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Dalenberg C.J.,Alliant International University | Brand B.L.,Towson University | Loewenstein R.J.,Sheppard Pratt Health System | Loewenstein R.J.,University of Maryland Baltimore County | And 7 more authors.
Psychological Bulletin | Year: 2014

We respond to Lynn et al.'s (2014) comments on our review (Dalenberg et al., 2012) demonstrating the superiority of the trauma model (TM) over the fantasy model (FM) in explaining the trauma- dissociation relationship. Lynn et al. conceded that our meta-analytic results support the TM hypothesis that trauma exposure is a causal risk factor for the development of dissociation. Although Lynn et al. suggested that our meta-analyses were selective, we respond that each omitted study failed to meet inclusion criteria; our meta-analyses thus reflect a balanced view of the predominant trauma- dissociation findings. In contrast, Lynn et al. were hypercritical of studies that supported the TM while ignoring methodological problems in studies presented as supportive of the FM. We clarify Lynn et al.'s misunderstandings of the TM and demonstrate consistent superiority in prediction of time course of dissociative symptoms, response to psychotherapy of dissociative patients, and pattern of relationships of trauma to dissociation. We defend our decision not to include studies using the Dissociative Experiences Scale-Comparison, a rarely used revision of the Dissociative Experiences Scale that shares less than 10% of the variance with the original scale. We highlight several areas of agreement: (a) Trauma plays a complex role in dissociation, involving indirect and direct paths; (b) dissociation-suggestibility relationships are small; and (c) controls and measurement issues should be addressed in future suggestibility and dissociation research. Considering the lack of evidence that dissociative individuals simply fantasize trauma, future researchers should examine more complex models of trauma and valid measures of dissociation. © 2014 American Psychological Association.


Severance E.G.,Johns Hopkins University | Gressitt K.L.,Johns Hopkins University | Stallings C.R.,Sheppard Pratt Health System | Origoni A.E.,Sheppard Pratt Health System | And 5 more authors.
Schizophrenia Research | Year: 2013

The origin of inflammation in psychiatric disorders is not well understood. The translocation of commensal microbiota across the gastrointestinal barrier can result in a persistent state of low-grade immune activation and/or inflammation. We measured serological surrogate markers of bacterial translocation (soluble CD14 (sCD14) and lipopolysaccharide binding protein (LBP)) in two psychiatric cohorts and compared these levels to C-reactive protein (CRP), body mass index (BMI), and food-related and autoimmune antibodies. The two cohorts were composed of the following: (1) n=141 schizophrenia, n=75 bipolar disorder, n=78 controls; (2) n=78 antipsychotic-naïve first-episode schizophrenia, n=38 medicated first-episode schizophrenia. sCD14 seropositivity conferred a 3.1-fold increased odds of association with schizophrenia (multivariate regressions, OR=3.09, p<0.0001) compared to controls. Case-control differences in sCD14 were not matched by LBP. Quantitative levels of LBP, but not sCD14, correlated with BMI in schizophrenia (R2=0.21, p<0.0001). sCD14 and LBP also exhibited some congruency in schizophrenia with both significantly correlated with CRP (R2=0.26-0.27, p<0.0001) and elevated in females compared to males (p<0.01). Antipsychotic treatment generally did not impact sCD14 or LBP levels except for significant correlations, especially sCD14, with gluten antibodies in antipsychotic-naïve schizophrenia (R2=0.27, p<0.0001). In bipolar disorder, sCD14 levels were significantly correlated with anti-tissue transglutaminase IgG (R2=0.37, p<0.001). In conclusion, these bacterial translocation markers produced discordant and complex patterns of activity, a finding that may reflect an imbalanced, activated innate immune state. Whereas both markers may upregulate following systemic exposure to Gram-negative bacteria, non-lipopolysaccharide-based monocyte activation, autoimmunity and metabolic dysfunction may also contribute to the observed marker profiles. © 2013 Elsevier B.V.


Samaroo D.,Cornell University | Dickerson F.,Sheppard Pratt Health System | Kasarda D.D.,U.S. Department of Agriculture | Green P.H.R.,Columbia University | And 3 more authors.
Schizophrenia Research | Year: 2010

A link between celiac disease and schizophrenia has been postulated for several years, based primarily on reports of elevated levels of antibody to gliadin in patients. We sought to examine the proposed connection between schizophrenia and celiac disease by characterizing the molecular specificity and mechanism of the anti-gliadin immune response in a subset of individuals with schizophrenia. Blood samples from individuals with schizophrenia and elevated anti-gliadin antibody titer were examined for celiac disease-associated biomarkers, including antibodies to transglutaminase 2 (TG2) enzyme and deamidated gliadin peptides, as well as the HLA-DQ2 and -DQ8 MHC genes. The anti-gliadin antibody response was further characterized through examination of reactivity towards chromatographically separated gluten proteins. Target proteins of interest were identified by peptide mass mapping. In contrast to celiac disease patients, an association between the anti-gliadin immune response and anti-TG2 antibody or HLA-DQ2 and -DQ8 markers was not found in individuals with schizophrenia. In addition, the majority of individuals with schizophrenia and anti-gliadin antibody did not exhibit antibody reactivity to deamidated gliadin peptides. Further characterization of the antibody specificity revealed preferential reactivity towards different gluten proteins in the schizophrenia and celiac disease groups. These findings indicate that the anti-gliadin immune response in schizophrenia has a different antigenic specificity from that in celiac disease and is independent of the action of transglutaminase enzyme and HLA-DQ2/DQ8. Meanwhile, the presence of elevated levels of antibodies to specific gluten proteins points to shared immunologic abnormalities in a subset of schizophrenia patients. Further characterization and understanding of the immune response to gluten in schizophrenia may provide novel insights into the etiopathogenesis of specific disease phenotypes. © 2009 Elsevier B.V.


Kreyenbuhl J.,University of Maryland Baltimore County | Kreyenbuhl J.,Care Network | Buchanan R.W.,University of Maryland Baltimore County | Dickerson F.B.,Sheppard Pratt Health System | And 2 more authors.
Schizophrenia Bulletin | Year: 2010

The Schizophrenia Patient Outcomes Research Team (PORT) project has played a significant role in the development and dissemination of evidence-based practices for schizophrenia. In contrast to other clinical guidelines, the Schizophrenia PORT Treatment Recommendations, initially published in 1998 and first revised in 2003, are based primarily on empirical data. Over the last 5 years, research on psychopharmacologic and psychosocial treatments for schizophrenia has continued to evolve, warranting an update of the PORT recommendations. In consultation with expert advisors, 2 Evidence Review Groups (ERGs) identified 41 treatment areas for review and conducted electronic literature searches to identify all clinical studies published since the last PORT literature review. The ERGs also reviewed studies preceding 2002 in areas not covered by previous PORT reviews, including smoking cessation, substance abuse, and weight loss. The ERGs reviewed over 600 studies and synthesized the research evidence, producing recommendations for those treatments for which the evidence was sufficiently strong to merit recommendation status. For those treatments lacking empirical support, the ERGs produced parallel summary statements. An Expert Panel consisting of 39 schizophrenia researchers, clinicians, and consumers attended a conference in November 2008 in which consensus was reached on the state of the evidence for each of the treatment areas reviewed. The methods and outcomes of the update process are presented here and resulted in recommendations for 16 psychopharmacologic and 8 psychosocial treatments for schizophrenia. Another 13 psychopharmacologic and 4 psychosocial treatments had insufficient evidence to support a recommendation, representing significant unmet needs in important treatment domains.


Koola M.M.,Sheppard Pratt Health System | Koola M.M.,George Washington University
Schizophrenia Research: Cognition | Year: 2016

The Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) project designed to facilitate the development of new drugs for the treatment of cognitive impairments in people with schizophrenia, identified three drug mechanisms of particular interest: dopaminergic, cholinergic, and glutamatergic. Galantamine is an acetylcholinesterase inhibitor and a positive allosteric modulator of the α7 nicotinic receptors. Memantine is an N-methyl-D-aspartate (NMDA) receptor antagonist. There is evidence to suggest that the combination of galantamine and memantine may be effective in the treatment of cognitive impairments in schizophrenia. There is a growing body of evidence that excess kynurenic acid (KYNA) is associated with cognitive impairments in schizophrenia. The α-7 nicotinic and the NMDA receptors may counteract the effects of kynurenic acid (KYNA) resulting in cognitive enhancement. Galantamine and memantine through its α-7 nicotinic and NMDA receptors respectively may counteract the effects of KYNA thereby improving cognitive impairments. The Single Nucleotide Polymorphisms in the Cholinergic Receptor, Nicotinic, Alpha 7 gene (CHRNA7), Glutamate (NMDA) Receptor, Metabotropic 1 (GRM1) gene, Dystrobrevin Binding Protein 1 (DTNBP1) and kynurenine 3-monooxygenase (KMO) gene may predict treatment response to galantamine and memantine combination for cognitive impairments in schizophrenia in the kynurenine pathway. © 2016 The Author.


McClam T.D.,Sheppard Pratt Health System | Marano C.M.,Johns Hopkins Bayview Medical Center | Rosenberg P.B.,Johns Hopkins Bayview Medical Center | Lyketsos C.G.,Johns Hopkins Bayview Medical Center
Harvard Review of Psychiatry | Year: 2015

Neurocognitive impairment due to Alzheimer's disease (previously termed Alzheimer's dementia) (AD) is the most common form of cognitive impairment worldwide. Given the anticipated increase in the population aged 65 and over, the prevalence of persons with AD is expected to increase exponentially during the next 30 years. Noncognitive neuropsychiatric symptoms (NPS) commonly occur in AD and are associated with adverse outcomes for patients and their caregivers. This review summarizes randomized, controlled trials (RCTs) published between 2004 and 2014 with a primary outcome measure of change in symptom severity for NPS in AD. Of the 388 articles initially identified through a literature search, 33 trials met inclusion criteria. Fifteen of these studies had agitation/aggression as a targeted symptom. Twenty-eight evaluated pharmacologic treatments, including psychotropics, cognitive enhancers, stimulants, and nutraceuticals. Nonpharmacologic interventions included bright light, music, exercise, and cognitive-stimulation therapies. Among the pharmacologic interventions, modest efficacy was reported with aripiprazole, citalopram, trazodone, methylphenidate, and scheduled analgesics. Significant reduction in symptom severity was reported with nearly all the nonpharmacologic interventions. Variations in methodology such as inclusion criteria, study setting, and outcome measures limit the generalizability of these results. Barriers to the implementation of nonpharmacologic interventions in clinical settings include resource and training limitations. Electroconvulsive therapy and dronabinol are promising as emerging treatment strategies. Randomized clinical trials are needed in order to validate the utility of electroconvulsive therapy and dronabinol, including where and with whom these interventions will prove most valuable. © Lippincott Williams & Wilkins.


News Article | November 1, 2016
Site: www.prnewswire.com

BALTIMORE, Nov. 1, 2016 /PRNewswire/ -- Sheppard Pratt Health System announced today the appointment of Ray Dziesinski as vice president and chief financial officer (CFO), effective November 7, 2016. Dziesinski joins Sheppard Pratt Health System from Vanderbilt University Medical Center,...


Dickerson F.B.,Sheppard Pratt Health System | Lehman A.F.,University of Maryland Baltimore County
Journal of Nervous and Mental Disease | Year: 2011

Many patients with schizophrenia have psychological distress and receive some form of psychotherapy. Several different psychotherapeutic approaches for schizophrenia have been developed and studied. Of these approaches, cognitive behavior therapy (CBT) has the strongest evidence base and has shown benefit for symptom reduction in outpatients with residual symptoms. In addition to CBT, other approaches include compliance therapy, personal therapy, acceptance and commitment therapy, and supportive therapy. Although usually studied as distinct approaches, these therapies overlap with each other in their therapeutic elements. Psychotherapy for schizophrenia continues to evolve with the recent advent of such approaches as metacognitive therapy, narrative therapies, and mindfulness therapy. Future research may also consider three different goals of psychotherapy in this patient population: to provide emotional support, to enhance functional recovery, and to alter the underlying illness process. Copyright © 2011 by Lippincott Williams & Wilkins.


Mendez T.,Sheppard Pratt Health System
Psychodynamic Psychiatry | Year: 2015

How is treatment complicated when both patient and therapist bring into the room multiracial identities that stand in contrast to their visible race or ethnicity? Using relational psychoanalysis's concepts of dissociation, enactment, and relational trauma, this article examines the way multiple racial realities, beyond the more familiar black/white binary, can coexist in the consulting room. The implications and potential pitfalls of a cross-cultural dyad, in which each participant carries a mixed-race identity, are considered through a clinical vignette. © 2015 The American Academy of Psychoanalysis and Dynamic Psychiatry.


Brand B.,Towson University | Loewenstein R.J.,Sheppard Pratt Health System | Loewenstein R.J.,University of Maryland Baltimore County
Journal of Trauma and Dissociation | Year: 2014

Proponents of the iatrogenic model of the etiology of dissociative identity disorder (DID) have expressed concern that treatment focused on direct engagement and interaction with dissociated self-states harms DID patients. However, empirical data have shown that this type of DID treatment is beneficial. Analyzing data from the prospective Treatment of Patients With Dissociative Disorders (TOP DD) Study, we test empirically whether DID treatment is associated with clinically adverse manifestations of dissociated self-states: acting so differently that one feels like different people, hearing voices, and dissociative amnesia. We show that, over the course of the study, there were significant decreases in feeling like different people and hearing voices. These results indicate that this form of DID treatment does not lead to symptomatic worsening in these dimensions, as predicted by the iatrogenic model. Indeed, treatment provided by TOP DD therapists reduced, rather than increased, the extent to which patients experienced manifestations of pathological dissociation. Because severe symptomatology and impairment are associated with DID, iatrogenic harm may come from depriving DID patients of treatment that targets DID symptomatology. © 2014 Copyright Taylor and Francis Group, LLC.

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