot of times, when you have ARFID, it can isolate you, or your treatment might interfere with your social participation or your leisure. You can't do the things that you want to do all the time, and OT can help reshape those routines and roles and habits to promote recovery from ARFID.

Content creators are raising ARFID awareness through social media. Have you seen public knowledge of this eating disorder increase since you began researching it?

ARFID is a newer DSM diagnosis. Once there’s a diagnosis, more people are bound to receive that diagnosis, and with more people receiving a diagnosis, more people will naturally know about ARFID.

I did a guest lecture for the Occupational Therapy in Mental Health course at the IHP in June, and when I was a student here, ARFID wasn't even mentioned. I added it into my presentation, and I asked, ‘Has anyone heard of ARFID?’ and almost everyone raised their hands. I was very shocked to see that progression because I know that none of my friends in grad school knew about it, but almost everybody knew about it in the current cohort in the OT program. That was cool.  

How did your background in research shape your clinical experience at the MGH Institute, as well as the client-facing work you do now?

Throughout grad school, all my field work and clinical experiences were such foundational components because I was drawn more to analysis, research, and theory.

I still want to be doing research, so I'm actively applying to PhD programs to try to teach eventually. Clinical experience is so important to have as a researcher and as a professor because, especially with clinical research, you can understand the barriers to implementing research in clinical practice, and you can understand what clinical practice needs. 

I gain a lot of perspective from working with my clients and hearing their stories, and it keeps you out of that, one-size-fits-all, monotonous, robotic approach because you have to individualize to make a difference in the daily life of a person, versus just taking a protocol and applying it to their case.  

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