First Hours of Treatment 2
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Claim of Exemption -Client Security Fund
CLAIM OF EXEMPTION CLIENT SECURITY FUND FEE JD-GC-22 Rev. 1-17 P.B. § 2-55, 2-55A, 2-70 C.G.S. § 51-81d EXEMPTIONS FROM THE CLIENT SECURITY FUND FEE A. FULL EXEMPTION - You are exempt from paying the client security fund fee if you meet any of the following requirements: 1. You have served or expect to serve on active duty in the armed forces of the United States for a period of more than six months during the calendar year for which the fee is due. If you serve on active duty for a shorter period of time during the calendar year, you are obligated to advise the office of the Client Security Fund Committee and pay the client security fund fee due for the year. Such payment shall be made no later than thirty days after the end of the calendar year, by sending a check in the amount of $75.00 payable to the Client Security Fund, to the office of the Client Security Fund, P.O. Box 1379, Hartford, CT 06143-1379. Your failure to do so may subject you to disciplinary action by the Superior Court. 2. You have retired from the practice of law in Connecticut by providing the required written notice of retirement to the Statewide Bar Counsel pursuant to Practice Book Section 2-55 or 2-55A. 3.You have resigned from the Bar of the State of Connecticut pursuant to the procedure set forth in Practice Book Section 2-52. 4. You have been disbarred. B. PARTIAL EXEMPTION - You are entitled to a 50% exemption if you meet the following requirements: You do not engage in the practice of law as an occupation* AND you have not and do not expect to earn more than $1000 in legal fees or other compensation for services involving the practice of law during the calendar year for which the fee is due. -
ABSTRACT Autism Spectrum Disorder (ASD)
ADLN - Perpustakaan Universitas Airlangga ABSTRACT Autism Spectrum Disorder (ASD) was a disturbance of pervasife development in children characterized by the disturbance and delayed in cognitive, language, behaviour, communication, and social interaction. In the past 10 to 20 years, increased the number of autism currently reached an average of 8 persons among 1000 resident or 1:125. The cause of autism is is yet not found until now. The purpose of this research is analize risk factor of the trigger autism in children. This research used case control design. In the case category (ASD) accounted for 35 children according to record data in special school and the control category as many as 105 children taken from public school. Independent variables were genetic, premature, postmature, antenatal bleeding, maternal age of pregnancy, caesar childbirth, low birth weight (LBW), interval of pregnancy, organic brain syndrome, asphyxia, vaccination, smoking, consumtion of medicine and medicinal herbs, and spontaneous abortion. Whereas dependent variable was ASD incident. The data analysis by calculated odds ratio with 95% CI. The result of the research obtained were genetic, postmature, antenatal bleeding, caesar childbirth, low birth weight, interval of pregnancy, organic brain syndrome, asphyxia, vaccination, smoking, consumtion of medicine and medicinal herbs, spontaneous abortion was not the risk factor of the trigger ASD incident. The result obtained on the variables that significally premature (OR= 7.12 , 95% CI: 2.56<OR<26.07) which means that the children born prematurely had a 7.12 times higher for the onset of autism than children born with normal gestational age and another variable maternal age over 35 years (OR=8.58 , 95% CI: 1.30 <OR< 92.57) which means that the mother was pregnant at the age over 35 years had a 5.58 times higher risk to had children had autism than the mother who become pregnant less than 35 years. -
Curriculum Vitae Peter Robert Martin Address
CURRICULUM VITAE PETER ROBERT MARTIN ADDRESS: Department of Psychiatry and Behavioral Sciences Vanderbilt Psychiatric Hospital Suite 3035, 1601 23rd Avenue South Nashville, Tennessee 37232-8650 U.S.A. Phone: 615-343-4527 Mobile: 615-364-7175 E-Mail: [email protected] [email protected] https://orcid.org/0000-0003-2292-4741 WEBSITES: https://wag.app.vanderbilt.edu/PublicPage/Faculty/Details/27348 http://www.vanderbilt.edu/ics/ DATE AND PLACE OF BIRTH: September 6, 1949, Budapest, Hungary FAMILY: Married Barbara Ruth Bradford, December 23, 1985 Alexander Bradford Martin, born October 21, 1989 EDUCATION: 1967 - 1971 Honours B.Sc. (Molecular Genetics) McGill University, Montreal, Quebec, Canada 1971 - 1975 M.D., C.M. McGill University, Montreal, Quebec, Canada 1975 - 1976 Resident in Internal Medicine, Sunnybrook Medical Centre, University of Toronto, Toronto, Ontario, Canada 1976 - 1978 Research Fellow in Clinical Pharmacology, Clinical Pharmacology Program, Addiction Research Foundation Clinical Institute - Toronto Western Hospital, University of Toronto 1976 - 1979 M.Sc. (Pharmacology) University of Toronto Dissertation: Intravenous phenobarbital treatment of barbiturate and other hypnosedative withdrawal: A pharmacokinetic approach. 1978 - 1979 Resident in Psychiatry, Affective Disorders Unit, Clarke Institute of Psychiatry, University of Toronto 1979 Resident in Psychiatry, Hospital for Sick Children, University of Toronto 1980 Resident in Psychiatry, Toronto General Hospital, University of Toronto LICENSURE AND CERTIFICATION: The College of Physicians and Surgeons of Ontario (License No. 28907), 1976. The Board of Medical Examiners of the State of Maryland (License No. D26685), 1981. The Board of Medical Examiners of the State of Tennessee (License No. MD17128), 1986. Fellow of the Royal College of Physicians (Canada), Psychiatry, 1981. -
PAVOL JOZEF ŠAFARIK UNIVERSITY in KOŠICE Dissociative Amnesia: a Clinical and Theoretical Reconsideration DEGREE THESIS
PAVOL JOZEF ŠAFARIK UNIVERSITY IN KOŠICE FACULTY OF MEDICINE Dissociative amnesia: a clinical and theoretical reconsideration Paulo Alexandre Rocha Simão DEGREE THESIS Košice 2017 PAVOL JOZEF ŠAFARIK UNIVERSITY IN KOŠICE FACULTY OF MEDICINE FIRST DEPARTMENT OF PSYCHIATRY Dissociative amnesia: a clinical and theoretical reconsideration Paulo Alexandre Rocha Simão DEGREE THESIS Thesis supervisor: Mgr. MUDr. Jozef Dragašek, PhD., MHA Košice 2017 Analytical sheet Author Paulo Alexandre Rocha Simão Thesis title Dissociative amnesia: a clinical and theoretical reconsideration Language of the thesis English Type of thesis Degree thesis Number of pages 89 Academic degree M.D. University Pavol Jozef Šafárik University in Košice Faculty Faculty of Medicine Department/Institute Department of Psychiatry Study branch General Medicine Study programme General Medicine City Košice Thesis supervisor Mgr. MUDr. Jozef Dragašek, PhD., MHA Date of submission 06/2017 Date of defence 09/2017 Key words Dissociative amnesia, dissociative fugue, dissociative identity disorder Thesis title in the Disociatívna amnézia: klinické a teoretické prehodnotenie Slovak language Key words in the Disociatívna amnézia, disociatívna fuga, disociatívna porucha identity Slovak language Abstract in the English language Dissociative amnesia is a one of the most intriguing, misdiagnosed conditions in the psychiatric world. Dissociative amnesia is related to other dissociative disorders, such as dissociative identity disorder and dissociative fugue. Its clinical features are known -
Social Cognition in Eating Disorders: Encoding and Representational Processes in Binging and Purging Patients
RESEARCH ARTICLE Social Cognition in Eating Disorders: Encoding and Representational Processes in Binging and Purging Patients Lily Rothschild-Yakar1,2*, Zohar Eviatar2, Adi Shamia2 & Eitan Gur3 1Safra Children’s Hospital, Sheba Medical Center, Tel Hashomer, Israel 2Department of Psychology, University of Haifa, Israel 3Sheba Medical Center, Tel Hashomer, Israel Abstract Objective: The present study investigates social cognition impairments in 29 women with bingeing/purging spectrum eating disorders (ED) compared to 27 healthy controls. Method: Measures were used to examine encoding and representational processes in relation to affect perception and affect attribution, as well as the ability to recognize mental causality in social relationships. Results: ED patients failed to correctly encode causality in interpersonal relations, exhibited deficits in their ability to ascribe behaviour to mental states, and showed a greater tendency to attribute negative affects in interpersonal relationships. Stepwise regression analyses suggested that ED symptoms could account for deficits in the recognition of causality in interpersonal relations. Conclusions: In addition to addressing ED symptoms, social cognition deficits should be addressed in the psychological treatment of EDs. Copyright # 2010 John Wiley & Sons, Ltd and Eating Disorders Association. Keywords eating disorders; social cognition; mentalization *Correspondence Lily Rothschild-Yakar, PhD, Department of Psychology, University of Haifa, Haifa 31905, Israel. Tel: 972-3-649-9563; Fax: 974-4-824-0966. Email: [email protected] Published online 29 July 2010 in Wiley Online Library (wileyonlinelibrary.com) DOI: 10.1002/erv.1013 cognition in AN (restricting type), suggesting similarities Introduction with autistic spectrum disorders. They suggested that Dysfunctional social cognition may play an important deficits in social cognition may be central to the role in eating disorders (ED). -
Expanding Employee Privacy to Protect the Attorney-Client Privilege from Employer Computer Monitoring
Protecting What You Thought Was Yours: Expanding Employee Privacy to Protect the Attorney-Client Privilege from Employer Computer Monitoring KARA R. WILLIAMS* 1. INTRODUCTION Ashlee has been working at her current job for almost two years, and she was confident that she understood her privacy rights as an employee of the company.1 However, she was completely unaware that one day, by sending a private e-mail to her private attorney from her work computer, she might have jeopardized the confidentiality of her conversations that had occurred in what she thought was strict confidence. 2 Recently, Ashlee had been experiencing some problems with her supervisor at work, and she feared that his conduct might be amounting to sexual harassment. Concerned about her safety and her job, Ashlee sought the advice of a private attorney, who instructed her to keep him informed of the conduct of her employer. One day at work, Ashlee's employer made a lewd remark to her about her body and the outfit she was wearing. Upset by this comment, Ashlee quickly went back to her office and e-mailed her private attorney from her work-provided computer, giving him a great deal of personal information, as well as information about her employer's conduct. In response, her attorney concluded that Ashlee had an actionable claim for sexual harassment, and Ashlee subsequently filed suit against her employer. Despite the private nature of the conversation, during discovery for the pending lawsuit, Ashlee's employer demanded the production of Ashlee's confidential e-mail exchange with her personal attorney. -
Amnesia: Its Detection by Psychophysiological Measures
Amnesia: Its Detection by Psychophysiological Measures BRIAN E. LYNCH, M.A.* and JOHN McD. W. BRADFORD, M.B., Ch.B. (VCT), D.P.M. (VCT), F.F. PSYCH. (SA), M.R.C. P S Y C H. ( V . K . ) ** Introduction The term amnesia encompasses many varied examples and causes of memory loss. In an edited text on amnesia, Whitty and Zangwill explore the subject in terms of cerebral disease, trauma, electroconvulsive therapy and psychogenesis. 1 It becomes obvious from the various causative factors involved in amnesia that such a multi-factorial problem requires an eclectic approach in answering. At present, one area being investigated in some detail is alcohoVdrug-induced memory loss. The focus of the present study is the exploration of memory dysfunction resulting from alcohoVdrug abuse. In any discussion of alcohoVdrug-induced amnesia certain features of the dysfunction become important for consideration. Before the amnesia can be examined it must be determined to be either a legitimate loss or a feigned amnesia state. The basis of feigned versus genuine amnesia rests with an individual's biological and psychological resources. Expediency suggests that genuine amnesia tends toward an organic base and feigned toward a psychogenic base. That is to say, the probability of a genuine amnesia is greatly increased when found in concert with organicity. Likewise, feigned memory loss is more likely to be found in individuals suffering from a psychogenic disorder. In addition to the issue of genuine versus feigned amnesia, the type of memory loss is important in any clinical assessment of the disorder. The present study utilizes a clinical breakdown of amnesia type in accordance with characteristics outlined by Bradford and Smith.2 The amnesia states are discussed in relation to the following category types: (A) hazy amnesia: no absolute amnesia either in circumscribed periods or in one complete period; (B) partial (patchy) amnesia: segments of memory loss with no complete period of amnesia; (C) complete amnesia: total ·Mr. -
Madness As Disability
HPY0010.1177/0957154X14545846History of PsychiatryGilman 545846research-article2014 Article History of Psychiatry 2014, Vol. 25(4) 441 –449 Madness as disability © The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0957154X14545846 hpy.sagepub.com Sander L Gilman Emory University, Atlanta, USA Abstract How does society imagine mental illness? Does this shift radically over time and with different social attitudes as well as scientific discoveries about the origins and meanings of mental illness? What happens when we begin to think about mental illness as madness, as a malleable concept constantly shifting its meaning? We thus look at the meanings associated with ‘general paralysis of the insane’ in the nineteenth century and autism today in regard to disability. In this case study we examine the claims by scholars such as the anthropologist Emily Martin and the psychiatrist Kay Jamison as to the relationship between mental illness, disability and creativity. Today, the health sciences have become concerned with mental illness as a form of disability. How does this change the meaning of madness for practitioners and patients? Keywords Autism, bipolar disease, disability, madness With interest in mental illness from the standpoint of the growing field of disability studies comes a problem for the medical humanities (Callard et al., 2012; Longmore and Umansky, 2001). Is it possible to discuss what may well be the most stigmatizing form of illness or disability in the West without understanding the complexity of the tradition in which it stands? The diagnostic history of mental illness is entangled with the history of madness as a social convention, a history that colours even the contemporary debates about the meanings and forms of mental illness in our age of brain imagery and neuro-anatomy. -
Delirium & Delirious Mania
Delirium & Delirious Mania; Differential Diagnosis. Delirium & Delirious Mania; Differential Diagnosis. Author: Eline Janszen. (s894226) Thesis-Supervisor: Ruth Mark Bachelorthesis Clinical Health Psychology Department of Neuropsychology, University of Tilburg September, 2011. 1 Delirium & Delirious Mania; Differential Diagnosis. ABSTRACT In the last few years, delirium in hospitals and in the elderly population has become an important subject of various studies, resulting in the recognition of several subtypes; hyperactive delirium, hypoactive delirium and mixed delirium. The first one of these subtypes, hyperactive delirium, shows a lot of overlap with another syndrome: Delirious mania. The current literature review examines both syndromes, discussing the overlap and the differences of their symptoms, while also looking at the neurological structures involved. Search engines including Sciencedirect, PSYCHinfo and medline were used to find the relevant literature. The data found in this examination reveals that, in spite of the several overlapping symptoms, delirious mania and hyperactive delirium are different syndromes; hyperactive delirium is associated with symptoms like hyperactivity, circardian rhythm disturbances and neurological abnormalities that include lesions of the hippocampus and dysfunction of the orbitofrontal cortex while delirious mania shows distinctive symptoms like pouring water and denudativeness (disrobing) with neurological abnormalities that also include orbitofrontal cortex dysfunction, but suffer mostly from an overall frontal circuitry dysfunction. This distinction is important for clinical outcome, seeing as that hyperactive delirium is treated with haloperidol and the preferred treatment for delirious mania is ECT. Keywords: delirium, hyperactive delirium, delirious mania. 2 Delirium & Delirious Mania; Differential Diagnosis. INTRODUCTION In recent years there has been a lot of research focused on diagnosing delirium. Since patients with delirium display fluctuating symptoms, the distinction from other conditions can be difficult. -
Clinical Practice Guidelines for the BC Eating Disorders Continuum of Services September 1, 2012
CLINICAL PRACTICE GUIDELINES for the BC EATING DISORDERS CONTINUUM OF SERVICES SEPTEMBER 1, 2012 < ONLY REVERSE OUT OF PHC BLUE, BLACK AND PHC OCHRE Ministry of Health (Project Leader) Gerrit van der Leer, MSW, Director, Mental Health and Addictions Authors Josie Geller, PhD, R. Psych, Director of Research, Eating Disorders Program, Providence Health Care. Associate Professor, Department of Psychiatry, University of British Columbia. Shawna Goodrich, MSW, Former Clinical Director, Eating Disorders Program, Providence Health Care Kathy Chan, MA, Graduate Student, University of Ottawa Sarah Cockell, PhD, R. Psych, Psychologist, Heart Centre, Providence Health Care Suja Srikameswaran, PhD., R. Psych, Professional Practice Leader, Psychology, Providence Health Care, Outpatient Psychologist, Eating Disorders Program, SPH, Clinical Associate Professor, Department of Psychiatry, University of British Columbia Provincial Advisory Committee Connie Coniglio, EdD, Clinical Director, Provincial Specialized Eating Disorder Program for Children and Adolescents, BC Children’s Hospital. Pei Yoong Lam, MD, FRACP, Assistant Clinical professor, Division of Adolescent Medicine, Department of Pediatrics, University of BC. Provincial Specialized Eating Disorders Program for Children and Adolescents, BC Children’s Hospital. Kim Williams, RD, Dietician, Eating Disorders Program, Providence Health Care Randy Murray, Practice Lead, Mental Health and Substance Use, Interior Health Shelagh Bouttell, MSc RD, Nutrition Therapist, Fraser South Eating Disorder Program, -
MILD TRAUMATIC BRAIN INJURY(Mtbi) TOPIC REPORT
MILD TRAUMATIC BRAIN INJURY(mTBI) TOPIC REPORT An Updated Review Independent Medical Expert Group th 19 February 2021 1 Contents Key Points ............................................................................................................................................................................ 3 Introduction ......................................................................................................................................................................... 5 mTBI in Military Populations ........................................................................................................................................... 7 Early Predictors of Persistent Post-Concussion Symptoms ................................................................................. 8 Biomarkers .......................................................................................................................................................................... 9 Neuroimaging ..................................................................................................................................................................... 9 Magnetic Resonance Diffusion Tensor Imaging in mTBI .................................................................................... 9 Positron Emission Tomography .............................................................................................................................. 11 MEG: Basic Considerations ..................................................................................................................................... -
The Effect of Epilepsy on Autistic Symptom Severity Assessed by The
Ko et al. Behav Brain Funct (2016) 12:20 DOI 10.1186/s12993-016-0105-0 Behavioral and Brain Functions RESEARCH Open Access The effect of epilepsy on autistic symptom severity assessed by the social responsiveness scale in children with autism spectrum disorder Chanyoung Ko1, Namwook Kim2,3, Eunjoo Kim4, Dong Ho Song2,3 and Keun‑Ah Cheon2,3* Abstract Background: As the prevalence of autism spectrum disorders in people with epilepsy ranges from 15 to 47 % (Clarke et al. in Epilepsia 46:1970–1977, 2005), it is speculated that there is a special relationship between the two disorders, yet there has been a lack of systematic studies comparing the behavioral phenotype between autistic individuals and autistic individuals with epilepsy. This study aims to investigate how the co-occurrence of epilepsy and Autism Spec‑ trum Disorder (ASD) affects autistic characteristics assessed by the Social Responsiveness Scale (SRS), which has been used as a measure of autism symptoms in previous studies. In this research we referred to all individuals with Autism or Autistic Disorder as individuals with ASD. Methods: We reviewed the complete medical records of 182 participants who presented to a single tertiary care refer‑ ral center from January 1, 2013 to July 28, 2015, and subsequently received complete child and adolescent psychiatric assessments. Of the 182 participants, 22 were diagnosed with Autism Spectrum Disorder and epilepsy. Types of epilepsy observed in these individuals included complex partial seizure, generalized tonic–clonic seizure, or infantile spasm. Using ‘Propensity Score Matching’ we selected 44 children, diagnosed with only Autism Spectrum Disorder, whose age, gender, and intelligence quotient (IQ) were closely matched with the 22 children diagnosed with Autism Spectrum Disorder and epilepsy.