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The Medical Metaverse, Part 1: Introduction, Definitions, and New Horizons for Neuropsychiatry.

Abstract: Back to table of contents Next article Windows to the BrainFull AccessThe Medical Metaverse, Part 1: Introduction, Definitions, and New Horizons for NeuropsychiatryWilfredo López-Ojeda, M.S., Ph.D., and Robin A. Hurley, M.D.Wilfredo López-OjedaSearch for more papers by this author, M.S., Ph.D., and Robin A. HurleySearch for more papers by this author, M.D.Published Online:12 Jan 2023https://doi.org/10.1176/appi.neuropsych.20220187AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail Editor’s note: This report is the first of a two-part series introducing the concepts of the medical metaverse. Part 1 covers the basic definitions and its current utility in mental health care. Part 2 will address the metaverse as it relates to clinical neurosciences and will appear in a subsequent issue of The Journal of Neuropsychiatry and Clinical Neurosciences.The “metaverse” was initially used in literature by the science fiction writer Neal Stephenson in his 1992 dystopian novel Snow Crash (8, 9). The metaverse denotes a digital platform as a new and alternative environment manifested through digital content delivered via advanced technological devices employing artificial intelligence (AI) (2). This platform encompasses highly immersive and collaborative environments based on three-dimensional and real-time digital worlds in which multiple users can engage in activities (e.g., social, economic, and cultural). The users interact via avatars in versatile settings without physical limitations (10, 11). A metaverse research organization, the Acceleration Studies Foundation (ASF), proposed thinking about the metaverse as a link or connection point between the real and virtual worlds (2, 12). In the metaverse, however, users are not limited by the typical rules of nature (e.g., age, gender, appearance, and species). Freedom from other restrictions, such as time and space, is also enabled by virtual reality (VR) technologies (both hardware and software). Thus, individuals can engage in a wide array of activities that are impossible in real life (2).Metaverse TechnologiesThe cybernetic progression continues to advance with support from major technology companies. According to the literature, within the next 5 years tens of billions of dollars will be invested to expand currently available platforms (13). This rapid progression of core technologies, including AI, “big data,” the Internet of things (IoT), edge computing, blockchain, digital twins (DT), extended reality (XR), and high-speed 5G Internet networks, underpins the metaverse’s existence, advancement, and sustainability (14–18). The coronavirus disease 2019 (COVID-19) pandemic stimulated additional advances (2). Therefore, it is necessary to understand the concept of the metaverse, its nuances, and its applications for medical education and health care delivery (19).According to the ASF, the metaverse roadmap distinguishes technologies along two separate dimensions, augmentation versus simulation and intimate versus external, to characterize four general types of metaverse technologies: augmented reality (AR), lifelogging, mirror worlds, and virtual worlds (1). In the metaverse, augmentation and simulation are defined by whether the information is presented in physical reality (via AR) or in VR (via simulation) (Figures 1 and 2) (1, 2). Conversely, intimate (identity-focused) technologies are centered on the actions of the individual or object; for example, the user or object (i.e., semi-intelligent object) engages by using an avatar or digital profile. In contrast, the external (world-focused) technologies are centered on the outside world, and they typically focus on the control of aspects of the surrounding world, such as the ability to provide information about the conditions of the external environment and how the user can control these conditions (Figures 1 and 2) (1, 2).FIGURE 1. Quadrant-based metaverse diagram.The horizontal axis includes metaverse technologies that facilitate the empirical relationship between technology and user. The left side reflects the external environment, and the personalized experience of the user is intensified toward the right, intimate side (1, 2). In the external milieu, the surrounding world is emphasized, and this outward perspective is user centered and provides guidance to the user on how to engage with these environmental features. The intimate element of the metaverse provides an inward perspective and focuses on individualized behaviors guided by customized data. The vertical axis includes technologies that exemplify the relationship between reality and innovation. Augmentation increases the human sensory experience by incorporating new functions into the real-world environment via visual, auditory, and other sensory stimuli. Conversely, simulation duplicates the real world by modeling reality in a virtual world (1, 2).FIGURE 2. Four categories of metaverse technology.A. Augmented reality (AR). AR uses virtual imaging and fetching technologies to integrate digital information into the real-world environment (3). B. Lifelogging. This technology obtains digital records of the user’s personal data (e.g., heart rate, breathing, and sleep patterns) by capturing, storing, and sharing information by using multimodal digital sensors integrated in high-tech devices, such as smart watches, smart phones, and wearables (2, 4). C. Mirror worlds. In this type of technology, the real world is depicted (i.e., simulated) with digital innovations (e.g., satellites and interactive software) to reflect the characteristics of the external world in the cybernetic world. These simulations replicate an accurate version of the real-world structures and human environments (i.e., mirror duplicates). Google Earth, Foldit, and Microsoft Teams are examples of digital applications simulating mirror worlds (2, 5, 6). D. Virtual worlds. The virtual world incorporates virtual reality (VR) technology. In VR, the user is fully immersed and is completely blinded to the real environment; this immersion is facilitated by a head-mounted display (digital lenses) in which the user receives visual, auditory, and other sensory inputs (1, 2, 7).COVER. Artistic depiction of the medical metaverse. On the right, various technologies of the digital biomedical world. On the left, the head-mounted display lenses and the brain symbolize the immersive experience of extended reality and its role in the metaverse.All images created under the terms of the Creative Commons Attribution License. Created with VH Dissector, Canva, and BioRender.com.Medical MetaverseMetaverse technologies have opened new horizons for innovations in medicine. Medical education and health care practices are embracing technological advancements to improve patient care (2, 20–22). A wide range of subspecialties, such as cardiology, emergency medicine, gastroenterology, gynecology, oncology, ophthalmology, and radiology, are employing metaverse technologies (4, 22–26). Mental health disciplines are also benefiting from metaverse innovations, specifically XR technologies (VR, AR, and mixed reality) (27). VR technologies are among the most widely used advances in mental health interventions. VR exposure therapy (VRET) and AR exposure therapy have proven effective in treating specific phobias, posttraumatic stress disorder (PTSD), anxiety, attention-deficit hyperactivity disorder, substance-related disorders, depression, and eating disorders (20, 28–31).VRET employs psychotherapeutic immersive paradigms that provide multisensory VR experiences to amplify the patient’s experiential engagement during treatment sessions (27). VRET interventions are effective in reducing PTSD symptoms of active-duty and combat soldiers after military trauma (32, 33). XR therapeutic benefits are based partly on its immersive capabilities that allow experiences at a digital multisensorial level and integrate a seamless human-computer interface (27). Deepak Chopra indicated that “the metaverse guides us past the notion that mind, body, and spirit are separate” because the metaverse incorporates technologies (e.g., AR and VR) to rectify one’s dysfunctional reality by using virtual (functional) reality (34). VR innovations allow for the reproduction of transcendental experiences (e.g., delivering joy, distraction, and positive affect in a soothing environment) (34–36). Higher-level cognitive functions (e.g., decision making and problem solving) may vary based on the body’s characteristics that the individual perceives as self-owned. A study performed by Banakou et al. used superintelligent (“Albert Einstein”) and average-intelligence virtual body avatars to illustrate this concept (37). Participants who embodied the Einstein avatar performed cognitively better than those who embodied an average-intelligence avatar of an age similar to their own (37). A similar influence of the owned body has been shown in social behavior studies. These experiments investigated whether acting through certain types of avatars (i.e., as players in video games) and the avatars’ actions could influence pro- or antisocial behaviors (194 subjects). Players choosing more heroic avatars were encouraged to behave in a more prosocial manner. The authors reported that after acting as a villain or superhero within the virtual world, participants modeled the behaviors of their chosen avatars when interacting with their fellow players in the real world. In addition, the investigators highlighted that role-taking activities supported behaviors consistent with the priming actions (i.e., activities of the heroic or villainous avatar) (38). The introduction of avatars may support treatment engagement during psychotherapy (39). Thus, the virtual world can serve as a vehicle for observation, simulation, and modeling, and avatars power these processes (38). Additional benefits of avatar-integrated therapies include increases in treatment seeking via anonymity, reductions in communication barriers, facilitation of expression and exploration of client identity, and improvements in interventional settings by allowing therapists to control and manipulate the treatment conditions within the virtual environment (39).Metaverse technologies may establish an ideal scenario for mental health research (e.g., sense of body ownership) and the development of new therapies. The fact that real-life situations are difficult to replicate in the real world (i.e., during psychotherapy sessions) but can be safely recreated in cyberspace opens many possibilities for new therapeutic interventions (28). For example, VRET has proven effective in replicating human reactions (e.g., fear-inducing situations generating social anxiety) in real social environments (40, 41). Furthermore, VRET has been successfully used to reduce social anxiety associated with stuttering when speaking to those with authority or during public speaking (42).The COVID-19 pandemic has resulted in significant lifestyle changes worldwide. By extension, health care systems have transformed traditional health education and clinical care settings in an effort to decrease face-to-face interactions. Metaverse technologies are an effective alternative for remote care of certain chronic conditions and biometrically enhance care models involving mental health treatment. These treatments include mindfulness and cognitive-behavioral therapy, either guided by a therapist or as a self-help program (43, 44). In addition, medical metaverse XR innovations may supplement current therapeutic approaches and expand mental health care access (31).ConclusionsIn conclusion, the world is experiencing a digital health care transformation with the development of core technologies (e.g., AI, IoT, DT, and XR). The metaverse is driving these innovations synergistically to increase access to health care services among multiple disciplines, supplement medical education and training, and optimize the experience of delivering and receiving medical care to meet the clinical needs of patients. Part 2 of this series will further explore the rapidly changing influence that the metaverse has on clinical neurosciences.Veterans Affairs Mid-Atlantic Mental Illness Research, Education and Clinical Center (MIRECC) and the Research and Academic Affairs Service Line, W. G. Hefner Veterans Affairs Medical Center, Salisbury, N.C. (López-Ojeda, Hurley); Departments of Psychiatry and Behavioral Medicine (López-Ojeda, Hurley) and Department of Radiology (Hurley), Wake Forest School of Medicine, Winston-Salem, N.C.; Menninger Department of Psychiatry and Behavioral Sciences, Baylor College of Medicine, Houston (Hurley).Send correspondence to Dr. Hurley ([email protected]).Supported by Veterans Integrated Services Network 6 MIRECC.The authors report no financial relationships with commercial interests.References1. Smart J, Cascio J, Paffendorf J: Metaverse Roadmap: Pathways to the 3D Web. Acceleration Studies Foundation, 2007. https://www.metaverseroadmap.org/MetaverseRoadmapOverview.pdfGoogle Scholar2. Kye B, Han N, Kim E, et al.: Educational applications of metaverse: possibilities and limitations. J Educ Eval Health Prof 2021; 18:32Crossref, Medline, Google Scholar3. Wirza R, Nazir S, Khan HU, et al.: Augmented reality interface for complex anatomy learning in the central nervous system: a systematic review. 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J Neuropsychiatry Clin Neurosci 2021; 33:A4, 173–177Link, Google Scholar21. Wiederhold BK: Metaverse games: game changer for healthcare? Cyberpsychol Behav Soc Netw 2022; 25:267–269Crossref, Medline, Google Scholar22. Skalidis I, Muller O, Fournier S: CardioVerse: the cardiovascular medicine in the era of metaverse. Trends Cardiovasc Med (Epub May 11, 2022). https://doi.org/10.1016/j.tcm.2022.05.004Google Scholar23. Zhang C, Feng S, He R, et al.: Gastroenterology in the metaverse: the dawn of a new era? Front Med 2022; 9:904566Crossref, Google Scholar24. McWilliam A, Scarfe P: The metaverse and oncology. Clin Oncol (R Coll Radiol) (Epub Jul 13, 2022). https://doi.org/10.1016/j.clon.2022.06.011Google Scholar25. Werner H, Arcoverde V, Ribeiro G, et al.: An interactive experiment combining ultrasound, magnetic resonance imaging, and force feedback technology to physically feel the fetus during pregnancy. Eur J Radiol 2019; 110:128–129Crossref, Medline, Google Scholar26. Tan TF, Li Y, Lim JS, et al.: Metaverse and virtual health care in ophthalmology: opportunities and challenges. Asia Pac J Ophthalmol 2022; 11:237–246Crossref, Medline, Google Scholar27. López-Ojeda W, Hurley RA: Cranial nerve zero (CN 0): multiple names and often discounted yet clinically significant. J Neuropsychiatry Clin Neurosci 2022; 34:A4, 95–99Link, Google Scholar28. Ifdil I, Situmorang DDB, Firman F, et al.: Virtual reality in metaverse for future mental health-helping profession: an alternative solution to the mental health challenges of the COVID-19 pandemic. J Public Health (Epub Apr 25, 2022). https://doi.org/10.1093/pubmed/fdac049Google Scholar29. Baus O, Bouchard S: Moving from virtual reality exposure-based therapy to augmented reality exposure-based therapy: a review. Front Hum Neurosci 2014; 8:112Crossref, Medline, Google Scholar30. Freeman D, Reeve S, Robinson A, et al.: Virtual reality in the assessment, understanding, and treatment of mental health disorders. Psychol Med 2017; 47:2393–2400Crossref, Medline, Google Scholar31. Usmani SS, Sharath M, Mehendale M: Future of mental health in the metaverse. Gen Psychiatr 2022; 35:e100825Crossref, Medline, Google Scholar32. Rizzo A, Shilling R: Clinical virtual reality tools to advance the prevention, assessment, and treatment of PTSD. Eur J Psychotraumatol 2017; 8:1414560Crossref, Medline, Google Scholar33. Reger GM, Holloway KM, Candy C, et al.: Effectiveness of virtual reality exposure therapy for active duty soldiers in a military mental health clinic. J Trauma Stress 2011; 24:93–96Crossref, Medline, Google Scholar34. Chopra D: Is the Metaverse the New Hope for Mental Health? SFGATE. https://www.sfgate.com/news/article/Is-the-Metaverse-the-New-Hope-for-Mental-Health-17221756.php. Accessed Sep 26, 2022Google Scholar35. Liu K, Madrigal E, Chung JS, et al.: Preliminary study of virtual-reality-guided meditation for veterans with stress and chronic pain. 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Kampmann IL, Emmelkamp PMG, Morina N: Meta-analysis of technology-assisted interventions for social anxiety disorder. J Anxiety Disord 2016; 42:71–84Crossref, Medline, Google Scholar41. Hartanto D, Kampmann IL, Morina N, et al.: Controlling social stress in virtual reality environments. PLoS One 2014; 9:e92804Crossref, Medline, Google Scholar42. Chard I, van Zalk N: Virtual reality exposure therapy for treating social anxiety: a scoping review of treatment designs and adaptation to stuttering. Front Digit Health 2022; 4:842460Crossref, Medline, Google Scholar43. Chapman JR, Wang JC, Wiechert K: Into the spine metaverse: reflections on a future metaspine (uni-)verse. Glob Spine J 2022; 12:545–547Crossref, Medline, Google Scholar44. Boettcher J, Carlbring P, Renneberg B, et al.: Internet-based interventions for social anxiety disorder: an overview. Verhaltenstherapie 2013; 23:160–168Crossref, Google Scholar FiguresReferencesCited byDetailsCited byNone Volume 35Issue 1 Winter 2023Pages A4-3 Metrics KeywordsMetaversevirtual realityaugmented realitymixed realitymedical educationhealth care technologiesPDF download History Received 25 October 2022 Accepted 9 November 2022 Published online 12 January 2023 Published in print 1 January 2023

Elimination of Refractory Aggression and Self-Injury With Contingent Skin Shock.

Abstract: Back to table of contents Previous article Next article Case ReportsNo AccessElimination of Refractory Aggression and Self-Injury With Contingent Skin ShockNathan Blenkush, Ph.D., and Miles Cunningham, M.D., Ph.D.Nathan BlenkushSearch for more papers by this author, Ph.D., and Miles CunninghamSearch for more papers by this author, M.D., Ph.D.Published Online:14 Feb 2023https://doi.org/10.1176/appi.neuropsych.21020049AboutSectionsView articleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail View article Access content To read the fulltext, please use one of the options below to sign in or purchase access. Personal login Institutional Login Sign in via OpenAthens Purchase Save for later Item saved, go to cart PPV Articles - Journal of Neuropsychiatry and Clinical Neurosciences $35.00 Add to cart PPV Articles - Journal of Neuropsychiatry and Clinical Neurosciences Checkout Please login/register if you wish to pair your device and check access availability. Not a subscriber? Subscribe Now / Learn More PsychiatryOnline subscription options offer access to the DSM-5 library, books, journals, CME, and patient resources. This all-in-one virtual library provides psychiatrists and mental health professionals with key resources for diagnosis, treatment, research, and professional development. Need more help? PsychiatryOnline Customer Service may be reached by emailing [email protected] or by calling 800-368-5777 (in the U.S.) or 703-907-7322 (outside the U.S.). FiguresReferencesCited byDetailsCited byNone Metrics KeywordsSelf-MutilationViolence/AggressionSelf-InjuryTreatment RefractorySkin ShockPDF download History Received 22 February 2021 Revised 24 March 2022 Accepted 27 November 2022 Published online 14 February 2023

A Brain Mechanism for Hate.

Abstract: Back to table of contents Previous article Next article OpinionFull AccessA Brain Mechanism for HateMario F. Mendez, M.D., Ph.D.Mario F. MendezSearch for more papers by this author, M.D., Ph.D.Published Online:14 Feb 2023https://doi.org/10.1176/appi.neuropsych.20220121AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail Hate, defined here as intense dislike that encourages the elimination of others, involves dehumanization, or the denial of human qualities to others. Despite the importance of understanding the neuropsychiatry of hate, clinicians and investigators have devoted relatively little effort to its study. A review of the existing, albeit limited, literature suggests that hate depends on sufficiently dehumanizing others in order to permit their elimination. A potential brain mechanism for hate appears to involve an “animalistic” infrahumanization that results in withholding empathy from the devalued targets; this mechanism may be mediated by the inferior frontal cortex (IFC) (1). What follows is an attempt to support this hypothesis.As hate crimes, exemplified by horrific shootings at houses of worship and other public venues, continue to plague the United States, neurologists and psychiatrists may have an increasingly important role in elucidating the brain mechanisms that underlie hateful behavior. Although hatred is a major scourge of humankind, there is limited consensus on the nature of this phenomenon. There is disagreement as to whether hate is even an emotion. While some define hate as a deep, enduring, intense emotion (2), others consider it a long-lasting attitude or disposition of intense dislike punctuated by negative emotions such as anger (3). Whether emotion or disposition, there is additional disagreement on whether hate necessarily leads to an impulse to socially, psychologically, or physically eliminate its target. Nevertheless, hate that leads to negative impulses toward others is the source of much human tragedy.Given the controversy over the definition of hate, it is not surprising that there are a wide range of theories that attempt to explain hateful behavior. First, there are theories that reflect social psychological principles such as the need to belong and conform to social groups, pressures, norms, and rules. These social influences promote compliance with hateful behavior through deindividuation and group anonymity, diffusion of responsibility, passive compliance, blind obedience to authority, and ingroup versus outgroup distinctions (4). Second, some personality theories view certain people as being predisposed to hateful behavior, having a negative view of others, and possessing personality attributes that include authoritarianism and social dominance (5). These people homogenize all members of an outgroup and attribute deficient and negative character traits to them; thus, hateful individuals devalue and morally exclude outgroup members. Finally, there are direct theories of hate, such as Sternberg’s duplex theory (6). This theory proposes that hate involves a negation of intimacy, a negation of passion, and a negation of commitment, which are derived through stories that involve prototypes of targets with negative characteristics. The major feature that all of these theories seem to have in common is the need to dehumanize others, which is best seen as a cognitive heuristic that denies the human qualities of a hated “them.”The literature on dehumanization and its relation to the brain distinguishes two main forms of dehumanization: treating others as animals (devaluing through infrahumanization) and treating others as objects (a mechanistic unawareness of their basic humanity) (7). Investigators describe infrahumanization as the perception that outgroup individuals lack uniquely human traits, particularly secondary emotions, while retaining the basic emotions evident in other animals (8). Haslam’s dual model (7) further applies the term “animalistic dehumanization” to this devaluing of others as subhuman or nonhuman animals (e.g., “swine,” “monkeys,” and “vermin”), which arouses feelings of disgust and revulsion toward outgroups and makes harming them easier (9). Animalistic dehumanization normally occurs as a restraint on empathy when needed, such as situations involving social dominance or self-protection (e.g., averting one’s eyes from a panhandler) (10) and probably originates from activity in the ventrolateral prefrontal region—most probably the IFC (1). Haslam’s dual model further distinguishes a second form of dehumanization that results from a perceived lack of human nature or a perceived lack of being a human with an intentional mind (7, 11). This form of “mechanistic dehumanization,” which denies the existence of a mental life (“mentalization”) with thoughts, feelings, beliefs, and agency in others, sees those who are hated as nonliving machines or objects, resulting in feelings of indifference toward them (7). Mechanistic dehumanization is associated with decreased mesial prefrontal activity involving the ventromedial prefrontal cortex and perigenual anterior cingulate cortex (12) and decreased parietal and default mode network function (1).Taking the theories of hate and the studies on dehumanization into consideration, hate may depend on animalistic infrahumanization with heightened activity in the IFC facilitating disdain and disgust for the devalued target. The absence of moral emotional engagement, including hate, among frontolimbic brain-injured patients, such as those with frontotemporal dementia (FTD) (13), highlights the differential association of hate with animalistic dehumanization rather than with mechanistic dehumanization. Although the neuropathology of FTD is centered in the mesial frontal, anterior insula, and anterior temporal lobe structures (14)—regions purported to overlap with a proposed hate network (15)—patients with damage to these structures may have prominent mechanical dehumanization and indifference to others without the presence of hate.Actions based on hate continue to have grave consequences and require a more studied approach to cognitive factors, such as the type and origin of an underlying dehumanization that encourages harm toward others. Hate may emerge from a heightened normal mechanism for devaluing others, possibly mediated by the IFC, rather than the adulteration of mentalization seen with disease involving predominantly frontal dysfunction. Clearly this is a proposed starting point, or a hypothesis, for approaching an understanding of hate; hopefully, this hypothesis can stimulate further investigation of the neuropsychiatric mechanisms underlying hate, with an eventual goal of guiding efforts to mitigate its expression.Departments of Neurology and Psychiatry and Behavioral Sciences, David Geffen School of Medicine, University of California, Los Angeles; Neurology Service, Neurobehavior Unit, VA Greater Los Angeles Healthcare System, Los Angeles.Send correspondence to Dr. Mendez ([email protected]).Dr. Mendez is supported by the National Institute on Aging (grant 1RF1AG050967).The author reports no financial relationships with commercial interests.References1. Bruneau E, Jacoby N, Kteily N, et al.: Denying humanity: the distinct neural correlates of blatant dehumanization. J Exp Psychol Gen 2018; 147:1078–1093Crossref, Medline, Google Scholar2. Reber AS, Reber E: The Penguin Dictionary of Psychology. New York, Penguin Books, 2002 Google Scholar3. Ekman P: Emotions Revealed. New York, Henry Holt and Company, 2003 Google Scholar4. Zimbardo PG: A situationist perspective on the psychology of evil: understanding how good people are transformed into perpetrators; in The Social Psychology of Good and Evil. Edited by Miller AG. New York, Guilford Press, 2004, pp 21–50 Google Scholar5. Altemeyer B: Highly dominating, highly authoritarian personalities. J Soc Psychol 2004; 144:421–447Crossref, Medline, Google Scholar6. Sternberg RJ, Sternberg K: The Nature of Hate. Cambridge, Cambridge University Press, 2008 Crossref, Google Scholar7. Haslam N: Dehumanization: an integrative review. Pers Soc Psychol Rev 2006; 10:252–264Crossref, Medline, Google Scholar8. Leyens J-P, Paladino PM, Rodriguez-Torres R, et al.: The emotional side of prejudice: the role of secondary emotions to ingroups and outgroups. Pers Soc Psychol Rev 2000; 4:186–197 Crossref, Google Scholar9. Goff PA, Eberhardt JL, Williams MJ, et al.: Not yet human: implicit knowledge, historical dehumanization, and contemporary consequences. J Pers Soc Psychol 2008; 94:292–306Crossref, Medline, Google Scholar10. Ligneul R, Girard R, Dreher J-C: Social brains and divides: the interplay between social dominance orientation and the neural sensitivity to hierarchical ranks. Sci Rep 2017; 7:45920Crossref, Medline, Google Scholar11. Harris LT, McClure SM, van den Bos W, et al.: Regions of the MPFC differentially tuned to social and nonsocial affective evaluation. Cogn Affect Behav Neurosci 2007; 7:309–316Crossref, Medline, Google Scholar12. Scalabrini A, Ebisch SJH, Huang Z, et al.: Spontaneous brain activity predicts task-evoked activity during animate versus inanimate touch. Cereb Cortex 2019; 29:4628–4645Crossref, Medline, Google Scholar13. Mendez MF, Anderson E, Shapira JS: An investigation of moral judgement in frontotemporal dementia. Cogn Behav Neurol 2005; 18:193–197Crossref, Medline, Google Scholar14. Seeley WW: Selective functional, regional, and neuronal vulnerability in frontotemporal dementia. Curr Opin Neurol 2008; 21:701–707Crossref, Medline, Google Scholar15. Zeki S, Romaya JP: Neural correlates of hate. PLoS One 2008; 3:e3556Crossref, Medline, Google Scholar FiguresReferencesCited byDetailsCited byNone Metrics Keywordsdehumanizationpsychopathyfrontotemporal dementiaviolenceaggressionneuropsychologyPDF download History Received 21 June 2022 Revised 20 September 2022 Accepted 9 November 2022 Published online 14 February 2023

Mania Following Traumatic Brain Injury: A Systematic Review.

Abstract: OBJECTIVE Traumatic brain injury (TBI) is a leading cause of mortality and morbidity worldwide. Mania is an uncommon, but debilitating, psychiatric occurrence following TBI. The literature on mania following TBI is largely limited to case reports and case series. In the present review, the investigators describe the clinical, diagnostic, and treatment characteristics of mania following TBI. METHODS A systematic search of MEDLINE, EMBASE, and PsycINFO was conducted for English-language studies published from 1980 to July 15, 2021. The included studies provided the required individual primary data and sufficient information on clinical presentation or treatment of manic symptoms. Studies with patients who reported a history of mania or bipolar disorder prior to TBI and studies with patients who sustained TBI before adulthood were excluded. RESULTS Forty-one studies were included, which reported information for 50 patients (the mean±SD age at mania onset was 39.1±14.3 years). Patients were more frequently male, aged <50 years, and without a personal or family history of psychiatric disorders. Although 74% of patients reported mania developing within 1 year following TBI, latencies of up to 31 years were observed. Illness trajectory varied from a single manic episode to recurrent mood episodes. Rapid cycling was reported in six patients. Mood stabilizers and antipsychotics were most frequently used to improve symptoms. CONCLUSIONS Heterogeneity of lesion locations and coexisting vulnerabilities make causality difficult to establish. Valproate or a second-generation antipsychotic, such as olanzapine or quetiapine, may be considered first-line therapy in the absence of high-level evidence for a more preferred treatment. Early escalation to combined therapy (mood stabilizer and second-generation antipsychotic) is recommended to control symptoms and prevent recurrence. Larger prospective studies and randomized controlled trials are needed to refine diagnostic criteria and provide definitive treatment recommendations.

NMDA Receptor Antibodies and Neuropsychiatric Symptoms in Parkinson's Disease.

Abstract: OBJECTIVE N-methyl-d-aspartate receptor (NMDAR) encephalitis is an autoantibody-mediated neurological syndrome with prominent cognitive and neuropsychiatric symptoms. The clinical relevance of NMDAR antibodies outside the context of encephalitis was assessed in this study. METHODS Plasma from patients with Parkinson's disease (PD) (N=108) and healthy control subjects (N=89) was screened at baseline for immunoglobulin A (IgA), IgM, and IgG NMDAR antibodies, phosphorylated tau 181 (p-tau181), and the neuroaxonal injury marker neurofilament light (NfL). Clinical assessment of the patients included measures of cognition (Mini-Mental State Examination [MMSE]) and neuropsychiatric symptoms (Hospital Anxiety and Depression Scale; Non-Motor Symptoms Scale for Parkinson's Disease). A subgroup of patients (N=61) was followed annually for up to 6 years. RESULTS Ten (9%) patients with PD tested positive for NMDAR antibodies (IgA, N=5; IgM, N=6; IgG, N=0), and three (3%) healthy control subjects had IgM NMDAR antibodies; IgA NMDAR antibodies were detected significantly more commonly among patients with PD than healthy control subjects (χ2=4.23, df=1, p=0.04). Age, gender, and disease duration were not associated with NMDAR antibody positivity. Longitudinally, antibody-positive patients had significantly greater decline in annual MMSE scores when the analyses were adjusted for education, age, disease duration, p-tau181, NfL, and follow-up duration (adjusted R2=0.26, p=0.01). Neuropsychiatric symptoms were not associated with antibody status, and no associations were seen between NMDAR antibodies and p-tau181 or NfL levels. CONCLUSIONS NMDAR antibodies were associated with greater cognitive impairment over time in patients with PD, independent of other pathological biomarkers, suggesting a potential contribution of these antibodies to cognitive decline in PD.

Posttraumatic Stress Symptoms Among COVID-19 Survivors After Hospitalization.

Abstract: OBJECTIVE Limited data are available on posttraumatic stress symptoms (PTSS) among COVID-19 survivors. This study aimed to contribute to this knowledge base. METHODS PTSS among COVID-19 survivors who had been hospitalized were investigated. Patients were identified as COVID-19 positive at hospital admission. COVID-19 survivors were surveyed with the Posttraumatic Stress Disorder Checklist (PCL-5) between March and October 2020 at 5- and 12-month postdischarge follow-up points. RESULTS Of 411 patients, 331 (81%) survived to hospital discharge. Of these survivors, 83 (25%) completed the PCL-5 at the 5-month follow-up. Of those patients, 12 (14%) screened positive for PTSS. At the 12-month follow-up, four of eight patients remained PTSS positive. Mean age of follow-up participants was 62±15 years; 47% were women, 65% were White, and 63% were Hispanic. PTSS-positive patients were predominantly non-White (67% vs. 30%, p=0.02), and although the differences were not statistically significant, these patients tended to be younger (56 vs. 63 years, p=0.08) and have shorter intensive care unit stays (2.0 vs. 12.5 days, p=0.06). PTSS-positive and PTSS-negative groups did not differ significantly in prehospitalization neurological diagnoses (11% vs. 8%), psychiatric diagnoses (17% vs. 21%), and intensive care admission status (25% vs. 25%). More patients in the PTSS-positive group had returned to the emergency department (50% vs. 14%, p<0.01) and reported fatigue at follow-up (100% vs. 42%, p<0.001). In the multivariate logistic regression model, non-White race (OR=11, 95% CI=2-91) and returning to the emergency department (OR=19, 95% CI=3-252) were associated with PTSS-positive status. CONCLUSION PTSS were twice as common among hospitalized COVID-19 survivors than among those in the general population.

Functional Movement Disorder: An Interdisciplinary Case-Based Approach

Abstract: Back to table of contents Previous article Next article Book ReviewFull AccessFunctional Movement Disorder: An Interdisciplinary Case-Based ApproachNy-Ying Lam, M.D.Ny-Ying LamSearch for more papers by this author, M.D.Published Online:7 Jul 2023https://doi.org/10.1176/appi.neuropsych.20220168AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail edited by Kathrin LaFaver, Carine W. Maurer, Timothy R. Nicholson, David L. Perez; Cham, Switzerland, Humana Press, 2022, 463 pages.Patients with functional movement disorders (FMDs) often embark on a long and costly diagnostic journey to determine the cause of their disabling condition. FMD, which is a subset of functional neurological disorder (FND), is a diagnosis that sits between the realms of neurology and psychiatry. Patients undergo complex medical workups, and if no structural cause is found, patients complain of being told “it’s all in your head.” People come out of this experience feeling demoralized and unheard. Historically, medically unexplained symptoms have been difficult to align with contemporary conceptualizations of disease. In the textbook under review, the authors expertly summarize the historical context and evolution of the diagnostic criteria and nomenclature for FND. This approach provides a crucial backdrop to better understand FMDs.Functional Movement Disorder: An Interdisciplinary Case-Based Approach is a practical clinical textbook that brings together worldwide experts from the fields of neurology, psychiatry, mental health, and rehabilitation. The editors have all contributed significantly to the growing body of research characterizing FND subtypes and the attempt to understand the biological basis of FND symptoms. Both Dr. Kathrin LaFaver and Dr. Carine Maurer are neurologists and movement disorder specialists who have researched and developed pragmatic multidisciplinary treatment programs for patients with FMD. Dr. Timothy Nicholson, a neuropsychiatrist, and Dr. David Perez, double-boarded in neurology and psychiatry, highlight the importance of breaking down barriers to treatment of this neglected patient group whose physical health and mental health are inextricably linked.The book is organized in a logical flow, with part 1 laying the framework for a foundational understanding of the history of FND, the pathophysiology underlying FMDs, and the biopsychosocial model of medicine as applied to FMDs. The chapters in part 2 describe the most common clinical presentations of FMD by using a case-based approach. Each clinical chapter highlights specific features of the physical examination that constitute positive signs for FMD, which is incredibly helpful. Key differentiating factors from similar neurological diagnoses are discussed, with information well organized in tables or figures. For instance, one table compares features of functional jerky movements, tics, myoclonus, dyskinesias, and restless legs. When available, epidemiology, risk factors, and diagnostic or objective testing are discussed. Considerations for pediatric and older adult populations are also presented.The largest and final section, part 3, expands on management and treatment plans. This section includes multiple chapters explaining at length how to communicate the diagnosis to the patient, while providing tips, pitfalls, and guidance for complex situations or circumstances in which patients disagree with the diagnosis. Other chapters outline interdisciplinary care approaches by describing rehabilitation (physical therapy, occupational therapy, and speech therapy) and psychological approaches to treatment. The practical tips for determining which treatment modalities are appropriate for particular patients and developing a unified treatment plan are well appreciated.One area that is not fully expanded on in this text is the spectrum of other FNDs and somatic symptoms such as pain, fatigue, dizziness, nonepileptic seizures, sensory abnormalities, or cognitive complaints. These somatic symptoms are lumped into one chapter in part 2. FMD patients rarely present with movement symptoms in isolation, and additional guidance on how to explain and address these functionally limiting somatic symptoms would have been useful. My only other critique is that redundant information is provided across the clinical chapters in part 2, although this repetition may be difficult to avoid because patients often present with multiple, overlapping FMD symptoms.As a physiatrist, I appreciate that a key message in this book is an emphasis on the importance of collaborative interdisciplinary care. I hope that this textbook can inspire more physiatrists to join neurologists, psychiatrists, and other rehabilitation specialists in conducting research and treating patients who have FMD.I would recommend this book for any clinician who sees patients with medically unexplained symptoms affecting movement. This practical handbook empowers the clinician to make a diagnosis of FMD more definitively, to initiate treatment, and to counsel patients on the diagnosis and treatment plan. By providing an evidence-based approach to the assessment and management of FMD, this textbook serves as a ready resource for the busy clinician.Department of Rehabilitation Medicine, University of Washington School of Medicine, Seattle.Send correspondence to Dr. Lam ([email protected]).Michael Schrift, D.O., M.A., is the editor of the Book Reviews section.Dr. Lam reports no financial relationships with commercial interests. FiguresReferencesCited byDetailsCited byNone Metrics KeywordsFunctional Neurological DisorderFunctional Movement DisorderSomatoform DisordersRehabilitationNeuropsychiatryConversion DisorderPDF download History Published online 7 July 2023

Case Study 4: A 68-Year-Old Woman With Progressive Cognitive Decline and Anxiety.

Abstract: Back to table of contents Previous article Next article Clinical Case Conference in Behavioral Neurology & NeuropsychiatryNo AccessCase Study 4: A 68-Year-Old Woman With Progressive Cognitive Decline and AnxietyRishab Gupta, M.D., Vihar Patel, M.D., Scott M. McGinnis, M.D., David Silbersweig, M.D., Michael B. Miller, M.D., Ph.D., Mel B. Feany, M.D., Ph.D., Kirk Daffner, M.D., Seth A. Gale, M.D.Rishab GuptaSearch for more papers by this author, M.D., Vihar PatelSearch for more papers by this author, M.D., Scott M. McGinnisSearch for more papers by this author, M.D., David SilbersweigSearch for more papers by this author, M.D., Michael B. MillerSearch for more papers by this author, M.D., Ph.D., Mel B. FeanySearch for more papers by this author, M.D., Ph.D., Kirk DaffnerSearch for more papers by this author, M.D., Seth A. GaleSearch for more papers by this author, M.D.Published Online:12 Jan 2023https://doi.org/10.1176/appi.neuropsych.20220151AboutSectionsView articleView Full TextSupplemental MaterialPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail View article Access content To read the fulltext, please use one of the options below to sign in or purchase access. Personal login Institutional Login Sign in via OpenAthens Purchase Save for later Item saved, go to cart PPV Articles - Journal of Neuropsychiatry and Clinical Neurosciences $35.00 Add to cart PPV Articles - Journal of Neuropsychiatry and Clinical Neurosciences Checkout Please login/register if you wish to pair your device and check access availability. Not a subscriber? Subscribe Now / Learn More PsychiatryOnline subscription options offer access to the DSM-5 library, books, journals, CME, and patient resources. This all-in-one virtual library provides psychiatrists and mental health professionals with key resources for diagnosis, treatment, research, and professional development. Need more help? PsychiatryOnline Customer Service may be reached by emailing [email protected] or by calling 800-368-5777 (in the U.S.) or 703-907-7322 (outside the U.S.). FiguresReferencesCited byDetailsCited byNone Volume 35Issue 1 Winter 2023Pages 4-11 Metrics KeywordsAlzheimer DiseaseAnxietyDementiaAlcohol UseNeuropathologyPDF download History Received 13 August 2022 Accepted 14 November 2022 Published online 12 January 2023 Published in print 1 January 2023

Changes in Posttraumatic Stress Disorder Symptoms With Integrative Psychotherapy for Functional Neurological Symptom Disorder

Abstract: Objective: Patients with functional neurological symptom disorder (FNSD) report high rates of traumatization and have high levels of posttraumatic stress disorder (PTSD) symptoms. Psychotherapy is a mainstay of treatment for persons with FNSD. In this study, the investigators explored changes in PTSD symptoms and health-related quality of life after psychotherapy among persons with FNSD and examined factors contributing to these changes. Methods: Data were prospectively collected for patients with FNSD attending a specialist outpatient psychotherapy service in the United Kingdom (N=210) as part of an ongoing routine service evaluation. Pre- and posttherapy questionnaires included self-report measures of PTSD symptoms (Posttraumatic Stress Disorder Checklist–Civilian version), depressive symptoms (Patient Health Questionnaire–9), anxiety symptoms (General Anxiety Disorder–7 scale), somatic symptoms (Patient Health Questionnaire–15), health-related quality of life (Short-Form Health Survey–36), and social functioning (Work and Social Adjustment Scale). Independent contributions to psychotherapy-related changes in PTSD symptoms and health-related quality of life were explored through multivariate analyses. Results: All outcome measures revealed improvements after psychotherapy (p<0.001). Psychotherapy-related changes in depression and somatic symptoms and employment status at baseline explained 51% of the variance in PTSD symptom changes. Changes in PTSD symptoms, depressive symptoms, and somatic symptoms made independent contributions to improvements in health-related quality of life (R2=0.54). Improvements were unrelated to FNSD subtype (dissociative seizures or other FNSD), age, marital status, or number of sessions attended. Conclusions: Reductions in self-reported PTSD, depressive, anxiety, and somatic symptoms, as well as improved health-related quality of life, were observed among patients who received one or more sessions of psychotherapy. Randomized controlled trials of psychotherapy for patients with FNSD are warranted.

Time for Brain Medicine.

Abstract: Unprecedented knowledge of the brain is inevitably contributing to the convergence of neurology and psychiatry. However, clinical training continues to follow a divergent approach established in the 19th century. An etiological approach will continue to shift more psychiatric patients to the care of neurologists who are untrained in psychiatric management. At the same time, this new era of diagnostic biomarkers and neuroscience-based precision treatments requires skills not readily available to those trained in psychiatry. The challenges in training the next generation of doctors include establishing competence involving aspects of the whole brain, fostering the subspecialized expertise needed to remain current, and developing programs that are feasible in duration and practical in implementation. A new 4-year residency training program proposed in this article could replace existing residency programs. The program includes 2 years of common and urgent training in various aspects of neurology and psychiatry followed by 2 years of elective subspecialty tracks. The concept is similar to internal medicine residencies and fellowships. No changes to existing departmental structures are necessary. In concert with the emerging biological approach to the brain, "brain medicine" is proposed as a new name to denote this practice in the simplest terms: a focus on all aspects of the brain.

Introversion and Neuroticism in Akinetic-Rigid Parkinson's Disease: Association With Frontal-Executive Dysfunction.

Abstract: OBJECTIVE Personality changes have often been reported among people with Parkinson's disease (PD); however, no studies have investigated the associations between personality traits, cognitive function, and specific motor symptoms. In this study, the investigators assessed whether particular personality traits were associated with specific motor subtypes of PD (e.g., tremor-dominant and akinetic-rigid phenotypes) and whether frontal-executive functions were associated with personality traits among patients with a specific motor phenotype. METHODS Forty-one people with PD and 40 healthy control participants were enrolled in the study. All participants underwent assessments of cognitive and psychological function and personality traits. The study was conducted in Italy. RESULTS Tremor-dominant symptoms occurred among 20 (48.8%) people with PD, whereas 21 (51.2%) patients exhibited akinetic-rigid symptoms. Multivariate analyses of variance revealed that participants with akinetic-rigid PD demonstrated significantly poorer performance on frontal-executive tests compared with those with tremor-dominant PD. Moreover, those with akinetic-rigid PD exhibited more psychopathological symptoms and higher neuroticism and introversion compared with those with tremor-dominant PD. Correlations revealed that among participants with akinetic-rigid PD, psychopathological symptoms and neuroticism and introversion personality traits were associated with frontal-executive dysfunction, whereas among those with tremor-dominant PD, no significant associations were found between personality traits and cognitive abilities. CONCLUSIONS These findings suggest that specific personality and frontal-executive profiles are associated with the akinetic-rigid motor subtype of PD, thus helping to refine the different clinical manifestations of PD. A better understanding of the psychological, personality, and cognitive mechanisms in PD could also help to develop more targeted treatments.

Alterations in Resting-State Interhemispheric Coordination With Refractory Auditory Verbal Hallucinations in Schizophrenia.

Abstract: OBJECTIVE The purpose of this study was to investigate resting-state interhemispheric functional connectivity in patients with schizophrenia and refractory auditory verbal hallucinations (RAVHs) by using voxel-mirrored homotopic connectivity (VMHC). METHODS Thirty-four patients with schizophrenia and RAVHs (RAVH group), 23 patients with schizophrenia but no auditory verbal hallucinations (non-AVH group), and 28 matched healthy volunteers (healthy control group) were recruited in China. VMHC analyses were used to identify brain areas with significant differences in functional connectivity among the three groups, and correlations between symptom scores and neurological measures were examined. RESULTS VMHC analyses showed aberrant bilateral connectivity between several homotopic brain regions: the RAVH and non-AVH groups showed differences in bilateral connectivity of the superior and middle temporal gyri, and the RAVH and healthy control groups showed differences in bilateral connectivity of the gyrus rectus, inferior frontal gyrus, and putamen. In addition, interhemispheric connectivity of the superior and middle temporal gyri correlated with patients' positive symptom scores. CONCLUSIONS These findings may help to elucidate the pathophysiological mechanisms underlying auditory verbal hallucinations. The results revealed interhemispheric functional dysconnectivity among patients with schizophrenia and suggest that the dysconnectivity of homotopic brain regions may play an important role in the development of auditory verbal hallucinations.

Suicidal Thoughts and Behaviors in Anti-NMDA Receptor Encephalitis: Psychopathological Features and Clinical Outcomes.

Abstract: OBJECTIVE A wide variety of neuropsychiatric symptoms are described during the acute phase of anti-N-methyl-d-aspartate receptor encephalitis (ANMDARE), including psychosis, mania, depression, and catatonia, but there are few reports on suicidal thought and behaviors in ANMDARE. To address this gap in the literature, the authors measured the presence of suicidal thoughts and behaviors among a large cohort of Mexican patients diagnosed with definite ANMDARE. METHODS This observational and longitudinal study included patients with definite ANMDARE hospitalized at the National Institute of Neurology and Neurosurgery of Mexico between 2014 and 2021. Suicidal thoughts and behaviors were assessed before and after treatment by means of a clinical interview with relatives and a direct clinical assessment with each patient. Thoughts of engaging in suicide-related behavior and acts of suicidal and nonsuicidal self-directed violence before and during hospitalization were recorded. RESULTS From a total sample of 120 patients who fulfilled the diagnostic criteria for definite ANMDARE, 15 patients (13%) had suicidal thoughts and behaviors during the acute phase of the disease. All 15 of these patients experienced psychosis and had suicidal ideation with intention. Three patients engaged in preparatory behaviors and seven carried out suicidal self-directed violence. Psychotic depression and impulsivity were more frequent among those patients with suicidal thoughts and behaviors than among those without any form of suicidality. Four patients engaged in self-directed violence during hospitalization. Remission was sustained in 14 of 15 patients, with suicidal ideation and self-directed violence persisting during follow-up in only one patient. CONCLUSIONS Suicidal thoughts and behaviors are not uncommon during the acute phase of ANMDARE. On the basis of our sample, the persistence of these features after immunotherapy is rare but may be observed. A targeted assessment of suicidal risk should be strongly considered in this population.

rTMS/iTBS and Cognitive Rehabilitation for Deficits Associated With TBI and PTSD: A Theoretical Framework and Review

Abstract: Rehabilitation of cognitive and psychosocial deficits resulting from traumatic brain injury (TBI) continues to be an area of concern in health care. Commonly co-occurring psychiatric disorders, such as major depressive disorder and posttraumatic stress disorder, create additional hurdles when attempting to remediate cognitive sequelae. There is increased need for procedures that will yield consistent gains indicative of recovery of function. Intermittent theta-burst stimulation (iTBS), a form of repetitive transcranial magnetic stimulation, has potential as an instrument that can be tailored to aid cognitive processes and support functional gains. The use of iTBS enables direct stimulation of desired neural systems. iTBS, performed in conjunction with behavioral interventions (e.g., cognitive rehabilitation, psychotherapy), may result in additive success in facilitating cognitive restoration and adaptation. The purpose of this theoretical review is to illustrate how the technical and physiological aspects of iTBS may enhance other forms of neurorehabilitation for individuals with TBI. Future research on combinatorial iTBS interventions has the potential to translate to other complex neuropsychiatric conditions.

Outcome in Pediatric Functional Tic Disorders Diagnosed During the COVID-19 Pandemic.

Abstract: OBJECTIVES The incidence of pediatric functional tics has surged during the COVID-19 pandemic with little known about prognosis. To address this knowledge gap, the investigators examined clinical courses of functional tics diagnosed during the pandemic and explored factors predicting prognosis. METHODS Study personnel reviewed electronic medical records of 29 pediatric patients diagnosed as having functional tics between March 1, 2020, and December 31, 2021, and estimated Clinical Global Impression-Improvement (CGI-I) scores at follow-up encounters. Twenty patient-guardian dyads completed telephone interviews. Logistic regression models were used to identify possible predictors of clinical trajectories. RESULTS Of the 29 patients, 21 (82%) reported at least some improvement since diagnosis at the time of the last follow-up, with a median CGI-I score of 2 (much improved). During the telephone interview, 11 of 20 patients noted ongoing interference from tics, and 16 of 20 agreed with the diagnosis of functional tics. Median time from symptom onset to diagnosis was 197 days, with most patients reporting at least a mild reduction of symptoms (CGI-I score <4) at a median of 21 days after diagnosis. At a median follow-up time of 198 days after diagnosis, patients reported significant but not complete improvement. Greater age and longer time to diagnosis decreased odds of improvement within 1 month of diagnosis. CONCLUSIONS Most patients showed improvements in but not the resolution of functional tic symptoms after diagnosis. These data support the importance of early diagnosis for functional tics.

Network Localization of Spontaneous Confabulation.

Abstract: OBJECTIVE Spontaneous confabulation is a symptom in which false memories are conveyed by the patient as true. The purpose of the study was to identify the neuroanatomical substrate of this complex symptom and evaluate the relationship to related symptoms, such as delusions and amnesia. METHODS Twenty-five lesion locations associated with spontaneous confabulation were identified in a systematic literature search. The network of brain regions functionally connected to each lesion location was identified with a large connectome database (N=1,000) and compared with networks derived from lesions associated with nonspecific (i.e., variable) symptoms (N=135), delusions (N=32), or amnesia (N=53). RESULTS Lesions associated with spontaneous confabulation occurred in multiple brain locations, but they were all part of a single functionally connected brain network. Specifically, 100% of lesions were connected to the mammillary bodies (familywise error rate [FWE]-corrected p<0.05). This connectivity was specific for lesions associated with confabulation compared with lesions associated with nonspecific symptoms or delusions (FWE-corrected p<0.05). Lesions associated with confabulation were more connected to the orbitofrontal cortex than those associated with amnesia (FWE-corrected p<0.05). CONCLUSIONS Spontaneous confabulation maps to a common functionally connected brain network that partially overlaps, but is distinct from, networks associated with delusions or amnesia. These findings lend new insight into the neuroanatomical bases of spontaneous confabulation.

Treatment of Comorbid Anxiety and Epilepsy.

Abstract: Tweet: Phenomenological overlap of anxiety and epilepsy is so compelling that common neurophysiological roots and treatment options seem intuitive.

Long-Term Changes in Poststroke Depressive Symptoms: Effects of Functional Disability and Social Support.

Abstract: OBJECTIVE Long-term changes in specific depressive symptoms have rarely been studied in stroke patients. Such changes and the effects of social support and functional disability on specific symptoms after a long-term follow-up period (LTP) were investigated. METHODS The Montgomery-Åsberg Depression Rating Scale (MADRS), ENRICHD Social Support Instrument, and modified Rankin Scale (mRS) for functional disability were administered at baseline, a 6-month follow-up, and an LTP (35-83 months). Effects of social support and poor functional outcome (mRS score of 3 to 6) on the 10 single items included on the MADRS were identified. RESULTS Among 222 patients, mRS score, total MADRS score, and all single-item scores except "concentration difficulties," "inability to feel," and "suicidal thoughts" improved at the 6-month follow-up. From the 6-month follow-up to the LTP, the total MADRS score and half of the single-item scores worsened, although the functional outcome measure continued to improve. In multivariable linear regression tests, low social support was associated with "reduced sleep" (standardized β=0.20; 95% CI=0.06 to 0.34, p=0.005) and "pessimistic thoughts" (standardized β=0.16, 95% CI=0.03 to 0.30, p=0.019), and poor functional outcome was associated with all specific symptoms (standardized β values=0.18-0.43, all p<0.02) except "reduced sleep." CONCLUSIONS Although total MADRS and single-item scores improved in parallel with improvements in functional outcome at the 6-month follow-up, these scores worsened afterward. The lack of social support and presence of functional disability were both associated with total MADRS scores. However, specific symptoms were differentially affected, suggesting that tailored strategies should be applied to manage depression in stroke patients.

Measuring Antisocial Behaviors in Behavioral Variant Frontotemporal Dementia With a Novel Informant-Based Questionnaire.

Abstract: OBJECTIVE Antisocial behaviors are common and problematic among patients with behavioral variant frontotemporal dementia (bvFTD). In the present study, the investigators aimed to validate an informant-based questionnaire developed to measure the extent and severity of antisocial behaviors among patients with dementia. METHODS The Social Behavior Questionnaire (SBQ) was developed to measure 26 antisocial behaviors on a scale from absent (0) to very severe (5). It was administered to 23 patients with bvFTD, 19 patients with Alzheimer's disease, and 14 patients with other frontotemporal lobar degeneration syndromes. Group-level differences in the presence and severity of antisocial behaviors were measured. Psychometric properties of the SBQ were assessed by using Cronbach's alpha, exploratory factor analysis, and comparisons with a psychopathy questionnaire. Cluster analysis was used to determine whether the SBQ identifies different subgroups of patients. RESULTS Antisocial behaviors identified by using the SBQ were common and severe among patients with bvFTD, with at least one such behavior endorsed for 21 of 23 (91%) patients. Antisocial behaviors were more severe among patients with bvFTD, including the subsets of patients with milder cognitive impairment and milder disease severity, than among patients in the other groups. The SBQ was internally consistent (Cronbach's α=0.81). Exploratory factor analysis supported separate factors for aggressive and nonaggressive behaviors. Among the patients with bvFTD, the factor scores for aggressive behavior on the SBQ were correlated with those for antisocial behavior measured on the psychopathy scale, but the nonaggressive scores were not correlated with psychopathy scale measures. The k-means clustering analysis identified a subset of patients with severe antisocial behaviors. CONCLUSIONS The SBQ is a useful tool to identify, characterize, and measure the severity of antisocial behaviors among patients with dementia.

Ketone Bodies and Brain Metabolism: New Insights and Perspectives for Neurological Diseases.

Abstract: Back to table of contents Next article Windows to the BrainFull AccessKetone Bodies and Brain Metabolism: New Insights and Perspectives for Neurological DiseasesWilfredo López-Ojeda, Ph.D., M.S., and Robin A. Hurley, M.D., F.A.N.P.A.Wilfredo López-OjedaSearch for more papers by this author, Ph.D., M.S., and Robin A. HurleySearch for more papers by this author, M.D., F.A.N.P.A.Published Online:14 Apr 2023https://doi.org/10.1176/appi.neuropsych.20230017AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail The brain accounts for only approximately 2% of total body weight. However, it consumes about 20% of the body’s energy, among the highest of all organs (1). Brain energy metabolism (neuroenergetics) is an essential process for neural function and higher brain functions, such as memory and cognition (6). The neuroenergetic requirements to sustain neural and brain function depend primarily on glucose consumption via glycolysis or mitochondrial respiration processes via oxidative phosphorylation. Glycolysis does not require oxygen, occurs in the cytosol, and results in two adenosine triphosphate (ATP) molecules. Mitochondrial respiration requires oxygen and generates a much higher energy yield of 30–36 ATP molecules (1, 7, 8).Glucose and oxygen are the primary energy substrates for the brain (8). However, under specific circumstances (e.g., breastfeeding, adult ketosis, and diabetes), ketone bodies (KBs), lactate, and pyruvate act as alternative substrates for neurons (1). These monocarboxylate substrates can sustain normal brain activity (e.g., neuronal function and synaptic activity) during glucose deprivation (9). However, when systemic blood glucose levels drop, low endogenous carbohydrate levels cannot meet the body’s energy requirements, causing ketogenesis (2, 3) (Figure 1A–B).FIGURE 1. Ketogenesis (simplified).A. When systemic blood glucose levels drop, the low endogenous carbohydrate levels are unable to sustain the energy requirements of the body, thereby ketogenesis begins. In these circumstances, the body responds by decreasing insulin secretion, increasing glucagon secretion, and mobilizing fats from adipocytes to the liver cells (hepatocytes) for the breakdown of fatty acid molecules. B. Dietary fatty acids undergo β-oxidation within hepatocytes in the hepatic lobules of the liver, resulting in the formation of ketone bodies (1). C. Ketone bodies (acetoacetate, acetone, and β-hydroxybutyrate) can substitute for glucose as the primary source of energy in the body, particularly in the heart and the brain (2). D. Ketogenic diets are high-fat, high-protein, low-carbohydrate diets that result in the modulation of glycemia, elevated fatty acid levels, and relative caloric restriction (2, 3).KBs such as acetoacetate, acetone, and β-hydroxybutyrate can substitute for glucose as the primary source of energy for the body, particularly in the heart and the brain (2) (Figure 1C). Neonatally, KBs act as precursors for production of biological molecules, such as fats (especially cholesterol) and amino acids (10). KBs enter nerve cells via monocarboxylate transporters and enter the mitochondrial metabolic pathway, resulting in the production of ATP (Figure 2A–B). In the central nervous system (CNS), brain cells can use KBs as respiratory substrates for oxidative metabolic processes (4). KB metabolic activity in the brain is regulated by the permeability of the blood-brain barrier, which depends on the abundance of cerebral monocarboxylate transporters, brain enzymatic processes, and other factors (e.g., diet, fasting, and exercise) (10).FIGURE 2 and COVER. Brain energy metabolism (simplified).A. Ketone bodies are transported in blood vessels. They cross the blood-brain barrier and access nervous tissue via monocarboxylate transporters located on the plasmalemma of vascular endothelial cells and brain cells (1). In the central nervous system, brain cells can use ketone bodies as respiratory substrates for oxidative metabolic processes (4). Astrocytes can perform fatty acid oxidation to produce ketone bodies, which are then transferred to neurons as their main energy substrate. Neurons express all degradation enzymes (e.g., d-β-hydroxybutyrate dehydrogenase, acetoacetate-succinyl-CoA transferase, and acetoacetyl CoA-thiolase) required for ketolysis (ketone body metabolism). B. Within the mitochondria of neurons, ketone bodies are converted into acetyl coenzyme A (acetyl-CoA), which enters the tricarboxylic acid cycle (TCA cycle), yielding adenosine triphosphate (ATP) molecules (1, 5).All images created under the terms of the Creative Commons Attribution License. Created with VH Dissector and BioRender.com.Ketogenic diets (KDs) are high-fat, high-protein, low-carbohydrate diets that result in the modulation of glycemia, elevated fatty acid levels, and relative caloric restriction (2, 3) (Figure 1D). Nutritionally, such diets increase the production of KBs, a process called ketosis (2). However, ketosis can also occur in people consuming a low-calorie diet or a modified low-carbohydrate, high-fat diet and in individuals undergoing prolonged fasting periods and strenuous exercise (although the last two do not induce nutritional ketosis) (11, 12). In addition, ketotherapeutic medicines (e.g., medium-chain triglycerides and ketone esters) are bioenergetic supplements that can induce ketosis and regulate energy metabolism (12). These interventions are considered safe and well-tolerated treatments, potentially serving as excellent metabolic alternatives that prevent, slow, halt, or even reverse the development of some neurodegenerative diseases (13, 14) (Figure 1A–D).Effects of Ketone Bodies in Neurological DiseasesKBs can provide neuronal protection during conditions of glucose deficiency, such as hypoglycemia (1). Thus, multiple reports have confirmed some potential therapeutic benefits of KDs for various neurological conditions (15–18). A meta-analysis of 170 animal studies concluded that KDs provide multiple benefits involving aspects of epigenetics; neurotransmitter function, neuroinflammation, neuroprotection, and neuroplasticity; nociception; signaling pathways and synaptic transmission; and vascular supply (18). Similarly, a systematic study summarizing trials of therapeutic use of KDs in traumatic brain injury (TBI) and other neurological disturbances (including aggressive brain tumors, ischemic stroke, and status epilepticus) concluded that KDs can be supportive in clinical management (2). Neurological conditions with preliminary evidence showing the benefits of KDs are discussed below.Traumatic Brain InjuryTBI is linked to a significant increase (∼85%) in the number of monocarboxylate transporter channels that facilitate the transport of KBs into neurons and is accompanied by a surge of β-hydroxybutyrate–metabolizing enzymes in these cells (19–22). These findings suggest that upon injury, the brain shifts to the energetic pathway involving the metabolism of KBs (2). In line with this concept, the β-hydroxybutyrate components of KBs have two well-known neuroprotective properties: supporting the biochemical reconstruction of the respiratory chain and providing at least some energy from KB metabolism when the first complex of the respiratory chain via ATP-sensitive potassium channels is disrupted (21, 22).Results from rodent studies of TBI indicate that KDs improve cerebral metabolism, neuroprotection, and behavioral outcomes; protect myelin-forming oligodendrocytes; and reduce axonal damage while mitigating cerebral edema and apoptosis (23–26). A preliminary clinical trial revealed that a KD could be effective and feasible in adults with TBI (26). However, clinical trial data supporting the widespread use of ancillary KDs in the clinical management of TBI remain limited (27).EpilepsyKDs have been associated with positive outcomes in patients with medication-resistant epilepsy and febrile infection–related epilepsy syndrome (3, 28, 29). KDs may be effective in treating infants and children with medication-resistant epilepsy by increasing levels of KBs, which in turn mechanistically contribute (at least in part) to seizure control, possibly due to anticonvulsant effects (30–32). Some of the anticonvulsant characteristics of KBs result from the amplification of brain messengers and neuroactive substances, such as gamma-aminobutyric acid, agmatine, and monoamines, thereby reducing neuronal hypersensitivity (33). Anticonvulsive effects also result from the regulation of glutamate, possibly by altering the behavior of vesicular glutamate transporters, regulation of the neuronal membrane potential via ATP-sensitive potassium channels (activated during conditions of low ATP), and optimization of the tricarboxylic acid cycle and the electron transport chain cellular energy systems (34).Alzheimer’s DiseaseThe success of ketogenic therapies in epilepsy has increased interest in testing their use for other neurological disorders, such as Alzheimer’s disease (AD) (12). Comorbid AD and epilepsy is being increasingly recognized in people of advanced age. Patients with comorbid epilepsy and AD may experience seizures and epileptiform discharges at any stage of AD (35). In AD, mitochondrial dysfunction and decreased respiratory chain function alter processing of the amyloid precursor protein, which leads to increased production and deposition of beta-amyloid fragments in the brain (36). In addition, high-sugar diets are linked to increased deposition of beta-amyloid fragments, suggesting that the brain’s insulin resistance may contribute to AD (37, 38).The synthesis of KBs may lead to specific neurological benefits, including reducing inflammatory and apoptotic mediators and improving mitochondrial functionality (39). Furthermore, KBs generated from KD consumption decrease deposition and plaque formation of beta-amyloid fragments by reversing beta-amyloid neurotoxicity. Thus, KDs (including low-carbohydrate diets) might be useful in the clinical management of AD (40).Parkinson’s DiseaseParkinson’s disease (PD) is the second most common progressive neurodegenerative disorder of the CNS, affecting over 1% of people over 60 years of age (41, 42). In addition to reductions in dopamine synthesis, the pathogenesis of PD seems to involve other contributing factors, such as abnormal glucose metabolism in the brain, inflammation in the CNS, mitochondrial dysfunction, and metabolic disturbances (42, 43). Approximately 50%–80% of patients with a PD diagnosis also have impaired carbohydrate metabolism. In addition, peripheral insulin resistance, which is typically linked to brain insulin signaling and neuronal bioenergetic issues, is often seen in early PD (43, 44).Two important factors should be considered regarding KDs as a treatment for PD. First, high-carbohydrate, low-fat diets facilitate the availability of tyrosine, a dopamine precursor, in the cerebrospinal fluid, thereby increasing brain dopamine (insulin induced) (45). This change improves one of the most important pathophysiologic hallmarks of PD, deficits in the neurotransmitter dopamine. Second, increased KBs (via KDs) may improve mitochondrial oxidative phosphorylation in the brain and bolster energy metabolism in central and peripheral neurons through mechanistic stimulation of mitochondrial biogenesis (22, 46). These changes may contribute to attenuating the substantia nigra and frontal cortex deficits in respiratory chain complex I activity that have been reported in patients with PD (42, 43, 47).Levodopa (L-DOPA) is considered the primary medication for PD (48). L-DOPA ameliorates PD motor symptoms but does not seem to have any neuroprotective effects (49) and, paradoxically, may promote aggregation of alpha-synuclein (via the metabolite 5-S-cysteinyldopamine), inducing oxidative stress that can further deplete dopamine in the brain (50). Some studies indicate that KDs improve the bioavailability of L-DOPA (49, 51). Other studies suggest that simultaneous use of L-DOPA and a KD may halt the progression of PD symptoms (49, 52, 53).Animal and human studies indicate that KDs and ketotherapeutic supplements have other benefits, including protection of dopaminergic neurons from degeneration and improvements in motor function (22, 51, 54). In a recent randomized controlled trial, 47 patients with PD were assigned to either a KD (high-fat diet) group or a low-fat diet group for 8 weeks. Both groups demonstrated significantly improved motor and nonmotor skills. However, the KD group showed greater improvements in nonmotor symptoms. In addition, the KD was confirmed to be a safe and reasonable intervention for patients with PD (55). Although these results are promising, more investigation is required (56).GliomasGliomas are highly heterogeneous brain tumors, and glioblastoma is the most aggressive type of glioma in adults. Glioblastomas have an extremely poor prognosis of approximately 12–15 months from the time of diagnosis, and the 5-year survival rate is below 5%. These tumors are characterized by a poor response to treatment (57–59). Glioma cells survive mainly on glucose and cannot function without it, suggesting that KDs could potentiate apoptosis. In a clinical trial, ketosis occurred in patients with glioblastoma who consumed a liquid KD 2 weeks before beginning chemoradiation therapy. These results suggested that a KD had some therapeutic effects and was both feasible and safe in combination with standard chemoradiation therapy (59). In addition, a recent systematic analysis indicated that KDs are beneficial for patients with malignant gliomas, mostly based on higher rates of survival (60).MigraineMigraine is a chronic disease, resulting from both genetic and environmental factors. Two systematic studies reported therapeutic potential for KDs, with one study noting that KD interventions reduced the number of attacks and the intensity of headaches among participants with migraine (2, 61).Multiple SclerosisMultiple sclerosis (MS) is a neurodegenerative and inflammatory condition of the CNS with an autoimmune origin (2, 62). A growing body of evidence suggests that a KD is beneficial for those with MS and is both safe and feasible (63–65). Additionally, the clinical evidence suggests that patients with relapsing MS who follow a KD over a 6-month period typically experienced neuroprotective and desirable disease-modifying effects, such as reduced fatigue, depression, neurological disability, and adipose-related inflammation (65).Limitations of Ketogenic DietsKD and ketotherapeutic interventions have some potential adverse effects and contraindications. Adults who consume a KD often report weight loss; gastrointestinal side effects, such as constipation, diarrhea, nausea, and vomiting; and a transient increase in lipids. Although rare, headaches, abdominal pain, irregular menstruation, drowsiness, nephrolithiasis, and pancreatitis also have been associated with KDs (2, 66, 67). Consuming low-carbohydrate diets may also lead to reduced appetite and suppressed hunger. Older people, especially those with dementia, typically have a lack of appetite and dysphagia. The use of KDs in such individuals may cause them to omit meals, resulting in malnutrition and other nutrient deficiencies, which may worsen their condition (68). In a study of patients with PD, KDs were associated with periodic tremors or stiffness, increased irritability, and exacerbated hunger or thirst (55). Long-term use of KDs may also cause more serious side effects, including hyperuricemia, proteinuria, and metabolic acidosis, especially among individuals with coexisting diabetes and inadequate insulin management. In addition, increased aminotransferase and other liver enzyme activity has been reported, suggesting a temporary increase in hepatic enzyme activity possibly associated with a KD-induced hypercholesteremia (67, 69).Finally, there is the so-called “keto flu,” a cluster of symptoms and side effects that appear within the first few weeks of KD initiation. Symptoms may include “brain fog,” headache, nausea, dizziness, fatigue, gastrointestinal discomfort, constipation, arrhythmias, or low energy (70). Overall, these symptoms are transient and seem to be mild (2, 70). Serious adverse effects of KDs seem rare and usually result from a lack of or inadequate clinical supervision. Thus, use of KDs and ketotherapeutic approaches should be individualized for each patient (2).ConclusionsIn summary, nutritional regimens (KDs and ketotherapeutic supplements) that generate increased KBs in plasma and the brain (ketosis) appear to have substantial potential to improve neuronal processes, such as mitochondrial metabolism, cell signaling, and neurotransmitter function. Additionally, KDs can reduce oxidative stress, inflammation, and toxicity, which can increase neural network stability and thereby improve cognitive function. There is a growing body of evidence supporting the benefits of KBs for some neurological conditions. However, there remains a lack of data from randomized, blinded trials in large populations and relevant subpopulations to determine the feasibility, sustainability, and long-term effects of ketotherapeutic interventions, either alone or as adjuvant treatments for CNS disorders.Veterans Affairs Mid-Atlantic Mental Illness Research, Education and Clinical Center (MIRECC) and the Research and Academic Affairs Service Line, W. G. Hefner Veterans Affairs Medical Center, Salisbury, N.C. (López-Ojeda, Hurley); Department of Psychiatry and Behavioral Medicine (López-Ojeda, Hurley) and Department of Radiology (Hurley), Wake Forest School of Medicine, Winston-Salem, N.C.; Menninger Department of Psychiatry and Behavioral Sciences, Baylor College of Medicine, Houston (Hurley).Send correspondence to Dr. Hurley ([email protected]).Supported by Veterans Integrated Services Network 6 MIRECC.The authors report no financial relationships with commercial interests.References1. 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Front Nutr 2020; 7:20Crossref, Medline, Google Scholar FiguresReferencesCited byDetailsCited byNone Volume 35Issue 2 Spring 2023Pages 104-109 Metrics KeywordsMetabolic DiseasesKetogenesisNeuroenergeticsBrain energyKetogenic DietNeurological DiseasesBrain MetabolismPDF download History Received 31 January 2023 Accepted 27 February 2023 Published online 14 April 2023 Published in print 1 April 2023

Neuropsychiatric Status of Patients With Multiple Sclerosis Across Disease Duration Intervals.

Abstract: OBJECTIVES The neuropsychiatric sequelae of multiple sclerosis (MS) are important predictors of morbidity and mortality. The authors examined how symptoms of depression, anxiety, fatigue, subjective cognitive impairment, and objective cognitive dysfunction varied with disease duration. They also explored changes in the use of disease-modifying therapies, psychotropic medications, and psychotherapies in relation to disease duration. METHODS A retrospective sample of 464 people with MS was stratified into three groups based on disease duration: <5 years (N=129), 5-10 years (N=101), and >10 years (N=234). Symptoms of depression and anxiety were recorded with the Hospital Anxiety and Depression Scale (HADS); fatigue, with the five-item version of the Modified Fatigue Impact Scale (MFIS-5); subjective cognitive impairment, with the five-item version of the Perceived Deficits Questionnaire (PDQ-5); and cognition, with the Minimal Assessment of Cognitive Function in MS (MACFIMS). RESULTS There were between-group differences in anxiety symptoms (p<0.01) and degree of cognitive impairment (p=0.03), but there were no differences in depressive symptoms, fatigue, or subjective cognitive difficulties. Anxiety was higher during the first 5 years after diagnosis, and cognitive dysfunction was higher when assessed more than 10 years after diagnosis. With longer disease duration, a greater proportion of participants received psychotropic medications (p<0.01), and lower proportions received disease-modifying therapies (p<0.01) or psychotherapies (p<0.01). CONCLUSIONS Findings indicated that rates of some neuropsychiatric symptoms, such as anxiety and cognitive dysfunction, may shift with disease duration, whereas other symptoms, such as fatigue and depression, may not. These findings highlight the importance of closely monitoring the mental state of people with MS over time.

Dimensional Assessment of Depression and Anxiety in a Clinical Sample of Adults With Chronic Tic Disorder.

Abstract: OBJECTIVE Among adults with Tourette syndrome, depression and anxiety symptoms are widely prevalent and consistently associated with poor quality of life. Important knowledge gaps remain regarding mood and anxiety dimensions of the adult Tourette syndrome phenotype. Taking a dimensional approach, this study sought to determine the prevalence, severity, and clinical correlates of depression and anxiety symptoms in a clinical sample of adults with Tourette syndrome and other chronic tic disorders. METHODS A retrospective chart review was conducted of all adults with a chronic tic disorder presenting to a tertiary care Tourette syndrome clinic between December 2020 and July 2022. Information extracted during chart review included data from scales administered as part of routine care: Quality of Life in Neurological Disorders (Neuro-QoL) Depression Short Form, Neuro-QoL Anxiety Short Form, Adult Attention-Deficit/Hyperactivity Disorder Self-Report Screening Scale, Dimensional Obsessive-Compulsive Scale, and Yale Global Tic Severity Scale. Relationships between variables were examined by conducting between-group, correlation, and multivariable regression analyses. RESULTS Data from 120 adult patients with a chronic tic disorder (77 men and 43 women) were analyzed. Neuro-QoL Anxiety scores were elevated in 66% of the cohort; Neuro-QoL Depression scores were elevated in 26%. Neuro-QoL Anxiety scores were significantly higher than general population norms, whereas Neuro-QoL Depression scores were not. After adjustment for covariates, depressive and anxiety symptom severity scores were significantly associated with each other and with obsessive-compulsive disorder symptom severity but not with tic severity. Sex-based differences emerged in the analyses. CONCLUSIONS Among adults with chronic tic disorder, anxiety symptoms were more prevalent and severe than depressive symptoms, co-occurring psychiatric symptoms were more tightly linked with each other than with tic severity, and sex-based differences were evident.

Adjunctive Memantine for Catatonia Due to Anti-NMDA Receptor Encephalitis.

Abstract: Back to table of contents Previous article Next article Case ReportNo AccessAdjunctive Memantine for Catatonia Due to Anti-NMDA Receptor EncephalitisKatherine Kim, M.D., Rachel Caravella, M.D., Allison Deutch, M.D., Lindsey Gurin, M.D.Katherine KimSearch for more papers by this author, M.D., Rachel CaravellaSearch for more papers by this author, M.D., Allison DeutchSearch for more papers by this author, M.D., Lindsey GurinSearch for more papers by this author, M.D.Published Online:7 Jul 2023https://doi.org/10.1176/appi.neuropsych.20220206AboutSectionsView articleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail View article Access content To read the fulltext, please use one of the options below to sign in or purchase access. Personal login Institutional Login Sign in via OpenAthens Register for access Purchase Save for later Item saved, go to cart PPV Articles - Journal of Neuropsychiatry and Clinical Neurosciences $35.00 Add to cart PPV Articles - Journal of Neuropsychiatry and Clinical Neurosciences Checkout Please login/register if you wish to pair your device and check access availability. Not a subscriber? Subscribe Now / Learn More PsychiatryOnline subscription options offer access to the DSM-5 library, books, journals, CME, and patient resources. This all-in-one virtual library provides psychiatrists and mental health professionals with key resources for diagnosis, treatment, research, and professional development. Need more help? PsychiatryOnline Customer Service may be reached by emailing [email protected] or by calling 800-368-5777 (in the U.S.) or 703-907-7322 (outside the U.S.). FiguresReferencesCited byDetailsCited byNone Metrics KeywordsAnti-N-Methyl-d-Aspartate Receptor (anti-NMDAR) EncephalitisCatatoniaExcitatory-Inhibitory ImbalanceN-Methyl-d-Aspartate (anti-NMDA) Receptor AntagonistsDrug/Psychotherapy Treatment of Neuropsychiatric DisordersImmunology (Neuropsychiatric Aspects)PDF download History Received 26 November 2022 Revised 10 February 2023 Accepted 2 May 2023 Published online 7 July 2023

Preexisting Depression and Ambulatory Status After Stroke: Florida-Puerto Rico Collaboration to Reduce Stroke Disparities.

Abstract: OBJECTIVE Stroke is a global public health burden, and therefore it is critical to identify modifiable risk factors to reduce stroke incidence and improve outcomes. Depression is such a risk factor; however, the association between preexisting depression and stroke outcomes, such as independent ambulation, is not well studied, especially among racial-ethnic minority groups. To address this gap in the literature, effects of preexisting depression on ambulatory status at hospital discharge after stroke were evaluated among individuals participating in the racially and ethnically diverse Florida-Puerto Rico Collaboration to Reduce Stroke Disparities project. METHODS Data were analyzed from a total of 42,031 ischemic stroke patients, who were independently ambulatory prior to their stroke, after discharge from 84 hospitals between 2014 and 2017. Preexisting depression was confirmed by medical history or antidepressant medication use. Multilevel multivariate logistic regression analyses were used to assess the association of preexisting depression with independent ambulation at hospital discharge. Effects of sex and race-ethnicity on this association were examined. RESULTS Of 42,031 participants (mean±SD age=70.4±14.2 years; 48% were female; race-ethnicity: 16% Black, 12% Hispanic living in Florida, and 7% Hispanic living in Puerto Rico), 6,379 (15%) had preexisting depression. Compared with participants without depression, those with preexisting depression were older, were more likely to be female and non-Hispanic White, and had a greater burden of vascular risk factors or comorbid conditions. Independent ambulation at hospital discharge was less frequent among women, Black participants, and individuals with vascular risk factors or comorbid conditions. In multivariate models, preexisting depression decreased the likelihood of independent ambulation at discharge (odds ratio=0.88, 95% CI=0.81, 0.97). No interactions were found between preexisting depression and race-ethnicity or sex. CONCLUSIONS Preexisting depression was independently associated with dependent ambulation at hospital discharge after stroke, regardless of sex and race-ethnicity. Treating depression may contribute to primary stroke prevention and could improve ambulatory status at discharge.