Lenore Boling
McLean Hospital
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Featured researches published by Lenore Boling.
The Journal of Pediatrics | 1954
John P. Jahn; Lenore Boling; Thomas R. Meagher; H. Parvey Peterson; Gregory Thomas; Bruce M. Fisher; Albert E. Thill; William A. Leovy; Harry E. Balch; Laurance W. Kinsell
Summary Data are presented which may support the concept that the addition of ACTH and cortisone therapy to wellindicated antibiotic therapy in patients suffering from severe infections results in reduction of morbidity and mortality in such patients. Such combined therapy should be used with a full knowedge of the potential hazards as well as the potential assets involved.
Annals of Internal Medicine | 1952
Laurance W. Kinsell; John W. Partridge; Lenore Boling; Sheldon Margen
Excerpt The accumulation of knowledge and the development of concepts regarding the place of ACTH and cortisone in clinical medicine have followed an interesting pattern during the past three years...
Psychopharmacology | 1992
Jonathan O. Cole; George Gardos; Lenore Boling; David W. Marby; David Haskell; Patricia Moore
Relative vulnerability to dyskinesia in terms of exposure to antipsychotic drugs prior to onset of dyskinesia was studied in a sample of 100 psychiatric patients with dyskinesia onset generally within a year or less of the point of study entry. Unipolar and bipolar patients were more vulnerable to dyskinesia than other diagnostic groups. In the total sample, lithium exposure did not appear to delay development of dyskinesia. Longer exposure to antiparkinson drugs was associated with delayed onset of dyskinesia. Past exposure to electroconvulsive therapy was related to decreased vulnerability to dyskinesia.
Schizophrenia Bulletin | 2017
Charity J. Morgan; Michael J. Coleman; Ayse Ulgen; Lenore Boling; Jonathan O. Cole; Fred Johnson; Jan E. Lerbinger; J. Alexander Bodkin; Philip S. Holzman; Deborah L. Levy
Thought disorder (TD) has long been associated with schizophrenia (SZ) and is now widely recognized as a symptom of mania and other psychotic disorders as well. Previous studies have suggested that the TD found in the clinically unaffected relatives of SZ, schizoaffective and bipolar probands is qualitatively similar to that found in the probands themselves. Here, we examine which quantitative measures of TD optimize the distinction between patients with diagnoses of SZ and bipolar disorder with psychotic features (BP) from nonpsychiatric controls (NC) and from each other. In addition, we investigate whether these same TD measures also distinguish their respective clinically unaffected relatives (RelSZ, RelBP) from controls as well as from each other. We find that deviant verbalizations are significantly associated with SZ and are co-familial in clinically unaffected RelSZ, but are dissociated from, and are not co-familial for, BP disorder. In contrast, combinatory thinking was nonspecifically associated with psychosis, but did not aggregate in either group of relatives. These results provide further support for the usefulness of TD for identifying potential non-penetrant carriers of SZ-risk genes, in turn enhancing the power of genetic analyses. These findings also suggest that further refinement of the TD phenotype may be needed in order to be suitable for use in genetic studies of bipolar disorder.
Schizophrenia Bulletin | 2015
Curtis K. Deutsch; Deborah L. Levy; Selya F. R. Price; J. Alexander Bodkin; Lenore Boling; Michael J. Coleman; Fred Johnson; Jan E. Lerbinger; Steven Matthysse; Philip S. Holzman
Several laboratories, including ours, have reported an overrepresentation of craniofacial (CF) anomalies in schizophrenia (SZ). How might this dysmorphology arise in a brain-based disorder? Because the brain and face derive from shared embryologic primordia and morphogenetic forces, maldevelopmental processes may result in both CF and brain dysmorphology.Our approach is 2-pronged. First, we have employed, for the first time in the study of psychiatric disorders, objective measures of CF morphology that utilize an extensive normative database, permitting computation of standardized scores for each subject. Second, we have rendered these findings biologically interpretable by adopting principles of embryology in the analysis of dysmorphology.Dependent measures in this investigation focused on derivatives of specific embryonic primordia and were contrasted among probands with psychotic disorders, their first-degree relatives, and normal controls (NC). Subject groups included patients with a diagnosis of SZ (N = 39) or bipolar (BP) disorder with psychotic features (N = 32), their clinically unaffected relatives (N = 82 and N = 41, respectively), and NC (N = 95) subjects.Anomalies involving derivatives of frontonasal and mandibular embryonic primordia showed a clear association with psychotic illness, as well as familial aggregation in relatives in both diagnostic groups. In contrast, one class of CF anomalies emerged only among SZ probands and their first-degree relatives: dysmorphology arising along the junction of the frontonasal and maxillary prominence derivatives, manifested as marked asymmetries. This class was not overrepresented among the BP patients nor among their relatives, indicating that this dysmorphology appears to be specific to SZ and not a generalized feature of psychosis. We discuss these findings in light of embryologic models that relate brain regions to specific CF areas.
Schizophrenia Research | 2010
Verena Krause; Olga Krastoshevsky; Michael J. Coleman; J. Alexander Bodkin; Jan E. Lerbinger; Lenore Boling; Fred Johnson; Anne Gibbs; Jonathan O. Cole; Zhuying Huang; Nancy R. Mendell; Deborah L. Levy
The delineation of schizophrenia-related symptomatology is critical to informative clinical phenotyping in linkage studies. A minority of first-degree relatives of schizophrenia and schizoaffective probands (RelSZSA) qualifies for a clinical diagnosis in the schizophrenia spectrum. Schizotypal personality disorder (SPD) is a key component of this spectrum, largely because of its relatively specific familial aggregation in relatives. The criteria for SPD were not developed for the purpose of identifying RelSZSA, however, and SPD is not a homogeneous clinical disorder, potentially introducing false positives and false negatives into affectedness classifications. In this study we used logistic regression (LR) to identify the combination of clinical signs and symptoms that maximized the discrimination between nonpsychotic first-degree RelSZSA (n=241) and controls (n=161). Three variables contributed significantly to optimizing this distinction: no close friends or confidants other than family members, social isolation and irritability. The combination of deviant LR scores and schizophrenia-spectrum psychotic disorders had greater sensitivity for identifying RelSZSA, 23.7%, than SPD and schizophrenia-spectrum psychotic disorders, 16%. Importantly, the diagnosis of SPD and deviant LR scores were not significantly correlated. Most individuals with deviant LR scores did not meet criteria for a diagnosis of SPD and only a minority of those who were diagnosed with SPD had deviant LR scores. Since misclassification of gene carriers as non-gene carriers in linkage analyses increases the risk of false negatives, it may be advantageous to tailor the definition of the clinical phenotype to those aspects of social-interpersonal dysfunction that optimize the discrimination of RelSZSA from controls.
Progress in Neuro-psychopharmacology & Biological Psychiatry | 1994
George Gardos; Jonathan O. Cole; Jacqueline A. Samson; Lenore Boling; Caitlyn Conley
1. Two types of psychiatric diagnoses were obtained in a study of the course of early dyskinesia: DSM-III-R and Dimensional Global Ratings of Schizophrenia, Paranoia, Mania and Depression. 2. The strength of association between measures of vulnerability to developing tardive dyskinesia (TD), and clinical components from each of the two methods of obtaining psychiatric diagnoses was established by canonical correlations. 3. Overall, little difference was obtained between DSM-III-R categories and Global Ratings in terms of correlations with TD vulnerability measures. Using components from global diagnostic ratings, the Depression and Schizophrenia Scales made stronger contributions to the canonical functions than Mania and Paranoia. 4. Unipolar depressed patients appear more sensitive to NL: they developed TD after less NL exposure. 5. Dimensional classification appears to be a promising approach to capturing important characteristics of psychoses.
Archive | 1979
Lenore Boling
Several approaches to violence are common to most cultures. Among them are punishment, containment, and channelling of aggression. Retaliation, protection, and sometimes hope of change are elements in these interventions. In our own individualistic society there is, historically, a good deal of ambivalence concerning expectations and sanctions in regard to harming others. It is generally accepted that an individual has choices; but if he wants to get anywhere he has to search out opportunities, make his presence felt, compete and win. There are moral and legal constraints on the degree and methods of competition, but also an unspoken admiration and envy of those who circumvent these limits. Just one example of this is documented in Matthew Josephson’s book, The Robber Barons, which describes the careers of a few men who amassed great fortunes and power on the fringes of dishonesty and public acceptance. We balance on a fine line between the use and misuse of aggression. However, uncontrolled aggression, and particularly physical violence, is not generally accepted and is considered “bad” except under certain ritualized circumstances. Yet we are aware to varying degrees of the potential presence of aggression in ourselves. Each, according to his biological and environmental experience, makes what peace he can with this valued and devalued attribute. For the most part, it is kept out of conscious awareness. Nonetheless, violence is a subject which has been attracting an increasing amount of attention in recent years.
The Journal of Clinical Endocrinology and Metabolism | 1952
Laurance W. Kinsell; John W. Partridge; Lenore Boling; Sheldon Margen; George D. Michaels; Florence Olson; Sadie Smyrl; N. Dawson
The Journal of Clinical Endocrinology and Metabolism | 1961
Alan Goldfien; Robert Moore; Sheref Zileli; Leston Havens; Lenore Boling; George W. Thorn